● Heart failure
o causes
▪ A common chronic health problem with acute episodes often causing
hospitalization. Acute coronary disease and other structural or functional
problems of the heart can lead to acute HF.
▪ Caused by systemic HTN in most cases
▪ Common causes and Risk factors for HF:
● HTN, coronary artery disease, cardiomyopathy, substance abuse,
valvular disease, congenital defects, cardiac infections and
inflammations, dysrhythmias, DM, smoking/tobacco use, family history,
obesity, severe lung disease, sleep apnea, hyperkinetic conditions
(hyperthyroidism)
o left vs right
▪ Left sided heart (ventricular) failure includes HTN, coronary artery disease, and
valvular disease. Decreased tissue perfusion from poor cardiac output and
pulmonary congestion from increased pressure in the pulmonary vessels
indicate left ventricular failure
● Formerly referred to as congestive HF; not all cases of LVF involve fluid
accumulation
● May be acute or chronic and mild to severe.
● Two types:
o Systolic: heart cannot contract forcefully enough during systole
to eject adequate amounts of blood into the circulation
o Diastolic: left ventricle cannot relax adequately during diastole-
ventricle can not fill with sufficient blood to ensure an adequate
cardiac output
▪ Right sided heart (ventricular) failure may be caused by left ventricular failure,
right ventricular MI, or pulmonary HTN (cor pulmonale). The right ventricle
cannot empty completely. Increased volume and pressure develop in the
venous system and peripheral edema results.
o diagnosis
▪ Labs:
● Electrolytes - may occur from complications or diuretics
● Hgb and HCT - identify HF resulting from anemia
● BNP - used when dyspnea to r/o HF
● U/A - proteinuria/high specific gravity
● ABGs- respiratory acidosis
▪ B-type natriuretic peptide (BNP)
● is used for diagnosing HF (in particular, diastolic HF), in patients with
acute dyspnea
▪ Microalbuminuria
● An early indicator of decreased compliance of the heart and occurs
before the BNP rises
, ● “early warning detector” that lets HCP know that the heart is
experiencing early signs of decreased compliance long before symptoms
occur
▪ CXR
●Helpful in diagnosing left ventricular failure because the heart is
enlarged, representing hypertrophy or dilation
▪ Echocardiography
● Best tool in diagnosing HF- ejection fraction between 50-70%
● Cardiac valvular changes, pericardial effusion, chamber enlargement,
and ventricular hypertrophy can be diagnosed with this noninvasive
technique
● Can also be used to determine ejection fraction
▪ Hemodynamic Monitoring
● PA catheter allows for assessment of cardiac function and fluid volume
● PAP (positive airway pressure) /PAWP (pulmonary artery wedge
pressure) elevated with L sided HF because volumes and pressures are
increased in the left ventricle
●
o s/s
▪Left HF:
● Decreased cardiac output:
o Fatigue, weakness, oliguria during the day (nocturia at night),
angina, confusion, restlessness, dizziness, tachycardia,
palpitations, pallor, weak peripheral pulses, cool extremities
o Priority problems:
▪ Impaired gas exchange r/t ventilation/perfusion
imbalance
▪ Decreased cardiac output r/t altered contractility,
preload, and afterload
▪ Fatigue/weakness r/t hypoxemia
▪ Potential for pulmonary edema r/t L sided HF
● Pulmonary congestion:
o Hacking cough, worse at night, dyspnea/breathlessness,
crackles or wheezes in lungs, frothy, pink-tinged sputum,
tachypnea, s3 s4 summation gallop
▪ Right HF:
● jugular neck vein distention, enlarged liver and spleen, anorexia and
nausea, dependent edema (legs and sacrum), distended abdomen,
swollen hands and fingers, polyuria at night, weight gain, increased BP
from excess volume or decreased BP from failure
o treatment
▪ Drugs:
● ACE inhibitors: increase stroke volume (can cause hyperkalemia)
, ● ARBs: block aldosterone decreased fluid overload (can cause
hyperkalemia)
● Human BNP: increases sodium loss in renal tubules
● Diuretics: reducing sodium and water retention to decrease the
workload of the heart
o Loop and thiazide
● Venous vasodilators - nitrates: nitrate free periods to reduce tolerance
● Digoxin:
o Increased contractility, decreased HR, slowing of conduction
through AV node, inhibition of sympathetic activity
o Possibility of toxicity
● Beta-adrenergic blockers:
o Improve morbidity, mortality, and QOL for patients
o Helps to increase activity tolerance
o Improvement in symptoms
● Morphine sulfate:
o Reduce anxiety, decrease preload and afterload, slow
respirations, and reduce pain associated with MI
▪ Nutrition therapy:
● Sodium and fluid restrictions
▪ CPAP: improve cardiac output and ejection fraction by decreased afterload and
preload, BP, and dysrhythmias
▪ CRT-biventricular pacing:
● Synchronous ventricular contractions to improve EF, CO, and mean
arterial pressure (EF less than 35%)
▪ Gene therapy:
● End-stage HF
● Replaces damaged genes with modified genes to improve regrown of
cardiac cells
▪ Heart transplant
▪ VADs- ventricular assist devices
o nursing interventions
▪ Promoting oxygenation and gas exchange:
● Ventilation assistance
● Monitor RR q 1-4 hr
● Auscultate breath sounds q 4-8hr
● Position in high Fowler’s if patient dyspneic
● Maintain oxygen sat of 90%
o education
▪ Activity schedule, indications of worsening or recurrent HF, drug therapy,
nutrition therapy, advanced directives, energy management
▪ MAWDS (medications, activity, weight, diet, symptoms)
▪ Indications of worsening or recurrent HF
● Rapid weight gain (3lbs in a week or 1-2 lbs overnight)
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