PATHOPHARM CH. 19: heart failure and cardiac dysrhythmias

left sided heart failure

• most common HF

• associated with left ventricular infarction, valvular heart disease, and systemic hypertension

left sided HF backward effects

PULMONARY CONGESTION AND EDEMA

• DOE, orthopnea, cough, paroxysmal nocturnal dyspnea, cyanosis, basilar crackles

left sided forward effects

• decreased delivery of oxygen and nutrients

• not enough blood reaches tissues → poor perfusion

  • fatigue, oliguria, increased HR, faint pulses, restlessness, confusion, anxiety

mechanism of left sided HF

• reduced ejection fraction → increased LEFT ventricle preload → increased LEFT atrial and pulmonary pressure → pulmonary congestion

• low output activates RAAS system as a compensatory response → fluid and water retention (leads to edema!)

• over time: increased pulmonary pressure → increased RIGHT ventricular afterload → RIGHT ventricle hypertrophy. left eventually affects right!!

right sided heart failure

• preceded by left sided HF OR

• caused by right ventricle damage from MI or lung disease

  • isolated RV failure is rare!

• UNLIKE LEFT, sitting up doesn’t really help

mechanism of right sided HF

right ventricle damage → increased pulmonary vascular resistance → high afterload → right ventricle hypertrophy → right ventricle failure

right sided HF backward effects

SYSTEMIC VENOUS CONGESTION

• impaired function of liver, portal system, spleen, kidneys, peripheral subQ tissues, and brain

  • impaired mental function, hepatomegaly, ascites, splenomegaly, anorexia, subQ edema, JVD

right sided HF forward effects

• low cardiac output

  • fatigue, oliguria, increased HR, faint pulses, restlessness, confusion, anxiety

biventricular HF

• starts at LV failure and progresses to right

• produces both pulmonary congestion and systemic venous congestion, as well as decreased cardiac output

diagnosis of HF

• no single test; relies on past history, present illness, physical exam findings (i.e. edema)

echocardiography

• gold standard for evaluation HF

• measures chamber size, volume, dynamic, ejection fraction

other diagnostic factors for HF

• BNP and NT-proBNP levels

  • chest x-ray and ECG

key findings of HF

dyspnea, pulmonary rales (crackles), cardiomegaly, pulmonary edema, S3 heart sound, tachycardia

clinical manifestations of HF

• FACES: fatigue, activity, limitation, congestion, edema, shortness of breath

• orthopnea; fluid retention’ cognitive changes (decreased cerebral perfusions)

goals of HF treatment

• improve cardiac output

• minimize congestion

• reduce cardiac workload

• prevent progression

HF is not curable; age and comorbidities make it hard to treat

**improve underlying factors

medications for HF treatment

STANDARD OF CARE

• ACEIs/ARBs: standard therapy. ACEIs can cause severe cough!!

• aldosterone antagonists, some b1 blockers

• diuretics: remove fluid, reduce congestion and workload

• positive inotropes and digitalis: improve myocardial contractility

devices for HF treatment

• pacemakers: invasive monitor of the heart

• delivers shock when heart falls under a certain set rate/number

cardiac dysrhythmia treatment

• depends on type and severity

• aims to control rate and rhythm and prevent reoccurence

  • beta blockers, calcium channel blockers

  • electrical cardioversion

  • ablation therapy and pacemaker implantation

  • defibrilation

  • lifestyle modifications

  • regular monitoring and follow up

interrelationship between HF and dysrhythmias

• HF increases risk of atrial and ventricular arrhythmias (creates substrate for arrhythmia)

• dysrhythmias worsen cardiac output

• treat both conditions concurrently!

cardiac dysrhythmias

• abnormalities in impulse generation or conduction

• range from benign → life threatening

• results from ischemia, electrolyte imbalance, or drug toxicity

• life-threatening when severely affecting perfusion or CO