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116 Cards in this Set
- Front
- Back
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What 3 factors go into SV?
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1. preload
2. afterload 3. contractility |
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T or F: under steady state conditions, cardiac output and venous return are equal.
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true
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Ventricular wall stress at the end of diastole is called what? At the end of systole?
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1. preload
2. afterload |
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What are the general physiological conditions that lead to HF?
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1. pressure overload
2. volume overload 3. loss of functional myocardial tissue 4. generalized decrease in myocardial contractility 5. restricted filling |
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What is an example of restricted filling that occurs in HF?
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constrictive pericarditis- prevents heart from moving around or relaxing
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What is the difference between systolic dysfunction and diastolic dysfunction in HF?
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1. systolic-weak squeeze
2. diastolic-can't relax |
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Diastolic dysfunction in HF is also known by what name?
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HF with preserved ventricular ejection fraction
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Where will fluid end up in right-sided HF? Left-sided HF?
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1. peripheral edema
2. pulmonary edema |
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SNS activation of alpha-1-receptors on vascular smooth muscle occurs via which catecholamine?
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NE (EPI binds to alpha-2)
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In addition to SNS stimulation, what other property causes vasoconstriction in response to decreased BP?
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endothelin-1
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When HF first develops, what happens?
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SNS stimulation and RAAS are too much for body to handle
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Explain some of the counter-regulatory effects that occur during HF.
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HF->increased wall A/V stretch from too much blood left in chambers->release of ANP and BNP->increased Na+ excretion and vasodilation
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What is a lab test that may show the degree of HF?
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BNP
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T or F: compensatory mechanisms in HF are long term and do not become maladaptive.
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false-they are short term and become maladaptive in the long run
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What are some long term consequences of maladaptive compensatory mechanisms of HF?
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1. increased HR
2. increased force of contraction 3. increased afterload and preload 4. vasoconstriction 5. increased Na+ retention (all of these will cause heart damage and lead to edema) |
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What are the events of cardiac remodeling?
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1. cardiac hypertrophy
2. fibrosis 3. myocyte apoptosis 4. ventricular chamber dilation (these changes are due to excess NE, Angiotensin II, and aldosterone) |
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What are the 2 states of HF?
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1. acute decompensation
2. stable chronic HF |
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What are the treatment goals of HF?
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1. improve ejection fraction
2. symptomatic relief of pulmonary edema 3. reduce cardiac remodeling |
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What are the 2 ways to improve ejection fraction?
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1. increase contractility-positive inotropic drugs
2. decrease afterload-arteriolar dilators |
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What are the 2 ways to relieve preload to help with pulmonary edema?
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1. reduce preload via diuretics
2. reduce preload via venous dilators |
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How can you reduce cardiac remodeling?
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block the remodeling effects of excess neurohormonal activation on the heart
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Does myocardial contraction occur during depolarization or repolarization?
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depolarization
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What is the sequence of events in depolarization?
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Na+ influx->Ca++ influx (this is "trigger" Ca++)->stimulates RyR on SR->SR Ca++ released->stimulates further Ca++ release->contraction
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What events occur in repolarization?
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1. Na+ extruded via Na+/K+/ATPase
2. Ca++ extruded via Na+/Ca++ exchanger 3. Ca++ taken up in SR via SERCA pump |
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Which intracellular Na+ level will inhibit the Na+/Ca++ exchanger? Which will stimulate it?
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1. high Na+ inhibits
2. low Na+ stimulates |
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What drives the Na+/Ca++ exchanger?
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transmembrane Na+ gradient
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What is the MOA for digoxin?
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inhibits Na+/K+/ATPase->increases intracelleular Na+->inhibits Na+/Ca++ exchanger->increases intracellular Ca++->increases SR Ca++->more powerful contraction
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What will increased extracellular K+ do to the Na+/K+/ATPase pump of the myocardial cell?
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inhibits
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What does hyperkalemia do to digoxin? Hypokalemia?
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1. reduces action
2. increases action |
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Which drugs can cause hyperkalemia? Hypokalemia?
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1. aldosterone antagonists and ACEI's
2. thiazides and loops |
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What indirect effects does digoxin have?
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1. increases vagal activity
2. sensitizes baroreceptors and decreases SNS activity (these will decrease SA/AV activity) |
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What neurohormonal effect does digoxin have on HF?
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decreases SNS activity->decreases NE->prevents remodeling
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What are digoxin's toxic effects on the heart?
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1. low doses: sinus bradycardia and AV block
2. high doses: increased SNS tone and Ca++ overload |
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What will happen if you get Ca++ overload?
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spontaneous release of Ca++ from SR->DAD->aftercontraction
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In a damaged heart, what can excessive SNS tone and Ca++ overload cause?
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arrhythmias
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A major concern of digoxin is its low ____ ____.
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therapeutic index
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Digoxin is used to treat HF in what stages?
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C and D
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Digoxin is usually used in conjunction with what drugs?
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1. ACEI
2. diuretics 3. BB |
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T or F: digoxin may be given to stabilize a patient.
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false-it may be given after a patient is stabilized
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What are the stages of HF?
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1. Stage A-high risk for HF, no structural damage
2. Stage B-structural damage 3. Stage C-structural damage w/HF 4. Stage D-end-stage HF |
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What are the NYHA classes for HF?
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1. Class I (mild)-no limitation of physical activity
2. Class II (mild)-slight limitation of physical activity 3. Class III (moderate)-marked limitation of physical activity 4. Class IV (severe)-symptoms at rest |
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Which arrhythmias can digoxin be used to treat?
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a-fib and a-flutter (increases vagal activity to slow ventricular rate)
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Digoxin can cause which arrhythmias?
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1. sinus bradycardia
2. AV block 3. a-tach 4. premature ventricular contractions 5. v-tach and v-fib |
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In addition to the heart adverse effects of digoxin, what are the other adverse effects?
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1. increased GI motility
2. CTZ stimulation-N/V 3. CNS problems 4. visual disturbances 5. gynecomastia |
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What is usually the first sign of digoxin toxicity?
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nausea and vomiting
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What are 3 factors that enhance digoxin toxicity?
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1. hypokalemia
2. hypercalcemia 3. hypomagnesemia |
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What can a patient be given if they exhibit digoxin toxicity? When?
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1. digoxin Fab->binds to digoxin, decreases free digoxin in bloodstream
2. only in life-threatening situations |
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How are ACEI's used to treat HF?
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1. arteriolar dilators->reduce afterload->increase CO
2. decrease angiotensin II->decrease aldosterone->decrease Na+ and H2O reabsorption->decrease preload->increase CO |
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T or F: ACEI's will decrease Na+ and H2O reabsorption, so pulmonary edema is relieved by these drugs.
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false-after several months, aldosterone levels will be elevated
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What do high levels of angiotensin II do to the heart?
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1. myocyte hypertrophy
2. myoctye apoptosis 3. fibroblast hyperplasia |
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What is the major effect of ACEI's on HF?
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prevents cardiac remodeling (will also reduce afterload and some preload)
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ACEI's are used for what stages of HF?
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1. certain patients in A and B
2. all patients in C and D |
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How should ACEI's be given for HF?
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start at low dose and titrate up
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When would you avoid ACEI's?
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kidney problems
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What are the biggest concerns of ACEI's in HF?
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1. hypotension
2. renal impairment 3. hyperkalemia |
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When might you use an ARB with an ACEI?
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patients with low LVEF and conventional treatment isn't helping
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What specific BB's are used in HF?
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1. metoprolol
2. bisoprolol 3. carvedilol |
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What have studies shown about using bucindolol for HF?
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increased mortality
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T or F: carvedilol is an alpha and beta blocker.
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true
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How does excessive SNS stimulation contribute to cardiac remodeling and HF?
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1. myocyte apoptosis
2. altered myocardial gene expression (reverts to fetal gene expression) 3. cardiac hypertrophy 4. fibroblast hypertrophy |
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Overstimulation of SNS will downregulate what?
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beta receptors
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What are some theories as to why BB's will help with HF?
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1. prevent or reverse cardiac hypertrophy and remodeling
2. prevent beta-1 receptor down regulation 3. correct impaired intracellular Ca++ handling 4. decrease cardiac workload 5. prevent atrial/ventricular arrhythmias |
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T or F: ACEI's and BB's will reduce HF mortality.
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true
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What patients should receive BB's for HF?
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1. Stage B post-MI or low EF
2. Stage C and D (stable) |
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How much would a starting dose of metoprolol be? Carvedilol?
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1. 12.5-25 mg QD
2. 3.125 mg BID |
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What populations with HF might have significant beneficial effects from BB's?
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diabetics
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What is a good 3-drug combo for mild HF patients?
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ACEI, BB, and diuretic
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Abrupt withdrawal of BB can have what effect on HF patients?
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deterioration of cardiac function
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BB's are contraindicated when?
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1. acutely decompensated HF
2. symptomatic bradycardia or heart block w/o pacemaker 3. asthma |
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Can patients with COPD or diabetes be given a BB?
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yes
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If a patient presents with acute decompensated HF, would you want to remove their BB?
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no
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If you reduce preload, what happens to pulmonary edema?
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decreased
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What effect will diuretics have on CO in a patient with HF?
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little or no effect
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What are the end results of diuretics on HF?
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1. reduce pulmonary and peripheral edema without adversely affecting CO
2. decrease in wall stress may also slightly improve systolic function |
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Which diuretic is most effective in treating HF?
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loops-only drugs that can control fluid retention in HF
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What stage of HF will get a diuretic?
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C or D
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What is one of the major problems associated with K+ or Mg++ depletion?
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arryhthmias
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Why might an aldosterone antagonist be considered for HF?
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ACEI's may cause only a transient aldosterone decrease
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What are the effects of aldosterone on the blood vessels?
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1. endothelial dysfunction
2. inflammation 3. vascular fibrosis 4. prothrombic effects |
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What is the overall effect of using aldosterone antagonists and ACEI's on HF?
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decreased hospitalizations and mortality
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When using ACEI's and aldosterone antagonists in HF, what should you be careful of?
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hyperkalemia
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What stage HF will you use ACEI's with aldosterone antagonists?
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Stage C and NYHA Class III-IV
(moderately severe to severe HF w/recent decompensation or w/LV dysfunction early after an MI) |
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Serum creatinine levels must be considered when giving an ACEI/AA combo. What are the levels that are ok?
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1. males <2.5 mg/dl
2. females <2.0 mg/dl |
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What are the vasodilators used in chronic HF?
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1. hydralazine
2. isosorbide dinitrate |
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What is the MOA of hydralazine in HF?
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arteriole dilator->decreases afterload->increases ejection fraction and decreases wall stress
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What is the MOA of isosorbide dinitrate in HF?
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venous dilator->decreses preload->decreases edema and wall stress
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What are 2 beneficial features of hydralazine in HF?
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1. may have antioxidant effect
2. prolongs NO effects |
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When might you try hydralazine in combination with isosorbide dinitrate?
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1. african americans on optimal therapy w/moderate to severe sx
2. Stage C patients who can not use an ARB or ACEI |
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What is the goal in the pharmacological treatment of acute decompensated HF?
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1. relieve pulmonary congestion if present
2. decrease pump failure if present |
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How can pulmonary edema be reduced in acute decompensated HF?
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reduce preload
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How can CO be increased in acute decompensated HF?
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reduce afterload or increase contractility
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What are 2 drug classes that can reduce preload?
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1. venous dilators
2. diuretic |
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What drug class can reduce afterload?
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arteriolar dilator
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What 5 drug classes are given in acute decompensated HF?
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1. loop diuretics
2. nitroglycerin 3. nitroprusside 4. nesiritide 5. + inotropic drugs |
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How do loops decrease pulmonary edema?
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1. diuresis->decreased LV filling pressure->reduced pulmonary edema
2. vasodilation (IV)->stimulates PG's->increased venous capacitance->decreased LV filling pressure->reduced pulmonary edema |
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What do you have to be concerned about when using loops for decompensated HF?
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1. excessive diuresis
2. hypotension 3. electrolyte disturbances 4. worsens renal function |
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What is the best choice for treating congestion or pulmonary edema in a patient with acute decompensated heart failure?
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loops; if already on a loop, give IV loop; if that doesn't work, give thiazides
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Nitroglycerine and nitroprusside work for HF by working on what vessels?
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1. nitroglycerine-veins
2. nitroprusside-arteries and veins |
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Nesiritide is also called what?
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Recombinant human B-type natriuretic peptide (BNP)
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BNP is released from the ventricles in response to what?
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in response to increased wall stress, hypertrophy, and volume overload
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What is the MOA for nesiritide?
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activates guanylyl cyclase on vascular smooth muscle cells->increases cGMP->dilates arteries and veins
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What effects does nesiritide have in the kidneys?
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1. constricts efferent arteriole and dilates afferent arteriole, increasing GFR
2. increases natriuresis |
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When would you use nitroglycerine, nitroprusside, or nesiritide?
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acutely decompensated HF:
1. added to diuretics for patients with evidence of severely symptomatic fluid overload in the absence of systemic hypotension 2. relief of angina (nitroglycerin) 3. control of HTN complicating HF |
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What are the adverse effects of nesiritide?
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1. hypotension
2. HA 3. worsening renal function 4. possible increase in mortality 5. not approved for intermittent IV use |
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Giving drugs that increase myocardial contractility is indicated in what Stage HF? Are these positive inotropic drugs for short or long term?
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1. D
2. short term |
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What are the positive inotropic drugs for HF?
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1. dobutamine
2. dopamine 3. PDE inhibitors (inamrinone and milrinone) |
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Dobutamine works on which receptors?
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1. beta-1 on heart to increase inotropy
2. beta-2 on vessels to increase vasodilation 3. alpha-1 receptors on arteries to vasoconstrict |
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What is the end result of using dobutamine?
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increases contractility without increasing HR
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Which receptors does dopamine work on?
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dopaminergic->increase dose->beta->increase dose more->alpha receptors
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What is dopamine's main action in HF?
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1. dilates renal arteries (among others)->better renal perfusion
2. acts on beta-1 receptors to increase contractility 3. acts on alpha-1 receptors to vasoconstrict aa.->raise BP |
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How do PDE inhibitors work?
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1. inhibits break down of cGMP, causing:
a. vasodilation b. increased contractility c. increased heart relaxation |
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What happens if you take PDE inhibitors in long term?
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increased mortality
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What does inamrinone cause?
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thrombocytopenia
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What can PDE inhibitors cause?
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arryhthmias and hypotension
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In what stage of HF would you use dobutamine, dopamine, or milrinone?
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Stage D patients with severe refractory HF (IV)
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T or F: positive inotropic drugs will reduce mortality and have proven benefits
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false
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