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Diagnostic Examinations
Non-invasive
Electrocardiogram (ECG)
1. Noninvasive ECG a graphic record of the electrical activity of the heart
2. Portable recorder (Holter monitor) provides continuous recording of ECG for up to 24 hrs. Three
electrodes are attached to the patient's chest and connected to a small portable EKG recorder by lead
wires.
Non-invasive: Types of Holter Monitor
1. Continuous recording - the EKG is recorded continuously during the entire testing period.
2. Event monitor, or loop recording - the EKG is recorded only when the patient starts the recording,when symptoms are felt.
Holter Monitor
Non-invasive-Hemodynamic Monitoring
Vital signs HR, BP, and RR
Arterial oxygen saturation
Transthoracic echocardiography
Invasive-Hemodynamic monitoring
Information obtained through hemodynamic monitoring:
Cardiovascular performance (right and left ventricular function)
Changes in hemodynamic status and organ perfusion
Pharmacologic and nonpharmacologic therapy
Prognosis
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Invasive-Hemodynamic monitoring
Indications:
Any deficit or loss of cardiac function: such as AMI, CHF, Cardiomyopathy
All types of shock; cardiogenic, neurogenic, or anaphylactic
Decreased urine output from dehydration, hemorrhage, G.I. bleed, burns, or surgery
Invasive-Hemodynamic Monitoring
Advantages:
Eliminates potential for error due to measurement technique
Assessment is not inhibited in low-flow states
Recommended for all ICU patients with cardiovascular instability
In 50% of shock patients non-invasive methods underestimate BP by > 30 mmHg
Invasive-Hemodynamic Monitoring
Swan Ganz Catheter/ Pulmonary Artery Catheter
Components of Swan-Ganz
Normally has four ports
Proximal port [Blue] used to measure central venous pressure/RAP and port for measurement of
cardiac output
Distal port [Yellow] used to measure pulmonary artery pressure
Balloon port [Red] used to determine pulmonary wedge pressure;1.5 special syringe is connected
Infusion port [White] used for fluid infusion
Components of the Monitoring System
Bedside monitor amplifier is located inside. The amplifier increases the size of signal
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Transducer changes the mechanical energy or pressures of pulse into electrical energy; should be level
with the phlebostatic axis you can estimate this by intersecting lines from the 4th ICS, mid axillary line
Recorder
PCWP
PCWP-Pulmonary Capillary Wedge Pressure
It is important to measure PCWP to diagnose the severity of left ventricular failure and to quantify the
degree of mitral valve stenosis
Above 20 mmHg - PULMONARY EDEMA
By measuring PCWP, the physician can titrate the dose of diuretic drugs and other drugs that are used to
reduce pulmonary venous and capillary pressure, and thereby reduce the pulmonary edema.
PCWP
Complete set -up
Nursing care to patients with Swan Ganz Catheter
1. a sterile dry dressing should be applied to site and changed every 24 hours; inspect site daily and
report signs of infection
2. if catheter is inserted via an extremity, immobilize extremity to prevent catheter dislodgment or
trauma
3.Observe catheter site for leakage.
Nursing care to patients with Swan Ganz Catheter
5. Continuously monitor PA systolic and diastolic pressures and report significant variations
6. Irrigate line before each reading of PCWP
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7. Maintain client in same position for each reading
8. Record PA systolic and diastolic readings at least every hour and PCWP as ordered.
CENTRAL VENOUS PRESSURE
Blood from the systemic veins flows into the right atrium.
The pressure in the right atrium is the CVP.
Purposes:
1. Reveals RA pressure,
2. to determine the venous return and intravascular volume of the right atrium
3. Provides an IV route for drawing blood samples, administering fluids or medication, and possibly
inserting a pacing catheter
CVP
CVP
Normal range is 4-10 cmH20;
elevation indicates hypervolemia,
decreased level indicates hypovolemia
CVP
Cardiac Catheterization
Cardiac Catheterization
Invasive
ABG
Perform Allens test to determine collateral circulation
Disorders
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Alterations in
Cardiovascular
Functions
TOPICS- CARDIAC DYSFUNCTIONS
CAD
Angina
Cardiac Failure
AMI
Incidence
Worldwide:
1 in every 5 deaths are
caused by Heart Attack
worldwide
Philippines:
#1 Killer
12 Million Filipinos are diagnosed with CAD
Every 7 minutes, a Filipino dies of Heart Attack
CORONARY ARTERY DISEASE (CAD)
A. General Information
refers to a variety of pathology that cause narrowing or obstruction of the coronary arteries, resulting in
decreased blood supply to the myocardium
affects the arteries that provide blood, oxygen, & nutrients to the myocardium
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Causes:
Atherosclerosis- fatty/ plaque deposition
Arteriosclerosis- hardening of arterial lumen
Stages of Development
If demand exceed supply = 02 deficit!!!!!!!!
Myocardial Injury
Myocardial Ischemia
when insufficient oxygen is supplied to meet the requirements of the myocardium
transient/reversible state
Myocardial Necrosis
when severe ischemia is prolonged & irreversible damage to tissue will result
Necrosis - tissue death
Normal vessels can dilate 5-6x normal
Stenotic diseased vessels cannot
Risk Factors- Modifiable
Diet- fats, cholesterol
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Exercise
Sedentary lifestyle
Stress
Cigarette Smoking
Diabetes Mellitus
Obesity
Contraceptive Pills
Type A personality: competitiveness, impatience, aggressiveness, time urgency
Uncontrolled Hypertension
Risk Factors- Non-Modifiable
Age- above 40 years old
Gender- male
Race- whites
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Heredity
Clinical Manifestations
CAD Surgical Management
Goal: Restore Blood Supply
1.Percutaneous transluminal coronary angioplasty (PTCA)
-balloon angioplasty flattens plaque against arterial walls
2.Coronary atherectomy - surgical removal of an atheroma (abnormal mass of fat or lipids) in a major
artery
3.Coronary artery stents a rod or threadlike device for supporting tubular structures during surgical
anastomosis (connection between 2 vessels )
PTCA
Candidates for PTCA:
Those with lesions that occlude at least 70% of the lumen of a major coronary artery
Those whose conditions do not respond to medical treatment and who meet criteria for CABG
Coronary Artery Disease
Angina
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chest pain from myocardial ischemia
caused by inadequate myocardial blood and 0xygen supply
s
4Es-Precipitating Factors
EXCESSIVE physical EXERTION
EXPOSURE to cold ENVIRONMENT
EXTREME EMOTIONAL response
EXCESSIVE intake of saturated food (EAT
Angina
Health History
1. Assess drug use amphetamines,
cocaine which cause excessive sympathetic
stimulation & cardiac work
2. Pt may describe S/s other than pain.
Ex-burning, aching, pressure, smothering
or indigestion
Angina
Pain Assessment
What precipitated pain
how do you describe pain
use scale 1-10 to rate
what relieves pain
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How long does pain last, how often does it occur
Do you carry NTG? Last taken, #tabs, relief
any other heart meds do you take
Limit ADLs?
Angina-S/s
Angina
ANGINA PECTORIS-MEDICAL MGMT
Drug therapy: nitrates, beta adrenergic blocking agents, and/or calcium blocking agents, lipid reducing
drugs if cholesterol is elevated
Cardiac Failure
Cardiac Output
CO = Stroke volume X heart rate
=70 ml X 60 beats/min
=4,200 ml/min.
Volume of blood ejected per minute
Each ventricle ejects approximately 70mL of blood/ beat
Averages between 4-8L/min
cardiac output (CO)- the amount of blood pumped in 1 minute.
stroke volume (SV),which is the amount of blood pumped out of the ventricle with each contraction.
Preload-stretching of the cardiac myocytes prior to contraction
Afterload- "load" that the heart must eject blood against
Heart Failure
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inability of the heart to maintain adequate circulation
to meet the metabolic needs of the body due to
impaired pumping ability
Etiology
It can be caused by :
Inappropriate work load (volume or pressure overload)
Restricted filling
Myocyte loss
Conditions that Precipitate and Exacerbate Heart Failure
Types of Heart Failure
Based on left ventricular functioning
Systolic heart failure- an alteration in ventricular contraction
Diastolic heart failure - an alteration in ventricular filling
Types of Heart Failure
Forward failure -diminished cardiac output, an inadequate output of the affected ventricle causes
decreased perfusion to vital organs
Backward failure- damming back of blood in the venous system ,blood backs up behind the left ventricle
causing increased pressure in the atrium
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Types of Heart Failure
Low output failure- not enough CO is available to meet the demands of the body
High output failure -occurs when a condition causes the heart to work harder to meet the demands of
the body
Types of Heart Failure
Left sided
Right sided
Biventricular
CLASSIFICATIONS- New York Heart Association (NYHA)Classification of Heart Failure
CONGESTIVE HEART FAILURE -
Diagnostic tests: RVF
- chest x-ray: reveals cardiac hypertrophy
-echocardiography: indicates size of
cardiac chambers
CVP, ALT(SGPT), PO2
Diagnostic tests: LVF
ECG, chest x-ray (cardiomegaly, pleural
effusion), echocardiography, cardiac catheterization, dec. PO2, inc. PCO2
- B-type natriuretic peptide
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CONGESTIVE HEART FAILURE
Medical Management:
1. determination and elimination/control of underlying cause
2. Drug therapy:
- Diuretics: Furosemide, Spironolactone
- Dilators: ACE inhibitors, nitrates
- Digitalis: digoxin
3. Diet: low salt, low cholesterol
If medical therapies unsuccessful, mechanical assist devices (intra-aortic balloon pump), cardiac
transplantation or mechanical hearts may be employed.
Diuretic Therapy
The most effective symptomatic relief
Mild symptoms
Block Na reabsorbtion in loop of henle and distal convoluted tubules
Thiazides are ineffective with GFR < 30 --/min
Side Effects
Pre-renal azotemia
Skin rashes
Neutropenia
Thrombocytopenia
Hyperglycemia
Uric Acid
Hepatic dysfunction
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Diuretics (cont.)
More severe heart failure loop diuretics
Lasix (20 320 mg QD), Furosemide
Bumex (Bumetanide 1-8mg)
Torsemide (20-200mg)
Mechanism of action: Inhibit chloride reabsortion in ascending limb of loop of Henle results in
natriuresis, kaliuresis and metabolic alkalosis
Adverse reaction:
pre-renal azotemia
Hypokalemia
Skin rash
ototoxicity
K+ Sparing Agents
Triamterene & amilorideacts on distal tubules to K secretion
Spironolactone (Aldosterone inhibitor)
recent evidence suggests that it may improve survival in CHF patients due to the effect on renin-
angiotensin-aldosterone system with subsequent effect on myocardial remodeling and fibrosis
Inhibitors of renin-angiotensin- aldosterone system
Renin-angiotensin-aldosterone system is activation early in the course of heart failure and plays an
important role in the progression of the syndrome
Angiotensin converting enzyme inhibitors
Angiotensin receptors blockers
Spironolactone
Angiotensin Converting Enzyme Inhibitors
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They block the R-A-A system by inhibiting the conversion of angiotensin I to angiotensin II
vasodilation and Na retention
Ace Inhibitors were found to improve survival in CHF patients
Delay onset & progression of HF in pts with asymptomatic LV dysfunction
cardiac remodeling
Side effects of ACE inhibitors
Angioedema
Hypotension
Renal insuffiency
Rash
cough
Angiotensin II receptor blockers
Has comparable effect to ACE I
Can be used in certain conditions when ACE I are contraindicated (angioneurotic edema, cough)
Digitalis
Mechanism of Action
+ve inotropic effect by intracellular Ca & enhancing actin-myosin cross bride formation (binds to the
Na-K ATPase inhibits Na pump intracellular Na Na-Ca exchange
Vagotonic effect
Arrhythmogenic effect
Effects of Cardiac Glycosides
Increased force of myocardial contraction
(+ INOTROPIC EFFECT)
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Increased renal perfusion
(DIURETIC EFFECT)
Slowed heart rate
(- CHRONOTROPIC EFFECT)
Decreased conduction velocity through the AV node
( -DROMOTROPIC EFFECT).
Nursing Responsibilities
Recognize signs and symptoms of digoxin toxicity
Cardiac
Sinoatrial arrest or block
Third-degree AV block (complete)
Ventricular arrhythmias
Bradycardia
Gastrointestinal
Abdominal pain
Anorexia
Diarrhea
Nausea
Vomiting
Nursing Responsibilities
Recognize signs and symptoms of digoxin toxicity
Neurologic
Blue-yellow color blindness
Blurred vision
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Colored dots in vision
Confusion
Depression
Disorientation
Flickering lights
Headache
Insomnia
White halos on dark objects
Nursing Management-CHF
Nursing Management
6. Monitor heart rate and presence of dysrhythmias by cardiac monitor.
7. Insert foley catheter as prescribed and monitor urine output.
8. MIO
9. Avoid unnecessary IV administration of fluids.
10. Monitor weight to determine response to treatment.
Nursing Management
Nursing Management
Check for Medical Emergency: Acute Pulmonary Edema: frothy sputum, impending doom, panic,
orthopnea, cough w/pink-tinged sputum
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TX: add morphine to relieve anxiety, slow respiratory rate, and decrease peripheral vascular resistance
plus cardiac glycoside (Digoxin), and loop diuretic(Lasix), bronchodilators, and oxygen for hypoxia
Nursing Management
Monitor Intake and output
Maintain bed rest for the first 24-36 hours
Assess respiratory rate and characteristics. This may indicate heart failure.
Provide reassurance to the family and client.
CARDIAC SURGERIES
CORONARY ARTERY BYPASS SURGERY
A. General information:
A coronary artery bypass
graft is the surgery of choice
for clients with severe CAD
New supply of blood brought
to diseased/occluded
coronary artery by bypassing
the obstruction with a graft
that is attached to the aorta
proximally and to the
coronary artery distally.
Coronary Artery Bypass Grafting (CABG)
Candidates for CABG
Angina cannot be controlled by medical Rx
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Unstable angina
A positive exercise tolerance test & lesions or blockage that cannot be treated by PTCA
A left main coronary artery lesion or blockage of more than 70%
Individuals who have complications from unsuccessful PTCAs
CORONARY ARTERY BYPASS SURGERY
B. Nursing interventions: preoperative
1. Explain anatomy of the heart, function of coronary arteries, effects of CAD
2. Explain events of the day of surgery
3. Orient to the critical and coronary care units and introduce to staff
4. Explain equipments to be used (monitors, hemodynamic procedures, ventilators, ET, etc)
5. Demonstrate activity and exercise
6. Reassure availability of pain medications
CORONARY ARTERY BYPASS SURGERY
C. Nursing interventions: post-operative
1. Maintain patent airway
2. Promote lung re-expansion-deep breathing & coughing, incentive spirometer
3. monitor cardiac status
4. maintain fluid and electrolyte balance/monitor drainage in chest tubes (report if 100-
150cc/hr)
5. maintain adequate cerebral circulation
6. provide pain relief-splinting,meds
7. prevent abdominal distension
CORONARY ARTERY BYPASS SURGERY
8. Monitor for and prevent the ff. complications:
a. Thrombophlebitis / pulmonary embolism
b. Cardiac tamponade
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c. arrhythmias
d. CHF
9. Provide client teaching and discharge planning concerning:
a. limitation with progressive increase in activities
CORONARY ARTERY BYPASS SURGERY
b. sexual intercourse can usually be resumed by 3rd or 4th week post-op
c. medical regimen
d. meal planning with prescribed modifications
e. wound cleansing daily and report for any signs of infection
f. Symptoms to be reported:
- fever, dyspnea, chest pain with minimal exertion
ALTERATION IN RESPIRATORY FUNCTION
VENTILATION & PERFUSION RATIO (V/Q)
PULMONARY/RESPIRATORY FAILURE
inability of the lung to meet the metabolic demands of the body. This can be from failure of tissue
oxygenation and/or failure of CO2 homeostasis.
Classification
Respiratory Failure
Symptoms
CNS:
Headache
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Visual Disturbances
Anxiety
Confusion
Memory Loss
Weakness
Decreased Functional Performance
Respiratory Failure
Symptoms
Pulmonary:
Cough
Chest pains
Sputum production
Stridor
Dyspnea
Respiratory Failure
Symptoms
Cardiac:
Orthopnea
Peripheral edema
Chest pain
Other:
Fever, Abdominal pain, Anemia, Bleeding
Clinical
Respiratory compensation
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Sympathetic stimulation
Tissue hypoxia
Hemoglobin desaturation
Clinical
Respiratory compensation
Tachypnoea RR > 35 Breath /min
Accessory muscles
Recesssion
Nasal flaring
Sympathetic stimulation
Tissue hypoxia
Haemoglobin desaturation
Clinical
Respiratory compensation
Sympathetic stimulation
sweating
Tissue hypoxia
Haemoglobin desaturation
Clinical
Respiratory compensation
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Sympathetic stimulation
Tissue hypoxia
Altered mental state
(late)
Haemoglobin desaturation
Clinical
Altered mental state
PaO2 +PaCO2 acidosis dilatation of cerebral resistance vesseles ICP
Disorientation
Headache
coma
asterixis
personality changes
Clinical
Respiratory compensation
Sympathetic stimulation
Tissue hypoxia
Hemoglobin desaturation
cyanosis
Respiratory Failure
Laboratory Testing
Other tests
Hemoglobin
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Electrolytes, blood urea nitrogen, creatinine
Creatinine phosphokinase, aldolase
EKG, echocardiogram
Electromyography (EMG)
Nerve conduction study
Respiratory Failure
Laboratory Testing
Arterial blood gas
PaO2
PaCO2
PH
Chest imaging
Chest x-ray
CT sacn
Ultrasound
Ventilationperfusion scan
Respiratory failure:
Interventions
Supportive therapy
Specific therapy
Supportive therapy
Secure the airway
Pulse oximetry
Oxygen: by mask, nasal cannula, head box
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Proper positioning
Nebulization if indicated
Blood sampling: Routine, electrolytes, ABG
Secure IV line
CXR: upright AP & lateral views
Hypoxemic / Non - Hypercapnic respiratory failure
The major problem is PaO2.
If due to low V/Q mismatch; oxygen therapy.
If due to pulmonary intra-parenchymal shunts (ARDS), assisted ventilation with PEEP may be needed.
If due to intracardiac R-L shunt: O2 therapy is of limited benefit. Surgical t/t is needed.
Hypercapnic Respiratory failure
Key decision is whether mechanical ventilation is required or not.
In Acute respiratory acidosis: Mechanical ventilation must be strongly considered.
Chronic Resp acidosis: patient should be followed closely, mech ventilation is rarely required.
In acute-on-chronic respiratory failure, the trend of acidosis over time is a crucial factor.
Mechanical Ventilation: Indications
PaO2< 55 mm Hg or PaCO2 > 60 mm Hg despite 100% oxygen therapy.
Deteriorating respiratory status despite oxygen and Nebulization therapy
Anxious, sweaty lethargic child with deteriorating mental status.
Respiratory fatigue: for relief of metabolic stress of the work of breathing
Nursing Management
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Note changes suggesting increased work of breathing (tachypnea, diaphoresis, intercostal muscle
retraction, fatigue) or pulmonary edema (fine, coarse crackles or rales, frothy pink sputum).
Assess breath sounds.
Diminished or absent sounds indicate inability to ventilate the lungs sufficiently to prevent
Analyze ABG and compare with previous values
Determine hemodynamic status (blood pressure, pulmonary wedge pressure, cardiac output)
Nursing Management
Administer oxygen to maintain Pao2 of 60 mm Hg or Sao2 > 90% using devices that provide increased
oxygen concentrations (aerosol mask, partial rebreathing mask, nonrebreathing mask).
MIO
Provide measures to prevent atelectasis and promote chest expansion and secretion clearance, as
ordered (incentive spirometer, nebulization, head of bed elevated 30 degrees, turn frequently, out of
bed).
Perform chest physiotherapy to remove mucus. Teach slow, pursed-lip breathing to reduce airway
obstruction.
ARDS
clinical syndrome also called noncardiogenic pulmonary edema in which there is severe hypoxemia and
decreased compliance of the lungs, which leads to both oxygenation and ventilatory failure
Fulminant form of respiratory failure characterized by acute lung inflammationand diffuse
alveolocapillary injury
Sudden and life-threatening deterioration of the gas-exchange function of the lungs
S/S
Develop progressively as follows:
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Hyperventilation
Respiratory alkalosis
Dyspnea & Hypoxemia
Metabolic acidosis
Respiratory acidosis
Further hypoxemia
Hypotension, decreased cardiac output ,death
Diagnostic Evaluation
The hallmark sign for ARDS is a shunt; hypoxemia remains despite increasing oxygen therapy.
Decreased lung compliance; increasing pressure required to ventilate patient on mechanical ventilation.
Chest X-ray exhibits bilateral infiltrates.
Pulmonary artery catheter readings: pulmonary artery wedge pressure >18 mm Hg.
Histopathologic Changes
Diffuse alveolar damage is the descriptive term for the histopathologic findings encountered in acute
lung injury.
MEDICAL MANAGEMENT
Primary Focus in the management of ARDS includes:
Identification and treatment of the underlying condition.
Aggressive, supportive care must be provided to compensate for severe respiratory dysfunction
SUPPORTIVE THERAPY
Intubation
Mechanical ventilation
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Circulatory support
Adequate fluid volume
Nutritional support
Monitor ABGs, Pulse Oximetry, bedside Pulmonary Function Test
Positive End-Expiratory Pressure (PEEP) is a critical part of the treatment of ARDS.
Uses of PEEP-
PHARMACOLOGIC THERAPY (Under Investigation
Human Recombinant Interleukin-1 receptor antagonists
Neutrophil Inhibitors
Pulmonary-specific vasodilators
Surfactant Replacement Therapy
Antisepsis Agents
Antioxidant Therapy
Corticosteroids (late in the course of ARDS)
NUTRITIONAL THERAPY
Patients with ARDS require 35-45 Kcal/kg per day to meet caloric requirements.
Enteral Feeding is the first consideration; however TPN also may be required.
NURSING MANAGEMENT
General Measures
Close monitoring and frequent assessment
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Positioning is important to improve ventilation and perfusion in the lungs and enhance secretion
drainage.
Restrict fluid intake
Provide rest
Reassurance especially with neuromuscular blocking agents
Prepare for intubation and mechanical ventilation using PEEP
Definition Acute Renal failure (ARF)
Inability of kidney to maintain homeostasis leading to a buildup of nitrogenous wastes
Different to renal insufficiency where kidney function is deranged but can still support life
ARF
Occurs over hours/days
Lab definition
Increase in baseline creatinine of more than 50%
Decrease in creatinine clearance of more than 50%
Deterioration in renal function requiring dialysis
ARF
Pre renal (functional)
Renal-intrinsic (structural)
Post renal (obstruction)
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ACUTE RENAL FAILURE
Stages of ARF
OLIGURIC PHASE
urine output = < 400cc/day
Usually lasts 1-2 weeks
BUN, Creatinine, hyponatremia
DIURETIC PHASE
Gradual return to glomerular filtration
Excretion of fluid: 1-2 liters/ day- 4-5L
Usually lasts 2-3 weeks
BUN, Creatinine
RECOVERY PHASE
Returns to prerenal failure activity level
3-12 months
ACUTE RENAL FAILURE
Assessment
Urine output
Ultrasound
Azotemia (increased BUN and crea)
Hyperkalemia
Metabolic Acidosis
Anemia
Prevention
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Drugs taken by client
Nephrotoxic drugs
NSAIDs
ACUTE RENAL FAILURE
Medical Management
Fluid maintenance
Avoiding fluid excess
Dialysis
Pharmacologic treatment
Kayexalate (sodium polystyrene sulfonate)
Retention enema
Reduction of drug doses
Nutrition: protein- 1g/kg of weight; potassium restriction
ACUTE RENAL FAILURE
Maintaning fluid and electrolyte balance
High calorie, low protein diet
Reducing metabolic rate
Promoting pulmonary function
Infection prevention
Skin care
Emotional support
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Monro-Kellie Hypothesis
because of the limited space for expansion within the skull, an increase in any one of the components
causes a change in the volume of the others. (B&S, p. 2169)
What does this mean?
Decreased Cerebral Blood Flow
What happens to brain cells as blood flow decreases?
Early compensatory mechanism:
Vasomotor stimulation
What assessment findings indicate this?
Changes in concentration of CO2
causes cerebral vasodilation
causes vasoconstriction
Decreased cerebral outflow
Cerebral Perfusion Pressure
What is cerebral perfusion?
Steady cerebral perfusion can be maintained if arterial systolic pressure is 50 150 mm Hg and ICP is
below 40 mm Hg.
CPP = MAP ICP
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Normal CPP is 70 100 mm Hg
Increased ICP
Pathophysiology:
Acute neurologic condition alters the equilibrium of components within the cranial vault
Causes
Primary
Secondary
Regardless of cause, ICP decreases cerebral perfusion, stimulates further swelling, and may cause
herniation
Background Information
The brain is contained within and protected by the rigid cranial vault
The cranial vault also contains blood and CSF
These components are usually in a state of equilibrium and produce the ICP
Usually measured in the lateral ventricles
Normal pressure 10 to 20 mm Hg
Increased ICP and Cushings Response
Increased ICP: Clinical Manifestations
Early Indicators:
Subtle changes in LOC
Pupillary changes
Weakness of one extremity or one side
Constant headache increasing in intensity and aggravated by movement or straining
Late Indicators:
Continuing decrease in LOC progressing to coma
Bradypnea, bradycardia, hypertension and fever
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Altered respiratory pattern
Projectile vomiting
Hemiplegia, decorticate or decerebrate posturing
Loss of brain stem reflexes
Diagnostic Tests
CT
MRI
PET
SPECT
Transcranial Doppler
Electrophysiologic monitoring
Evoked potential monitoring
Contraindicated Diagnostic Test
Which diagnostic test is contraindicated in a patient with increased intracranial pressure?
Why?
Complications
Brain stem herniation
Diabetes insipidus
Syndrome of Inappropriate ADH (SIDAH)
What is the cause of these complications?
How will they be treated?
Medical Management
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Increased ICP is a true medical emergency
Treatment must be promptly initiated
Invasive monitoring of ICP
Manipulating one or more cranial vault component
Decrease cerebral edema
Maintain cerebral perfusion
Reduce CSF and intracranial blood volume
Controlling fever
Maintaining oxygenation
Reducing metabolic demands
Nursing Care
Maintaining a patent airway
Achieving an adequate breathing pattern
Optimizing cerebral tissue perfusion
Maintaining negative fluid balance
Preventing infection
Monitoring and managing potential complications
cEREBROvaSCULAR ACCIDENT
refers to a functional abnormality of the CNS that occurs when the normal blood supply to the brain is
disrupted
types
Ischemic stroke-little blood flow
Thrombotic
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Embolic
Hemorrhagic stroke-disrupted blood flow
Intracerebral
Subdural
types
Ischemic stroke-little blood flow
1. Thrombotic formation of a blood clot with coagulation the results in the narrowing of the lumen of a
blood vessel with eventual occlusion
2. Embolicocclusion of a cerebral artery by an embolus, resulting in necrosis and edema of the area
supplied by the involved vessel
types
Hemorrhagic stroke-disrupted blood flow
1. Intracerebral hemorrhage stroke-bleeding within the brain caused by a rupture of vessels
2. Subarachnoid hemorrhagic stroke-cause by aneurysm or AV malformation
cEREBROvaSCULAR ACCIDENT
Pathophysiology and Etiology
Cerebrovascular insufficiency is caused by atherosclerotic plaque or thrombosis, increased PCO2,
decreased PO2, decreased blood viscosity, hyperthermia/hypothermia, increased ICP.
Carotid arteries, vertebral arteries, major intracranial vessels, or microcirculation may be affected.
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Cardiac causes of emboli include atrial fibrillation, mitral valve prolapse, infectious endocarditis, and
prosthetic heart valve.
Development of CVA
1.Transient Ischemic attack-brief episodes of
neurologic manifestations which clear completely in
less than 24 hours
2. Reversible ischemic neurologic deficit-neurologic
deficits remain after 24 hours but leaves no residual
signs and symptoms after days to weeks
3. Stroke in-evolution-progressing stroke which
develops over a period of hours or days;
manifestations dont resolve and leave residual
neurologic effects
4. Completed stroke- when neurologic deficits remain
unchanged over 2-3 day period
Risk Factors
Prior ischemic episodes
Cardiac disease
DM
Atherosclerotic diseasae
Hypertension, hypercholesterolemia
Polycythemia
Smoking
Oral contraceptives
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Emotional stress
Obesity
Family history of stroke
Age
Assessment and diagnostic findings
Physical and neurologic exams (focus on airway patency and cough and gag reflex)
TIA (transient ischemic attack)
CT scan
ECG
Carotid ultra sound
Transesophageal echocardiography to rule out emboli from heart.
Tia s/s
History of intermittent neurologic deficit, sudden in onset, with maximal deficit within 5 minutes and
lasting less than 24 hours.
Carotid bruit
History of headaches of duration of days before ischemia.
Tia s/s
Carotid system involvement:
amaurosis fugax,
homonymous hemianopsia,
unilateral weakness, unilateral numbness or paresthesias,
aphasia
dysarthria.
Tia s/s
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Vertebrobasilar system involvement: vertigo, homonymous hemianopsia, diplopia, weakness that is
bilateral or alternates sides, dysarthria, dysphagia, ataxia, perioral numbness
Warning signs that may precede CVA
Paresthesia
Transient loss of speech
Hemiplegia
Severe occipital or nuchal headaches
Vertigo or syncope
Motor or sensory disturbances (tingling transient paralysis)
Epistaxis
Cva S/S
Cva S/S
Cva S/S
Treatment for Ischemic Stroke
tPA=Thrombolytic agent
Document time of symptom onset. (If awoke with symptoms, must go by time when last seen normal)
Immediate head CT (check for blood)
Evaluate for tPA administration (review exclusion/inclusion criteria)
Treatment for Ischemic Stroke
If not a tPA candidate, ASA in ED. Rectal ASA if fails swallow eval. or if swallow eval. not complete.
Keep NPO, until a formal swallow eval. is done.
Admit as Inpatient and perform diagnostic testing: Carotid US, Echo, TEE, ECG monitoring for a-fib, MRI,
fasting Lipid, Clotting disorder blood work (Antiphospholipid, Factor V, Antithrombin III)
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Rehabilitation
Treatment for Ischemic Stroke
Surgery carotid endarterectomy (removal of an atherosclerotic plaque or thrombus from the carotid
artery if with TIA symptoms)
tPA Administration Considerations
Must be started before 3 hours from onset
No blood on head CT
Review patients history for other risk factors
Accurate weight recorded
Foley catheter prior to tPA
tPA Cont
Consent explained and signed
(BP>185/110) treat with labetolol 10-20mg IV over 1-2 min. May repeat x1 or nitro paste 1-2 inches. If
treatment does not lower BP, do not give tPA
shows significant deficits to merit treatment.
tPA Contraindications
Any recent surgery185/110)
Seizure at the onset of stroke
Active internal bleeding (
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Use of anticoagulants with PT>15 or INR >1.7
Platelet count
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Improve Mobility and prevent joint deformities
Correctly position patient to prevent contractures
Place pillow under axilla
Hand is placed in slight supination- C
Change position every 2 hours
CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
NURSING INTERVENTIONS
2. Enhance self-care
Carry out activities on the unaffected side
Prevent unilateral neglect
Keep environment organized
Use large mirror
CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
NURSING INTERVENTIONS
3. Manage sensory-perceptual difficulties
Approach patient on the Unaffected side
Encourage to turn the head to the affected side to compensate for visual loss
CEREBROVASCULAR ACCIDENTS: Ischemic Stroke
NURSING INTERVENTIONS
4. Manage dysphagia
Place food on the UNAFFECTED side
Provide smaller bolus of food
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Manage tube feedings if prescribed
5. Help patient attain bowel and bladder control
Intermittent catheterization is done in the acute stage
Offer bedpan on a regular schedule
High fiber diet and prescribed fluid intake
CVA: Hemorrhagic Stroke
Normal brain metabolism is impaired by interruption of blood supply, compression and increased ICP
Usually due to rupture of intracranial aneurysm, AV malformation, Subarachnoid hemorrhage
CVA: Hemorrhagic Stroke
Normal brain metabolism is impaired by interruption of blood supply, compression and increased ICP
Usually due to rupture of intracranial aneurysm, AV malformation, Subarachnoid hemorrhage
CVA: Hemorrhagic Stroke
Sudden and severe headache
Same neurologic deficits as ischemic stroke
Loss of consciousness
Meningeal irritation
Visual disturbances
General manifestations
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Hemorrhagic Stroke Treatment
Do not give antithrombotics or anticoagulants
Monitor and treat blood pressure greater than 150/100
NPO, until swallow eval is completed
Anticipate Neurosurgical consult
Possible administration of blood products
CVA: Hemorrhagic Stroke
NURSING INTERVENTIONS
1. Optimize cerebral tissue perfusion
2. relieve Sensory deprivation and anxiety
3. Monitor and manage potential complications
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Increased Intracranial pressure
Intracranial pressure more than 15 mmHg
Brunner= Normal intracranial pressure 10-20 mmHg
Causes:
Head injury
Stroke
Inflammatory lesions
Brain tumor
Surgical complications
Increased Intracranial pressure
Pathophysiology
The cranium only contains the brain substance, the CSF and the blood/blood vessels
MONRO-KELLIE hypothesis- an increase in any one of the components causes a change in the volume of
the other
Any increase or alteration in these structures will cause increased ICP
Increased Intracranial pressure
Pathophysiology
Compensatory mechanisms:
1. Increased CSF absorption
2. Blood shunting
3. Decreased CSF production
Increased Intracranial pressure
Pathophysiology
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Decompensatory mechanisms:
1. Decreased cerebral perfusion
2. Decreased PO2 leading to brain hypoxia
3. Cerebral edema
4. Brain herniation
S/s Cushings triad
HPN
Bradycardia
Widening of pulse pressure
Decreased cerebral blood flow
Cerebral Edema
Abnormal accumulation of fluid in the intracellular space, extracellular space or both.
Herniation
Results from an excessive increase in ICP when the pressure builds up and the brain tissue presses down
on the brain stem
Cerebral response to increased ICP
Steady perfusion up to 40 mmHg
Cushings response
Vasomotor center triggers rise in BP to increase ICP
Sympathetic response is increased BP but the heart rate is SLOW
Respiration becomes SLOW
Increased Intracranial pressure
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CLINICAL MANIFESTATIONS
Early manifestations:
Changes in the LOC- usually the earliest
Pupillary changes- fixed, slowed response
Headache
vomiting
Increased Intracranial pressure
CLINICAL MANIFESTATIONS
late manifestations:
Cushing reflex- systolic hypertension, bradycardia and wide pulse pressure
bradypnea
Hyperthermia
Abnormal posturing
Increased Intracranial pressure
Nursing interventions:
Maintain patent airway
1. Elevate the head of the bed 15-30 degrees- to promote venous drainage
2. assists in administering 100% oxygen or controlled hyperventilation- to reduce the CO2 blood
Increased Intracranial pressure
Nursing interventions
3. Administer prescribed medications- usually
Mannitol- to produce negative fluid balance
corticosteroid- to reduce edema
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anticonvulsants-p to prevent seizures
Increased Intracranial pressure
Nursing interventions
4. Reduce environmental stimuli
5. Avoid activities that can increase ICP like valsalva, coughing, shivering, and vigorous suctioning
Increased Intracranial pressure
Nursing interventions
6. Keep head on a neutral position. ACOID- extreme flexion, valsalva
7. monitor for secondary complications
Diabetes insipidus- output of >200 mL/hr
SIADH
Altered level of consciousness
Consciousness
Requires:
1. Arousal: alertness; dependent upon
reticular activating system (RAS); system of
neurons in thalamus and upper brain stem
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2. Cognition: complex process, involving all
mental activities; controlled by cerebral
hemispheres
It is a function and symptom of multiple pathophysiologic phenomena
Causes: head injury, toxicity and metabolic derangement
Disruption in the neuronal transmission results to improper function
Altered level of consciousness
Assessment
Orientation to time, place and person
Motor function
Decerebrate
Decorticate
Sensory function
Altered level of consciousness
Patient is not oriented
Patient does not follow command
Patient needs persistent stimuli to be awake
COMA= clinical state of unconsciousness where patient is NOT aware of self and environment
Altered level of consciousness
Etiologic Factors
Head injury
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Stroke
Drug overdose
Alcoholic intoxication
Diabetic ketoacidosis
Hepatic failure
Altered level of consciousness
ASSESSMENT
Behavioral changes initially
Pupils are slowly reactive
Then , patient becomes unresponsive and pupils become fixed dilated
Glasgow Coma Scale is utilized
Altered level of consciousness
Nursing Intervention
1. Maintain patent airway
Elevate the head of the bed to 30 degrees
Suctioning
2. Protect the patient
Pad side rails
Prevent injury from equipments, restraints and etc.
Altered level of consciousness
Nursing Intervention
3. Maintain fluid and nutritional balance
Input an output monitoring
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IVF therapy
Feeding through NGT
4. Provide mouth care
Cleansing and rinsing of mouth
Petrolatum on the lips
Altered level of consciousness
Nursing Intervention
5. Maintain skin integrity
Regular turning every 2 hours
30 degrees bed elevation
Maintain correct body alignment by using trochanter rolls, foot board
6. Preserve corneal integrity
Use of artificial tears every 2 hours
Altered level of consciousness
Nursing Intervention
7. Achieve thermoregulation
Minimum amount of beddings
Rectal or tympanic temperature
Administer acetaminophen as prescribed
8. Prevent urinary retention
Use of intermittent catheterization
Alteration In Metabolism
DKA
HHNK
TERMS
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Gluconeogenesis
is a metabolic pathway that results in the generation of glucose from non-carbohydrate carbon
substrates such as lactate, glycerol, and glucogenic amino acids.
Glycogenolysis
takes place in the muscle and liver tissues, where glycogen is stored, as a hormonal response to
epinephrine (e.g., adrenergic stimulation) and/or glucagon, a pancreatic peptide triggered by low blood
glucose concentrations, and produced in the alpha cells of the islets of Langerhans.
Lipolysis
is the breakdown of lipids and involves the hydrolysis of triglycerides into free fatty acids followed by
further degradation into acetyl units by beta oxidation. The process produces Ketones, which are found
in large quantities in ketosis, a metabolic state that occurs when the liver converts fat into fatty acids
and ketone bodies, which can be used by the body for energy.
Lipolysis testing strips such as Ketostix are used to recognize ketosis.
Role of Insulin
Required for transport of glucose into
Muscle
Adipose
Liver
Inhibits lipolysis
Absence of insulin
Glucose accumulates in the blood
Liver
Uses amino acids for gluconeogenesis
Converts fatty acids into ketone bodies
Acetone, Acetoacetate, -hydroxybutyrate
Increased counterregulatory hormones
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Diabetes Mellitus
group of metabolic diseases characterized by elevated levels of glucose in the blood (hyperglycemia)
resulting from defects in insulin secretion, insulin action, or both ((American Diabetes Association )
Classification of Diabetes
DM1- IDDM - formerly insulin dependent diabetes mellitus
- near absolute/ absolute deficiency of insulin
- juvenile onset
-if insulin is not given,fats are metabolized ,resulting into ketonemia(acidosis)
DM2- NIDDM formerly non-insulin dependent DM - relative lack of insulin or
resistance to action of insulin
-usually sufficient to stabilize fat and protein metabolism ,but not to deal with carbohydrate metabolism
- adult-onset
Risk Factors
Family History
Diet
Obesity
Sedentary lifestyle
Age
Stress
4 Cardinal Signs
Polyuria
Polydipsia
Polyphagia
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Weight Loss
Diabetic Ketoacidosis
acute, life-threatening hyperglycemic crisis
Develops when severe/ absolute insulin deficiency occurs
Complication of DM 1
main characteristics:
hyperglycemia over 300 mg/dL (300-800)
low bicarbonate level (
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Medical Stress
Counterregulatory hormones
Oppose insulin
Stimulate glucagon release
Hypovolmemia
Increases glucagon and catecholamines
Decreased renal blood flow
Decreases glucagon degradation by the kidney
Diabetic Ketoacidosis
Due to:
Severe insulin deficiency
Excess counterregulatory hormones
Glucagon
Epinephrine
Cortisol
Growth hormone
3 Lines of defense against Acidosis
1st Line: Immediate buffering (converts H ions-CO2& H2O)
Lungs: excrete CO2
Kidneys: excrete acetoacetate in urine
2nd Line: Resp.: acetone & CO2 exhaled
depth & rate Kussmauls
fruity/ acetone breath
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3rd Line: Renal System: excretes 30-100g ketones/day
ammonia mechanism is activated
-excretion of excess hydrogen
Inadequate insulin
Clinical manifestations
Management
Goals:
Correct fluid & electrolyte imbalances-
Restore normal circulating blood volume
Shift from a state of fat catabolism to a state of carbohydrate catabolism by providing insulin
Identify and correct those factors that precipitated ketoacidosis
Management
Correct Fluid and Electrolyte Imbalances:
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Intravenous infusion of Isotonic saline (0.9% or 0.45% NaCl) started immediately
usually 1000 ml/first hour- then 2000-8000ml over the next 24 hours
Dextrose is added (D5NSS or D5 0.45 saline) when blood glucose level reaches 250-300 mg/dl
Clients with compromised cardiac function may require slower intravenous fluid replacement
Potassium Administration
Hypokalemia occurs Once Intervention begins due to re-entering of potassium back to the cells along
with insulin
Nursing Intervention
Monitor Vital signs, neurovital signs ( ICP)
2. Assess weight, skin turgor, and hematocrit
3.Administer Oxygen therapy
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Start Intravenous line; (0.9% PNSS/ 0.45% NSS)
Client Education
Take insulin or oral antidiabetic medications as prescribed
Monitor blood glucose frequently
Monitor urine ketones when blood glucose levels rise (above 250mg/dl)
Schedule regular appointments with the physician for regular review of blood glucose tests, weight gain
or losses, and general health and well-being.
Recognize signs/symptoms of infection ( a major cause of DKA)
Call the physician/ seek consultation if any of the following develops:
Anorexia
Nausea, vomiting or diarrhea
Ketonuria persisting for more than 8 hours
A febrile illness or infection
Any sign or symptom of acidosis
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Hyperosmolar Nonketotic Syndrome
Extreme hyperglycemia and dehydration
Unable to excrete glucose as quickly as it enters the extracellular space
Maximum hepatic glucose output results in a plateau of plasma glucose no higher than 300-500 mg/dl
When sum of glucose excretion plus metabolism is less than the rate which glucose enters extracellular
space.
HHNK
Hyperglycemic, HyperOsmolar, NonKetotic Coma
Occurs in DM2 (NIDDM)
Extreme hyperglycemia 800-2000 mg/dl
No ketosis and no acidosis
Polyphagia, polydipsia, glycosuria,hypotension, shock
Major difference of DKA and HHNK is
LACK of KETONURIA in HHNK
Treatment is similar with DKA
Hyperosmolar Nonketotic Syndrome
Extreme hyperglycemia and hyperosmolarity
High mortality (12-46%)
At risk
Older patients with intercurrent illness
Impaired ability to ingest fluids
Urine volume falls
Decreased glucose excretion
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Elevated glucose causes CNS dysfunction and fluid intake impaired
No ketones
Some insulin may be present
Extreme hyperglycemia inhibits lipolysis
Hyperosmolar Nonketotic Syndrome Presentation
Extreme dehydration
Supine or orthostatic hypotension
Confusion coma
Neurological findings
Seizures
Transient hemiparesis
Hyperreflexia
Generalized areflexia
Hyperosmolar Nonketotic Syndrome Presentation
Glucose >600 -1200mg/dl
Sodium
Normal, elevated or low
Potassium
Normal or elevated
Bicarbonate >15 mEq/L
Mental status changes
Seizures neurological deficts
Treatment of HHS
Hydration!!!
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Even more important than in DKA
Find underlying cause and treat!
Insulin drip
Should be started only once aggressive hydration has taken place.
Switch to subcutaneous regimen once glucose < 200 and patient eating.
Serial Electrolytes
Potassium replacement.
Hyperosmolar Nonketotic Syndrome Treatment
Fluid repletion
NS 2-3 liters rapidly
Total deficit = 10 liters
Replete in first 6 hours
Insulin
Make sure perfusion is adequate
Insulin drip 0.1U/kg/hr
Treat underlying precipitating illness
Clinical Errors
Fluid shift and shock
Giving insulin without sufficient fluids
Using hypertonic glucose solutions
Hyperkalemia
Premature potassium administration before insulin has begun to act
Hypokalemia
Failure to administer potassium once levels falling
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Recurrent ketoacidosis
Premature discontinuation of insulin and fluids when ketones still present
Hypoglycemia
Insufficient glucose administration