CHF Flashcards
non cardiac causes of HF
Severe anemia (high output HF) *
Nutritional Deficiencies: K+, Ca2+
Drugs:
-chemotherapy agents (i.e. doxorubicin)
-COX-2 inhibitors
-NSAIDs
-thiazolidinediones (“glitazones”)
Causes of HF: cardiac - systolic vs diastolic
Usually a consequence of underlying CV disorders
Systolic:
- heart’s ability to CONTRACT is diminished
- EF <40%
- MCC of systolic HF: MI
Diastolic:
- heart muscle stiffens and cannot relax/fill properly
- normal EF
systolic dysfunction HF examples
Reduction in muscle mass (MI)*
Dilated cardiomyopathies
Ventricular Hypertrophy from pressure overload:
- systemic and pulmonary HTN
- aortic/pulmonic valve stenosis
Ventricular Hypertrophy from volume overload:
- valvular regurgitation
- shunts
- high-output states (hyperthyroidism)
diastolic dysfunction HF examples
Ventricular hypertrophy
Infiltrative myocardial disease:
- amyloidosis
- sarcoidosis
MI and infarction: stiff muscle
Mitral and tricuspid valve stenosis:
- restrict flow of blood into ventricles during filling phase
Pericardial disease:
- physically restricts the heart’s ability to expand and fill
Left sided HF pathophysiology
1) LV doesn’t adequately pump blood forward -> increase pulmonary circulation pressure
- elevated pressure forces fluid into lung interstitium -> congestion and edema
2) Gas exchange impairment from fluid congestion in lungs -> reduction of diffusion of O2 and CO2 between alveoli and pulmonary capillaries -> HYPOXEMIA (decrease oxygenation in blood) -> tissue hypoxia
3) tissue hypoxia and organ dysfunction; Dyspnea
Right sided HF pathophysiology
1) RV doesn’t pump well leading to congestion in peripheral veins
2) Peripheral edema:
-hepatojugular reflex: increase in JVD when pressure applied over the liver
- hepatosplenomegaly
- ankle edema (ambulatory pt)
- sacral edema (bedridden pt)
often caused by LEFT SIDED HF
example of R sided HF:
- left to right shunt
- chronic lung ds (cor pulmonale)
compensatory neurohormonal responses in HF
Triggered in response to reduction in CO/tissue perfusion
Activation of systems:
-SNS
- RAAS
- vasopressin secretion (ADH)
- proinflammatory cytokines
Effect:
- increase vasoconstriction
- tachycardia
- increase Na+ and H2O retention
- increase preload and SV
- ventricular hypertrophy and remodeling
Outcome:
- increase plasma volume and venous pressure
- decrease CO and increases circulatory CONGESTION
- compensatory mechanisms will exacerbate and worsen existing HF
risk factors to HF
- hyperlipidemia
- HTN
- diabetes/insulin resistance
- metabolic syndrome
these all can lead to atherosclerosis -> CAD -> MI -> loss of muscle contraction -> systolic HF
staging of HF: American College of Cardiology/American Heart Association (ACCF/AHA)
stages A-D
Stage A
- At high risk for HF WITHOUT structural heart disease or signs and sx of HF
Stage B
- STRUCTURAL heart disease w/o signs and sx of HF
Stage C: symptomatic!
- Structural heart disease WITH prior or current sx of HF
Stage D
- REFRACTORY HF requiring specialized interventions
staging of HF: heart failure society of america (HFSA)
class I-IV
CLASS I
- No limitations of physical activity
- Ordinary Physical Activity does NOT cause symptoms
CLASS II
- Slight limitations of physical activity
- Ordinary physical activity results symptoms
CLASS III
- Marked limitation of physical activity
- Pts are comfortable at rest but LESS THAN ORDINARY physical activity will lead to symptoms
CLASS IV
- Symptomatic at rest!
- discomfort increases with ANY physical activity
Diuretics MOA and which types
MOA
- reduce plasma volume and edema -> relieve symptoms of circulatory congestion
Loop diuretics (IV /PO)
-more potent natriuretic activity
- Carefully titrate doses to avoid excessive diuresis, dehydration and electrolyte imbalances
- IV loop as initial tx for pt with acute decompensated HF
- PO diuretics for stage C HF
Thiazide diuretics (HCTZ)
- for milder cases
Aldosterone antagonists/Potassium sparring: spironolactone
- use for pts w sx at rest despite med use (class 4)
loop diuretics MOA + drug names
- administered IV/PO
-more potent natriuretic activity
-Carefully titrate doses to avoid excessive diuresis, dehydration and electrolyte imbalances
Examples:
-Furosemide (Lasix) *
-Torsemide
-Bumetanide
ADRs for loops and thiazides diuretics
Tachycardia
Electrolyte imbalances:
-hypokalemia
-hypomagnesaemia
-hypocalcemia (loop)
-Common to give K+ and Mg+ supplements to CHF patients
diuretics: aldosterone antagonists; indication, dosing
Indication:
- for pts with symptoms at rest despite the use of diuretics, digoxin, ACE inhibitors and beta-blockers
- stage 4 CHF
- stage C HF with reduced LVEF
Dosing:
-Use low dose and closely monitor potassium for hyperkalemia
diuretics: aldosterone antagonists CI
- hyperkalemia
- CKD
vasodilators class names (7)
ACEi
Angiotensin receptor blockers (ARB)
Angiotensin Receptor Neprolysin Inhibitor (ARNI)
Isosorbide dinitrate (ISDN)
Hydralazine (HYD)
HCN channel blocker
Hydralazine/isosorbide combo (BIDIL)
“AAA I HHH I”
ACE inhibitors MOA + indication
1) decreases angiotensin II
- counteract the activation of RAAS system (compensatory mechanism of HF)
- Vasodilation = ↓ Plasma Volume, ↓ Venous Pressure = ↓ Preload & ↓ Afterload = ↑ CO and ↓ arterial pressure
- DECREASES MORTALITY
2) blocks degradation of bradykinin
- increases vasodilation -> decrease PVR -> lowers BP
Indication:
-Stage A HF*
ACEi ADR
nonproductive cough (20%) *
hyperkalemia *
angioedema*
decrease renal function
rash
abnormal taste
dizziness
angiotensin receptor blockers
-sartan
-used in pts intolerant to ACE inhibitors!!
indication:
- Stage A HF
ARNI- angiotensin receptor neprolysin inhibitor (combination) MOA
Valsartan / Sacubitril (ARB + Neprilysin combo drug)
- DECREASES morbidity + mortality*
MOA
- Valsartan: blocks effects of angiotensin II -> decreases RAAS (dec Na & H20 retention, dec vasoconstriction, dec fibrosis)
- Sacubitril increases natiuretic peptides (↑ natriuresis, ↑ diuresis, ↑ vasodilation, inhibits fibrosis)
ARNI ADRs
hypotension
hyperkalemia
Acute Renal Failure
cough
dizziness
ARNI= “High Highs And Cough Dizzy”
- arni is a guy with high highs and a cough that makes him dizzy
ARB: hyperkalemia, Acute Renal Failure, cough
Sacubitril: dizziness + hypotension
ARNI indications
Move pt from ACEi/ARB to this combo med if BP is adequate
- DUAL MOA: decreases fibrosis and mortality
- good med for HFrEF
isosorbide dinitrate (ISDN) moa
MOA:
-Relaxes VENOUS smooth muscle MORE THAN arterial smooth muscle
- ↓ venous volume + pressure = ↓ pulmonary congestion
drugs: Isordil, Ismo, Imdur
“IS kids are VEIN + need to lower pulmonary congestion (vapers)”
- DIVE -> DInitrate + VEins
Indication of isosorbide dinitrate (ISDN)
-Often combined w/ hydralazine in pts who CANNOT TOLERATE ACEi in Stage C HF
- add on tx after BAD tx in Stage C HF
- AA: hydralazine + ISDN decreases mortality as add on tx to ACEi and BBs
HYD/ISDN:
- improve outcomes for stage C HF with reduced LVEF sx on optimal tx (BAD)
- Stage C HF and cannot tolerate ACEi/ARBs to reduce mortality
- AA population with class III-IV HFrEF on optimal tx
beta blockers MOA
MOA:
- reduce excessive SNS stimulation
- REDUCES MORTALITY in CHF
Reducing SNS stimulation:
- decrease HR + contractility -> decrease O2 demand
- decrease stimulation of renin-angiotensin-aldosterone system
