Heart failure/Cardiogenic Pulmonary Edema Heart Failure

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NOTES Heart Failure/Pulmonary Edema

Module #4: Nursing Care of the Individual with Cardiovascular Disorders

Heart failure/Cardiogenic Pulmonary Edema
Heart Failure

(click here for more information)

A. Etiology/Pathophysiology/Incidence
1. Definition: Inability of heart to pump sufficient blood to meet metabolic demands of body resulting in decreased tissue perfusion

a. Acute or chronic

b. Common term= Congestive Heart Failure (CHF)

c. Leading causes= HTN and CHD

d. Affects 5 million people in USA; 6 – 10% of person older than 65

2. Etiology

a. Impaired myocardial contraction; CAD and myocardial infarction resulting in left ventricular damage

b. Inflammatory conditions: cardiomyopathy, myocarditis

c. Long-standing excessive workload; valvular disorders or congenital heart defects; HTN

d. Acute excess demands: volume overload; hyperthyroidism; massive pulmonary embolism

3. Key concepts:

a. CO= SV x HR: in heart failure it is insufficient to meet the metabolic needs of the body

b. SV; determined by preload, afterload and myocardial contractility

c. Systolic failure (most common type); decreased contractility of left ventricle; unable to generate enough pressure to eject blood forward through high-pressure aorta; Key- left ventricular ejection fraction (percentage of blood in ventricles that is ejected during systole; normal is approx 60%; less than 40% = heart failure (determined by ECHO)

d. Diastolic failure- impaired filling ability of ventricles during diastole; due to decreased stroke volume, normal systolic function; high filling pressures; normal ejection fraction (ejection “ok”; not much to eject)

e. Preload:

  • Volume of blood in ventricles at end diastole.

  • Depends on venous return

  • Depends on compliance

What durgs primarily affect pre-load…diuretic…why?
f. Afterload:

  • Force needed to eject the blood into the circulation

  • Arterial B/P, pulmonary artery pressure

  • Valvular disease increases afterload

What drugs affect primarily afterload…ACE inhibitors, niprides…vasodilators…why?...understand this concept)
4. Pathophysiology: Key understanding-body responds by *compensation

(See p. 872, Table 30-2, Compensatory Mechanisms of Heart Failure) *look carefully at this table!

  1. Frank-Starling mechanism: Increased ventricular filling and myocardial stretch eventually results in ineffective contraction (usually increased venous return increases force of contraction)

  2. Activation of sympathetic nervous system and renin-angiotensin system

1) Release of norepinephrine increases heart rate and contractility; arterial and venous vasoconstriction

2) Decreased renal perfusion (blood is redistributed to maintain adequate circulation to brain and heart) activates renin release from kidneys

  1. Renin-angiotensin system results in salt and water retention; somewhat offset by atrial natriuretic factor (ANF) hormone secreted by atria in response to stimulation of stretch receptors in atria caused by excess fluid volume and also by B-type natriuretic factor (*BNP-note measure in CHF)secreted by ventricles due to fluid volume overload; help to counteract negative effects of sympathetic nervous system and rennin-angiotensin-aldosterone system by producing vasodilatation and diuresis.

1) Ventricular remodeling: chambers dilate to adapt to excess fluid volume (Ace inhibitors prevent this…why important?)

2) Ventricular hypertrophy occurs as muscle cells enlarge

d. Initially compensation improves cardiac output but long-term results in deterioration of cardiac function and decompensation

e. With heart function deterioration, decrease in tissue and heart perfusion leads to further weakening of heart, cycle perpetuates

  1. Normal heart can adjust output to meet increased demands up to 5 times basic level; if heart failure: minimal to no cardiac reserve which results in activity intolerance

5. Causes of Heart Failure (See p. 870, Table 30-1)
a. Impaired cardiac function

1) Coronary heart disease

2) Cardiomyopathies

3) Rheumatic fever

4) Endocarditis

b. Increased Cardiac workload

1) Hypertension

2) Valvular disorders

3) Anemias

4) Congenital heart defects

c. Acute non-cardiac conditions

1) Volume overload

2) Hyperthyroid, Fever, infection
6. Classifications of heart failure *Make sure you understand the difference! See above also.
a. Systolic versus Diastolic Failure

*Read text p. 873 and see above.

What is the difference between systolic and diastolic failure?

b. Left-sided versus right sided failure **(see text p. 873, fig. 30-1; Hemodynamic Effects Left sided Heart Failure & p. 874, fig. 30-2; Hemodynamic Effects Right Sided Heart Failure & p. 875 Multisystemic effects Heart Failure)

1) Depending on cause, one ventricle may be primarily affected; left sided results from CAD, hypertension; right sided: results from restricted blood flow to lungs, as with acute or chronic pulmonary disease

2) In chronic heart failure, both sides are involved

3) Left sided failure can lead to right sided failure [LUNGS]

4) Manifestations of left-sided heart failure result from decreased cardiac output: dizziness and syncope; pulmonary congestion with dyspnea, shortness of breath, cough, orthopnea (lungs; dec. CO

5) Manifestations of right-sided heart failure result from right sided heart distension: distended neck veins, peripheral tissue edema seen in dependent tissues: feet and legs or sacrum, if client bedridden; GI congestion: nausea and anorexia; liver engorgement: RUQ pain [PERIPHERY}

c. High-output versus low-output failure

1) Occurs in situations requiring increased cardiac output, but heart is unable to meet increased oxygen demands

2) Occurs with hypermetabolic states including hyperthyroidism, infection, anemia, and pregnancy

d. Acute versus chronic failure (Acute also known as Pulmonary edema)

1) Due to acute MI; chronic due to chronic cardiomyopathy

*What kind of heart failure is likely to occur when a patient is septic? (see text p. 874)
B. Common Manifestation/Complications (depends upon type and extent)

1. Left sided heart failure: pulmonary congestion; dyspnea, tachypnea, orthopnea PND (paroxysmal nocturnal dyspnea due to fluid reabsorption during night), Cheynes Stokes breathing, fatigue, anxiety, arrhythmia, rales, pale and cool skin, decreased peripheral pulses and pulse pressure, S3 and S4 gallop, (NOTE L FOR LEFT AND L FOR LUNGS). Can progress to right sided heart failure and Pulmonary Edema (acute heart failure characterized by significant overload in the lungs, acute restlessness, anxiety, increased crackles, tachypnea, tachycardia, pink frothy sputum, decreased SO2 and Po2)

2. Right sided heart failure: distended neck veins, peripheral tissue edema seen in dependent tissues (feet and legs or sacrum if client bedridden); GI congestion: nausea and anorexia; liver engorgement: RUQ; pain; fatigue, weakness, lethargy; wt. gain, inc. abdominal girth, distended neck veins (JVD or jugular vein distention, visible more than a few millimeters above the clavicle with client supine at a 45 degree angle); hepatomegaly + HJR (hepatojugular reflex); may not see signs of LVF; *atrial dysrthymias common

Right-sided heart failure without left sided heart failure- called Cor Pulmonale; how does this affect afterload? What causes cor pulmonale? (text p. 1134)

3. Manifestations related to increased salt and water retention

a. Nocturia: voids more than once during night as fluid reabsorbed from dependent tissues when client is supine

b. Paroxymal nocturnal dyspnea (PND): client awakens with acute shortness of breath that occurs when fluid is reabsorbed into circulation while client is supine

c. Dyspnea at rest (little or no cardiac reserve)

d. Audible S3 and S4 (Click here to listen to S3 S4)

4. Manifestations related to compensatory mechanisms: hepatomegaly and splenomegaly; ascites, impaired liver function: nausea, vomiting, anorexia; myocardial distension: dysrhythmias, pleural effusion, acute pulmonary edema

5. Disease can progress to biventricular failure (end stage heart failure) see p. 876, Table 30-3 stages of Heart Failure
C. Therapeutic Interventions/Collaborative Care
1. Goals of Collaborative Care:

a. Slow progression of heart failure

b. Reduce cardiac workload

c. Improve cardiac function

d. Control fluid retention
2. Diagnostic tests:

a. Diagnosis based on client history, physical examination and diagnostic findings

b. Atrial natriuretic factor (ANF) also known as atrial natriuretic hormone (ANH); however measure **B-type natriuretic peptide (BNP) (greater than 100 indicate HF)- released by heart muscle in response to changes in blood volume; blood levels elevated with heart failure (values measured in ER setting) ;determine if problem is heart failure; evaluate response to treatment (*understand this!)

c. Serum electrolytes and osmolarity: monitoring of electrolytes to evaluate treatment; osmolarity may be decreased with fluid retention and due to decreased renal perfusion

d. Urinalysis, BUN, Creatinine: renal function evaluation (change due to decreased renal perfusion)

e. Liver function tests: effects of heart failure on liver function

f. Arterial blood gases: evaluation of effectiveness of gas exchange

g. Chest x-ray: show pulmonary vascular congestion, cardiomegaly

h. Electrocardiography: changes associated with ventricular enlargement and dysrhythmias, ischemia, infarction

i. Echocardiography with Doppler flow studies: evaluation of left ventricular function (EF); blood flow across valves and great vessels

j Radionuclide imaging: evaluation of ventricular function and size

k. Cardiac enzymes

l. Hemodynamic Monitoring; CVP and Swan-Ganz (evaulate status….see below for typical findings)

m. Cardiac cath for heart pressures

  1. Assessment: depends upon if acute or chronic and severity: if typical chronic left sided heart failure (systolic) with acute exacerbation:

    1. Vital signs: HR ^ to compensate; O2 sat dec; Resp ^ to compensate; BP initially up with inc systemic vascular resistance (renin-angiotensin, sympathetic nervous system stimulation)

    2. Urine output: decreased due to compensatory mechanism with rennin-angiotensin system causing vasoconstriction leading to adrenal cortex to produce aldosterone and posterior pituitary to release ADH which both lead to sodium and water retention.

Findings from Hemodynamic Monitoring…. (review from Lab #4)

    1. PA readings: (evaluate left ventricular function (normal is 25/10 mmHg with mean of 15 mmHg) is *elevated in left ventricular failure; PAWP (measures pressures generated by felt ventricle); normal is 8-12 mmHg is increased in left ventricular failure and pericardial tamponade (decreased in hypovolemia

    2. SVR: Initially increased as compensatory mechanism with renin-angiotensin and sympathetic stimulation. Need MAP (mean arterial pressure of 50/60 or greater to maintain perfusion to vital organs (CO X SVR); calculate by Systolic BP + (diasolic BP) X 2


    1. CVP: Measurement of blood volume and venous return; right heart filling pressure; elevated in right-sided heart failure, may develop as individual develops biventricular failure (both sides of heart fail); (normal is 2-8 mmHg); used primarily to monitor fluid volume status

  1. Medications (see text p. 879-880; Medication Administration; Heart failure); (see p. 818-819; Medication Administration: Antianginal); (see p. 987-988; Medication Administration: Antihypertensives) **Know your cardiac drugs…how they work and why!!!

a. Angiotensin-converting enzyme (ACE) inhibitors (decrease SVR & heart workload); decrease afterload

1) Block renin-angiotensin system activity, decrease cardiac work and increase cardiac output

2) Reduce manifestations and progression of heart failure (stops remodeling of heart!); end in pril or ril

b. Action of Beta-blockers (prevent ventricular remodeling)

1) Prevents bad effects of sympathetic nervous system stimulation

2) Used in low doses; reduce the force of myocardial contraction

c. Action of Diuretics (reduce preload by decreasing total blood volume and circulatory congestion)

1) Relieve symptoms related to fluid retention

2) May cause serious electrolyte imbalance and rapid fluid loss

3) Types

a) Loop diuretics: used with severe heart failure, i.e. furosemide (Lasix), bumetanide (Bumex), torsemide (Demadex), Ethacrynic acid (Edecrin)

b) Thiazide diuretics: used to treat less severe heart failure

d. Action of Vasodilators (increase cardiac ouput by reducing impedance to ventricular outflow, thus decrease afterload)

1) Arterial dilation: reduces PVR and afterload

2) Venous dilation: reduces venous return and preload

3) Pulmonary vascular relaxation: allows reabsorption of fluid from interstitial tissues and alveoli

4) Types

a) Nitrates (intravenous sodium nitroprusside in treatment of acute heart failure)

b) Hydralazine (Apresoline) (arteriole smooth muscle relaxant)

c) Prazosin (alpha-adrenergic blocker) (Minipress) decrease vasomotor tone and vasoconstriction

e. **Action of Inotropic medications (increase cardiac output)

1) Increases the strength of myocardial contraction by increasing intracellular calcium concentration

2) Digitalis glycosides

a) Decreases SA node automaticity and slows conduction through AV node, increasing ventricular filling time

b) Has narrow therapeutic range, excreted through kidneys

c) Digitalis toxicity

(1) Early manifestations: anorexia, nausea and vomiting, headache, altered vision, confusion

(2) Dysrhythmias: sinus arrest, supraventricular and ventricular tachycardia, high AV blocks

(3) Risk increased by hypokalemia, hypomagnesia, hypercalcemia, increased age

3) Positive inotropic agents such as IV dopamine (Intropine) or dobutamine (Dobutrex) used with end-stage heart failure and waiting heart transplant

4) ***Nesiritide (Natrecor) human B type natriuretic peptide, augment diuresis and decrease afterload(vasodilator); ***Primacor also (milrinone lactate; classified as bipyridine phosphodiesterase inhibitor; inotropic vasodilator to produce vasodilation by relaxing vascular smooth muscle)
g. Action of Anti-dysrhythmic medications (usually negative inotropic drugs)

1) PVC’s with heart failure frequently left untreated (Why?)

2) Amiodarone is drug of choice for non-sustained ventricular tachycardia
h. Keys to management in heart failure: (click here for update on HF classification and current therapies)

1) Cardiac Glycoside-Digoxin

2) Positive inotropes- dobutamine (late stage); also Primacor. Natrecor

3) Antihypertensives

4) ACE inhibitors- stops remodeling (pril or ril); Catopril, enalapril, cozar, lisinopril

5) **Preload reduction *Morphine- if acute PE (remember this drug, important in early management of pulmonary edema!...decrease preload…and anxiety!)

a) Vasodilators-nitrates

b) Diuretics-lasix, HCTZ

c) Beta blockers- dec. effects of SNS

    • **Typically NO CALCIUM CHANNEL BLOCKERS (decrease contractility of myocardium!) Remember this!! However do use beta blockers but with caution.

5. Diet and Activity (Important to understand management)
a. **Sodium-restricted diet moderate at 1.5 – 2 gm of sodium/ low cholesterol/ fluid restriction (1200 cc daily); may require increased potassium (diuretics)

b. Moderate, progressive activity program; improve myocardial function; bed rest may be necessary during acute episodes

c. Oxygen; intubation for pulmonary edema, supplemental

d. **Positioning include high Fowler’s to facilitate breathing, elevate legs to promote increased venous return, lower to decrease afterload

In what type of heart failure would it be appropriate to elevate legs (systolic or diastolic)?

e. Space Nursing Care

6. Heart Transplant and other Interventions (click here to try transplant)

a. Only effective treatment for end-stage heart failure

b. Survival rates: 80% at one year; 70% at five years

c. Chief causes of mortality with transplants: infection and rejection

d. Client requires immunosuppressive drugs even with good match

e. Donor heart is denervated; will not respond to position changes, stress, exercise, and some drugs

f. Other Surgical Procedures/Emergency Interventions

1) Intraaortic balloon pump (IABP) used for cardiogenic shock; allows heart to rest **need to understand principle of operation…IABP temporarily supports cardiac function….IABP inflates during diastole, increasing perfusion of the coronary and renal arteries and deflates druig systole, decreasing afterload and cardiac workload…inflation-deflation triggered by ECG pattern see text p. 834 fig 29-7

2) Ventricular assist device (VAD) used to take over for the ventricles; used as a bridge to transplant…can supplement cardiac output by 10-15% (see text)

3) Artificial heart (click here to see how the artificial heart works!)

4) Cardiomyoplasty- wrap latissimus dorsi around heart (promote more effective pumping of heart); muscle stimulated in synchrone with heart; providing more forceful contraction and increasing CO; does NOT improve prognosis or quality of life in patients with end-stage heart failure.

5) Ventricular reduction surgery- ventricular wall resected; promote more effective pumping of heart; doesn’t improve prognosis or quality of life if end stage heart failure; used on enlarged or hypertrophied hearts.

6) Biventricular pacing to improve left ventricular function *Access this site to gain more information on how/why it works!)

7) Implantable defibrillator: when ejection fraction falls to less that 40% person at high risk for sudden cardiac arrest due to arrhythmia; implant defibrillator. (See text p. 856-857) How does the ICD work?

7. Nursing Diagnosis/Nursing Care (Text p. 882-885…carefully read this)
a. Decreasing risk factors for CHD

b. Screening and effective management of HPT and diabetes

c. Nursing Diagnoses (What interventions ware imortant? See text)

1) Decreased Cardiac Output

2) Excess Fluid Volume: monitoring daily weight: 1 liter of fluid = 1 kg or 2.2 lb of weight

3) Activity Intolerance: providing nursing care and teaching client and family to function with frequent rest periods

4) Deficient Knowledge regarding low sodium diet and medications including home care education regarding self monitoring for cardiac decompensation; daily weights (notify physician if 2 pound gain in daily weight); maintaining medications, diet, progressive exercise with rest periods, cardiac rehabilitation, continued medical care

Pulmonary Edema

A. Etiology/Pathophysiology
1. Definition : Abnormal accumulation of fluid in the interstitial tissue and alveoli of the lung

a. Medical emergency with onset either gradual or acute

1) Causes

a) Cardiac

(1) Acute myocardial infarction

(2) Acute heart failure

(3) Valvular disease

b) Non-cardiac causes

(1) Acute respiratory distress syndrome (ARDS)

(2) Trauma

(3) Sepsis

(4) Drug overdose or neurologic sequellae
2. Pathophysiology of cardiogenic pulmonary edema

a. Severe impairment of left ventricular contractility

b. EF falls- rise in end-diastolic volume and pressure

c. Pulmonary pressure rises; fluid leaks from pulmonary capillaries into interstitial tissues, decreasing lung compliance and interfering with gas exchange

d. Fluid enters alveoli disrupting ventilation and gas exchange

e. Death by suffocation if untreated; caused by *left-sided heart failure, rapid administration of IV fluids most common cause.

Pathophysiology of Cardiogenic Pulmonary Edema

 End-diastolic blood volume (inc) (approx 30 mmHg)

 Left ventricular end-diastolic pressure (inc)

Pressure reflected back to pulmonary capillary bed (inc)

Pulmonary intravascular hydrostatic pressure (inc)

Pulmonary artery wedge pressure (PAWP) (inc)

Fluid forced into interstitium (inc)

Pulmonary congestion (inc)

Increased pressure forces fluid into alveoli (inc)
(Pulmonary edema)

B. Common Manifestation/Complications

1. Manifestations

a. Dyspnea, shortness of breath, orthopnea, tachycardia

b. Skin is cyanotic, cool, clammy, and diaphoretic

c. Productive cough: pink, frothy sputum (*know whyfluid, RBC’s and plasma proteins in alveoli and airway!)

d. Audible crackles with lung sounds; S3 gallop (click to listen)

e. Mental changes: often restless and highly anxious, may be confused or lethargic
C. Therapeutic Interventions/Collaborative Care

1. Goals of Collaborative Care:

a. Slow progression of heart failure

b. Reduce cardiac workload

c. Improve cardiac function

d. Control fluid retention

e. Restore effective gas exchange

f. Reduce fluid and pressure in pulmonary vascular system

g. Intervention: upright position sitting with legs dependent to decrease blood return
2. Diagnostic tests: (see above to determine cardiac function and degree heart failure) for Acute failure!

a. Arterial blood gases

b. Continuous monitoring of oxygen saturation

c. Chest x-ray

d. Hemodynamic monitoring (PAWP often > 25 mm Hg.)
3. Medication and Treatment (MAD DOG) M(orphine to decrease anxiety, slow respiration and decrease venous return by vasodilation) A (irway including aminophylline for bronchodilation) D (italis to slow and strengthen contraction) D (irusesis to decrease venous return and preload) O (oxygen) G (blood gases for evaluation and treatment) **know why this works!!

(increase gas exchange; O2; intubate; elevate HOB)
a. Medication: intravenous morphine: dec. anxiety, improve breathing, to vasodilate, which reduces venous return and left atrial pressure

b. Oxygen administration to achieve 100% oxygen concentration

c. Continuous positive airway pressure (CPAP) with mask

d. Intubation and mechanical ventilation

e. Semi-fowler’s/Fowlers position, legs dependent; maybe phlebotomy to remove 300-500 cc blood;

f. CVP/hemodynamic monitoring

g. Other medications

1) Loop diuretics for rapid diuresis

2) Vasodilators such as intravenous nitroprusside to reduce afterload and improve cardiac output

3) Dopamine or dobutamine infusion or digoxin to improve myocardial contractility

4) Intravenous aminophylline cautiously to reduce bronchospasm and decrease wheezing

4. Nursing Diagnosis/Nursing Care

a. Goals: improve oxygenation, reduce fluid volume, support emotionally

b. Requires early recognition and initiation of treatment; emergent care is ABC (Airway, Breathing, Circulation)

c. Nursing Diagnoses

1) Impaired Gas Exchange: work of breathing is increased which leads to fatigue and decreased effort

2) Decreased Cardiac Output

*When cardiogenic in nature, cause is acute decrease in myocardial

contractility or increased workload for left ventricle

*Accurate intake and output with indwelling catheter

3) Fear

4) Knowledge deficit: Teaching related to cause, usually CHD or acute MI

Go here to access these case studies to review your understanding of CHF
Client with MI develops CHF
CHF Overview

RNSG 2432 

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