CCRNPart1

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“Never let what you cannot do

interfere with what you can do”

- John Wooden -

CCRN REVIEW PART 1

Sherry L. Knowles, RN, CCRN, CRNI

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TOPICS Acute Coronary Syndromes

Acute Myocardial Infarction

Heart Blocks

Heart Failure

Cardiac Alterations

Aortic Aneurysms

Cardiomyopathy Shock States

Peripheral Vascular Disease

Hemodynamics

ARDS

Chronic Lung Disease

Drowning

Pneumonia

Pneumothorax

Pulmonary Embolism

Respiratory Failure Gastrointestinal Alterations

GI Bleeding

Pancreatitis

CCRN REVIEW PART 1

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OBJECTIVES1. Understand the different types of acute coronary syndromes.

2. Identify basic coronary circulation and how it relates to different types ofmyocardial infarctions.

3. Anticipate potential complications associated with an AMI.4. Identify the standard treatment of an AMI.

5. Distinguish between various AV blocks.

6. Recognize the signs & symptoms of heart failure.

7. Identify the treatment of heart failure.

8. Recognize the general definition and classifications of aortic aneurysms.

9. Understand the different types of aortic dissections.

10. Recognize the signs & symptoms of cardiomyopathy.

11. Differentiate between the different types of cardiomyopathy.

12. Identify the treatment for the different types of cardiomyopathy.

13. Understand the different stages of shock.

14. Differentiate between different types of shock.

CCRN REVIEW PART 1

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OBJECTIVES15. Distinguish between arterial and venous peripheral vascular disease.

16. Identify the various treatments for peripheral vascular disease.

17. Define respiratory failure.

18. Identify the various treatments for acute respiratory failure.

19. Recognize the signs & symptoms and causes of various respiratoryalterations.

20. Identify the standard treatment for various respiratory alterations.

21. Identify the components of cardiac output and stroke volume.

22. Recognize the pulmonary artery catheter waveforms.

23. Recognize the basic treatments used for commonly seen hemodynamicprofiles.

24. Explain the common causes of gastrointestinal bleeding.

25. Describe the most commonly seen treatments for GI bleeding.

26. Describe the signs & symptoms of acute pancreatitis and availabletreatments.

CCRN REVIEW PART 1

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Acute Coronary

Syndromes

Acute MI

Aortic Aneurysms

Cardiac Alterations

Cardiovascular Conditions

Cardiomyopathy

Heart Blocks

Heart Failure

Shock States

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DEFINITIONS

– Term used to cover a group of symptomscompatible with acute myocardial ischemia

– Acute myocardial ischemia is insufficient blood

supply to the heart muscle usually resulting from

coronary artery disease

Acute Coronary Syndrome

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DEFINITION

– Infarction occurs due to mechanical obstructionof a coronary artery (or branch) caused by a

thrombus, plaque rupture, coronary spasm

and/or dissection.

– STEMI vs. NSTEMI (non-STEMI)


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SIGNS & SYMPTOMS

– Complains Vary

May include crushing chest pain (which may or may

not radiate), back, neck, jaw, teeth and/or epigastric

pain, SOB, nausea/vomiting and dizziness

– ST elevations on ECG – Elevated cardiac enzymes


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SIGNS & SYMPTOMS

– PAWP, CO, SVR, dysrhythmias, S4,

cardiac failure, cardiogenic shock

– Diaphoresis, pallor, referred pains

– Diabetics and women often present abnormalsymptoms


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Coronary Circulation

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I AVR V1 V4

II AVL V2 V5

III AVF V3 V6

II

V

12 Lead ECG

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ST ELEVATIONS

– Anterior Wall MI

Leads V1-V4

Reciprocal changes in leads II, III, and aVF

Area supplied by the LAD

– Inferior Wall MI Leads II, III and aVF

Reciprocal changes in leads I, and aVL

Area usually supplied by the RCA


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ST ELEVATIONS

– Lateral Wall MI

I, aVL, V5 and V6

Area supplied by the Circumflex artery

– Posterior Wall MI

Reflected on the opposite walls

Opposite deflections


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Coronary Arteries

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Anterior Wall MI

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Inferior Wall MI

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COMPLICATIONS

– Dysrhythmias, heart failure, pericarditis,ventricular aneurysms, ventricular thrombus,

VSD, mitral regurgitation, papillary muscle (or

chordae tendineae) rupture, pericardial

effusions, pericarditis


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NURSING INTERVENTIONS – O2

– Bedrest – Serial ECG’s

– Serial cardiac enzymes

– Keep pain free (NTG. MSO4)

– MONA (Morphine, O2, Nitroglycerin, Aspirin), Heparin, beta-blockers, and ace inhibitors. May also

include thrombolytics or Gp2b3a inhibitors

– PCI, PTCA, IABP, CABG


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TREATMENT

– Time Is Heart Muscle

– Prompt ECG

– Goals: Relieve pain, limit the size of the

infarction and to prevent complications(primarily lethal dysrhythmias)


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TREATMENT

– MONA (Morphine, O2, Nitroglycerin, Aspirin),

Heparin, beta-blockers, and ace inhibitors. May

also include thrombolytics or Gp2b3a

inhibitors

– Cardiac Catheterization (with angioplasty,atherectomy and/or stent)

– IABP, CABG, Education


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Balloon Angioplasty

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Vascular Stent Deployment

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Atherectomy

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SPECIFIC TREATMENTS

– Inferior Wall (IWMI)

Fluids (with RV infarct)

Inotropics

Afterload reducing medications

– Anterior Wall (AWMI)

Diuretics

Inotropics

Afterload reducing medications


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Aortic Aneurysms

DEFINITION

– A bulge or ballooning of the aorta

When the walls of the aneurysm include all three

layers of the artery, they are called true aneurysms

When the wall of the aneurysm include only the

outer layer, it is called a pseudo-aneurysm

– May be thoracic or abdominal

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Aortic Aneurysms

CAUSES

Atherosclerosis

Marfan syndrome

Hypertension

Crack cocaine usage

Smoking

Trauma

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Aortic Aneurysms Rupture

An aortic aneurysm, depending on its size, mayrupture, causing life-threatening internal bleeding

The risk of an aneurysm rupturing increases as theaneurysm gets larger

The risk of rupture also depends on the location ofthe aneurysm

Each year, approximately 15,000 Americans die of aruptured aortic aneurysm.

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Aortic Aneurysms

CLASSIFICATIONS

– Classified by shape, location along the aorta,and how they are formed

– May be symmetrical in shape (fusiform) or a

localized weakness of the arterial wall (saccular)

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Aortic Aneurysms

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Aortic Aneurysms

SIGNS & SYMPTOMS

– Often produces no symptoms

– If an aortic aneurysm suddenly ruptures it presents

with extreme abdominal or back pain, a pulsating

mass in the abdomen, and a drastic drop in blood

pressure

– An increase in the size of an aneurysm means an

increased in the risk of rupture

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Aortic Aneurysms

THORACIC SIGNS & SYMPTOMS

– Back, shoulder or neck pain

– Cough, due to pressure placed on the trachea

– Hoarseness

– Strider, dyspnea

– Difficulty swallowing

– Swelling in the neck or arms

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Aortic Dissections

DEFINITION

– Tearing of the inner layer of the aortic wall, whichallows blood to leak into the wall itself and causes

the separation of the inner and outer layers

– Usually associated with severe chest pain

radiating to the back

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Aortic Dissections

A. Dissection

beginning in the

ascending aorta

B. Whenever the

ascending aorta

is not involved

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Aortic Dissections

A. Dissection

beginning in the

ascending aorta

B. Whenever the

ascending aorta

is not involved

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Aortic Dissections

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Aortic Dissections

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Aortic Aneurysms

COMPLICATIONS

Rupture

Peripheral embolization

Infection

Spontaneous occlusion of aorta

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Aortic Aneurysms

TREATMENT

Medical management

– Controlled BP (within specific range)

Surgical repair

> 4.5 cm in Marfan patients or > 5 cm in non-Marfan patients will require surgical

correction or endovascular stent placement

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Cardiomyopathy

DEFINITION

– Diseases of the heart muscle thatcause deterioration of the function of

the myocardium

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Cardiomyopathy

CLASSIFICATIONS – Primary / Idiopathic (intrinsic)

Heart disease of unknown cause, although viralinfection and autoimmunity are suspected causes

– Secondary (extrinsic)

Heart disease as a result of other systemic diseases,

such as autoimmune diseases, CAD, valvular

disease, severe hypertension, or alcohol abuse

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Cardiomyopathy

Hypertropic Cardiomyopathy

Restrictive Cardiomyopathy

Dilated Cardiomyopathy

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Bizarre hypertrophy of the septum

– Previously called IHSS

Idiopathic Hypertropic Subaortic Stenosis

– Known as HOCM

Hypertropic Obstructive Cardiomyopathy

Positive inotropic drugs Should Not Be Used

– Contractility will outflow tract obstruction

Nitroglycerin Should Not Be Used

– Dilation Will Worsen The Problem

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Harley

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TREATMENT – Relax the ventricles

Beta Blockers

Calcium Channel Blockers

– Slow the Heart Rate Increase filling time

– Use Negative Inotropes Optimize diastolic filling

– Do Not use NTG Dilation will worsen the problem

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Rigid Ventricular Wall

– Due to endomyocardial fibrosis

– Obstructs ventricular filling

Least common form

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TREATMENT

– Positive Inotropics

– Diuretics

– Low Sodium Diet

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Grossly dilated ventricles without hypertrophy

– Global left ventricular dysfunction

– Leads to pooling of blood and embolic episodes

– Leads to refractory heart failure

– Leads to papillary muscle dysfunction secondary

to LV dilation

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TREATMENT

– Positive Inotropes

– Afterload Reducers

– Anticoagulants with Atrial Fib

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Cardiomyopathies

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Cardiomyopathy

GENERALIZED TREATMENT – Positive Inotropes

Except with Hypertropic Cardiomyopathy

– Vasodilators Except with Hypertropic Cardiomyopathy

– Reduce Preload & Afterload – Diuretics

– Beta Blockers

– Calcium Channel Blockers

– IABP

– Vasodilators (as indicated) – Fluid Restriction

– Daily weights, prn O2, planned activities,education, and emotional support

– Consider Heart Transplant

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Conduction Defects

STABLE VS UNSTABLE

– Stable Start with medications

– Unstable

Shock (cardioversion or defibrillation)

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Normal Sinus Rhythm

Heart Rate 60 - 100 bpm

Rhythm Regular

P Wave Before each QRS & identical

PR Interval (in seconds) 0.12 to 0.20

QRS (in seconds) < 0.12

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Atrial Fibrillation

AFib

– Multifocal atrial impulses at rate 300-600/min

– Irregular conduction to ventricles

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Atrial Flutter

AFL

– Atrial impulses at rate of 250-350/min

– Regularly blocked impulses at the AV node

– Saw tooth flutter waves

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Wandering Atrial Pacemaker

WAP

– Multiple ectopic foci in the atria

– Three or more p wave morphologies

– Rate < 100

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Supraventricular Tachycardia

SVT

– Supraventricular rhythm at rate 150-250

– P waves cannot be positively identified

Atrial Tach = supraventricular rhythm with p wave morphology

that is noticeably different from the sinus p wave

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Ventricular Tachycardia

VT

– Ventricular rate of 100-250/min

– Wide QRS

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Torsades de Pointes

Polymorphic VT

– VT with alternating ventricular focus

– Often associated with prolonged QT Rate < 100

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Heart Blocks (AV Blocks)

Sinus Rhythm with First Degree AV Block

Sinus Rhythm with Second Degree AV Block, Type 2

Sinus Rhythm with Second Degree AV Block, Type 1

Third Degree AV Block

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DEFINITION

– A condition in which the heart cannot pump

sufficient blood to meet the metabolic needs of

the body

– Pulmonary (LVF) and/or systemic (RVF)

congestion is present.

Heart Failure

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DEFINITION

– Pulmonary Edema

Fluid in the alveolus that impairs gas exchange byaltering the diffusion between alveolus and capillary

Acute left ventricular failure causes cardiogenicpulmonary edema

Non-cardiogenic pulmonary edema is a synonym for Adult Respiratory Distress Syndrome (ARDS)

Heart Failure

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COMPENSATORY MECHANISMS – Sympaththetic nervous system stimulation

Tachycardia Vasoconstriction and increased SVR

– Renin-angiotensin-aldosterone system

activation (RAAS)

Hypo perfusion to the kidneys (renin) Vasoconstriction (angiotensin) Sodium and water retention (kidneys) Ventricular dilation

Heart Failure

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FUNCTIONAL CLASSIFICATIONS

– Class I

– Class II

– Class III

– Class IV

Heart Failure

(without noticeable limitations)

(symptoms upon activity)

(severe symptoms upon activity)

(symptoms at rest)

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COMPLICATIONS

– Hypotension

– Dysrhythmias

– Respiratory Failure

– Progressive Deterioration

– Acute Renal Failure

– Fluid & Electrolyte Imbalances

Heart Failure

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TREATMENT

– Improve Oxygenation

– Decrease Myocardial Oxygen Demand

– Decrease Preload

– Decrease Afterload

– Increase Contractility

– Manage Dysrhythmias

– Educate!

Heart Failure

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Vascular Disease

Aorto/Iliac Disease: Pre & Post PTA/Stent

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SYMPTOMS

PAIN

PAIN RELIEF

EDEMA

PULSES

INTEGUMENTCHANGES

ULCERS

SKIN TEMPERATURE

SEXUAL ISSUES

ARTERIAL

Upon walking

On resting, standing ordependent position of lower limbs

None

Decreased or absent

Hair lossSkin shinyNail thickeningPallor when elevatedRed when dependent

Ulcers located on toes, lateralareas or site of traumaGangrene possible

Cool

ImpotencySexual dysfunction

VENOUS

While standing

Elevation of extremities

Present, edematous

May be difficult to palpate

Brownish pigmentationMay be cyanotic whenextremities are dependent

Ulcers located on ankles,medial or pre-tibial areas

Normal or warm

Not present

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TREATMENTS

– Medical

Are they taking ASA, Coumadin, Ticlid, Plavix,Oral Contraceptives, Hormones?

– Invasive

PTA, atherectomy, stents

– Surgical Grafts

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Bypass Grafts

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TYPES OF SHOCK

– Hypovolemic Shock

– Cardiogenic Shock

– Distributive Shock

– Obstructive Shock

Shock

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Shock

COMPENSATORY MECHANISMS

– Tachycardia

Attempts to deliver more blood to the tissues – Vasoconstriction

Attempts to maintain adequate BP in order to

adequately perfuse the body tissues

– Increased ADH Secretion

ADH makes the body hold onto water in an effort to

maintain volume and thus enough blood pressure to

perfuse the body tissues

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Types of Shock

Hypovolemic Shock – Inadequate perfusion to the tissues due to insufficient

intravascular volume

Cardiogenic Shock – Inadequate perfusion to the tissues due to heart failure

Distributive Shock – Inadequate perfusion to the tissues due to blood flow out of the

intravascular space causing insufficient intravascular volume – Anaphylactic, Septic, and Spinal Shock

Obstructive Shock – Inadequate perfusion to the tissues due to obstruction of blood flow

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Hypovolemic Shock

SIGNS & SYMPTOMS Low BP Tachycardia

Orthostatic Hypotension RestlessnessConfusion Agitation (or listless)

Thirst Pallor

Cool, Clammy Skin Resp. Rate

UOP CO

PAWP CVP

SVR Lactate Levels

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Hypovolemic Shock

TREATMENT

– Volume (IVF, Blood)

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Cardiogenic Shock

SIGNS & SYMPTOMS

Low BP Restlessness

Agitation (or listless) Confusion

Tachycardia Pallor

UOP CO

PAWP (low with RVF) CVP

SVR Lactate Levels

JVD Peripheral Edema

Ventricular Gallop (S3) Dyspnea

Pulmonary Crackles

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TREATMENTBedrest O2

CO Positive Inotropes

Preload & Afterload Diuretics

Vasodilators Positioning

Myocardial Demand IABP

Cardiogenic Shock

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Anaphylactic Shock

SIGNS & SYMPTOMS

Low BP Tachycardia

Restlessness Confusion

Agitation (or listless) ThirstPallor Warm Feeling

Pruritus Hives

Angioedema Bronchoconstriction

Wheezing Laryngeal Edema

Dyspnea Cool, Clammy Skin

UOP CO

PAWP CVP

SVR Lactate Levels

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TREATMENT – Epinephrine

– IVF

– Vasoconstrictors

– Support/Maintain Airway

Anaphylactic Shock

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Obstructive Shock

SIGNS & SYMPTOMS

Low BP Tachycardia

Restlessness ConfusionAgitation (or listless) Pallor

Cool, Clammy Skin CO , UOP

Symptoms related to cause

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Obstructive Shock

CAUSES

Pulmonary Embolus Tamponade

Tension Pneumothorax Aortic Aneurysm

TREATMENT

Treat the Cause

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Cardiogenic Shock is the only shock with PAWP

Early (Hyperdynamic) Shock is the only shock with CO and SVR

Neurogenic Shock is the only shock with Bradycardia

Anaphylactic Shock has the definitive characteristic of wheezing dueto bronchospasm

Parameter Hypovolemic Cardiogenic Neurogenic Anaphylactic Early Septic Late Septic

CVP/RAP

PAWP or Norm

CO

BP

SVR

HR Normal

Shock Profiles

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SIRS Sepsis Severe Septic MODS DeathInfection Sepsis Shock

Sepsis Syndrome

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Sepsis – SIRS’ response with presumed/confirmed infection

Severe Sepsis – Sepsis associated with organ dysfunction, hypoperfusion

(lactic acidosis, oliguria, altered mental status etc.), or

hypotension (SBP < 90 mmHg or ↓ SBP > 40 mmHg)

Septic Shock – Sepsis with perfusion abnormalities and hypotension

despite adequate fluid resuscitation

Sepsis Syndrome

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EARLY STAGE (Hyperdynamic)Normal BP Tachycardia

Confusion Agitation (or listless)

Respiratory Rate Temperature

Normal Color Normal or

UOPNormal PAWP CO SVR

LATE STAGE (Hypodynamic)Low BP Tachycardia

Orthostatic Hypotension Restlessness

Confusion Agitation (or listless)

Thirst Pallor

Cool, Clammy Skin UOP

CO PAWP

CVP SVR

Lactate Levels

Septic Shock

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3. Improve Perfusion

– Prevent organ dysfunction

– Treat temp as needed

2. Treat The Cause – Pan culture, antibiotics

– Seek primary site of infection

– Direct therapy to primary cause

1. Stabilize The Patient

– Fluids (lots of fluids) 150ml/hr or more

– Vasoconstrictors

Treatment for Sepsis

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HEMODYNAMICS

Invasive PA Catheter

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Invasive PA Catheter

CONTRAINDICATIONS

Mechanical Tricuspid or Pulmonary Valve

Right Heart Mass (thrombus and/or tumor)

Tricuspid or Pulmonary Valve Endocarditis

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Stroke Volume

Components Stroke Volume

– Preload: the volume of blood in the ventricles

at end diastole and the stretch placed on themuscle fibers

– Afterload: the resistance the ventricles must

overcome to eject it’s volume of blood

– Contractility: the force with which the heart

muscle contracts (myocardial compliance)

PAC Insertion Sequence

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PAC Insertion Sequence

Phl b i A i

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Phlebostatic Axis

4th ICS Mid-chest, regardless of head elevation

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RAP (CVP)

RVP

PAP

PAWP

SVR

0-8 mmHg

15-30/0-8 mmHg

15-30/6-12 mmHg

8 - 12 mmHg

700-1500 dynes/sec/cm2

Normal Hemodynamic Values

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Normal Hemodynamic Values

Values normalized for body size (BSA)

CI: 2.5 – 4.5 L/min/m2

SVRI: 1970 – 2390 dynes/sec/cm-5/m2

SVI or SI: 35 – 60 mL/beat/m2

EDVI: 60 – 100 mL/m2

Mixed Venous Oxygen Saturation

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Mixed Venous Oxygen Saturation

SvO2

End result of O2 delivery and

consumption

Measured in the pulmonary artery

An average estimate of venous saturation for

the whole body.

Does not reflect separate tissue perfusion oroxygenation

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Measuring PA Pressures

Measure All Hemodynamic Valuesat End-Expiration

– “Patient Peak”

– “Vent Valley”

S t R i ti

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Spontaneous Respirations

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Measure all pressures at end-expiration

At top curve with Spontaneous Respiration

“patient-peak”

Intrathoracic pressure decreases duringspontaneous inspiration

– Negative deflection on waveforms

Intrathoracic pressure increases during spontaneous expiration

– Positive deflection on waveforms


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Measure all pressures at end-expiration

At bottom curve with mechanical ventilator

“Vent-

Valley”

Intrathoracic pressure increases duringpositive pressure ventilations (inspiration)

– Positive deflection on waveforms

Intrathoracic pressure decreases duringpositive pressure expiration

– Negative deflection on waveforms


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a-wave

– Atrial contraction

– Correct location for measurement of PAWP Average the peak & trough of the a-wave

– Begins near the end of QRS or at the QTsegment

Delayed ECG correlation from CVP sincePA catheter is further away from left atrium

PAWP Waveform

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PAWP Waveform

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BREAK!

CCRN REVIEW PART 1

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ARDS

Drowning

Pneumothorax

Respiratory

Failure

Respiratory Alterations

Chronic Lung

Disease

Pneumonia

Pulmonary Embolism

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ARDS

DEFINITIONS

– Severe respiratory failure associated with pulmonary

infiltrates (similar to infant hyaline membrane disease)

– Pulmonary edema in the absence of fluid overload or

depressed LV function (Non-cardiogenic pulmonary edema)

– Originates from a number of insults involving damage to thealveolar-capillary membrane

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Acute Respiratory Distress Syndrome

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ARDS

PATHOPHYSIOLOGY

– Inflammatory mediators are released causing extensive

structural damage

– Increased permeability of pulmonary microvasculature

causes leakage of proteinaceous fluid across the alveolar –

capillary membrane

– Also causes damage to the surfactant-producing type II cells

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ARDS

CXR CHARACTERISTICS

– Normal size heart

– No pleural effusion

– Ground Glass appearance

– Often normal early in the disease but may rapidly

progress to complete whiteout

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ARDS

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ARDS

SIGNS & SYMPTOMS – Symptoms develop 24 to 48 hours of injury

Sudden progressive disorder

Pulmonary edema Severe dyspnea

Hypoxemia REFRACTORY to O2

Decreased lung compliance

Diffuse pulmonary infiltrates

– Symptoms may be minimal compared to CXR – Rales may be heard

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ARDS

Common Risk

Factors Other Risk Factors Sepsis

Massive

Trauma

Shock

Multiple

TransfusionsPneumonia

Aspiration

Infection

Smoke inhalationInhaled toxins

Burns

Near Drowning

DKA

PregnancyEclampsia

Amniotic Fluid Embolus

Drugs

Acute PancreatitisDIC

Head Injury

ICP

Fat Emboli

Blood ProductsHeart/Lung Bypass

Tumor Lysis

Pulmonary Contusion Narcotics

RISK FACTORS

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ARDS

TREATMENT

– Respiratory Support

– PEEP, CPAP

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Chronic Lung Disease

COPD

– Presents with hyper-inflated lung fields

Due to chronic air trapping May be barrel chested

– May lead to cor pulmonale (right-sided heart failure)

Due to chronic high pulmonary pressures

– Often hypercarbic (high pCO2)

Often dependent upon hypoxic drive

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Near Drowning

Salt Water

– Causes body fluids to shift into lungs

Osmosis: From low to high concentration

Results in hemoconcentration & hypovolemia

– Results in acute pulmonary edema

Fresh Water

– Fluids shift into body tissues

Results in hemodilution & hypervolemia

Can result in gross edema

– Damaged alveoli fill with proteinaceous fluid

May lead to pulmonary edema

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Pneumonia

Lung infection (bacterial, viral, or fungal)

– Most commonly caused by Streptococcus

pneumoniae

Symptoms include fever, pleuretic chest

pain, productive cough, and tachypnea

– Often presents bronchial breath sounds over the

lung area

Treatment involves giving the right antibiotic

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P th

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Pneumothorax

T i P th

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Tension Pneumothorax

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P th

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Pneumothorax

SIGNS & SYMPTOMS

– Standard Pneumothorax Sharp "pleuritic" chest pain, worse on breathing

Sudden shortness of breath Dry, hacking cough (may occur due to irritation

of the diaphragm)

May cause mediastinal shift

– Tension pneumothorax Signs of standard pneumothorax with signs of

cardiovascular collapse

Immediately life threatening

May cause mediastinal shift

P th

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Pneumothorax

TREATMENT

Spontaneous pneumothorax

– Depends on symptoms & size of pneumothorax

– Provide respiratory support

– May need chest tube or needle decompression

Some resolve without intervention

Tension pneumothorax

– Requires immediate intervention

– May cause cardiovascular collapse

– May need chest tube or needle decompression

2nd intercostal space

P th

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TREATMENT

– Pleurodesis

Pneumothorax

Chemical or surgical adhesion of the lung

to the chest wall

Used for multiple collapsed lungs or

persistent collapse

Fl il Ch t

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Flail Chest

P l E b li

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Definition

Signs & Symptoms

Pulmonary Embolism

– Arterial embolus that obstructs blood flow to the lung

– Symptoms include sudden dyspnea, cough, chest

pain, hemoptysis and sinus tachycardia

– Blood gas shows low pO2 & low pCO2

– May present positive Homan’s Sign

– May present loud S2

P l E b li

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Diagnostic Tests

– CXR

– VQ Scan

– Spiral CT

– Pulmonary arteriogram/angiogram

– Venous ultrasound of the lower extremities

– ABG with low pO2 & low pCO2

– D-Dimer

Pulmonary Embolism

P l E b li

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Treatment

– Requires immediate intervention

– Provide respiratory support

– Treat pain & comfort – Usually includes intravenous heparin

Heparin reduces risk of secondarythrombus formation while clot is reabsorbed

– May require embolectomy

– May require thrombolysis

– May need umbrella filter

– May need long term anticoagulants

Pulmonary Embolism

R i t F il

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Respiratory Failure

DEFINITIONS

– Failure to maintain adequate gas exchange

– Inadequate blood oxygenation or CO2 removal

– PaO2 < 50 mmHg and/or PaCO2 > 50 mmHg

and/or pH < 7.35 on Room Air

Respirator Fail re

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Respiratory Failure

TYPE I Hypoxemia without hypercapnia

TYPE II Hypoxemia with hypercapnia

Respiratory Failure

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Respiratory Failure

CAUSES

– V/Q Mismatching

– Intrapulmonary Shunting

– Alveolar Hypoventilation

Respiratory Failure

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Respiratory Failure

V/Q MISMATCHING

– COPD

– Interstitial Lung Disease

– Pulmonary Embolism

Respiratory Failure

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Respiratory Failure

PULMONARY SHUNTING

– AV fistulas/malformations

– Alveolar collapse (atelectasis)

– Alveolar consolidation (pneumonia)

– Excessive mucus accumulation

Respiratory Failure

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Respiratory Failure

SIGNS & SYMPTOMS

– Restlessness / Agitation

– Confusion / LOC

– Tachycardia / Dysrhythmias

– Tachypnea / Dyspnea

– Cool, clammy, pale skin

Respiratory Failure

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Respiratory Failure

ARTERIAL BLOOD GASES

– pH 7.30 / pO2 45 / pCO2 80

– pH 7.30 / pO2 55 / pCO2 65

– pH 7.32 / pO2 50 / pCO2 50

– pH 7.55 / pO2 65 / pCO2 22

Respiratory Failure

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Respiratory Failure

TREATMENT

– Ensure Adequate Ventilation

– FiO2 Ineffective with shunting

Prolonged O2 > 40% causes O2 toxicity

Must use caution with CO2 retainers

– Chronic hypercapnia causes CO2 retainers

to use hypoxic drive

– Too much O2 can depress respirations

CCRN REVIEW PART 1

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BREAK!

CCRN REVIEW PART 1

Gastrointestinal Alterations

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GI Bleed

Pancreatitis

Gastrointestinal Alterations

Gastrointestinal Bleeding

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CAUSES

– UGI Bleeding

Includes the esophagus, stomach, duodenum

– Peptic Ulcer Disease (PUD), or Esophageal Varices

– ASA, NSAID’s, Anticoagulants, Alcohol

– H. Pylori

– LGI Bleeding

Includes the jejunum, ileum, colon, rectum

– Colorectal cancer, Polyps, Hemorrhoids, IBD



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Hematemesis – vomiting of blood (or coffee groundmaterial) (indicates bleeding above the duodenum )

Melena – passage of black tarry stools > 50ml (indicates

degradation of blood in the bowel)

Hematochezia – passage of red blood (rectal bleeding)

Occult Bleeding – bleeding that is not apparent to thepatient and results from small amounts of blood

Obscure Bleeding – occult or obvious but source notidentified


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Hematemesis – always UGI source

Melana – indicates blood has been in GI tract

for extended periods – Mostly UGI – Small bowel

– Rt colon (if bleeding relatively slow)

Hematochezia

– Mostly colon

– Massive UGI bleeding (not enough time for degradation)


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TREATMENT – Find the underlying cause

– Fluid volume replacement

– Endoscopy or colonoscopy

– Medical and /or surgical therapy Somatostatin

IV or intra-arterial vasopressin

Sclerotherpay

Angiography with embolization Electrocoagulation

Band ligation

Balloon tamponade (Sengstaken-Blackmore tube)


The Pancreas

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The Pancreas

The Pancreas secretes digestive enzymes,

bicarbonate, water, and some electrolytes into

the duodenum via the pancreatic duct

– Lipase, Amylase, Trypsin

The Pancreas also produces

and secretes insulin

Pancreatitis

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Pancreatitis

DEFINITION

– An autodigestive process resulting

from premature activation ofpancreatic enzymes

Pancreatitis

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Pancreatitis

PATHOSHYSIOLOGY

• Inactive pancreatic enzymes are activated outside

of the duodenum

• The swelling pancreas causes fluids to shift into

the retro peritoneum and bowel

• Fluid shifts can cause severe hypovolemia and

hypotension

• Inflammation cause commotion around pancreas

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Pancreatitis

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Pancreatitis

SIGNS & SYMPTOMS

– Abdominal Pain

– Nausea & Vomiting – Abdominal Distention

– Jaundice

– Malnutrition

– Hematemesis

– Grey Turner’s Sign

– Cullen’s Sign

– Elevated Amylase,

Lipase, LDH, AST, WBC’s

BUN, and Glucose

Pancreatitis

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Pancreatitis

COMPLICATIONS – Hypocalcemia

– Hypotension

– Acute Tubular Necrosis

– DIC

– Obstructive Jaundice

– Erosive Gastritis

– Paralytic Ileus

– Pseudocyst or Abscess – Bowel Infarction

– Internal Bleeding

– Fat Necrosis

– Pleural Effusion (left)

– Pulmonary Infiltrates

– Hypoxemia

– Atelectasis

– ARDS

– Pericardial Effusion

– Mediastinal Abscess

– Hyperglycemia

– Hypertriglyceridemia

– Encephalopathy

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Pancreatitis

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Pancreatitis

FULMINATING PANCREATITIS

• Signs & Symptoms

Tachycardia & low BP (may be the only sign)

Pulmonary & cerebral insufficiency

Acute diabetic ketosis or oliguria

Hemorrhagic pancreatitis may appear

CCRN REVIEW

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THE ENDPART 1

CCRN REVIEW PART 1

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THANK YOU

References

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References

American Heart Association. (2005). Guidelines 2005 for CardiopulmonaryResuscitation and Emergency Cardiovascular Care. Available at:www.americanheart.org.

Bridges EJ.(2006) Pulmonary artery pressure monitoring: when, how, andwhat else to use. AACN Adv Crit Care. 2006;17(3):286 –303.

Chulay, M., Burns S. M. (2006). AACN Essentials of Critical Care Nursing.McGraw-Hill Companies, Inc., Chapter 23.

Finkelmeier, B., Marolda, D. (2004) Aortic Dissection, Journal ofCardiovascular Nursing: 15(4):15 –24.

Hughes E. (2004). Understanding the care of patients with acute pancreatitis.Nurs Standard: (18) pgs 45-54.

Sole, M. L., Klein, D. G. & Moseley, M. (2008). Introduction to Critical CareNursing. 5th ed. Philadelphia, Pa: Saunders.

Thelan, L. A., Urden, L. D., Lough, M. E. (2006). Critical care: Diagnosis andTreatment for repair of abdominal aortic aneurysm. St. Louis, Mo.:Mosby/Elsevier. pg 145-188.

References Continued

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References Continued

Urden, L., Lough, M. E. & Stacy, K. L. (2009). Thelan's Critical Care Nursing:Diagnosis and Management (6th ed). St. Louis, Mo.: Mosby/Elsevier.

Woods, S., Sivarajan Froelicher, E. S., & Motzer, S. U. (2004). Cardiac Nursing.5th ed. Philadelphia, Pa: Lippincott Williams & Wilkins.

Wynne J, Braunwald E. (2004). The Cardiomyopathies in Braunwald's Heart

Disease: A Textbook of Cardiovascular Medicine (7th Edition). Philadelphia:W.B. Saunders, vol. 2, pps. 1659 –1696, 1751 –1803.

Zimmerman & Sole. (2001). Critical Care Nursing (3rd Edition). WB Saunders.,pgs. 41-80, 176-180, 242-266.

Anderson, L. (July 2001). Abdominal Aortic Aneurysm, Journal ofCardiovascular Nursing:15(4):1 –14, July 2001.

Irwin, R. S.; Rippe, J. M. (January 2003). Intensive Care Medicine. LippincottWilliams & Wilkins Philadelphia: pgs 35 548

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