Heart Failure Flashcards
What are the characteristics of Systolic Heart Failure (HF-REF)?
- weakened heart muscle
- left ventricle loses ability to generate enough pressure to eject blood forward through aorta
- reduced ejection fraction <40% (N = >55%)
What are the characteristics of Diastolic Heart Failure (HF-PEF)?
- inability of ventricles to relax and fill during diastole (can’t fill enough)
- decreased filling results in decreased stroke vol & CO
- results in venous engorgement in both pulmonary and vascular systems
What is the most common form of HF?
Systolic (HF-REF)
What are the four compensatory mechanisms in HF?
(1) SNS: increases catecholamines
(2) Neurohormonal responses
- RAAS: increases renin
- Posterior Pituitary gland: secretes ADH
(3) Ventricular dilation
(4) Ventricular hypertrophy
Explain the SNS compensatory mechanism
increases epinephrine & norepinephrine to improve CO by increasing
- HR
- myocardial contractility
- and peripheral vasoconstriction
leads to increased cardiac workload and need for oxygen (vasoconstriction causes an increase in preload)
Explain the RAAS (neuro-hormonal) compensatory mechanism
kidneys respond to decreased blood flow by producing more renin
renin converts angiotensin I -> II by ACE and in response, the adrenal cortex releases aldosterone resulting in
- Na and H20 retention
- peripheral vasoconstriction
- increased BP
Explain the Posterior Pituitary Gland (neuro-hormonal) compensatory mechanism
responds to decreased cerebral perfusion pressure and secretes ADH (causes sodium and water retention) creating increased blood volume in an already overloaded state
Explain the Ventricular dilation compensatory mechanism
Heart chambers enlarge due to chronically elevated pressure
Initially adaptive to cope with increasing blood volume but eventually muscle fibers become overstretched and lose the ability to contract effectively = decreased CO
Explain the Ventricular hypertrophy compensatory mechanism
Increase in muscle mass and cardiac wall thickness in response to overwork and strain
Initially adaptive but over time hypertrophic heart muscle has poor contractility requiring more oxygen to perform
Coronary artery circulation becomes poor, and the heart is prone to dysrhythmias
Explain the counter-regulatory mechanisms (hormones)
Natriuretic peptides (atrial natriuretic peptide and brain natriuretic peptide [BNP]) are hormones produced by heart muscle in response to increased blood vol
These hormones regulate renal, cardiovascular, and hormonal compensation
Cardiac decompensation occurs when these mechanisms can no longer maintain CO and tissue perfusion becomes insufficient
Explain left-sided HF
- LV cannot pump blood effectively to the systemic circulation
- Causes blood to back up to the left atrium and pulmonary veins
- Pulmonary congestion and edema
-> dyspnea, cough, crackles, and impaired O2 exchange
Explain right-sided HF
- RV cannot eject sufficient amounts of blood
- Causes blood to back up in the right atrium and venous system
-> peripheral edema, hepatomegaly, ascites, JVD, anorexia, GI distress, weight gain
Clinical manifestations of Acute Decompensated HF
- Pulmonary edema: decreases lung compliance and increases resistance in small airways = mild increase in RR and decrease in PaO2
- As pulmonary venous pressure increases, more fluid leaks into interstitial space = tachypnea & SOB
- If pulmonary pressure continues to increase, fluid moves into alveoli and disrupts gas exchange = respiratory acidosis
- Affected patients are anxious, pale, cyanotic, clammy, cold, severe dyspnea and orthopnea, wheezing, coughing, blood-tinged sputum
- Auscultation will reveal crackles, wheezes, and ronchi throughout the lungs
- HR is rapid and BP may be elevated or decreased
Clinical Manifestations of Chronic HF
- Fatigue: poor CO, anemia
- Dyspnea at rest or mild exertion
- Orthopnea
- Paroxysmal nocturnal dyspnea
- Cough: dry, nonproductive
- Tachycardia
- Edema
- Nocturia: impaired renal perfusion during the day, when lying flat blood moves back into CVS
- Skin Changes: dusk, lower extremities are shiny, swollen, and diminished hair growth
- Behavioural changes: restlessness, confusion, impaired memory d/t decreased cerebral perfusion
- Chest pain: decreased coronary artery perfusion
- Weight changes: progressive gain
Complications of HF
(1) Pleural Effusion
(2) Dysrhythmias - enlargement of heart changes normal electrical pathways
(3) Left Ventricular Thrombus - increased LV and decreased CO increase risk of formation and stroke
(4) Hepatomegaly - venous system backing up into liver leading to impaired liver function and possibly cirrhosis
(5) Renal failure - decreased CO leads to hypoperfusion of kidneys = renal insufficiency or failure