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What is the formula for blood pressure?
BP = CO x TPR
Explain the "vicious cycle of heart failure"
Poor ventricular performance --> poor perfusion --> body increases vasoconstriction, increases Na retention --> increases ventricular dilation...

This is a "non-correcting cycle"
According to the Starling Curve, ______ _______ increases with LVFP.
According to the Starling Curve, CARDIAC OUTPUT increases with LVFP.
Name four important inotropes
1. Digoxin
2. Dobutamine
3. Dopamine
4. Inamrinone
Digoxin: M of A
Na/K ATPase
Dobutamine: what does it do?
beta-1 agonist
Dopamine: what does it do?
beta-agonist, NE release
Digoxin: M of A
Inhibit Na/K ATPase --> intracellular Na up --> Na/Ca exchanger can't function, so intracellular Ca rises --> contractility up
Digoxin: derived from what?
Foxglove
Digoxin: pharmacology
Long half-life (1.5 -2 days, thus hard to get rid of if things go wrong)
Typically given as a loading dose followed by maintenance.
Digoxin: Major clinical impact
Reduction in the number of hospitalizations due to CHF
Digoxin: What does it do?
Improves contractility
Inhibits AV node conduction
Digoxin: elimination
Renal - may require dose adjustment
Digoxin: alternate names?
Digitalis, Foxglove
Digoxin: AE
- Increased automaticity
- Heart block
- Hyperkalemia ("You can't have Dig tox without hyperK)
- "Van Gogh" like visual changes
- GI effects
Digoxin: drug interactions
Interacts with many other CV agents (amiodarone)
Digoxin: antidote
Binding antibody
"You can't have digoxin toxicity without ____________."
"You can't have digoxin toxicity without HYPERKALEMIA."
Dobutamine: route
IV
Dobutamine: what is it?
Potent beta-1 agonist with peripheral alpha-1 activity (keeps BP steady)

Good because doesn't stimulate beta-2 receptors in the skeletal muscules, causing hypotension.
Dobutamine: what does it do?
- Increases CO

- Reduces heart filling pressures

- Lowers TPR (i.e. the increased tone seen with hypoperfusion goes away)
Dobutamine: major problems associated with what?
With increased HR and myocardial oxygen demand
"Dobutamine Holiday": what is it?
When a patient is admitted and put on IV dobutamine to transiently improve myocardial performance.
Dobutamine: does it improve mortality?
No.
Dopamine: route
IV
Dopamine: what does it do?
Beta-1 agonist, releases NE

Raises BP, improves contractility.
Dopamine: used most often to do what?
To raise BP
Dopamine: AE
Tachycardia, increased myocardial oxygen demand, can lower the threshold for arrhythmias.

Dopamine is essentially "flogging the system"

Can make those with coronary artery stenosis very ischemic
Dopamine: effects at low dose, effects at high dose
At low dose: can cause some vasoconstriction

At high dose: beta-1 activity and NE release.

NE release is not so good, so is only used in the short term
Dopamine: used mainly for what?
BP control
Inamrinone: what is it?
A phosphodiesterase inhibitor used to treat CHF

An agent of last resort, after dobutamine
Inamrinone: route
IV
Oral forms not available due to toxicity and increased mortality (milrinone)
Inamrinone: AE
Cardiac arrhythmias, hypotension
Inamrinone: M of A?
Inhibits phosphodiesterase (which degrades cAMP) --> increased intracellular cAMP.

Targets both the vasculature and the heart.

cAMP up in the heart = revs up
cAMP in periphery = vasodilation
Levosimendan: availability
Only available outside the US
Levosimendan: what does it do?
Sensitizes myocytes to ambient Ca levels --> works to provide more inotropy from endogenous levels of catecholamines.
Levosimendan: M of A
Binds to cardiac troponin C in a calcium-dependant manner

Also produces vasodilation by activating ATP-sensitive K channels in smooth muscle cells
Levosimendan: used for whom?
Very decompensated CHF patients (Class IV).
Levosimendan: AE
Hypotension
Arrhythmias
Hypokalemia (b/c of effects on K channels)
Excess preload reduction comes at the expense of what?
Cardiac output.
Thiazides: AE
Hypokalemia
c/c potency of loop diuretics and thiazides.
Loop diuretics are much more potent
c/c the hypokalemia associated with loop diuretic use vs. thiazide use
Hypokalemia due to loop diuretic use is more severe.
Nitroprusside: route
IV only
Nitroprusside: dilates which vessels?
Both arterial and venous
Nitroprusside: AE
Liberation of cyanide from the thiocyanide complex with NO leads to toxicity.
Nitroprusside: what does it do?
Drops blood pressure and filling pressures.
What the general philosophy about how to lower preload?
By increasing venous pooling (nitroglycerine/nitroprusside) or by reducing intravascular volume (diuretics)
Aldosterone antagonists: mortality and morbidity with CHF
Both reduced!
Spironolactone: what is it?
A K-sparing aldosterone antagonist. A synthetic steriod.
Spironolactone: AE
Can cause hyperkalemia and gynecomastia
Eplerenone: what is it?
A non-steroidal aldosterone receptor antagonist.
Eplerenone: pharmacology
- Longer half-life (4-6 hrs) than Spironolactone

- Metabolized by CYP3A4
Eplerenone: AE
Hyperkalemia
Eplerenone: drug interactions
Metabolized by CYP3A4, so can interfere with other CYP-metabolized drugs like cyclosporine, simvastatin
ACEi: primarily reduce _______.
ACEi: primarily reduce AFTERLOAD.
ACEi: benefits
- Prevents pathologic remodeling of the heart (interrupt neurohumoral stimulation)

- Improves outcomes in patients with low ejection fraction.
Both aldosterone antagonists and ACEi have what affect on potassium?
Increase
ACEi: have to keep an eye on what?
Creatinine
ACEi: AE
Cough and renal toxicity (ACEi --> GFR down --> creatinine up)
ARBs: name two
Losartan, valsartan
ARBs: predominantly reduce what?
Afterload.
ARBs: benefits
- Prevent pathologic remodeling of heart

- Improve outcomes in patients with a low ejection fraction
ARBs: AE
Renal toxicity (but no cough)
ARBs: what are they?
Antagonists to the AII type 1 receptor.
Every CHF that can tolerate them should be on what?
Beta-blockers
c/c magnitude of benefit of ACEi vs. beta-blockers
Beta-blockers have a greater magnitude of benefit.
What is a good way to think about ANP and BNP?
As the "damage signals" of the myocytes
Beta-blockers: used for what class of HF?
Class II and Class III
Nesiritide: what is it?
Recombinant B-type (brain) natriuretic peptide. Produced from bacteria
Nesiritide: what does it do?
Reduces filling pressures and dyspnea in acute decompensated CHF (Class IV)
Nesiritide: route
IV
Nesiritide: AE
Reduces renal function --> increased creatinine.
Why is BNP called "brain" natriuretic peptide?
Because it was discovered there first.
What are three components that are part of "neurohumoral stimulation"?
- The sympathetic nervous system
- The renin-angiotensin system
- The aldosterone system
Hydralazine: what is it?
Vasodilator
Hydralazine: M of A
Unknown
Hydralazine: best paired with what?
With a beta-blocker (due to reflex tachycardia)
An effect similar to that caused by beta-blockers can be achieved with what durg combination?
Hydralazine (direct vasodilator)+ nitrates

(But ACEi and ARBs are better)
Hydralazine: AE
A "wicked" reflex tachycardia
LVH: women vs. men
Women have more of a propensity to remodel pathologically
How do we treat diastolic heart failure?
Almost the same way as systolic heart failure:

1. Reduce the congestive state
2. Maintain atrial contraction
3. Treat and prevent ischemia
4. Control HTN
What are the drugs that increase longevity?
1. ACEi
2. Beta-blockers
3. Aldosterone antagonists