CHF Flashcards
causes of HF
-usually a consequence of underlying CV disorders
-Myocardial infarction – MC cause of systolic dysfunction
-Other cardiovascular causes
-non cardiac causes:
-1. Severe anemia
-2. Nutritional Deficiencies- K and Ca
-3. Drugs:
-chemotherapy agents (i.e. doxorubicin)
-COX-2 inhibitors
-NSAIDs
-thiazolidinediones (“glitazones”)- DM
systolic dysfunction
-decrease contractility
-Reduction in muscle mass (MI)
-Dilated cardiomyopathies
-Ventricular Hypertrophy – pressure overload (systemic and pulmonary HTN, aortic or pulmonic valve stenosis)
-Ventricular Hypertrophy – volume overload (valvular regurgitation, shunts, high-output states)
diastolic dysfunction
-restriction in ventricular stiffness
-increased ventricular stiffness
-ventricular hypertrophy
-infiltrative myocardial disease (amyloidosis, sarcoidosis)
-myocardial ischemia and infarction
-mitral and tricuspid valve stenosis
-pericardial disease
pathophysiology of HF
-Reduction in stroke volume and CO by measurement of ventricular end-diastolic pressure (preload)
-1. Reduced stroke volume caused by either diastolic or systolic dysfunction
-Left-sided failure:
-LV doesn’t adequately pump blood forward -> increase pulmonary circulation pressure -> fluid forced into lung insterstitium -> congestion and edema -> reduction of diffusion of O2 and CO2 between alveoli and pulmonary capillaries -> hypoxemia (decrease oxygenation in blood) -> tissue hypoxia and organ dysfunction OR dyspnea (exertional, orthopnea, paroxysmal nocturnal)
-right HF- congestion in peripheral veins -> hepatojugular reflex (increase in jugular vein distension when pressure applied over the liver) OR ankle edema (ambulatory pt and sacral edema (bedridden pt))
-compensatory neurohormonal responses- triggered in response to reduction in CO
-reduction in tissue perfusion -> activation of SNS, RAAS, vasopressin, proinflammatory cytokines -> increase vasoconstriction, increase tachycardia, increase Na and H2O retention, increase preload, and SV, ventricular hypertrophy and remodeling -> increase plasma volume and venous pressure OR decrease CO and increase circulatory congestion
risk factors to HF
-risk factors- hyperlipidemia, HTN, diabetes, insulin resistance ->
-atherosclerosis LVH ->
-CAD ->
-Myocardial ischemia ->
-coronary thrombosis ->
-MI -> arrhythmia and loss of muscle
-arrhythmia -> sudden death
-loss of muscle -> remodeling -> ventricular dilation -> HF -> death
staging of HF: American College of Cardiology/American Heart Association (ACCF/AHA)
-Stage A – At risk for HF w/o structural heart disease or signs & symptoms of HF
-Stage B – Structural heart disease w/o signs & symptoms of HF
-Stage C – Structural heart disease with prior or current symptoms of HF
-Stage D – Refractory HF requiring specialized interventions
staging of HF: heart failure society of america (HFSA)
-CLASS I – No limitations of physical activity. Ordinary Physical Activity does not cause undue fatigue, dyspnea or palpitations
-CLASS II – Slight limitations of physical activity. Ordinary physical activity results in fatigue, palpitation, dyspnea or angina
-CLASS III – Marked limitation of physical activity. Although patients are comfortable at rest, less-than-ordinary physical activity will lead to symptoms
-CLASS IV – Symptomatic at rest. Symptoms of CHF are present at rest and the discomfort increases with any physical activity
stages, phenotypes and treatment of HF
treatment of HF stage C and D
classes of drugs used to treat HF: diuretics
-MOA- reduce plasma volume and edema -> relieve symptoms of circulatory congestion
-Thiazide diuretics (HCTZ) – for milder cases
-Loop diuretics (IV/PO)
-aldosterone antagonists (spironolactone)
loop diuretics
-IV/PO
-more potent natriuretic activity
-Carefully titrate doses to avoid excessive diuresis, dehydration and electrolyte imbalances
-Examples:
-Furosemide (Lasix)
-Torsemide (Demadex)
-Bumetanide (Bumex)
general side effects for loops and thiazides
-hypokalemia
-hypomagnesaemia
-hypocalcemia (loops)
-tachycardia
-Important ions to maintain normal cardiac function are Ca2+, Mg+and K+
-Common to give K+ supps and Mg+ supps in CHF patients
-Refer to HTN handout for full list of ADRs
diuretics: aldosterone antagonists
-spironolactone
-reserve for pts with symptoms at rest despite the use of diuretics, digoxin, ACE inhibitors and beta-blockers
-Use low dose and closely monitor potassium.
-HFSA guidelines: Use IV loop diuretics as initial tx for pts w/ ADHF and evidence of fluid overload
-ACC/AHA guidelines:
-Use PO diuretics to maximize standard HF therapies (ACE inhibitors, BBs) in patients w/ Stage C Heart Failure
-Use aldosterone antagonist in selected Stage C HF pts w/ moderately severe to severe symptoms of HF and reduced LVEF who can be carefully monitored for preserved renal fn and normal K+ concentration
vasodilators
-ACE inhibitors- prils
-ARB- sartan- used in pts intolerant to ACE inhibitors
-ARNI- angiotensin receptor neprolysin inhibitor (combination)
-isosorbide dinitrate (ISDN)
-hydralazine (HYD)
-hydralazine/isosorbide combo (BIDIL)
-HCN channel blocker
ACE inhibitors
-prils
-reduce formation of Angiotensin II, therefore counteract the activation of the renin-angiotensin aldosterone system, which occurs during compensatory mechanism of heart failure
-results in venous and arterial dilation, reduction in plasma volume, venous pressure and edema as well as increase in CO by reducing arterial pressure and cardiac afterload.
-Several studies demonstrate reduced mortality in pts with heart failure
-SEs - nonproductive cough (20%), rash, abnl taste, hyperkalemia, dizziness, decrease renal function, angioedema.
-ACC/AHA guidelines: ACE inhibitors/ARBs should be used in appropriate patients starting at Stage A HF (i.e. HTN, MI)
