TCHP Education Consortium · 2018-01-10 · renal, and endocrine systems including the anatomy,...

Disruption of Organ Systems in Critical Care: Pulmonary, GI,

Renal, and Endocrine February 1st, 2018

7:30 a.m. to 4:00 p.m. Minneapolis VA Health Care System

Room 4U–106 (in the Medical Library) Description/Learning Outcomes The lungs oxygenate all the cells in our body and help in the excretion of waste products. Any disruption of this process can cause a rapid decline into critical illness. Likewise, disruptions in other organs such as the GI, renal, and endocrine systems can lead to profound illness and threaten life. The learning outcome of this class is to improve the learner’s ability to assess and manage adults experiencing disorders of the pulmonary, GI, renal, and endocrine systems.

Target Audience This class is designed for primarily novice critical care or telemetry nurses, although others are welcome to attend.

Before You Come to Class It is highly recommended that you complete the Pulmonary System Review and GI, Renal, and Endocrine System Review prior to attending. It will be assumed that you have this knowledge. You can find the primer on the TCHP website; it will be attached to your pre-class materials: http://tchpeducation.com/coursebooks/preclass_docs.html

Schedule 7:30 - 7:45 a.m. Registration 7:45 - 8:45 a.m. ABG Interpretation Andrea Leszko 8:45 - 9:00 a.m. Break

9:00 – 9:30 a.m. Chest Tubes Andrea Leszko 9:30 – 10:45 a.m. Pulmonary Pathologies (Pneumonia, Aspiration Pneumonia, COPD,

ARDS) Andrea Leszko

10:45 – 11:45 a.m. Pulmonary Pathologies (Asthma, Pulmonary Embolism, Pulmonary Hypertension, Ventilatory Failure

Cleo Bonham

11:45 - 12:30 p.m. Lunch 12:30 - 1:30 p.m. Liver and Gastrointestinal Problems Colleen Adams 1:30 - 1:45 p.m. Break 1:45 – 2:45 p.m. Renal Failure Colleen Adams 2:45 - 4:00 p.m. Disorders of the Endocrine System Marybeth Einess

Continuing Education Credit For attending this class,

you are eligible to receive:

7.00 contact hours Criteria for successful completion: All participants must attend the program and complete an online evaluation form to receive contact hours. Note that you must attend the ENTIRE activity to receive contact hours. The Twin Cities Health Professionals Education Consortium is an approved provider of continuing nursing education by the Wisconsin Nurses Association, an accredited approver by the American Nurses Credentialing Center's Commission on Accreditation.

If you complete the primers for this class, you are eligible to receive an additional:

Criteria for successful completion: You must read the primer and complete the online post-test and evaluation.

Continued on next page

TCHP Education Consortium

You must print out your own course materials! None will be available at the class. Click on the link below to access:

www.tchpeducation.com/coursebooks/coursebooks_main.htm If the link does not work, copy and paste the link (web page address) into your internet browser. Available 1 week prior to class.

Please Read! Check the attached map for directions to the class and assistance with parking. Certificates of attendance will be emailed to class participants once the online evaluation is completed. You should dress in layers to accommodate fluctuations in room temperature. Food, beverages, and parking costs are your responsibility. If you are unable to attend after registering, please notify the Education Department at your hospital or TCHP at 612-873-2225. In the case of bad weather, call the TCHP office at 612-873-2225 and check the answering message to see if a class has been cancelled. If a class

has been cancelled, the message will be posted by 5:30 a.m. on the day of the program. More complete class information is available on the TCHP website at www.tchpeducation.com.

Minneapolis VA Health Care System –4U-106 One Veterans Drive

Minneapolis, MN 55417

Directions to the MVAHCS

From the East (St. Paul): Take 35E south

to West 7th

/Highway 5 exit. Turn right at

the top of the exit ramp. Continue on 5 to

the Fort Snelling exit and stay to the right as

you follow the exit around. You will “Y”

into traffic coming from the Mendota

bridge. Move to the right and exit on 55

west. As you exit on 55 west, it will “Y”

almost immediately. Stay to the left and go

straight through the stoplight. You will be

on Minnehaha. Follow Minnehaha to the

stoplight in front of the VA and turn left

into the parking lot. If you miss the “Y”

continue to the next stoplight (54th

) and turn

left. Go to stop sign (Minnehaha) and turn

left again. Go to the stoplight in front of the

VA and turn right into the parking lot.

From the Southeast: Take 35E to 110

west. Take the 55 west/Fort Snelling exit.

Go to the far righthand lane as soon as you

exit to continue on 55 west. Go over the

Mendota Bridge, move to the right lane and

exit to follow 55 west. As you exit on 55 west, it will “Y” almost immediately. Stay to the left and go straight

through the stoplight. You will be on Minnehaha. Follow Minnehaha to the stoplight in front of the VA and turn left

into the parking lot. If you miss the “Y” continue to the next stoplight (54th

) and turn left. Go to stop sign

(Minnehaha) and turn left again. Go to the stoplight in front of the VA and turn right into the parking lot.

From the North: Take 35W south to 62 east. *Follow directions below.

From the South: Take 35W north to 62 east. *Follow directions below.

From the West: Take 494 east to 35W north. Take 62 east. *Follow directions below.

*Directions, continued: Get into the right lane on 62 and exit on 55 west. At the top of the exit ramp, turn left to

continue on 55 west. Go to the stoplight (Minnehaha) and turn left. Follow Minnehaha to the stoplight in front of the

VA and turn left into the lot.

For All: Park in the Visitor’s Parking Lot to the left (parking is free). Enter through the outpatient entrance and take

the elevator to the 4th

floor. Enter the Medical Library that is next to the bank of elevators. 4U-106 is located at the

back of the library.

Light Rail Transit: The LRT line stops right in front of the VA. Feel free to utilize the park and ride lots and take

the LRT to the VA. Go to the LRT website for information about where to park, fares, and how to ride:

http://www.metrocouncil.org/transit/rail/index.htm

N

W E

S

= stoplight

= stop sign

62

55 west

Minnehaha

54th

St

55 east

VA Health

Care System

GI, Endocrine & Renal Systems Review

© 2000 TCHP Education Consortium; revised 2007, 2015.

This educational activity expires April 30, 2018. All rights reserved. Copying, electronic transmission and sharing without permission is forbidden.


This home study is pre-reading for a class. Please complete before class time. If contact hours are desired, follow the directions at the end of the packet.

Introduction/Learning Outcome

Gastrointestinal (GI), endocrine, and renal problems may

occur in any critically ill adult. The learning outcome of

this home study is for learners to self-report an

improvement in their knowledge base related to the GI,

renal, and endocrine systems including the anatomy,

physiology, and pathophysiology of GI bleeding, diabetic

ketoacidosis, hyperglycemic-hyperosmolar, non-ketotic

coma, renal insufficiency and failure, liver failure, and

other metabolic problems.

Target Audience This home study was designed for the novice critical care

or telemetry nurse; however, other health care

professionals are invited to complete this packet.

Content Objectives 1. Describe the pathophysiology of selected GI

problems.

2. Describe the pathophysiologic process of cirrhosis and

hepatic failure.

3. Identify the pathophysiologic process of renal

insufficiency and failure.

4. Define pancreatitis.

5. Differentiate between DKA and HHNK.

6. Identify three causes of hypothermia.

Disclosures

In accordance with ANCC requirements governing

approved providers of education, the following disclosures

are being made to you prior to the beginning of this

educational activity:

Requirements for successful completion of this


In order to successfully complete this activity you

must read the home study and complete the online

post-test and evaluation.

Conflicts of Interest

It is the policy of the Twin Cities Health Professionals

Education Consortium to provide balance,

independence, and objectivity in all educational

activities sponsored by TCHP. Anyone participating in

the planning, writing, reviewing, or editing of this

program are expected to disclose to TCHP any real or

apparent relationships of a personal, professional, or

financial nature. There are no conflicts of interest that

have been disclosed to the TCHP Education

Consortium.

Expiration Date for this Activity:

As required by ANCC, this continuing education

activity must carry an expiration date. The last day that

post tests will be accepted for this edition is April 30,

2018—your envelope must be postmarked on or

before that day.

Planning Committee/Editors* *Linda Checky, BSN, RN, MBA, Program Manager for

TCHP Education Consortium.

*Lynn Duane, MSN, RN, Assistant Program Manager

for TCHP Education Consortium.

Michelle Davenport, RN, BSN, PHN, FCN, Clinical

Care Supervisor, Cardiac-Renal and Cardiac Medical

Intermediate Care Units at Hennepin County Medical

Center.

Author

Karen Poor, MN, RN, Former Program Manager of the

Twin Cities Health Professionals Education Consortium

Content Experts *Michelle Davenport, RN, BSN, PHN, FCN, Clinical

Care Supervisor, Cardiac-Renal and Cardiac Medical

Intermediate Care Units at Hennepin County Medical

Center.

Tom Scullard, RN, Clinical Care Supervisor, MICU at

Hennepin County Medical Center.

*Denotes content expert for the current edition.

Contact Hour Information

For completing

this Home Study and evaluation,

you are eligible

to receive:

1.50 contact hours

Criteria for successful

completion: You must read the

home study packet and complete

the online post-test and evaluation.

The Twin Cities Health Professionals

Education Consortium is an approved

provider of continuing nursing

education by the Wisconsin Nurses

Association, an accredited approver by

the American Nurses Credentialing

Center’s Commission on

Accreditation.

Please see the last page of the packet for information on

submitting your post-test and evaluation for contact hours.

GI, Endocrine & Renal Critical Care Primer

2000 TCHP Education Consortium; 2015v.2 edition

Page 3

Gastrointestinal Problems

Mrs. Sylvia Scotch comes into the Emergency Room with

extreme nausea. She has had one bright red blood emesis

of 250 cc. Her husband states that she vomited bright red

blood three to four times at home. She is at 17 weeks

gestation, and reportedly has been severely nauseated

throughout her pregnancy.

What are the causes of GI bleeding?

Eighty-five to ninety percent of all GI bleeding occurs in

the upper GI tract. Erosive gastritis (23.4 %), gastric or

duodenal peptic ulcer (50%), esophageal varices (10 %),

Mallory Weiss tear, and aortointestinal fistula are all

problems that can result in GI bleeding.

The remaining percentage of GI bleeding occurs in the

lower GI tract. Problems resulting in bleeding are:

Diverticulosis

Neoplasm: carcinoma, polyp

Inflammatory bowel disease such as ulcerative

colitis or Crohn’s disease

Ischemic colitis and Mesenteric Ischemia

Angiodysplasia

Meckel’s diverticulum

Hemorrhoids

A Mallory-Weiss tear was diagnosed in Mrs. Scotch’s case.

This type of GI bleeding occurs when persistent or violent

vomiting occurs, tearing the junction between the

esophagus and stomach (GE junction). Arterial blood

vessels are exposed and torn.

Why is she vomiting bright red blood?

Bleeding manifests in different ways related to the

physiologic processes the blood undergoes.

1. Bright red blood = has not undergone any chemical

degradation. The site of bleeding is very close to the

site of exit (hemorrhoids), or the bleeding is very fast

(i.e. arterial bleed).

2. Maroon/dark red blood = has been through at least

one chemical process, such as degradation by

hydrochloric acid in the stomach or enzymes in the

intestine.

3. Maroon/dark red blood with clots = has been

through a chemical process and has coagulated.

4. Black/tarry blood = has been through multiple

chemical processes. Excreted as melena after passing

through the large intestine where water is removed.

How is the gastrointestinal system supplied

with blood?

The heart, via the abdominal aorta, supplies the GI system

with arterial blood. The branches of the abdominal aorta

are responsible for certain organ systems:

Celiac artery: supplies the esophagus, stomach,

spleen, and pancreas. The celiac artery branches into

the hepatic artery, which supplies the liver with blood.

Superior mesenteric artery: supplies the pancreas,

small intestine, and colon

Inferior mesenteric artery: supplies the colon

The liver is supplied differently than the remainder of the

GI system. The liver receives arterial blood through the

hepatic artery, but also receives venous blood from the

portal vein. The portal vein receives blood from the

gastric, splenic, superior and inferior mesenteric veins.

The liver is in charge of processing this venous blood and

extracting its nutrients. The hepatic vein drains the

processed blood into the inferior vena cava.

Bowel Obstruction

There are two general types of obstruction in the GI tract:

functional obstruction and mechanical obstruction. Either

type of obstruction may lead to ischemia, necrosis, and

perforation of the bowel.

Functional Obstruction

In functional obstruction, the gut is unable to provide

absorption, motility, or secretion to digest food.

Adynamic Ileus

One of the most common occurrences in the critically ill

patient, an adynamic (paralytic) ileus occurs after surgical

manipulation, trauma, or shock states. Peristalsis is greatly

diminished; peristalsis is the mechanism by which

nutrients and fluids are moved down the GI tract. This

leads to a build-up of secretions and gas inside the GI tract.

The bowel becomes distended and painful. Nausea and

vomiting usually occur, potentially leading to fluid and

electrolyte imbalances.

Peritonitis

The peritoneum is a serous membrane that covers the

abdominal wall and abdominal organs. It encloses a

normally sterile environment and contains only a small

amount of lubricating fluid. In peritonitis, substances have

entered into the peritoneum, either through the bowel,


© 2000 TCHP Education Consortium; 2015v.2 edition Page 4

accessory organs, genitourinary tract, or from outside of

the body.

The open, warm, and moist environment of the peritoneum

is ideal for the spread of contaminants throughout the

peritoneum and also into the bloodstream. The peritoneum

begins to “weep” or cause serous fluid to enter into the

peritoneum, potentially leading to hypovolemia. When

contaminants enter the peritoneum, a thick, sticky mucus is

secreted to “wall off” the opening that is spilling the

contaminants. Sympathetic nervous system stimulation

causes a decrease in bowel motility, which will decrease

the spread of contamination.

Untreated peritonitis can quickly lead to sepsis, septic

shock, and death.

Disturbances in the nutritional state occur because of

decreased bowel motility, increased caloric need from the

inflammatory response, and the nausea and vomiting that

normally accompany peritonitis.

Narcotic use

The most commonly used narcotic analgesics, including

morphine (IV or po), meperidine (IV or po), and codeine

can cause a decrease in bowel motility, leading to

constipation. The decreased bowel motility, combined

with bowel distention from the constipation, can lead to

malabsorption of nutrients.

Bowel ischemia

Bowel ischemia can result from either a systemic or local

decrease in blood flow to the intestine. The most common

cause is shock. In shock, the sympathetic nervous system

vasoconstricts the mesenteric arterial bed in order to get the

most circulating volume into the main blood vessels.

Ischemia results in a hypotonic, edematous bowel with

little or no motility.

Inflammatory bowel disease

Crohn’s disease, diverticulitis, and ulcerative colitis are all

diseases in which the bowel is inflamed and irritable. The

bowel becomes hypertonic and hypermotile, leading to

frequent small, painful diarrheal stools. The inflammation

on the intima of the bowel causes a decreased absorption

of nutrients.

Mechanical Obstruction

In mechanical obstruction, the gut is physically blocked,

preventing nutrients from reaching those parts of the

intestine that digest and absorb food and liquid. There is

typically hyperperistalsis as the bowel attempts to force

nutrients and fluids past the area of obstruction.

Adhesion: A stricture of the bowel caused by

scar tissue which wraps around the bowel and

connects to another organ or the peritoneum.

Volvulus: A twisting of the bowel.

Tumors: A tumor anywhere in the GI tract can

cause mechanical obstruction; the larger the

tumor, the more potential blockage occurs.

Intussusception: Telescoping of the bowel onto

itself.

Liver Failure

Anatomy of the Liver

The liver is located directly below the lung on the right side

of the thorax. It weighs approximately 3 pounds in the

adult, and is composed of two lobes: the right and the left.

Normally, the liver is protected by the rib cage and is not

palpable. The liver is protected by a tough, fibrous coating

called Glisson’s capsule.

The liver receives approximately 400 ml of blood each

minute from the hepatic artery and the portal vein. This

blood oxygenates the liver tissues, and passes through the

lobules of the liver to be processed. Blood that has been

processed is collected in the sinusoids, where it is passed

through the central hepatic vein and into the vena cava.

Functions of the Liver

Inferior vena cava

Falciform ligament

Caudate lobe

Lesser omentum

Quadrate lobe

Gall bladder



Page 5

Production of bile salts

Elimination of bilirubin

Metabolism of steroid hormones

Metabolism of drugs

Carbohydrate metabolism

Fat metabolism

Protein metabolism

Synthesis of plasma proteins

Synthesis of clotting factors

Storage of minerals and vitamins

Filtration of blood and removal bacteria

and particulate matter

Pathophysiology of Hepatitis

Hepatitis is an inflammation of the liver caused by either a

reaction to drugs or toxins (such as alcohol), by infections

such as malaria, mononucleosis, or salmonellosis, or by a

virus. Patients with hepatitis are generally not seen in the

critical care areas unless they are in the acute stage of

fulminant hepatitis.

Pathophysiology of Cirrhosis

In cirrhosis, the liver architecture has been altered through

a diffuse process of fibrosis and scarring into structurally

abnormal nodules. There are three types of cirrhosis:

1. Postnecrotic cirrhosis is characterized by nodules of

fibrous tissue rather than normal liver nodules. It can

be a result of viral hepatitis, an auto-immune disease,

or as a toxic response to drugs and chemicals.

2. Biliary cirrhosis results when the bile is obstructed

from flow, either through a primary or secondary

pathology. Regardless of the cause, bile is unable to

flow from the liver, backing up into the liver and

causing lobule damage.

3. Portal or alcoholic cirrhosis (Laennecs) occurs as a

result of chronic and heavy ingestion of alcohol. The

stages of development are:

Fatty liver changes: the alcohol replaces fat for

fuel in liver metabolism, leading to a build-up of

fat on and in the liver.

Alcoholic hepatitis occurs, causing inflammation

and necrosis of liver cells.

Cirrhosis is the end result of the fatty liver

changes and hepatitis. In cirrhosis, the liver

becomes yellow-orange, fatty, and is filled inside

and out with scar tissue. The blood flow that

normally goes through the liver is blocked,

causing further damage to the liver.

Regardless of the cause, cirrhosis always leads to hepatic

failure.

Pathophysiology of Liver Failure

Although only 10% of the liver is needed to survive,

damage beyond that will cause total hepatic failure. Each

of the functions that the liver normally performs fails,

leading to multi-focal patient problems.

Production of bile salts: Bile salts are not produced,

leading to inadequate or absent breakdown of fat in the

intestine. Fatty, odorous stools (steatorrhea) are produced.

Elimination of bilirubin: Bilirubin is a breakdown product

of the heme unit in hemoglobin. Normally, bilirubin is

transferred to the liver, where it is conjugated with

glucuronide and is excreted into the bile. With liver failure,

bilirubin is not conjugated in the liver, and therefore cannot

be excreted.

Metabolism of steroid hormones: The liver should bind the

steroid hormones to proteins, rendering the hormones

inactive. This does not occur in liver failure, leading to a

build-up of hormones, including aldosterone, ADH,

estrogens, and glucocorticoids.

Metabolism of drugs, including alcohol: One of the

primary functions of the liver is to metabolize drugs,

including alcohol. When the liver is not functioning, drugs

are not metabolized or excreted. This leads to a build-up

of certain drugs, or abnormal metabolism of others, which

can cause serious damage to other organs.

Carbohydrate metabolism: About 70% of ingested glucose

is taken up into the peripheral tissues (mostly muscle). The

remaining 30% is taken up by the splanchnic organs,

mostly the liver. The liver stores about 70-80% of the

glucose ingested as glycogen. The liver also synthesizes

glucose from lactic acid, amino acids, and glycerol.

Increased levels of circulating glucose result in the patient

who is receiving nutrition, decreased levels of glucose

result when the patient is not receiving any nutrition.



Fat metabolism: The liver forms lipoproteins and converts

carbohydrates and proteins to fat in starvation; synthesizes

cholesterol and forms ketones from fatty acids.

Protein metabolism: Proteins are broken down into amino

acids -- the liver deaminates these acids, forming ammonia

and conjugating the ammonia into urea, which can be

excreted.

Synthesis of plasma proteins: The liver is the only organ

that can make albumin, as well as other plasma proteins, as

a result of conjugation of the amino acids. A decrease in

the amount of plasma proteins leads to edema formation

because of the loss of oncotic pressure inside the blood

vessels.

Synthesis of clotting factors: Fibrinogen, prothrombin, and

factors V, VII, IX, and X are all formed by the liver. In the

absence of proper function, coagulation times increase

because of the lack of clotting factors.

Storage of minerals and vitamins: The liver normally

stores minerals and fat soluble vitamins. Without adequate

function, the body cannot store or use these vitamins and

minerals.

Filtration of blood and removal of bacteria and particulate

matter: With the normal function of the Kuppffer cells

destroyed, the patient is at higher risk for infection related

to active bacteria and particulate matter.

Portal hypertension

In the normal system, blood is delivered to the liver via the

hepatic artery (400 ml/min) and the portal vein (1,000

ml/min). Venous blood is drained from the liver via the

hepatic vein.

Normally, blood from all of the gastrointestinal organs

comes through the liver to be processed. In portal

hypertension, there is a mechanical blockage in the liver,

due to cirrhosis, scarring, hepatitis, or sarcoidosis. This

blockage causes the incoming low pressure blood to “back

up”because the blood does not have the pressure to

overcome the elevated pressure in the portal vein. The

result of portal hypertension is distended veins throughout

the GI system – hemorrhoids, varices, caput medusae, and

leakage of fluid into the peritoneum – ascites and edema.

Disorders of the Kidney

Definitions

Glomerular filtration rate (GFR): Rate at which

solutes are filtered from the glomerulus into the

nephron. Measured by the creatinine clearance.

Acute renal failure (ARF): A broad term used to

denote a rapid decrease in glomerular filtration rate

(GFR) as a result of insult to renal parenchyma.

Acute tubular necrosis (ATN): A specific form of

ARF in which insult to renal parenchyma (e.g., renal

ischemia, hemorrhage, drug effects) results in necrosis

of renal tubules. There is an abrupt decrease in GFR.

Regeneration of renal function can take weeks to

months following removal of insult.

Azotemia: Presence of nitrogenous waste products

(urea, creatinine) in the blood at elevated levels.

Uremia: Toxic condition in which patient develops

clinical symptoms resulting from nitrogenous waste

build-up.

Classification of ARF

There are three types of conditions which may cause acute

renal failure:

1. Pre-renal

2. Intra-renal

3. Post-renal

Splenic vein

Pancreatic vein

Inferior mesenteric v.

Inferior vena cava

Hepatic veins

Cystic vein

Pyloric vein Portal vein

Superior mesenteric v.

Gastric blood supply



Page 7

Pre-Renal ARF

In acute renal failure caused by pre-renal etiologies, there

is a decrease in renal blood flow that results in decreased

GFR. There are three major causes of pre-renal ARF:

1. Decreased intravascular volume from

hemorrhage, sepsis, and extra-cellular volume

depletion/dehydration

2. Cardiac dysfunction with decreased cardiac

output, such as MI, arrhythmias, tamponade,

cardiogenic shock, CHF, and afterload reduction

therapy

3. Obstruction of flow to the kidney, such as by a

renal artery embolus

Intra-Renal ARF

A severe parenchymal insult from disease or nephrotoxic

agent resulting in damage to glomerulus and/or tubules

may cause acute renal failure. There are many etiologies

of this type of ARF, including:

1. Glomerulonephritis (5-10%)

2. Hypertension

3. Diabetes mellitus

4. Vasculitic diseases, such as polyarteritis nodosa,

Wegener’s granulomatosis, scleroderma, lupus

5. Acute tubular necrosis from ischemia, nephrotoxic

agents (drugs, contrast media, heavy metals),

myoglobins and hemoglobin in the urine

Heme pigment ATN, which is an episode of

hemolysis resulting in the release of heme

pigment, seen in transfusion reaction, venous

snake/insect bites, extracorporeal circulation, and

faulty heart valves.

Nephrotoxic ATN: drugs implicated in

nephrotoxicity:

Acetaminophen

Aminoglycosides

Amphotericin B

Analgesics

Cephalothin

Cisplatin

Contrast media

Cyclosporin

Dextran

Lithium

Methotrexate

NSAIDS

Penicillins

Plicamycin

Tetracyclines

Post-Renal ARF

Post-renal ARF is caused by an obstruction anywhere

along the urinary tract (renal pelvis to urethra). This

obstruction results in the blockage of flow of urine and

ultimately, damage to renal parenchyma secondary to

hydronephrosis.

Causes of post-renal failure include:

1. ureteral and pelvic blood clots, stones, and fungus

balls;

2. ureteral and pelvic malignancy and retroperitoneal

fibrosis;

3. bladder stones, blood clots, carcinoma;

4. urethral strictures or prostatic hypertrophy

5. neurogenic bladder with inadequate emptying

What anatomical structures are involved in

renal failure?

The kidneys have an extraordinarily different system of

perfusion. The renal system receives 20-25% of the

cardiac output (about 1200 ml/min) at any given time. The

descending aorta is the first blood vessel involved in

delivering arterial blood to the kidneys. The aorta gives off

a branch called the renal artery, which enters the kidney

beside the ureter.

The afferent arteriole branches to form the capillary

network. This network sits inside “Bowman’s capsule.”

The afferent (incoming) and efferent (outgoing) capillaries,

endothelial membrane and Bowman’s capsule make up the

glomerulus.

Blood flows through the kidneys at a regulated rate; the

renal vasculature has an autoregulating mechanism. As the

blood flows through the glomeruli, osmotic, hydrostatic,

and electrical gradients will determine the elements to go

into the urine. Blood will flow through the efferent

arteriole after water products and/or water have been

Glomerulus Bowman’s capsule

Proximal tubule

Distal tubule

Loop of Henle

Collecting duct

Pelvis

Vasa recta

Efferent arteriole

Peritubular capillaries

Afferent arteriole

Arcuate artery



excreted and will exit through the interlobular vein into the

arcuate vein, the interlobar vein and finally into the renal

vein.

Disorders of the Pancreas

Functions of the Pancreas

There are two major functions of the pancreas: the

exocrine and endocrine. The exocrine pancreas is made

up of acinar cells which secrete pancreatic enzymes. These

enzymes are designed to enter the duodenum and begin the

initial breakdown of fats (by lipase), carbohydrates (by

amylase), and proteins (by trypsin, chymotrypsin, and

others). The enzymes are secreted through the pancreatic

duct into the Ampulla of Vater. The common bile duct also

enters into the Ampulla of Vater. The endocrine pancreas

is composed of the islet of Langerhans, which has four

types of cells:

Alpha cells: secrete glucagon, which breaks down

glycogen into glucose, adipose tissue to triglycerides

and stimulates gluconeogenesis

Beta cells: secrete insulin, which facilitates entrance

of glucose into the cells

Delta cells: secrete somatostatin, which inhibits

insulin, glucagon and growth hormone secretion

PP cells: secrete a polypeptide, which causes

hypermotility

Pancreatitis

Mr. George Statin is a 47-year-old male with a history of

gallbladder disease. He is admitted to the unit with severe

flank pain, accompanied by nausea, vomiting, diaphoresis,

and pallor. The initial diagnosis is pancreatitis.

What is the connection between gallbladder disease and

pancreatitis?

Acute pancreatitis can be caused by a number of different

problems, including:

Blunt and penetrating trauma

Infections such as infectious mononucleosis, mumps,

viral hepatitis

Drugs, such as thiazides, estrogens, sulfonamides,

tetracycline

Hyperlipidemia, hyperparathyroidism, hypercalcemia

Ischemia

Operative injury / ERCP diagnostic test

The most common causes of pancreatitis are alcohol

use and gallbladder disease.

The pancreatic duct, which carries the enzymes to the

duodenum, connects with the same outlet (the Ampulla of

Vater) as the common bile duct. A blockage in the

Ampulla of Vater from a gallstone, or sludgy bile from the

gallbladder can also block the pancreas.

What happens in pancreatitis?

There is a blockage, either through inflammation or

mechanical obstruction, of the path through which the

pancreatic enzymes travel through to the intestine. The

enzymes build-up in the pancreas and in the pancreatic

duct, leading to activation of their proteolytic action. The

enzymes begin to “digest” the protein base of the pancreas.

If the enzymes destroy tissues around and through the

blood vessels of the pancreas, the pancreatitis is called

hemorrhagic.

What are the complications of pancreatitis?

Among the complications of acute pancreatitis are:

Chronic pancreatitis

Pseudocyst formation: an accumulation of

pancreatic enzymes in a membranous sac that

protrudes from the pancreas

Abscess formation: either in, on, or around the

pancreas

Respiratory insufficiency as a result of the

changes in capillary permeability from the

enzymatic digestion; can result in Adult

Respiratory Distress Syndrome (ARDS).

Diabetic Ketoacidosis (DKA)

Body Tail

Pancreatic duct

Superior mesenteric a.

Superior mesenteric v.

Head

Hepato-

pancreatic

ampulla

Major

duodenal

papilla

Common bile duct Duodenum



Page 9

Joshua Springer is a 16-year-old male who was playing

basketball when he suddenly fainted. The paramedics were

called when Joshua was difficult to arouse. When he

entered the emergency room, he was found to have a blood

sugar of 1600 mg/dL and an arterial pH of 7.03. His

parents stated that he had had flu-like symptoms for

several days. Joshua was previously undiagnosed with

diabetes.

What is Diabetic Ketoacidosis?

DKA is a condition in which the body is not supplied with

and does not manufacture insulin with which glucose can

enter the cells. It occurs in people with uncontrolled Type

I diabetes mellitus, with severe metabolic stress, and in

people who have not been diagnosed with Type I diabetes.

What is the pathophysiologic process of DKA?

There are two main problems associated with DKA:

1. There is too much circulating glucose.

2. There is not enough glucose in the cells.

The amount of circulating glucose rises because of (1)

continued dietary intake and (2) the attempt by the liver to

increase the amount of glucose by gluconeogenesis and

glycogenolysis. The liver does not understand that the

body is unable to utilize the glucose; it is only stimulated

because the tissues are not receiving glucose. The high

amount of glucose causes:

Osmotic diuresis: the osmotic pressure inside the

vascular is much higher than in the interstitium and the

cells, causing fluid to be pulled into the blood from the

cells and tissues. This leads to increased urine output,

resulting in hypovolemia.

Increased catabolism of proteins.

Increased lipolysis, leading to overproduction of free

fatty acids.

The lack of glucose entering the cells leads to the

production of ketoacids, which can act as an energy source

for the cells. This leads to:

Metabolic acidosis from the overabundance of

ketoacids.

Hyperkalemia: as the potassium leaves the cells and

hydrogen enters the cells to try to buffer the metabolic

acidosis.

Decreased level of consciousness: the brain can use

only glucose for metabolism; it cannot store glucose

and will not use any other substrate for energy.

Hyperglycemic, Hyperosmolar NonKetotic

Coma (HHNK)

Mrs. Cecelia Post is an 89-year-old female nursing home

patient who is brought by ambulance into the hospital

because of decreasing level of consciousness and anuria.

Her serum glucose is 1200 mg/dL, her pH is 7.34, and her

bicarbonate level is 23 mEq/L. The initial diagnosis of

HHNK is made.

How is HHNK different from DKA?

In DKA, there is no insulin production or supply; in

HHNK, there is a relative lack of insulin. There is just

enough insulin in the patient with HHNK that ketoacids are

not manufactured; thus, metabolic acidosis does not occur.

The steady increase in glucose levels, however, causes the

same osmotic diuresis as in DKA, leading to a large volume

deficit. There is a gradual decrease in the level of

consciousness in the patient with HHNK, rather than the

acute neuro changes of DKA.

What will cause HHNK?

HHNK occurs in patients with known or undiagnosed Type

II (non-insulin dependent) diabetes. The majority of the

patients with HHNK are elderly; the ability to manufacture

“normal” insulin diminishes, as does the attention to

increased thirst and increased urine output. This type of

hyperglycemia is often misdiagnosed in the elderly as a

gradual decline in their physical state.

Metabolic Disorders

The thyroid gland is located immediately beneath the

larynx on either side of the trachea. It is made up of two

lobes, which are made up of two different cell types: the

follicular cells, which produce triiodothyronine (T3) and

thyroxine (T4); and the parafollicular cells, which produce

thyrocalcitonin.

External carotid a.

Superior thyroid a.

Veins leading to

internal jugular v.

Inferior thyroid a.

Common carotid a.

Subclavian a. Trachea

Isthmus Left lobe

Right lobe

Thyroid cartilage



The thyroid hormones initiate and increase metabolic

activity in all cells and tissues. T3 is the most active of the

hormones, and is converted from T4. The actions of the

thyroid hormones are to:

1. Increase the metabolic activity, oxygen consumption,

rate of chemical reactions, and heat production of all

cells.

2. Promote growth by working with insulin, growth

hormone, and the sex steroids.

3. Stimulate metabolism of carbohydrates, fats, and

proteins.

4. Increase metabolism and clear hormones and drugs

Thyrotoxicosis (Thyroid Storm)

In thyrotoxicosis, or thyroid storm, the actions of the

hormones are greatly accentuated. This is a life-

threatening condition which may be caused by

decompensation of a preexisting hyperthyroid state,

insufficient provision of antithyroid therapy, or

administration of an iodine load to a patient who has an

underlying thyroid disease.

Alterations in Temperature

There are three zones of temperature in the human body:

(1) the superficial zone, (2) the intermediate zone, and (3)

the core zone. The superficial zone is the temperature of

the skin; the intermediate zone is the temperature of the

muscles; and the core zone is the temperature of organs

such as the brain, heart, and liver. The oral temperature is

normally between 36.0 and 37.0 degrees Celsius.

Heat is produced through cellular metabolism. The

ingestion and metabolism of food, basal metabolic rate,

muscle activity, hormones, and sympathetic nervous

system all produce heat. Heat production is increased

during higher metabolic rate periods, such as with exercise,

excessive food intake, and the release of catecholamines.

Less heat than normal is produced when the patient has a

lower metabolic rate than normal, such as in starvation or

with a lack of thyroid hormones.

The hypothalamus is in charge of regulating heat

production and responding to heat loss through the

thermoregulatory center. The possible responses of the

hypothalamus are to cause vasodilation or

vasoconstriction, shivering, and activating the

neuroendocrine response to balance heat production and

heat loss.

Hypothermia

Hypothermia is a body temperature below 37 degrees C

(98.6 degrees F). Hypothermia can be either accidental or

elective. Elective hypothermia is frequently used in the OR

for cardiovascular and neurosurgery; it may be indicated

for multiple trauma, cerebral ischemia, and graft

preservation. Accidental hyperthermia is related to a

number of problems:

Near-drowning

Exposure or prolonged exposure to cold

temperatures

Rapid infusion of cold intravenous solutions or

blood products

Dysfunction of thermoregulatory mechanisms

Drugs, such as alcohol, antidepressants,

antipyretics, sedatives, and barbiturates

The patient with mild hypothermia (34 to 36.5 degrees C)

may have an increased risk for shivering, altered

mentation, a clouded LOC, and altered electrodynamics.

The patient experiencing moderate hypothermia (28 to 33.5

degrees C) will experience atrial dysrhythmias, a 50%

decrease in body metabolism, a 50% degree in heart rate,

and nonreactive pupils. Deep hypothermia is a temperature

between 17 and 27.5 degrees C, and is characterized by

ventricular fibrillation, inactivation of thermoregulatory

centers, absent muscle reflexes, and cardiac and respiratory

arrest. The last stage, profound hypothermia, is when the

patient’s body temperature is between 0 and 16.5 degrees

C. The chance of survival is slim at this stage.

Hyperthermia

Hyperthermia is defined as a body temperature that is

above the normal physiologic level of 37.2 degrees Celsius.

In mild hyperthermia (37.2 to 38.8 degrees C), the patient

has a potential for dehydration and dysrhythmias. In

moderate hyperthermia (38.8 to 40 degrees C), the patient

may be confused and experiencing dysrhythmias and

dehydration. With a temperature above 40.5 degrees, the

patient is experiencing critical hyperthermia. At this stage,

the patient has increased dysrhythmias, altered mentation,

confusion, and is at risk for seizures and cardiac arrest.

Malignant hyperthermia is a specific kind of critical

hyperthermia, characterized by a rise of 0.5 degrees C

every 15 minutes to 42.7 degrees C (109 degrees F). This

type of hyperthermia tends to be genetic in origin and is

related to general anesthesia.

Summary

Although not as “glamorous” as other systems in the body,

the gastrointestinal, endocrine, and renal systems can



Page 11

certainly cause as significant of a critical illness as any

other system. In this program, you learned about the

anatomy and physiology of these organ systems and the

pathophysiology of selected GI, endocrine, and renal

diseases.

Recommended Reading

1. Bacon B.R. (2012). Chapter 308. Cirrhosis and Its

Complications. In Longo D.L., Fauci A.S., Kasper

D.L., Hauser S.L., Jameson J, Loscalzo J (Eds),

Harrison's Principles of Internal Medicine, 18e.

Retrieved from:

http://accessmedicine.mhmedical.com/content.aspx?b

ookid=331&Sectionid=40727103

2. Brozenee S, Russell SS. (1999). Core Curriculum for

Medical-Surgical Nursing, 2nd ed. Academy of

Medical-Surgical Nurses, Janetti NJ.

3. Dickson, S. (1995, Oct.). Understanding the

oxyhemoglobin dissociation curve. Critical Care

Nurse, pp. 54-58.

4. LeBlond R.F., Brown D.D., DeGowin R.L. (2009).

Chapter 9. The Abdomen, Perineum, Anus, and

Rectosigmoid. In LeBlond R.F., Brown D.D.,

DeGowin R.L. (Eds), DeGowin's Diagnostic

Examination, 9e. Retrieved from:


ookid=370&Sectionid=40499502.

5. Lo B.M. (2011). Chapter 79. Lower Gastrointestinal

Bleeding. In Tintinalli J.E., Stapczynski J, Ma O,

Cline D.M., Cydulka R.K., Meckler G.D., T (Eds),

Tintinalli's Emergency Medicine: A Comprehensive

Study Guide, 7e. Retrieved from:


ookid=348&Sectionid=40381546.

6. Phipps WJ, Sands JK, Marek JF, eds.

(1999)..Medical-Surgical Nursing: Concepts &

Clinical Practice, 6th ed. St. Louis: Mosby, Inc.

7. Saltzman, J.R. (2012). Chapter 30. Acute Upper

Gastrointestinal Bleeding. In Greenberger, N.J.,

Blumberg, R.S., Burakoff, R (Eds), Current diagnosis

& treatment: Gastroenterology, hepatology, &

endoscopy, 2e. Retrieved August 04, 2014 from

http://accessmedicine.nhmedical.com/content.aspx?b

ookid=390&Sectionin=39819265.

8. Seidel HM, Ball JW, Dains JE et al, eds.(2002)

Mosby's Guide to Physical Examination, 5th ed. St.

Louis: Mosby, Inc.

9. Stillwell, S. (2006). Mosby’s Critical Care Nursing

Reference. 4th ed. St. Louis, Mo: Mosby/Elsevier.

10. Cheever K.H. & Hinkle J.L. (2013) Brunner &

Suddarth's Textbook of Medical-Surgical Nursing,

13th ed. Philadelphia: Lippincott William and

Wilkins.

11. Wiegand, D.J.L. & Carlson, K.K. (eds.) (2011).

AACN Procedure Manual for Critical Care. 6th ed.

Philadelphia: Elsevier.

Directions for Submitting Your Post

Test for Contact Hours

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the electronic post-test:

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html

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and easy Survey Monkey post-test and evaluation.

Fill in your answers and click “done.” Your

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hospital (consult www.tchpeducation.com if you are

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http://accessmedicine.nhmedical.com/content.aspx?bookid=390&Sectionin=39819265

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Paid Participants If you are not an employee of one of the TCHP

hospitals, you will need to submit a payment of

$15.00 to TCHP in order to have your home study

processed. If submitting a check, please make it

payable to TCHP Education Consortium and indicate

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Pulmonary System Review

© 2002 TCHP Education Consortium. Revised 2007, 2014, 12/2017

This educational activity expires April 30, 2018. All rights reserved. Copying, transmitting electronically or sharing without permission is forbidden.


This home study is pre-reading for a class. Please complete before class time. If contact hours are desired, follow the instructions at the end of the packet.


2002 TCHP Education Consortium; 2017 edition Page 20

Introduction/Learning Outcomes The lungs are responsible for oxygenating all 50 billion

cells in the body and for helping in the excretion of waste

products. Primary or secondary insults to the lungs can

cause a rapid decline into critical illness. The learning

outcome of this home study is for learners to self-report an

improvement in their knowledge base related to pulmonary

anatomy, physiology, and pathophysiology of problems

such as pulmonary embolism, pneumonia, COPD, asthma,

and ARDS, as well as an increased understanding of blood

gas analysis.

Target Audience

This home study was designed for the novice critical care

or telemetry nurse; however, other health care

professionals are invited to complete this packet.

Content Objectives 1. Define the process of oxygenation and ventilation.

2. Identify acid-base disturbances based on blood gas

analysis.

3. Review oxygenation and ventilation modalities used

for the critically ill patient.

4. Differentiate between the pathophysiologies of

asthma, bronchitis, and emphysema.

5. Describe the pathophysiology of pulmonary

embolism, pneumonia, idiopathic pulmonary fibrosis,

and acute respiratory distress syndrome (ARDS).

Disclosures In accordance with ANCC requirements governing

approved providers of education, the following disclosures

are being made to you prior to the beginning of this


Requirements for successful completion of this

educational activity: In order to successfully complete this activity you must

read the home study and complete the online post-test and

evaluation.

Conflicts of Interest It is the policy of the Twin Cities Health Professionals

Education Consortium to provide balance, independence,

and objectivity in all educational activities sponsored by

TCHP. Anyone participating in the planning, writing,

reviewing, or editing of this program are expected to

disclose to TCHP any real or apparent relationships of a

personal, professional, or financial nature. There are no

conflicts of interest that have been disclosed to the TCHP

Education Consortium.

Expiration Date for this Activity:

As required by ANCC, this continuing education activity

must carry an expiration date. The last day that post tests

will be accepted for this edition is April 30, 2018—your

envelope must be postmarked on or before that day.

Planning Committee/Editors* *Linda Checky, BSN, RN, MBA, Program Manager for


*Lynn Duane, MSN, RN, Assistant Program Manager

for TCHP Education Consortium

Kelly Kreimer, MSN, RN, ICU Educator, Minneapolis

VA Medical Center

Author Karen Poor, MN, RN, Former Program Manager of the


Content Expert/Reviewer Amanda Piersak, RN, MHL, CCRN, Nurse Educator at

the Minneapolis VA Health Care System.

*Kelly Kreimer, MSN, RN, ICU Educator, Minneapolis

VA Medical Center

*Denotes the content expert for the current edition

Contact Hour Information

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this Home Study and evaluation,

you are eligible

to receive:

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Criteria for successful

completion: You must read the

home study packet and complete

the online post-test and evaluation.

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submitting your post-test and evaluation for contact hours.


2002 TCHP Education Consortium; 2017 edition

Page 2

Review of Pulmonary Anatomy and

Physiology

Upper Respiratory Tract

The upper respiratory tract is comprised of the nose,

mouth, pharynx, larynx, and trachea. Air enters the body

through the nose or mouth and moves through the pharynx.

The respiratory tract is lined with ciliated mucosal cells.

These cells cleanse the airway by moving debris and mucus

up and out. This mechanism is called the “mucociliary

escalator.” The upper respiratory tract:

conducts and conditions air

protects the airways

makes speech and smell possible

Lower Respiratory Tract

The air moves past the epiglottis, larynx, and through the

trachea into the lungs. The epiglottis covers and protects

the airway by preventing aspiration of food or foreign

bodies. The larynx is a structure that houses the vocal

cords, which are designed to produce sound through

vibration and movement. The trachea is 10-12 cm long

and consists of 16-20 C-shaped rings made of cartilage that

cover its anterior side.

The lower respiratory tract begins when the trachea

bifurcates into the right and left mainstem bronchi, at a

site called the carina. The right mainstem bronchus is

shorter, wider, and more vertical than the left. The bronchi

are made of cartilage and are surrounded by muscles that

run longitudinally and spirally around the bronchi. The

main bronchi each branch into five lobar bronchi. The

lobar bronchi branch into segmental bronchi, which divide

into terminal bronchioles, which then divide into

respiratory bronchioles.

At the end of each respiratory bronchiole lies a cluster of

several alveoli, called an acinus. The acinus is the area

where gas exchange takes place. Adults have 200-600

million alveoli with a total surface area of 40-100 square

meters. The alveolar membrane is about 0.2 microns thick.

The lungs themselves are air-filled, spongy structures that

are divided into lobes. The right lung has three lobes and

normally accounts for 55% of total ventilation. The left

lung has two lobes and accounts for 45% of ventilation.

The Mechanics of Ventilation

Inspiration is an active process -- muscles have to contract

to cause air to flow into the lungs. The diaphragm is the

major muscle of inspiration. This large muscle is located

just underneath the rib cage and contracts to pull the rib

cage down and out. This produces a negative pressure

(vacuum) inside the thorax, which pulls air in. Nerves

coming from the spinal cord at the C3-C5 level innervate

the diaphragm. Seventy percent of the tidal volume is

provided by the action of the diaphragm.

Another group of muscles that is normally used in

inspiration is the internal intercostal group. These

muscles are located between the ribs and elevate the ribs

when contracted, increasing the antero-posterior diameter.

If you place your hand on your ribs and deeply inspire, you

will note that your ribs come up and out. These muscles

are innervated at the T1-T11 level of the spinal cord.

The third group of muscles is not used in normal

inspiration. The scalene and sternocleidomastoid

muscles are called “accessory muscles,” and pull up the

sternum and ribs when used. Think of a long distance

runner after a race. The runner will stand with his hands

on his knees and breathe deeply, so that you can see the

sternocleidomastoid bulge and the clavicles rise. These

muscles are used when additional volume of inspiration is

needed (as in exercise), when the body’s demand for

oxygen is greater than the supply, when the airway is

obstructed, or there are lung compliance problems.

Exhalation is a passive process. The relaxation of the

inspiratory muscles will “push” air out of the thorax. In the

event of difficulty in breathing, the abdominal muscles and

external intercostal muscles can contract to push up and

back, which will press the air out of the lung.

Control of Ventilation

There are several mechanisms that control ventilation:

1. The cerebral cortex controls

voluntary breathing, which

makes holding breath and

hyperventilation possible.

2. Brain stem:

The lower pons (pacemaker or apneustic center)

produces sustained inspiration when stimulated.



Page 3

The upper pons (pneumotaxis center) initiates

expiration when stimulated by the apneustic

center.

The medulla (the “manager”) receives messages

from the chemoreceptors to stimulate inspiration.

3. Chemoreceptors are receptors that are sensitive to

hydrogen ion and oxygen concentration. They are

located in the aorta and carotid arteries, and medulla.

Changes in the PaCO2, pH, and PaO2 cause the

respiratory rate and tidal volume to change to maintain

adequate oxygenation and acid-base balance. The

central chemoreceptors in the medulla are most

sensitive to hydrogen ions and CO2. Those in the aorta

and the carotid bodies (peripheral chemoreceptors) are

most sensitive to oxygen.

Lung Volumes and Capacities

The amount of air moving in and out of the lungs can be

broken down into specific volumes. Two or more volumes

combine to form a capacity. Many of these volumes and

capacities are measured using Pulmonary Function Tests

(PFT’s) and can be used for diagnostic purposes.

The following chart shows the volumes and capacities and

describes what each one measures.

TLC = Total Lung Capacity

air in lungs after full inspiration ~ 6,000 ml

IRV = Inspiratory Reserve Volume

air forcibly inhaled above VT

VT = Tidal Volume

air inhaled or exhaled with each breath

ERV = Expiratory Reserve Volume

air forcibly exhaled above VT

RV = Residual Volume

air that always remains in lung

IC = Inspiratory Capacity

max amount of air inhaled after a normal exhalation

FRC = Functional Residual Capacity

amount of air in lungs after tidal breath

VC = Vital Capacity

amount of air that can be forcibly inhaled and

exhaled with one breath

Physiology of Ventilation There are two parts to gas exchange: ventilation (V) and

perfusion (Q). Ventilation refers to the movement of air in

the pulmonary airways; perfusion refers to the movement

of blood in the pulmonary vasculature. The pulmonary

arteries, veins, and capillaries are a low-pressure system

and together contain about 500-750 ml of blood, 10-15%

of the cardiac output.

The capillary bed in the lung is a network of very thin, fine

vessels that enclose each alveolus. The alveolar-capillary

membrane is approximately 0.2 microns thick. This

extremely fine membrane allows the easy diffusion of

gases. Gases, primarily oxygen and carbon dioxide, move

from areas of high pressure to areas of lower pressure. For

exchange of gases to occur, ventilated alveoli must be

located next to perfused capillaries.

The amount of ventilation (V) and perfusion (Q) is

expressed by the ratio V/Q. The normal amount of

ventilation is 4 LPM, and normal amount of perfusion is

about 5 LPM, so V/Q overall = 4/5 or 0.8. There are,

however, regional differences in the different parts of the

lung depending on position. With normal lung function,

ventilation and perfusion is greater in the bases of the lungs

when the person is in an upright position.

Changes in the V/Q ratio occur when perfusion does not

match ventilation. There are two reflexes that work to keep

V/Q normal:

1. Pulmonary vasoconstriction: when there are

alveoli not helping with gas exchange, the blood

vessels supplying those alveoli constrict (e.g.,

pneumonia, COPD)

2. Terminal bronchiole constriction: When blood

is not flowing past the alveoli, the smooth muscle

in that area constricts (e.g., pulmonary embolism)

ERV

TLC

IRV

VT

RV

IC

FRC

VC



Page 4

Alterations in the VQ ratio (often referred to as a “V/Q

mismatch”) can occur from one of two physiologic

mechanisms: shunting or increased dead space.

Shunting

A “shunt” occurs when a portion of the cardiac output

(blood) does not participate in gas exchange. An

“anatomical shunt” occurs when a portion of the cardiac

output bypasses the alveolar-capillary unit.

Abnormal shunting occurs with structural abnormalities,

such as pulmonary AV fistula (intrapulmonary), Tetralogy

of Fallot (intracardiac), or shunts related to neoplasms. In

a “physiological shunt,” blood is circulating through non-

ventilated alveoli. This is common in patients with

atelectasis, pleural effusions, pulmonary edema, or

pneumonia.

Dead Space

Dead space is the volume of air not participating in gas

exchange. Dead space is normally 2 ml/kg. Anatomical

dead space refers to the portion of each breath that fails to

reach the alveoli for perfusion. This is normal in the

trachea and large airways, such as the bronchi. Anatomical

dead space is increased in persons with large airways or

long ventilator tubing. Physiological dead space exists

when the alveoli receive air but do not connect with the

capillary membrane. Patients with emphysema have

increased physiologic dead space -- the alveolar walls and

capillary beds have been destroyed, leaving a large amount

of air space that doesn't connect with a capillary.

Compliance

Compliance is to the ability of the lungs to stretch

(elasticity or distensibility) and recoil. It is measured as the

volume of air per unit of pressure change (i.e., ml/cm H20).

Normal lung compliance is 200 ml/cmH2O. Increased

compliance indicates that the pressure needed to stretch

the lungs is less than normal, from:

“stretched out” lungs (as is seen in emphysema) –

this makes it more difficult for the patient to

exhale

Decreased compliance indicates that the pressure needed

to stretch the lungs is greater than normal or that the lungs

are “stiff” (e.g. ARDS). As compliance decreases, the

pressure required to deliver the same volume increases.

Resistance

Resistance is the pressure inside the airways as air flows

into the lungs. To a certain extent, the normal airway

“resists” the entrance of air, simply because the airways

become smaller. Resistance is measured in terms of cm

H2O/liters of flow. An increase in the resistance to air flow

can be measured with a peak pressure. Factors that

influence resistance include:

Airway:

flow rate of the gas: noninvasive oxygen delivery,

CPAP, or mechanical ventilation

size/diameter of airway: bronchospasm increases

resistance

obstruction: kinks or H2O in ventilator tubing,

excessive secretions

Lung:

chest size

volume of gas

elasticity/compliance

Chest wall:

deformities

position of patient

external compression of chest wall or diaphragm

(such as with ascites, obesity, and/or pregnancy)

Work of Breathing

The work of breathing (WOB) refers to how much energy

the ventilatory muscles require. At rest, the work of

breathing consumes 1-3% of the cardiac output. The work

of breathing can be either increased or decreased; however,

we are more concerned about increases in the work of

breathing. Work of breathing can be increased by a variety

of factors:

1. Hypoxemia, acidosis, hypercarbia

2. Airway resistance problems: secretions,

bronchospasm, artificial airway

3. Lung compliance problems: ARDS

4. Increased metabolic work: hyperthermia,

hyperthyroidism

No shunt

Normal

ventilation and

perfusion

Physiologic shunt

NO ventilation

Normal perfusion

Anatomic shunt

Normal

ventilation

NO perfusion



Page 5

Increased WOB may lead to respiratory muscle fatigue and

decompensation. If the oxygen demands of the body

continue to be higher than the supply, the patient may

exhibit hypoxemia, tissue hypoxia, acidosis, and

hypercarbia, resulting in arrhythmias and cardiac arrest.

Oxygenation The amount of oxygen can be measured in different ways

in the blood: the partial pressure of oxygen (PaO2) and O2

saturation (SaO2).

1. The PaO2 is the pressure (P) exerted by oxygen (O2)

dissolved in the arterial blood (a).

2. Oxygen saturation (SaO2) is the percent (%) of

oxygen that the hemoglobin is carrying.

PaO2

The PaO2 (pO2) represents the amount of oxygen that is

physically dissolved in the blood -- about 3% of the total

oxygen. The greater portion of oxygen (about 97%) is

chemically bound to hemoglobin as oxyhemoglobin. The

PaO2 reflects gas exchange in the lung and is the driving

force behind hemoglobin saturation.

A normal range for PaO2 on room air is 70-100 mm Hg.

This measurement can be affected by:

age: as people age, their “normal" PaO2 decreases

altitude: the higher the altitude, the lower the pressure

to push oxygen into the blood

FiO2: the Fraction of inspired oxygen (FiO2) is the

amount of oxygen that is being inhaled. Decreases in

the amount of oxygen will lead to a decrease in the

PaO2.

Oxygen Saturation and Oxyhemoglobin

Oxygen saturation (SaO2) calculates the percentage of

oxygen that hemoglobin is transporting. Each gram of

hemoglobin can carry 1.34 ml of oxygen.

Oxyhemoglobin can be determined when the hemoglobin

(Hgb), SaO2, and the cardiac output (CO) are known. The

formula is:

Oxyhemoglobin saturation =

(1.34 X Hgb X SaO2) X CO/100

Pulse oximetry uses light-emitting devices to detect the

saturated hemoglobin and non-saturated hemoglobin. The

percentage of saturated hemoglobin is usually 90-100%.

Because it is a percentage, the SaO2 can never be more

than 100%. The SaO2 reflects oxygenation status, not

ventilation status (pH, PaCO2).

Benefits of SaO2 Monitoring

Noninvasive

Accurate with an SaO2 > 70%

Can have continuous monitoring

Limitations of SaO2 Monitoring

Affected by a poor pulsatile signal (hypotension,

shock, vasopressors)

Affected by high bilirubin levels (such as in liver

failure)

Excessive movement will limit accuracy of monitor

Oxyhemoglobin Dissociation Curve

The oxyhemoglobin dissociation curve defines the

relationship between dissolved oxygen (PaO2) and the

oxygen actually carried by the hemoglobin

(oxyhemoglobin). This curve reflects how easily Hgb

gives up oxygen to the tissues.

The flat upper portion of the curve illustrates that if the

PaO2 drops from 100 to 70, the saturation decreases only

slightly. Adequate amounts of oxygen will be carried to

the tissues even with a lower PaO2. The steep midportion

of the curve demonstrates that slight reductions in PaO2

result in large reductions in the saturation of Hgb.

Many physicians write orders to keep the SaO2 > 90%.

This is because an SaO2 of 90% is roughly equal to a

PaO2 of 60. A PaO2 of 60 will keep tissues alive.

100 80 60 40 20 0

Left shift pH PaCO2 temp 2,3 DPG

Right shift pH PaCO2 temp 2,3 DPG

20 40 80 100

PaO2

S a O

2

90

60

Normal



Page 6

The relationship between PaO2 and SaO2 is affected by

alterations in the pH, temperature, CO2, and 2,3 DPG (a

substance that facilitates dissociation of O2 from

hemoglobin at the tissues). If the hemoglobin-oxygen

affinity is high, oxygen is easily bound to hemoglobin and

does not want to release to the tissues. This is called a

“shift to the left”. When the hemoglobin-oxygen affinity

is low, oxygen is not easily bound to hemoglobin; however,

the hemoglobin readily unloads its O2 at the tissue level.

This is called a “shift to the right”.

Hypoxemia/Hypoxia

The terms “hypoxia” and “hypoxemia” are sometimes used

interchangeably, but they represent different concepts.

Hypoxia is an inadequate amount of oxygen available

at the tissue level (We can’t measure this)

Hypoxemia is an inadequate amount of oxygen in the

blood (We can measure this)

Hypoxia occurs for a variety of reasons:

Pulmonary causes:

1. Alveolar hypoventilation

2. Diffusion defects at the alveolar-capillary

level

3. Right to left shunt

4. V/Q mismatch (the most common cause)

Nonpulmonary causes:

1. Reduced blood flow: commonly from

myocardial infarction, shock, or

dysrhythmias

2. Anemia

3. Nonfunctioning hemoglobin: Hgb is bound

to other substances, such as CO poisoning

4. Mitochondrial failure: cyanide poisoning

Compensatory Mechanisms to Prevent

Hypoxia

The body has a number of compensatory mechanisms that

it uses to correct hypoxia.

1. The respiratory system will increase the minute

ventilation by increasing the respiratory rate

and/or the tidal volume, and will change the blood

flow to optimize the VQ ratio.

2. The heart rate and contractility will increase, and

selective vasoconstriction and vasodilation will

take place to pump oxygenated blood to the

priority organs.

3. The kidneys will excrete erythropoietin,

which increases red blood cell

production in the bone marrow

(erythrocytosis). This increases the

body’s oxygen carrying capabilities.

With the exception of the kidneys’ response, all of the

compensatory mechanisms to correct hypoxemia increase

the tissue demand for oxygen, thus increasing workload.

Measures to Increase Oxygenation

Administration of Oxygen

The fastest way to increase oxygenation is to administer

oxygen! Oxygen therapy is used to treat hypoxemia, to

decrease the work of breathing, and to decrease the work

of the heart.

Nasal Prongs (Cannula)

Nasal prongs (cannula) are used when an exact

concentration of oxygen does not need to be guaranteed.

Adults and pediatric patients are put on a flow of 1-6 liters

per minute (LPM), while infants can be put on up to 2

LPM. Nasal prongs are indicated for supplemental oxygen,

not patients in acute distress. The approximate

concentrations of oxygen per liter of flow per minute are:

1 L = 24% 2 L = 28% 3 L = 32%

4 L = 36% 5 L = 40% 6 L = 44%

A "bubbler" humidifier can be used for flow rates of 4 liters

or higher. CAUTION: a bubbler humidifier should not be

used with any device other than a nasal cannula, as it may

cause harm to the patient.

Simple mask

The simple mask can be used to deliver 6 - 10 LPM of

oxygen, which approximates 35-55% fraction of inspired

oxygen (FiO2). The actual amount of oxygen delivered

can vary greatly with changes in the patient’s ventilatory

pattern.

Non-rebreather (partial) mask

The mask of choice for emergency situations is the non-

rebreather mask. This mask delivers nearly 100% oxygen

as long as the following criteria are met:

1. The mask fits the patients face snugly

2. The flow to the reservoir bag is adjusted so that

the bag does not totally collapse when the patient

inhales (the bag is always partially inflated)



Page 7

The partial non-rebreather mask consists of a pliable mask

with a reservoir bag and two one-way valves. For safety's

sake, there is only one valve on the side of the mask so if

the source of the oxygen fails, the patient can entrain room

air. The second one-way valve is located on the reservoir

bag so the patient cannot "rebreathe" exhaled gas.

Venturi mask

The Venturi mask is considered a "high flow system." This

mask is used when a consistent FiO2 is needed and the

patient does not require added humidity. The mask has

either an adjustable Venturi, or individual Venturis that can

be changed to allow different oxygen concentrations. Be

sure to set the flowmeter to the appropriate liter flow. Each

Venturi requires different flows; this is usually stamped

with the concentration of oxygen it will deliver; e.g. 50%

FiO2/15 LPM.

High flow humidifiers

A high flow humidifier is indicated for patients whose

natural mechanism for heating and humidifying inspired

gas has been bypassed (i.e. intubated or tracheostomy

patients). It can also be used for patients whose natural

mechanism is not sufficient to prevent retention of

secretions due to mucosal drying. The tubing, reservoir,

sterile water, and "mask" must be changed at the frequency

required by Infection Control policies and prn. Heated

humidity devices will cause condensation in the tubing;

this condensate must be drained from the circuit and not

drained back into the reservoir to prevent contamination.

Aerosol (nebulizers)

Aerosol therapy is indicated for the following conditions:

The presence of upper airway edema; i.e.

laryngotracheobronchitis, subglottal edema, post-

extubation edema, post-operative management of

the upper airway.

The presence of one or more of the following:

stridor, brassy croup-like cough, hoarseness

following extubation, upper airway irritation

(smoke inhalation) or airway insult.

Continuous aerosol therapy may be delivered via face

mask, face tent, hood, or blow-by. An oxygen analyzer

must be used on all infant hoods. Condensate must be

drained frequently from tubing to avoid contamination.

Contamination with an aerosol can cause the contaminates

to become airborne.

Ventilation Ventilation is the movement of air, both into and out of the

lungs. Ventilation is dependent on:

Respiratory effort

Respiratory rate

Lung compliance

Lung resistance

Ventilation is measured by the PaCO2 on the ABG and by

end-tidal CO2 monitoring (capnography).

PaCO2

Measurement of the PaCO2 is done on the arterial blood

gas. Like the PaO2, the PaCO2 is measured as a pressure,

in mm of Hg. The normal PaCO2 is between 35 and 45 mm

Hg.

End-Tidal CO2 Monitoring

End-tidal CO2 monitoring or "capnography" is useful for

determining that tracheal, rather than esophageal,

intubation has taken place. Capnography can also be used

to evaluate the efficiency of mechanical ventilatory support

and for monitoring the severity of pulmonary disease and

response to therapy.

Ways to Improve Ventilation

Effective Coughing Techniques

In the old days, we were taught to have the patient cough

with every deep breath, and to have patients blow up

balloons in an effort to prevent pneumonia. We know now

that those techniques are not helpful. Coughing is effective

only when there is something to cough out. Deep

exhalation and needless coughing cause the alveoli to

collapse, causing more atelectasis. Coughing also causes

an increase in the intracranial pressure and pain in surgery

patients.

There are several methods of coughing that are effective in

clearing the smaller airways of mucous. They are:

1. Cascade cough: have the patient inhale deeply

through the nose, hold for 1-3 seconds, then cough

forcefully several times.

2. Huff cough: have the patient inhale deeply through the

nose, hold for 1-3 seconds, then say "huff" forcefully

several times.

3. End-expiratory cough: have the patient take a normal

breath, then at the end of a normal exhalation, have the

patient cough once. Follow by a cascade or huff

cough.



Page 8

Deep Breathing and Incentive Spirometry

Effective deep breathing and incentive spirometry will aid

in alveolar expansion, will help to clear the smaller

airways, and will improve stress. The patient should be

encouraged to breathe deeply at least ten times every hour.

For patients who cannot breathe and are on the ventilator,

the "sigh" button can be used to give them a breath that is

1 1/2 times the normal tidal volume. Check with the

physician before doing this.

Chest Physiotherapy

Often done by respiratory therapists, chest physiotherapy

is designed to mobilize secretions by a sequential

application of "cupping" or "thumping" the posterior, and

sometimes anterior, chest.

Nasal Pharyngeal Airway (Trumpet)

The trumpet is an excellent ventilation and suctioning aid.

It can be used in conscious or unconscious patients. The

trumpet is placed, using a water-soluble lubricant, into the

patient’s nare, using a gentle back and forth motion.

Optimally, the trumpet should be moved from nare to nare

every 24 hours to prevent skin breakdown.

Oral Airway

The oral airway is a good tool to keep the tongue out of the

airway. It can be used only for patients who are

unconscious and who are not gagging. The oral airway can

be dangerous to use in patients who may vomit, as it

provides a more open channel for aspiration. Generally, an

oral airway is used as a temporary measure until the patient

wakes up or is intubated.

Endotracheal Intubation/Mechanical Ventilation

Endotracheal intubation with mechanical ventilation may

be used when other methods of airway maintenance have

failed. Endotracheal intubation keeps the airway open and

protected. Mechanical ventilation decreases the work of

breathing and improves ventilation and gas exchange,

increasing PaO2 and decreasing PaCO2.

Tracheostomy

The ultimate in invasive ventilation techniques, the

tracheostomy is used for a wide variety of purposes.

Patients may require a tracheostomy for long-term

mechanical ventilation or as a result of neck, throat, or

mouth surgery.

CPAP or BiPAP

Another way of improving oxygenation and ventilation is

by using non-invasive positive pressure, such as CPAP or

BiPAP. CPAP stands for "Continuous Positive Airway

Pressure," and BiPAP stands for "Bilevel Positive Airway

Pressure." Both will provide positive pressure or "PEEP"

for spontaneously breathing people. PEEP (Positive End

Expiratory Pressure) is the pressure left in the lungs at the

end of expiration. Increasing PEEP helps to keep the

alveoli from collapsing. It is important to differentiate

between CPAP and BiPAP. CPAP provides positive

pressure on exhalation to help keep the airways open,

BiPAP is essentially "Bi-level" ventilation - or CPAP with

pressure support. BiPAP provides both pressure support

on inhalation to decrease the work of breathing AND

positive pressure on exhalation to help keep the airways

open.

Indications for positive airway pressure are to:

1. Reduce air trapping in patients with asthma and/or

COPD.

2. Help mobilize retained secretions in patients with

cystic fibrosis or chronic bronchitis.

3. To prevent or reverse atelectasis.

4. Optimize bronchodilator delivery in patients

receiving bronchial medication therapies.

5. Help redistribute extra-vascular water, such as in

pulmonary edema.

6. Assist with breathing for those with ventilatory

muscle weakness, but who do not wish to be

intubated.

CPAP can be delivered a number of ways, either with a

nasal or full-face mask or with a mechanical ventilator via

an endotracheal tube or tracheostomy. Patients, such as

those with obstructive sleep apnea (OSA), may also have a

small bedside CPAP machine for the home care setting.

These patients use the CPAP at night and when napping.

One of the major complications of CPAP and BiPAP use

relates to skin breakdown because of the tight-fitting nasal

or facial mask. For this reason, these machines have been

designed to have a small leak when placed on the patient.

In the critical care setting, patients who are alert and

cooperative may benefit greatly from this type of

ventilation. Patients who are at risk for vomiting, who have

facial trauma, who are unable to independently remove the

mask if they need to, or who are not able to comply with

the treatment should not be on CPAP/BiPAP treatment.



Page 9

Arterial Blood Gas Analysis Arterial blood gases (ABG’s) provide information about

oxygenation and acid-base balance. Acid-base status

reflects physiologic processes and chemical reactions.

Acid-base balance refers specifically to the regulation of

hydrogen ion concentration in the body.

Obtaining an ABG

1. Identify the pulsating arterial site (radial and brachial

sites most common).

2. Perform the Allen's test.

3. Thoroughly cleanse area with an alcohol prep pad for

one minute.

4. Stabilize the artery by pulling the skin taut and

bracketing the pulsating area with the first two fingers

of your non-dominant hand.

5. Holding the syringe like a pencil, puncture the skin

slowly (at about a 45 degree angle). Advance the

needle with the bevel up.

6. Wait for flash of arterial blood to occur.

7. If no flash occurs, withdraw slowly until the needle is

almost out, and redirect.

8. When flash occurs, allow syringe to fill with at least

one ml of blood.

9. Withdraw needle and apply pressure to the site for five

minutes. While holding pressure, carefully rotate the

syringe to mix the blood and heparin.

10. Using universal precautions, remove the needle from

the syringe and place cap (see your unit policy).

Immediately send to the lab. The ABG is no longer

valid after 30 minutes.

11. If point of care lab equipment (e.g., ISTAT) is

available, it should be utilized.

Do's and Don'ts

DO document the SaO2 at the exact time the ABG is

drawn. The SaO2 is calculated on the ABG from the

pH and HCO3- and should correspond closely with the

oximeter measurement.

DO document the respiratory rate, effort, and use of

accessory muscles.

DO document patient temperature

DO document amount of oxygen the patient is on.

DON'T draw ABG's if patient just suctioned.

DON'T draw ABG's if patient receiving nebulizer

treatment.

DON'T draw ABG's if patient became short of

breath doing an activity (or if SaO2 dropped while

YOU were doing something to the patient).

DON'T draw ABG's if patient is not on the amount

of oxygen or device you want to assess (wait 20

minutes after any O2 or device change).

Acid-Base Balance and the ABG

pH

The pH on the ABG is inverse logarithmic number of

hydrogen ions in the blood. Normally, the pH should be

7.35-7.45. A lower pH indicates that the blood is more

acidic. A higher pH indicates that the blood is more

alkaline.

Maintaining a Normal pH

The body’s organ systems function best with a normal pH.

In order to maintain the blood pH between 7.35-7.45, the

body has a buffering system. There are two major chemical

buffers, regulated by the respiratory and renal systems, in

the body:

carbon dioxide (CO2) is primarily regulated by the

respiratory system. The normal PaCO2 on the ABG

is 35 - 45 mm/Hg

bicarbonate (HCO3-) is primarily regulated by the

renal system. The normal HCO3- level on the ABG

is 22 - 26 mEq/L

The respiratory system responds within 1-3 minutes to

changes in acid-base balance. If the chemo-receptors sense

too many hydrogen ions (acidosis), it will stimulate the

respiratory center to breathe faster and deeper – to “blow

off” CO2. If the chemoreceptors sense too few hydrogen

ions (alkalosis), it will depress the respiratory center,

slowing respiration and reducing tidal volume to keep

CO2.

The kidneys compensate over 24-48 hours to correct

imbalances. If the kidneys see acidosis, they will retain,

regenerate or synthesize HCO3- and excrete H+. If the

kidneys see alkalosis, they will excrete HCO3- and retain

H+.

If the body sees acidosis, it will:

Increase the respiratory rate to blow off CO2

Retain, regenerate or make bicarbonate

Excrete hydrogen ions

If the body sees alkalosis, it will:

Decrease the respiratory rate to keep CO2

Excrete bicarbonate



Page 10

Retain hydrogen ions

When there is an acid-base disturbance and either the lungs

or kidneys react, it is called compensation. Compensation

can be complete or partial. The body will compensate so

that the pH reaches the edges of normal. For example, if

the pH is 7.10 (acidosis), the body will try to compensate

so that the pH will reach 7.35, not greater than 7.35. Partial

compensation means that the pH has not reached a normal

level.

Respiratory Acidosis

In acute respiratory acidosis, the lungs don’t get rid of

enough CO2. This is the most common acid-base balance

disturbance in the hospital setting.

Causes: oversedation, head trauma, respiratory and

cardiac arrest

What to look for: PaCO2, pH, normal HCO3-

Examples:

pH 7.29, PaCO2 57, HCO3- 28

pH 7.06, PaCO2 98, HCO3- 28

In compensated respiratory acidosis, the lungs still don't

get rid of enough CO2, but the kidneys have had enough

time to save bicarbonate.

Causes: COPD, spinal cord injury, respiratory muscle

paralysis

What to look for: PaCO2, pH, HCO3-

Examples:

pH 7.31, PaCO2 76, HCO3- 39

pH 7.34, PaCO2 60, HCO3- 33

Respiratory Alkalosis

In acute respiratory alkalosis, the lungs are “blowing off”

too much CO2, leading to an increased pH.

Causes: stress, pain, fever, and hypoxemia

What to look for: PaCO2, pH, normal HCO3-

Examples:

pH 7.52, PaCO2 27, HCO3- 22

pH 7.65, PaCO2 23, HCO3- 24

Compensated respiratory alkalosis occurs when the lungs

"blow off" too much CO2, but the kidneys have time to

excrete bicarbonate and save hydrogen ions.

Causes: uncommon, but can occur in the patient with

neurological damage


Examples:

pH 7.49, PaCO2 16, HCO3- 11

pH 7.45, PaCO2 23, HCO3- 16

Metabolic Acidosis

Metabolic acidosis occurs where there is either too much

acid (such as in shock, hypoxemia, diabetes [especially

DKA], overdose, renal failure) in the system, or when there

is a loss of bicarbonate (diarrhea, NG suction, renal tubular

acidosis).

Acute metabolic acidosis without compensation may be

seen in the mechanically ventilated, sedated, or comatose

patient. Because of the altered mental status, there is no

compensatory response by the respiratory system.

What to look for: normal PaCO2, pH, HCO3-

Examples:

pH 7.05, PaCO2 37, HCO3- 7

pH 7.23, PaCO2 40, HCO3- 12

Compensated metabolic acidosis is much more common.

The respiratory rate and depth increases to blow off CO2.

There is a limit to how much the respiratory system can

compensate. The PaCO2 may be quite low, but it is still not

able to bring the pH back to normal.


Examples:

pH 7.19, PaCO2 22, HCO3- 8

pH 6.96, PaCO2 9, HCO3- 2

Metabolic Alkalosis

In metabolic alkalosis, there is a gain of base or increased

loss of acid, resulting in an increased pH. If there is a gain

of base, such as in sodium bicarbonate (baking soda)

ingestion or administration of NaHCO3 during CPR, the



Page 11

HCO3- will be elevated. If there is loss of an acid, such as

in vomiting or NG suction, the HCO3- will be normal in the

acute phase.

Acute metabolic alkalosis is uncommon, but can been seen

if the patient is not neurologically intact and is unable to

increase the respiratory rate.

What to look for: normal PaCO2, pH, HCO3-

Examples:

Gain of a base: pH 7.55, PaCO2 40, HCO3- 42

Loss of acid: pH 7.52, PaCO2 37, HCO3- 28

Compensated metabolic alkalosis can look like:


Examples:

Gain of a base: pH 7.47, PaCO2 46, HCO3- 42

Loss of acid: pH 7.46, PaCO2 44, HCO3- 26

There is also a limit to the compensation of the respiratory

system in metabolic alkalosis. The body will not tolerate

CO2 levels over 50-55 mm Hg, and will increase the rate

and depth of breathing after that point.

Now, you might notice that metabolic alkalosis from loss

of an acid and respiratory acidosis look a lot alike. Here’s

how to tell the difference. There is an increase in CO2 in

both metabolic alkalosis and respiratory acidosis, but the

pH will be relatively normal. In compensated respiratory

acidosis, though, the pH will be on the low side of normal,

not the high, and the HCO3- level will be high, not normal.

Analyzing the ABG

1. Look at the PaO2.

2. Look at the pH.

a) Is it normal?

b) Is it low normal or high normal? Look for

changes in the PaCO2 and HCO3- to see if there is

compensation for a problem.

c) If it is low (less than 7.35), the patient is in

acidosis.

d) If it is high (more than 7.45), the patient is in

alkalosis.

3. Look at the PaCO2.

a) The pH and PaCO2 have a "teeter-totter"

relationship. If the problem is respiratory, one

will be up, and the other will be down.

b) If the pH and PaCO2 are both up or both down, the

problem is metabolic. The teeter-totter isn't

there, so it can't be a primary respiratory problem,

instead, it is a metabolic problem with respiratory

compensation.

4. Look at the HCO3-.

a) The pH and HCO3- go up and down together in a

metabolic problem.

b) If the pH and the HCO3- are opposite (one is up

and the other is down), the problem is primarily

respiratory, and the HCO3- is trying to

compensate.

Examples:

1) pH 7.01; PaCO2 69; HCO3- 24

a) The pH is very low, so it is acidosis.

b) The PaCO2 is high, making a teeter-totter with the

pH, so it is a respiratory problem.

c) The HCO3- is normal, so there is no

compensation.

d) Respiratory acidosis without compensation.

2) pH 7.33; PaCO2 72; HCO3- 36

a) The pH is low, so it is acidosis.



c) The HCO3- is high, so there is compensation, but

not enough to bring the pH to normal.

d) Respiratory acidosis with partial compensation.

3) pH 6.99; PaCO2 20; HCO3- 2

a) The pH is very low, so it is acidosis.

b) The PaCO2 is low; it is not a teeter-totter with the

pH, so it is a metabolic problem with respiratory

compensation.

c) The HCO3- is low, confirming a metabolic

problem.

d) Metabolic acidosis with partial compensation.

4) pH 7.35; PaCO2 65; HCO3- 32

a) The pH is low normal.



c) The HCO3- is high, so there is compensation.

d) Respiratory acidosis with compensation.

5) pH 7.51; PaCO2 15; HCO3- 8

a) The pH is high, so it is alkalosis.

b) The PaCO2 is low, making a teeter-totter with the




Page 12

c) The HCO3- is low, so there is compensation.

d) Respiratory alkalosis with partial compensation.

6) pH 7.78; PaCO2 59; HCO3- 40

a) The pH is very high, so it is alkalosis.

b) The PaCO2 is high; it is not a teeter-totter with the

pH, so it is a metabolic problem with respiratory

compensation.

c) The HCO3- is high, confirming a metabolic

problem.

d) Metabolic alkalosis with partial compensation.

7) pH 7.45; PaCO2 37; HCO3- 24

a) The pH is normal.

b) The PaCO2 is normal

c) The HCO3- is normal.

d) Normal acid-base balance.

Venous Blood Gases Venous blood gases (VBGs) are another way to obtain

information about oxygenation and acid-base balance.

They are collected in the same manner as a venous blood

sample for other lab draws and are labeled and sent as

directed for ABGs. The “Do’s and Don’ts” for VBGs are

the same as for ABGs, however, the normal values differ

slightly.

Normal Values ABG VBG

pH 7.35-7.45 (7.40) 7.31-7.41 (7.36)

PO2 80-100 mm Hg 35-40 mm Hg

SO2 95% 70-75%

PCO2 35-45 mm Hg 41-51 mm Hg

HCO3 22-26 mEq/L 22-26 mEq/L

Although VBG analysis is limited in assessing

oxygenation, a normal venous pH, PCO2, and HCO3 are

useful in ruling out severe acid-base disturbances.1

Acute Respiratory Distress Syndrome

(ARDS) Larry Leakey is a 21-year-old man who was involved in a

severe car accident. He underwent emergency surgery to

repair a lacerated liver, perforated bowel, and tension

hemopneumothorax. He received 15 units of blood during

surgery. He was rapidly extubated after surgery and sent

to the ICU.

The next day, Larry became increasingly short of breath

and was using all accessory muscles. He had O2

saturations in the 80's. His PaO2 on blood gases was 34

mm Hg. His heart rate was 180 beats/min. Larry’s chest

x-ray showed diffuse, patchy infiltrates throughout his lung

fields. His diagnosis was ARDS.

What is ARDS?

Acute Respiratory Distress Syndrome (ARDS) and its less

severe cousin Acute Lung Injury (ALI) have been

documented in medical history for at least two thousand

years. It became better known during the Vietnam War,

when soldiers would develop respiratory failure and die

after being wounded. Although over twenty years of

extensive research and study have been given to ARDS and

its treatment, the mortality for ARDS remains high.

What happens in ARDS?

ARDS always occurs as a secondary problem. Four to 48

hours after the initial insult, the immune system is

activated, causing inflammation in the lung. The white

blood cells (particularly neutrophils) release chemical

mediators which cause increased vascular permeability. In

the lung, this becomes disastrous.

Fluid and proteins enter into and around the alveoli through

the very thin vascular membrane, causing pulmonary

edema. Pulmonary edema increases the space between the

alveoli and the alveolar capillary beds, decreasing gas

exchange. Damage caused by pulmonary edema, combined

with a decreased amount of surfactant, causes “stiff” lungs

at risk of barotrauma, alveolar collapse, and atelectasis.

The combination of pulmonary edema and atelectasis leads

to intrapulmonary shunting, decreased compliance, and

increased work of breathing. The patient begins to become

more and more hypoxemic, even on high levels of oxygen.

As a result of hypoxemia, the pulmonary vasculature

constricts through the capillary beds. This causes

pulmonary hypertension. As the pressure builds in the

pulmonary artery, more and more fluid is forced out into

the alveoli and interstitium. The lung becomes even less

compliant, causing an increased work of breathing and an

increased oxygen demand.

What causes ARDS?

There are certain injuries, diseases, and interventions that

are more likely to cause ARDS. The most common causes

are listed below.

Most Common

1) Sepsis

2) Gastric aspiration

3) Pneumonia

4) Trauma

Other Drug overdose (e.g., ASA)

Near-drowning



Page 13

Massive blood transfusion/transfusion reaction

Inhalation of toxic gases and vapors

Pancreatitis

Asthma exacerbation

Batt Atsma is a 37-year-old mother of two who has had

asthma for many years. She is classified as a Step 3 -

moderate persistent asthmatic. She enters the hospital with

shortness of breath and wheezing unrelieved by her usual

asthma medications.

What is asthma?

One of the diseases that can be considered both acute and

chronic is asthma. People with asthma chronically have

the underlying disease, but also have exacerbations of

asthma.

The conducting airways (bronchi, bronchioles) of the

pulmonary system are hyperreactive in persons with

asthma. With a precipitating factor, the smooth muscle of

the airways constrict, causing decreased air conduction and

increased breathing difficulty. With the smooth muscle

contraction comes increased mucous production, mucosal

cell swelling, and ventilation-perfusion abnormalities.

Because of the pressure dynamics in the chest, air will flow

into the patient with an asthma exacerbation much more

easily than it will flow out. Air becomes “trapped” inside

the lungs, causing lung hyperinflation. The resistance to

airflow increases, causing the patient to work harder at

breathing. The pressure inside the alveoli becomes greater

(because of the air trapping) than the pressure in the

airways, so more air becomes trapped in the alveoli.

What are the causes of asthma?

Respiratory infection

Allergic reaction to inhaled antigen

Inappropriate bronchodilator management

Idiosyncratic reaction to aspirin or other

nonsteroidal anti-inflammatory agents

Emotional stress

Exercise

Environmental exposure

Occupational exposure

Nonselective beta blocking agents

Mechanical stimulation (coughing, laughing,

cold air inhalation)

Reflux esophagitis

Sinusitis

Batt Atsma has been classified as a Step Three - moderate

persistent asthmatic. She is on multiple inhalers through

the day, and typically has two to three asthma "attacks" per

week. She is no longer able to do many of the sporting

activities that she used to do with her children.

Is there a classification system for how bad

asthma is?

The National Asthma Education and Prevention Program,

which is sponsored by the National Heart Lung and Blood

Institute, has published guidelines to determine the severity

of illness for adults and children older than 5 years. This

classification helps clinicians determine what treatments

would best suit the patient.

Step One - Intermittent

In this level, patients have symptoms twice a week or less,

but are asymptomatic with a normal PEF between

exacerbations. The exacerbations last from a few hours to

a few days, and the intensity may vary. They have

symptoms at night less than twice a month. The FEV1/PEF

is greater than 80% of predicted.

Step Two - Mild Persistent

Patients with mild, persistent asthma have symptoms more

than twice a week but not daily and not more than once on

any day. Exacerbations of their asthma may interfere with

activities. They are prone to having nighttime symptoms

3-4 times a month, but still have an FEV1/PEF ratio of

greater than 80% of predicted.

Step Three - Moderate Persistent

These patients have symptoms every day and use inhaled

short-acting beta2-agonists every day. When they have

exacerbations (>2 times/week), they affect the patient’s

activities and may last for days. They have nighttime

symptoms more than once a week, and have an FEV1/PEF

ratio of >60% and < 80% of predicted.

Step Four - Severe Persistent

The most severe of all of the asthma classifications,

patients with severe, persistent asthma experience

continual symptoms, have limited physical activity, and

have frequent exacerbations. They have frequent nighttime

symptoms and have a FEV1/PEF ratio of less than 60% of

predicted.



Page 14

Pulmonary Function Assessment

One of the best indicators of asthma symptom severity is

the FEV1 on the spirometer. Standing for "Forced

Expiratory Volume" in one second, it measures how much

the patient is able to exhale forcibly after a normal

inhalation. The amount exhaled in one second in normal

lungs is approximately 80% of the total exhaled amount -

that's where the 80% of predicted value comes from on the

classification above.

Another measure of day-to-day function is the PEF - the

peak expiratory flow rate. This is the fastest rate at which

air can move through the airways in a forced exhalation.

The day-to-day rate is measured against the patient’s

personal best, and should be > 80% of the patient’s

personal best. Measurements of the PEF can and should be

done by the patient on a daily basis. Typically, a PEF

>80% of the personal best is in a "green" zone - which

indicates that the asthma is stable. A PEF of 60-80% is in

the "yellow" zone and indicates that the patient should take

extra caution or medications. A PEF of <60% is in the

"red" zone and indicates that the patient is having a

significant exacerbation.

What is status asthmaticus?

This is the term used to describe an asthma exacerbation

that is refractory to bronchodilator therapy, including

aminophylline IV and beta-adrenergic agents

(epinephrine). Status asthmaticus is often an emergency

requiring further treatment, such as intubation and

mechanical ventilation.

Chronic obstructive pulmonary disease Joe Chroniclung is a 60 year-old male with end stage

COPD. He was recently hospitalized for pneumonia and a

COPD exacerbation and was sent to a transitional care

facility for rehabilitation. Joe was a long-time smoker, but

has not smoked since his last hospitalization.

In chronic obstructive pulmonary disease (COPD), there is

an obstruction to air flow either into or out of the lungs.

Chronic bronchitis and emphysema are the major diseases

that cause COPD. Although the pathophysiology for each

is discussed separately, please be aware that the two most

commonly appear together.

What is chronic bronchitis?

In chronic bronchitis, persistent injury to the alveoli causes

an overstimulation of mucus production, accompanied by

a persistent cough. As the disease progresses, the bronchial

walls thicken, reducing airspace and causing an increase in

airway resistance. The results of the bronchial wall

thickening and excessive mucus production are:

Hypoxemia and hypercapnia

Chronic cough with sputum production

Pulmonary hypertension from hypoxemia,

leading to cor pulmonale and right-sided heart

failure

The diagnosis of chronic bronchitis is made when there is

a history of a chronic productive cough for three months of

the year in each of two successive years.

What is emphysema?

In emphysema, the alveolar walls are destroyed, causing

the very small alveoli to enlarge into large air sacs, called

blebs. During the wall destruction, the capillary beds are

also destroyed. The results of this are:

Hypercapnia without hypoxemia (in the early stages)

Bleb formation with potential for pneumothorax

Air trapping within the blebs with constriction of the

smooth muscle of the bronchioles

What are the causes of COPD?

Cigarette smoking

Environmental pollution or occupational

exposure

Alpha1-antitrypsin deficiency (genetic marker for

familial emphysema)

What type of tests can be done to assess

Joe's pulmonary function?

Joe's last documented FVC was 3.12 and FEV1 was 1.29.

The FEV1 was 32% of predicted.

Pulmonary function tests can be very useful in determining

the function of the lungs in COPD, just as they can in

asthma. The FEV1 is the same test as for COPD as it is for

asthma - the amount of air that can be forcibly exhaled in

one second. In people with normal lungs, the FEV1 should

be > 80%. The FVC (Forced Vital Capacity) is also

measured. Where the FEV1 was the amount of air exhaled

in one second, the FVC is the total amount of air that is

exhaled quickly. This volume represents the patient's

ability to breathe deeply and cough. This number is

reduced in people with obstructive disease.



Page 15

Pneumonia S.A. Pneumo is a 67 year-old male who enters the hospital

with shortness of breath, a cough, and a 1½ week history

of flu-like symptoms. He is diagnosed with pneumonia.

What causes pneumonia?

Pneumonia has a number of causes. It can be caused by

microorganisms such as bacteria, viruses, and fungi.

Streptococcus pneumoniae, Mycoplasma pneumoniae, and

Histoplasma capsulatum may all cause pneumonia in a

normally healthy person. Pneumococcus, Escherichia coli,

Pseudomonas, Serratia, Proteus, and Acinetobacter usually

occur as pneumonias in patients who have a chronic

disease, poor nutrition, trauma, surgery, or who are

immunosuppressed.

Aspiration is one of the most common causes of

pneumonia. Gastric contents contain caustic substances

and bacteria. Entry into the airway causes the conducting

airways to be blocked and the alveoli to be “burned”

causing inflammation.

Chemical inhalation is another cause of pneumonia.

Inhalation of smoke, cleaning chemicals and industrial

chemicals causes caustic damage to the airways and

alveoli. Inflammation and formation of exudate results,

blocking the airways and alveoli.

What is the pathophysiology of

pneumonia?

Once the foreign substance has entered the lungs, the

immune response is initiated. First, certain alveolar cells

begin to produce large amounts of mucous to try to coat the

foreign substance. Second, white blood cells will attempt

to "wall off" the foreign substance. Third, the

inflammation triggered by the immune system will

increase blood flow to the area and increase capillary

permeability.

If these normal mechanisms don't work, the patient

becomes progressively more ill. Mucus and fluid from the

capillaries fill the alveoli and the space around the alveoli.

This increases the space through which gas must travel. At

the same time, the increased blood flow goes past alveoli

that aren't contributing to gas exchange (physiologic

shunting). And lastly, if the patient has a bacterial

pneumonia, the bacteria may produce exudates that further

clog the alveoli. These problems culminate in hypoxemia.

Hypoxemia will cause the patient to breathe faster, leading

to hypocapnia (blowing off CO2).

What's the difference between a

"community" and "nosocomial"

pneumonia?

Pneumonias that begin outside of the hospital setting are

called "community acquired" and pneumonias that start in

health care facilities are known as "nosocomial"

pneumonias. People who are at risk for acquiring

pneumonia in the hospital are those who:

are > 70 years old

are intubated and/or on mechanical ventilation

have a depressed level of consciousness

have an underlying chronic lung disease

have had a previous large volume aspiration

are being given cimetidine for stress-bleeding

prophylaxis

are being given antimicrobials

have an NG tube and/or are receiving tube

feedings

have had a recent bronchoscopy

Idiopathic Pulmonary Fibrosis Audrey L. is a 62 y.o. with a long 1 pack per day smoking

history. While Audrey has been smoke-free for 7 years, she

has been experiencing a progressive shortness of breath on

exertion and a non-productive cough over the last 6

months. It has gotten so bad that she feels all out of breath

just cooking dinner and performing other daily activities.

What is Idiopathic Pulmonary Fibrosis and

who is at risk for it?

Idiopathic pulmonary fibrosis (IPF) is a disorder of

unknown cause characterized by inflammation of the lower

respiratory tract that usually leads to the formation of scar

tissue. History of cigarette smoking increases the risk of

development and it affects more men than women.

Typically it first appears between ages of 50 and 70 years.

What symptoms do IPF patients have and

how is it diagnosed?

Patients usually present with a gradual onset of exertional

dyspnea and/or a nonproductive cough. Inspiratory

crackles and clubbing of the fingers may be present on

examination. A chest x-ray may show a variety of findings

from peripheral reticular densities to end-stage

honeycombed lung. The Gold Standard for diagnosis is an

open lung biopsy using video assisted thoracic surgery

(VATS) to help confirm pathology.



Page 16

What is the prognosis and treatment for IPF?

The clinical course is variable and prognosis is poor. The

5-year survival rate after diagnosis is 30%-50%. As the

disease progresses common complaints are fatigue,

weakness, anorexia, and weight loss. The optimal medical

therapy for the treatment of IPF has yet to be identified. No

proven effective therapies are available for the treatment of

IPF beyond lung transplantation. Initial treatment may

consist of a corticosteroid (prednisone), sometimes in

combination with other drugs that suppress the immune

system (e.g. methotrexate, cyclosporine). Another

treatment strategy is the assessment and management of

comorbid conditions, including chronic obstructive

pulmonary disease (COPD), obstructive sleep apnea,

gastroesophageal reflux disease (GERD), and coronary

artery disease.

Pulmonary embolism Clottia Breathless is a 28 year-old woman who was

admitted at 0500 for shortness of breath and chest pain.

She has right calf tenderness, and her right leg is swollen

and warm. The Homan's sign is positive on the right. Her

tentative diagnosis is pulmonary embolism.

What is the most likely cause of Ms.

Breathless’ illness?

Perfusion to the lung may be disturbed by an embolus in

the pulmonary vasculature. Pulmonary emboli are

generally made of blood clots, which may form in the

vasculature in the:

Popliteal vein

Ileofemoral vein

Right side of the heart

Pelvic area

Pulmonary emboli may also consist of fat, air, or amniotic

fluid.

What will favor the development of a

pulmonary embolus?

The three factors, called Virchow’s triad, favoring the

development of venous thrombosis include:

Blood stasis

Blood coagulation abnormalities

Vessel wall abnormalities

Emboli may also be formed from other substances that

enter into the blood stream. Fat emboli can form when the

long or flat bones of the body are broken; air emboli can

occur with traumatic injury (pneumothorax) or leak in a

central line; and amniotic fluid emboli may occur with an

abruptio placentae.

How does blood normally flow in the lung?

Ninety-nine percent of the blood in the body goes through

the pulmonary circulation to be re-oxygenated. The

remaining 1% feeds the pulmonary tissues with

oxygenated blood through the bronchial circulation. De-

oxygenated blood enters into the lung through the

pulmonary artery and travels to the capillary bed. The

capillary bed is a network of very thin, fine vessels that

enclose each alveolus (think of a spider web around a

grape), which is optimal for gas exchange.

Oxygen, CO2, and other waste products are exchanged

between the alveolus and capillary through a pressure

gradient system. Re-oxygenated blood travels out of the

capillary system, through the pulmonary vein and into the

left heart.

A feature vital to efficient gas exchange is called

“autoregulation,” that refers to the ability of the arteries in

the lung to constrict when blood is flowing by alveoli

which are not contributing to gas exchange (i.e., an

atelectatic alveolus), and to dilate when stimulated by the

sympathetic nervous system. Vasoconstriction in response

to non-gas exchanging alveoli is important to prevent

shunting, which is blood moving from the venous to

arterial side without receiving oxygen.

Ms. Breathless is experiencing hypoxemia as the blood

supply to some of her alveoli is shut off. Although she is

ventilating appropriately, the gases cannot diffuse into the

blood stream.

What is the pathophysiologic process of a

pulmonary embolism?

The embolus forms, enters into the venous system and

travels through the right heart into the pulmonary

vasculature. A large embolus tends to lodge in the upper

part of the lung and causes rapid and severe deterioration,

leading to cardiac arrest and death. Small, or micro, emboli

tend to lodge in the lower part of the lung. With micro

emboli, deterioration is slower and less severe.

What caused Ms. Breathless' symptoms?

The patient entered the ER with labored respirations

(dyspnea) and a rapid respiratory rate (tachypnea). As the

embolus blocked perfusion to a large number of alveoli, it

decreased the amount of gas exchange. The resulting

hypoxemia and hypercapnia triggered the chemoreceptors

in the aortic arch, medulla, and carotid bodies to increase



Page 17

respiratory rate and effort to attempt to keep the body

tissues oxygenated.

As the chemoreceptors trigger an increased respiratory rate

and effort, the sympathetic nervous system is also

stimulated to force the heart to pump the limited amount of

oxygen faster. The increased heart rate and increased

blood pressure are compensatory responses to hypoxemia.

Skin color may be a late indicator of oxygenation status.

Cyanosis indicates that there are more desaturated

hemoglobin molecules (blue) than saturated hemoglobin

molecules (red). If the patient is anemic, there will be no

cyanosis; rather, the patient will be pale.

What are the potential complications?

Pulmonary vascular pressure rises because of the

mechanical blockage of a blood vessel. This elevation is

called pulmonary hypertension. As the hypertension

increases, the work of the right heart increases. This

increased workload can lead to angina, myocardial

infarction, or heart failure.

Summary Without the lungs and proper lung function, every organ in

the body would cease to function in minutes. The

respiratory system is responsible for oxygenating the

bloodstream and for removing excess gases from the

circulation. Understanding how oxygenation and

ventilation occur and how to interpret ABG's can help you

determine how best to assess and manage your critically ill

patient. Knowing the causes, pathophysiology, and some

of the tests for selected pulmonary illnesses provides you

with a foundation of knowledge for managing the acutely

and critically ill pulmonary patient.

References

1. ----(2007). Expert Panel Report 3: Guidelines for the

Diagnosis and Management of Asthma (EPR-3). National

Institutes of Health: National Heart, Lung, and Blood

Institute. www.nhlbi.nih.gov/guidelines/asthma.

2. Anderson, J. M. (1996, June). Management of four arterial

blood gas problems in adult mechanical ventilation:

Decision-making algorithms and rationale for their use.

Critical Care Nurse, 16(3), 62-72.

3. Chhabra, S. (July-Sept, 2011) Agreement and differences

between venous and arterial gas analysis. Annals of Thoracic

Medicine 6(3): 154. Available online at www.ncbi.nlm.nih.gov/pmc/articles/pmc3131761

4. Craven, H. (ed.) (2009). Core Curriculum for Medical-

Surgical Nursing, 4th ed. Academy of Medical-Surgical

Nurses, Janetti NJ.

5. Fanta, C.H. (20160. Overview of asthma management. In

B.S. Bochner & R.A. Wood (Eds.) UpToDate. Retrieved

12/30/2017, from http://www.uptodate.com/home.

6. Godfrey, A.M. (2014). Idiopathic Pulmonary Fibrosis.

Medscape. Retrieved June 2014 from

http://emedicine.medscape.com/article/301226-

overview#showall

7. Kabrel, C. & Thompson, B. (2017). Clinical presentation,

evaluation, and diagnosis of the nonpregnant adult with

suspected acute pulmonary embolusm. In J. Mandel & R.

Hockberger (Eds.) UpToDate. Retrieved 12/30/17, from

http://www.uptodate.com/home.

8. Phipps WJ, Sands JK, Marek JF, eds. (1999). Medical-

Surgical Nursing: Concepts & Clinical Practice, 6th ed. St.

Louis: Mosby, Inc.

9. Seidel HM, Ball JW, Dains JE et al, eds.(2010) Mosby's

Guide to Physical Examination, 7th ed. St. Louis: Mosby,

Inc.

10. Siegel, M. (2016). Acute respiratory distress syndrome

epidemiology, pathophysiology, pathology, and etiology in

adults. In D. Parsons (Ed.) UptoDate. Retrieved 12/30/17

from http://www.uptodate.com/home.

11. Hinkle, J. and Cheever, K. (2014). Brunner & Suddarth's

Textbook of Medical-Surgical Nursing, 13th ed.

Philadelphia: Lippincott William and Wilkins.

12. Wiegand, D.J.L. & Carlson, K.K. (eds.) (2011). AACN

Procedure Manual for Critical Care. 6th ed. Philadelphia:

Elsevier.

Directions for Submitting Your Post Test

for Contact Hours

1. Go to the TCHP website Home Study page to

get the electronic post-test:

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Your certificate of completion will be sent to you

in a week or 2 (Note: This process is not

automatic so do not expect an immediate return

of a certificate of completion).

Please Note: Survey Monkey does not save

your work so plan to do the post-test all the

way through.

If you are having difficulty with Survey Monkey,

please contact [email protected] for help.

http://www.ncbi.nlm.nih.gov/pmc/articles/pmc3131761

http://www.uptodate.com/home

http://emedicine.medscape.com/article/301226-overview#showall

http://emedicine.medscape.com/article/301226-overview#showall





http://tchpeducation.com/homestudies/homestudies.html

mailto:[email protected]



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TCHP is not responsible for lost or misdirected

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TCHP Consortium Hospital Employees

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hospital (consult www.tchpeducation.com if you

are unsure), your certificate of completion will be

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