Term
| What drugs would you use to lower cholesterol and triglycerides (first line, second line, ect.) |
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Definition
1) Start them on a statin (HMG-coA reductase inhibitor).
- look out for rhabomyolysis, but 95% well tolerated.
2a) Add Ezetimibe if LDL-C levels don't lower enough
2b) Add Niacin too raise HDL-C and to lower TG levels
2c) Try adding Bile acid resins, but look out for increased TG.
3a) Use Fibrates if patient HDL-C is low and if patient does not response/responds negatively to Niacin. |
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Term
| Under what conditions might you prescribe Niacin, and how does it work? |
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Definition
1) Either to replace statin (myopathy) or as an adjuvent to raise HDL-C and lower TG
2) Niacin a) prevents release of free fatty acids from adipose, thereby limiting hepatic TG synthesis, b) limits VLDL release (because of TG effect) and c) increases HDL (limits apoA metabolism). |
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Term
| When might you prescribe a fibrate drug and how do they work? |
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Definition
1) In patients with low HDL-C who do not respond to Niacin treatment. WATCH OUT FOR MYOPATHY IF THEY ARE ON A STATIN.
2) Increase peripheral lipolysis and decrease hepatic TG synthesis |
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Term
| Under what conditions might you prescribe a statin, and how does it work? |
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Definition
1) First line to lower LDL-C and prevent CHD.
2) HMG-coA reductase inhibitor prevents cholesterol synthesis and leads to increased LDL-receptor synthesis (leading to more non-HDL lipoprotein metabolism as well). |
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Term
| Under what conditions might you prescribe a bile acid sequsterant, and how does it work? |
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Definition
1) To lower LDL-C further in patients on a statin.
**may increase TG levels, however**
2)Prevents bile acid circulation from intestine to liver, leading to increased bile acid synthesis from cholesterol in liver (7-alpha hydroxylase mediated). This leads to increased LDL-receptor expression and further free cholesterol elimination. |
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Term
| Under what conditions might you prescribe Ezetimbe, and how does it work? |
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Definition
1) To further lower LDL-C in patient on a statin
2) Prevents micelle uptake of cholesterol in intestine (inhibits sterol transporter), decreasing delivery to liver. Liver then starts to take up more cholesterol from blood as a result. |
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Term
When should you prescribe Beta-blockers?
How do you choose which ones to use?
When should they NOT be used? |
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Definition
1) Effective to treat
- Systolic heart failure (blunts cardiotoxic effects of elevated catecholamines)
- HOCM
- HTN
- ACS/Ischemic heart disease (Reduce oxygen demand by decreasing HR and preventing RAAS and sympathetic effects on LV remodeling)
- A fib/Tachyarrhythmias
- Chronic exertional angina
2) In diabetes or peripheral vascular disease, use a beta-selective drug like Metoprolol, but in HTN or LV dysfunction use a drug with alpha activity to cause vasodilation.
3) Avoid in conditions of volume overload (aortic insufficiency, mitral regurgitation) or LV dysfunction (aortic stenosis) |
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Term
True or False:
Digoxin is effect in treating diastolic heart failure. |
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Definition
False.
Digoxin treats systolic HF by increasing contractility (mechanical) and may treat arrhythmia by slowing AV conduction velocity (electrical) |
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Term
| What drug(s) tend to cause delayed afterdepolarizations at high doses? |
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Definition
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Term
| Why might you use dobutamine in heart failure? |
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Definition
Does not have a large effect on HR, so it is favorable for a sensitive oxygen supply/demand balance.
For severe, cold wet failure (volume overloaded with low CO), you may want the positive inotrope to "whip" the heart. |
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Term
| Why not give verapamil with a beta blockers after an acute MI? |
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Definition
| They are both negative inotropes. Dont ever give beta blockers with ISA activity after an MI, because the vasoconstriction will be a problem (increasing afterload). |
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Term
| Why not give a volume-depleted CHF patient an ACE-inhibitor? |
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Definition
| They already don't have enough volume, so you will make them even more hypotensive and you may cause renal insufficiency |
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Term
| Why might HR decrease following NE addition? |
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Definition
| The NE will bind alpha receptors and increase MAP. The central baroreceptors will sense this and fire less. This will slow down the HR. However, if you give a ganglionic blocker, this reflex will be prevented! |
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Term
| Under what conditions should you be careful giving beta blockers? |
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Definition
1) Diabetes (hypoglycemia)
2) Peripheral vascular disease (cause claudication/raynaud's if alpha block)
3) Asthma (B2 block could cause vasospasm)
4) LV dysfunction (make contractility even worse).
5) Volume overload (decreasing heart rate and contractility may worsen pulmonary edema) |
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Term
| What agents should be given following an acute MI? |
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Definition
| 1) Ace-inhibitor, Aspirin, Beta blocker, Statin and diuretic. |
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Term
True or False:
Digoxin and ACE-inhibitors increase tolerance to exercise. |
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Definition
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Term
| When do you give hydralazine with isosorbide dinitrate? |
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Definition
| To african americans in heart failure to cause vasodilation and decrease ROS damage. |
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Term
How should you alter each of the following in Aortic Stenosis?
1) HR
2) Heart rythm
3) Contractility
4) Preload
5) Afterload
Good drugs/Bad drugs? |
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Definition
Remember, issue in aortic stenosis is diastolic dysfunction, with elevated LVEDP leading to concentric hypertrophy and ultimately to decompensated heart failure.
1) Leave it alone (keep it 50-80)
2) Sinus rhythm is a MUST- when exercise demands more blood from atrium, and it is not kicking correctly due to A fib, there won't be enough
3) Leave it alone
4) Increase preload
5) Increase afterload (need to maintain DBP to keep perfusion since coronary perfusion= DBP- LVEDP
Phenylephrine would be a good idea to increase afterload, but avoid beta blockers, because they will decrease HR and contractility. |
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Term
How should you alter each of the following in Aortic Insufficiency?
1) HR
2) Heart rythm
3) Contractility
4) Preload
5) Afterload
Good drugs/Bad drugs? |
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Definition
Here there is too much blood rushing back into the LV, so you need to speed things up an get it out of there.
1) Increase HR to prevent fluid buildup
2) rhythm doesn't really matter here
3) Increase contractility for same reason as 1
4) Preload doesn't really matter
5) Decrease afterload (get blood systemically when you can)
Beta agonists would be good here, since they will increase HR and decrease TPR (dobutamine)
Avoid beta blockers which will decrease HR and contractility |
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Term
How should you alter each of the following in Mitral regurgitation
1) HR
2) Heart rythm
3) Contractility
4) Preload
5) Afterload
Good drugs/Bad drugs? |
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Definition
Here there is too much blood rushing back into the LA, so you need to speed things up an get it out of there.
1) Increase HR to prevent fluid buildup
2) rhythm doesn't really matter here
3) Increase contractility for same reason as 1
4) Decrease preload (already too much fluid here)
5) Decrease afterload (same reason)
Beta agonists would be good here, since they will increase HR and decrease TPR (dobutamine)
Avoid beta blockers which will decrease HR and contractility |
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Term
How should you alter each of the following in HOCM?
1) HR
2) Heart rythm
3) Contractility
4) Preload
5) Afterload
Good drugs/Bad drugs? |
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Definition
In HOCM, you have a dynamic LVOT obstruction (SAM), so you don't want to let LVEDV get too small (opposite of MR).
1) Slow it down to increase filling and keep LVEDV
2) Keep them in sinus rythm
3) Decrease contractility to keep LVEDV high enough
4) Increase preload to keep LVEDV high
5) Increase afterload to maintain perfusion pressure for CA.
Don't give beta-agonists (slow that HR down!). Try Beta blockers perhaps or phenylephrine with fluids. |
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Term
| What is the treatment for chronic post-MI management? |
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Definition
A2BC2D & N
1a) Aspirin (or warfarin, depending on risk) for clotting
1b) Ace-inihibitor (prevent sympathetic remodeling and control BP)
2) Beta blocker to limit O2 demand
3a) Cholesterol-lowering statin to stabalize plaques over time (first reverses endothelial damage, then later stabalizes plaque)
3b) Clopidogrel for clotting
4) Diuretic for volume control
5) Nitrates may also be added for comfort. |
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Term
| What is the correct chronic management of ischemic heart disease? |
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Definition
1) Start with a beta blocker (perhaps with a1 activity for HTN or LV dysfunction).
2) Add nitrate if necessary for further afterload reduction
3) If beta blocker cannot be tolerated, try calcium channel blocker |
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Term
| What is the appropriate pharmacological management of heart failure? |
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Definition
Need to stop RAAS and Sympathetics from remodeling LV
Depends on stage
A (high risk factors): ACE-i, ARB or nitrate/hydralazine
B (Structural changes): A + Diuretic + beta blocker (carvedilol) so long as patient is NOT hypervolemic
C (Symptomatic): B + Warfarin and Defibrillator + Digoxin (for symptoms)
** may add dobutamine/milrinone if cold and wet**
D (Symptoms as rest): C + IABP or transplant |
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Term
| What drugs can be added to HF treatment to improve symptoms as needed, but are also dangerous because of SE? |
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Definition
1) Diuretics for edematous patient (not too dangerous)
2) Digoxin to get that heart to contract, but watch out for "nausea, yellow halo vision and arrhythmia"
3) + Inotropes (milrinone and dobutamine) for COLD and WET, but they will demand more O2 and increase mortality |
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Term
Do you treat a patient with atypical anginal chest pain following a negative stress test?
What about a patient with non-anginal chest pain? |
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Definition
1) 50% pretest probability for atypical angina, so a negative stress test would make you run more tests before treating.
2) 15% pre-test probability for non-anginal chest pain, so a negative test would mean don't treat. |
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Term
| When should you give Aspirin, Clopidogrel and/or Abcixumab for acute coronary syndromes?? |
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Definition
Anti-platelet drugs
- Aspirin and Clopidogrel (stop after 1 year) for all ACS patients!
- Abcixumab in acute situation is given acutely during stenting. |
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Term
| How should anti-thrombin drugs be used for patients with acute coronary syndromes? |
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Definition
1) Heparin (and analogs) are used acutely and during stenting procedures;may be continued several days as prophylaxis for DVT until MI patients are fully ambulatory.
2) Warfarin is used instead of aspirin in patients
with more severe embolism risk (A-fib, mechanical valve,
decompensated ventricle, prior stroke). |
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Term
When should you use class II or IV anti-arrythmic drugs?
What about Class 1A/1C/III? |
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Definition
1) Beta or Calcium channel blockers for supraventricular arrhythmia involving AV node (WPW & AVNRT)
2) Sodium or Potassium blockers for all other supraventricular arhythmias
1A like procainamide increases refractory period (broad use), while 1C doesn't (only for severe tachyarrhythmias) |
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Term
| When can Ranolazine be prescribed? |
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Definition
Delayed Na+ channel inhibitor used to treat ischemic heart disease (prevent calcium overload).
Use in high WALL-stress conditions (high preload or decompensated HF) |
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Term
| When might you want to increase the "preload" of a patient in heart failure? |
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Definition
If it was 1) an acute MI with low volume and low cardiac output (a cold dry case) or 2) a RV infarct
You would want to venoconstrict in this case, perhaps with phenylephrine. |
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