CAD - Wendt Flashcards by Kelly Weaver

What factors contribute to increased oxygen consumption?

Increased HR, contractility, afterload, and preload

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What is afterload?

The pressure in the veins that the heart has to match to push blood through the body

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What is preload?

The volume of blood that enters the heart during diastole

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If veins are dilated preload is (increased/decreased)?

Decreased

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If preload is (increased/decreased), oxygen consumption increases?

Increased

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What are risk factors for angina?

Age (>55 for men, >65 for women)
Cigarette smoking
Diabetes
HTN
Kidney disease
Obesity
Sedentary lifestyle

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What two factors will increased coronary perfusion when they decrease?

HR and preload

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How does preload increase the demand of the heart?

The heart has to stretch more to accommodate a larger blood volume

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Why does a decreased HR increase coronary perfusion?

It allows the heart to spend more time in diastole, when blood can flow into coronary vessels

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What are the 3 types of angina?

Printzmetal's Variant
Chronic stable (fixed stenosis--narrowing of blood channel)
Unstable (from thrombus)

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What causes stable angina?

Atherosclerosis which causes oxygen demand to exceed supply

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What factors precipitate stable agnina?

Exertion, food, emotions (stress, anger, etc)

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What are the characteristics of variant angina?

Sudden and transient constriction; often occurs at rest and at night; hard to diagnosis because vessels look healthy

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Is variant angina supply ischemia or demand ischemia?

Supply–cardiac myocytes don’t receive enough oxygen

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What are characteristics of unstable angina?

A sudden worsening of angina at rest

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What causes unstable angina?

Thrombosis or plaque rupture

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What treatment strategy is used for unstable angina?

Inhibit platelet function, dissolve clot

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Which type of angina often comes before an MI?

Unstable angina

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What drug classes are used to increase oxygen delivery?

Vasodilators (CCBs, nitrates)

Anti-thrombotics (anticoags, antiplatelets)

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What drug classes are used to decrease oxygen demand?

Vasodilators
Cardiac depressants (beta blockers, CCBs, HCN channel inhibitor)

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How does vasodilation occur via NO?

Endothelial cells produce eNOS –> increased NO production –> NO –> moves to VSM –> causes vasodilation by activating cGMP –> MLCP–> dephosphorylates MLC –> can’t bind to actin –> vasodilation

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What are the organic nitrate drugs?

Glyceryl trinitrate
Isosorbide mononitrate
Isosorbide dinitrate

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Which of the nitrates is longest acting?

Isosorbide mononitrate

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Which of the nitrates is shortest acting?

GNT

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Which of the nitrates are used for angina prophylaxis?

5-ISMN, ISDN

Which of the nitrates develop tolerance?

All organic nitrates

What is the mechanism of GTN tolerance?

mtALDH is sulfated irreversibly to activate GTN--run out of the enzyme as it is permanently inactivated

How long does GTN tolerance last?

a few hours

Are organic nitrates more effective in the veins or the arteries? Why?

Veins | Veins are more flexible/able to dilate

How do CCBs work?

Decrease Ca influx in myocytes

What do CCBs do?

Dilate arteries and decrease HR

CCBs primarily effect (preload/afterload)?

Afterload (dilating arteries decreases BP)

Why do CCBs not affect veins as much?

Veins have a larger calcium store in SR; rely less on extracellular calcium

How do CCBs work?

Block Ca--Ca is needed to phosphorylate MLC (via CAM) to allow binding to actin and contraction. No Ca means no contraction --> dilation

Which class of CCB is most effective for treating angina?

Dihydropyridines (effect vessels rather than heart)

Beta blockers block ______ stimulation of myocardium to ___ HR and ____ coronary perfusion

Block epinephrine stimulation to lower HR and increase coronary perfusion

How do beta blockers affect angina?

Reduce oxygen usage

When during a heart beat is coronary perfusion highest?

Diastole

What is the MOA of beta blockers in VSM cells?

Blocks this pathway: Epinephrine binds to receptor --> increase in cAMP --> increase in PKA --> decrease in MLCK --> Relaxation (no binding with actin)

What is the MOA of beta blockers in cardiac myocytes?

Blocks this pathway: Beta agonist binds to receptors --> active AC --> increased cAMP --> PKA --> Ca released from SR --> contraction in myocytes (CAM)

What are the cardioselective Beta blockers?

Atenolol Metoprolol Acebutolol

What are the non-selective beta blockers?

Propranolol Carvedilol Pindolol Labetalol

What patient population is it particularly important to use cardio-selective beta blockers?

Patients with COPD/asthma (non-cardioselective cause bronchiole constriction)

What are the problems with nitrates, Beta blockers, and CCBs?

Reflex tachycardia Increased preload Constipation

Which drug classes cause reflex tachycardia? Why?

Nitrates and DHP CCBs | They affect BP only - not heart

What medications can be used to prevent reflex tachycardia?

Beta-blockers

What medication causes an increase in preload?

Beta-blockers (by decreasing HR/contractility, filling time increases)

What medication can prevent an increase in preload caused by Beta blockers?

Nitrates! (They dilate vessels, so more blood can be stored in them)

Why are most angina drugs used in combinations?

To counteract the negative effect of one with the other

What are the major side effects of non-specific beta-blockers?

LV dysfunction, bradycardia, bronchoconstriction

What are the major side effects of nitrates?

Hypotension/Flushing headaches (from drop in BP)

What are the major side effects of diltiazem?

generally well-tolerated--some flushing/HA, LV dysfunction, bradycardia

What are the major side effects of DHPs?

Hypotension, flushing/HA

What are the major side effects of verapamil?

LV dysfunction, bradycardia, GI ditress

Which angina treatment option has the most potential for GI distress?

Verapamil

Which angina treatment option has the most potential for hypotension/flushing/HA?

Nitrates, DHP CCBs

Which angina treatment medications may cause bradycardia?

Beta-blocker, verapamil

What do HCN Channels transport? Where?

Sodium into the cell in the SA Node

How are HCN Channels activated?

Hyperpolarization

What is an HCN Channel inhibitor?

Ivabradine

How do HCN channels help treat angina?

``` Slow HR (reduced oxygen consumption) Prolong diastole and improve ventricular filling (increase perfusion) ```

What can HCN channel inhibitors be used for?

Angina Inappropriate sinus tachycardia Heart failure

What is a major benefit of ivabradine?

No hemodynamic abnormalities (no changes in blood pressure/vasculature)

What is the NCX?

A channel that takes in Na and releases Ca - used to balance Ca concentrations

When myocytes don't have enough oxygen, they ____ sodium uptake, which decreases ______. This ____ Calcium flow and ___ heart function

increase sodium uptake; decreases sodium gradient. Increases calcium flow and increases heart function (b/c calcium stimulates heart)

Which drug is an NCX blocker?

ranolazine

What are side effects of ranolazine?

Dizziness and QT prolongation

Does ranolazine affect blood pressure?

No--it is specific to myocytes

What drugs are used in treating unstable angina?

ASA, heparin, P2Y12 antagonists

Statins cause increased ____ receptors, more ____ deliver to the liver, and _____

LDL receptors; LDL; decreased plasma cholesterol

What are the treatment goals of unstable angina?

Block thrombus formation | Dissolve existing thrombi

What is the mechanism of action of aspirin?

Blocks platelet activation

What is the mechanism of action of PSY12?

Blocks platelet activation

What is the mechanism of action of GPIIb/IIIa antagonists?

Block platelet aggregation

What is the mechanism of action of Heparin?

Inhibit thrombin formation (which is needed for fibrinogen formation, which causes platelet aggregation)

Blocking ___ synthesis is key to antiplatelet activity of ASA

TXA2 (thromboxane)

ASA irreversibly inactivates ____ through ____

COX-1; acetylation

What class is clopidogrel?

PSY12: ADP Receptor inhibitor

How long does clopidogrel's action last?

Several days

What is clopidogrel used for?

ACS, recent MI, stroke, PVD

What 3 classes of medications are used to treat acute coronary syndrome?

Aspirin P2Y12 GP IIb/IIIa inhibitors

Which drugs are GP IIb/IIIa inhibitors?

eptifibatide tirofiban abciximab

What is heparins structure?

Straight chain, polysaccharide

How does heparin work?

Binds to AT-III, which increases plasma proteases