Exam 3 - Chronic HF Flashcards
Define Heart Failure. What is #1 cause?
1 cause=CAD
Inability to provide enough oxygenated blood to body.
What is the most common form of HF and its result?
Systolic HF. LV can’t get blood to body due to dialation and hypertrophy.
Define Cardiac Index. Normal range? What is the CI in HF patients?
Measure of pumping ability from left ventricle to deliver O2. In HF patients their Cardiac Index is low.
Normal range: 2.5-4
What is Ejection Fraction? What percent is normal? Systolic and Diastolic HF values?
Amount of blood pumped/end diastolic volume. Below 40% is bad.
Normal=70%
Systolic HF is 3/10 and 30%
Diastolic HF is problem of filling, pumping 3 but can only hold 5, 3/5 for 60%. Looks normal but isn’t.
What is mortality of rate in 5 years of heart failure if nothing done? What if everything is done?
Nothing done=50% after 5 years
Everything done=35% after 5 years
What are the 4 compensatory mechanisms of HF?
- RAAS
- SNS
- Ventricular Hypertrophy
- Frank-Starling Law (increase end diastolic pressure)
Which four drugs reduce HF mortality?
- ACEI/ARBs
- BBs
- Aldosterone blocking agents
- Vasodilators (in AAs)
Two drugs which reduce HF morbidity?
- Digoxin
2. Diuretics
Treatments for Stages A and B of HF?
A=Treat risk factors. ACEI/ARBs
B=ACEI/ARBs or BBs
Routine treatment for Stage C HF? Selected PTs?
Treatment for Stage D HF?
Routine C: ACE/ARBs, BB, diuretics.
Selected C PT: Aldosterone antagonist, digitalis, hydralazine/nitrates
Stage D: End-of-life care. Hospice, transplant, IV Dobutamine
ACEI/ARB MOA? Effects on kidneys, H2O/Na, BP, Afterload? Place in therapy?
Interference with RAAS ending by disrupting Angiotensin II.
Decrease BP, decrease Na/H2O retention, decrease Afterload.
Highly excreted with kidneys. Only modify dose if K+ bad.
Used in all stages of HF.
ACEI/ARB absolute contraindications?
Preggers, K+ above 5, bilateral renal artery stenosis, angioedema
Sacubitril/valsartan (Ernesto) MOA and place in therapy? Time to convert from ACE to Ernesto?
Valsartarn=ARB
Sacubitril=Blocks neprilysin causing vasodilation
Together they add more vasodilation than ARB or ACEi alone.
Used in newly diagnoses with EF less than 40%. Wait 36 hours.
Beta-Blocker MOA? Effect on coronary areries? Which three can be used?
Block beta receptors decreasing HR and BP. Increased coronary artery blood flow.
- Metoprolol Succinate
- Bisoprolol
- Carvedilol
What stages are Beta Blockers used in? ADR? Why not Metoprolol Tartrate?
A, B, C.
ADRs=Bradycardia, worse HF is BB dose started too high, respiratory issues
Metoprolol Succinate has better outcomes.
MOA and place of Ivabradine?
MOA: selectively inhibits “funny channel” in SA and AV nodes and reduces HR
Place: All other meds maxed out and EJ less than 35%. Further enhances Beta-Blockers.
Aldosterone MOA and place in which stages? Preload? CI?
MOA: Competes with Aldosterone for intracellular mineralcorticoid receptors. Decrease Na/H2O, increase K. Decreases Preload.
Place: In Stages C and D if on max ACEi/BB and still symptomatic.
CI: Hyperkalemia
Hydrazaline and Isosorbide are what class of drugs? Where does each work? Who used in?
Vasodilators.
Hydrazaline=coronary, cerebral, renal arteries
Isosorbide=vasodilation via NO
Used in African Americans.
Which diuretics best in HF? Does it improve morbidity or mortality?
Loop Diuretics best. Morbidity.
Loop Diuretic MOA? Preload and edema effect? Kidneys?
Increase Na/H2O excretion in Loop of Henle. Reduce preload and edema. Can be used with bad kidneys!
What stages get Loop Diuretics? What might you have to do with dose for diuretics and renal failure?
Stages C or D, only if symptomatic.
Increase dose with renal failure.
Four most common Loop Diuretics electrolyte abnormalities?
Hyperglycemia, Hyperuricemia
Hypokalemia, Hypomagnesemia
Digoxin MOA? Which VD and who gets toxic? How excreted?
MOA: Positive inotropic (+CO), negative chronotropic. Increased Intracellular Na and Ca causes inotrope.
Elderly become toxic due to small VD.
Renally excreted.
Signs of Digoxin toxicity? Hyper/hypokalemia and Digoxin?
Bradycardia, heart failure, and hypokalemic.
Hyperkalemia=decrease effects of digoxin
Hypokalemia=increase effects of digoxin
How to treat Diastolic HF?
No gold standard. Goal to treat underlying condition.
What are 4 the ACC/AHA stages of HF? Which most commonly seen in hospital or clinic?
Class A=at risk, no structural changes
Class B=ventricular hypertrophy and found incidentally
Class C=the typical PT seen in clinicals
Class D=end-of-life
Define Preload and Afterload. What happens to LV from afterload?
Preload=amount of blood at end of diastole (end diastolic volume)
Afterload=amount of pressure heart pumps against for systole (measurement of systemic resistance). LV hypertrophy.
Define Pulmonary Capillary Wedge Pressure. What will it be in HF patients? Normal range?
Measurement of what’s happening in the capillaries as volume status in the lungs. In acute decom HF PCWP will be high!
Normal range: 8-12
Which 4 meds renally excreted
- ACEi
- ARB
- Aldosterone blocker
- Digoxin
When to reduce or d/c loop diuretics?
When excess fluid gone
ACEi/ARB decrease which load?
Aldosterone-blocker deceases which load?
ACEi/ARB=Afterload
Aldosterone=Preload
Most common ADE of Digoxin?
Stomach funk
