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Circulatory > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

angina pectoris

A

Ischemic heart disease
Myocardial oxygen supply insufficient to match, myocardial, oxygen demand
Manifestation of coronary artery disease from untreated atherosclerosis

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2
Q

Chronic stable angina

A

Pain over sternum spreading to chest
Radiating to arms, neck, jar, or any combination
Pain subsides in 1 to 15 minutes
Pain is described as a pressure or heavy discomfort
Precipitating factors: exertion, emotion, eating, cold weather, lying down
Relief: stopping effort, nitroglycerin

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3
Q

Chronic stable angina ECG

A

Transient S-T depression, disappearing with relief of pain

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4
Q

Unstable angina

A

Increase frequency and duration
Angina at rest
Rupture of atherosclerotic plaque

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5
Q

Silent ischemia

A

Asymptomatic
Most common type of angina

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6
Q

Vasospastic angina

A

Rare
Episodic coronary artery spasm

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7
Q

Goal of pharmacologic therapy for angina

A

Immediate relief of anginal attacks
Prevention of anginal attacks
Increased exercise tolerance
Decreased CV mortality
Focus on increasing oxygen supply and/or decreasing oxygen demand

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8
Q

Drugs for angina work, mainly by

A

Reducing myocardial oxygen demand

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9
Q

Main drug classes for angina

A

Organic nitrates
Calcium channel blockers
Beta blockers

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10
Q

Other strategies to prolong survival of patients with angina

A

Antiplatelet agents, statins, ACE inhibitors (stabilize/regress atherosclerotic plaques)
Reduce risk factors (smoking, obesity, hypertension, diabetes, influenza)

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11
Q

Acute treatment of unstable angina (acute coronary syndrome)

A

Anti-ischemic and analgesic therapy
Antiplatelet drugs and antithrombotic drugs

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12
Q

What are the determinant of myocardial oxygen demand?

A

Heart rate
Contractility
Ventricular wall stress
-preload: sarcomere stretch just prior to contraction
-Afterload: ventricular systolic wall tension

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13
Q

Determinants of myocardial oxygen supply

A

Most available oxygen is extracted at rest, increase demand during exercise is Met by increasing coronary blood flow via arteriolar dilation (autoregulation)
-Severe CAD, arterials in ischemic regions maybe fully dilated at rest
-When exertion continues there’s no way to increase CBF deliver more oxygen to ischemic areas
CBF is negligible during systole, duration of diastole is the limiting factor for myocardial perfusion during tachycardia

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14
Q

What triggers the release of NO to cause VSM dilation?

A

ACh

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15
Q

NO causes VSM to

A

Relax

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16
Q

Organic nitrates prototype drug

A

Nitroglycerin

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17
Q

Nitroglycerin mechanism of action

A

Prodrug metabolized to NO by ALDH2
NO induces vascular smooth muscle relaxation to cause Venus and arterial vasodilation
-venous dilation predominates over arterial
-Decreased venous return reduces preload thus reducing oxygen demand

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18
Q

Effects of nitroglycerin on CBF

A

Dilation of large arteries, promotes redistribution of blood to ischemic areas of endocardium
Minimal effects on smaller vessels already that are already maximally dilated to maintain resting blood flow
Direct dilating affect on vasospastic coronary arteries

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19
Q

Hemodynamic effects of nitroglycerin

A

At typical doses- no direct inotropic or chronotropic effects; no changes in MAP
At higher doses - reflux tachycardia, if there is sufficient dilation of systemic arteries to reduce MAP

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20
Q

Pharmacokinetics of sublingual nitroglycerin

A

Tablets in sprays circumvent first pass metabolism, attaining therapeutic blood levels in 1 to 2 minutes
Provide relief of acute attacks
Duration less than one hour
Tablets unstable to heat light and moisture, tingling sensation when active tablets put under tongue
EMS should be contacted if the first does not alleviate symptoms within five minutes

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21
Q

Pharmacokinetics of oral and cutaneous nitroglycerin

A

Used for a cute relief and prophylaxis
Onset and 30 to 60 minutes
4 to 24 hour duration of action

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22
Q

Pharmacokinetic tolerance of nitroglycerin

A

Overuse of oral/transdermal formulations or continuous infusions
Documented in workers exposed to nitroglycerin explosives who developed Monday morning headaches
Mechanism: nitrate mediated inactivation of ALDH2
minimize using a centric dosing schedules that provide nitrate free intervals of 10 to 12 hours

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23
Q

ALDH2 polymorphism

A

Low activity polymorphism
High prevalence in Asian patient population
Decreased efficacy in patients due to decreased formation of NO

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24
Q

Clinical efficacy of nitroglycerin

A

Effective in preventing in terminating, a cute anginal attacks
Improves exercise tolerance
Abolishes ST segment depression
No survival benefit or prevention of MI

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25
Q

Adverse effects of nitroglycerin

A

Headache, facial flushing- can be severe due to arterial or dilation in face/neck and meningeal arterys
Orthostatic hypotension - due to suppressed ability of veins to constrict
Reflex tachycardia- increases O2 demand, negating therapy (prescribed with a beta blocker to control this effect)

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26
Q

Nitroglycerin drug interactions

A

Drugs for ED- nitroglycerin can trigger severe refractory hypotension impossible am I if taken within 24 hours of PDE-5 inhibitor
Alcohol- inhibits ALDH2 and accentuates orthostatic hypotension

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27
Q

Calcium channel blocker subclasses

A

Dihydropyridines: nifedipine (1st generation)
Heart rate lowering : verapamil

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28
Q

Calcium channel blocker mechanism of action

A

Block inward flow of calcium through L type calcium channels by binding office of unit
Produce a decrease in transmembrane calcium current in VSM , HRL CCBs also reduce calcium current in myocytes and nodal tissue
Vasodilators of peripheral in coronary arteries (decrease after a load to reduce oxygen demand)
Useful and relaxing, coronary artery spasms , increasing oxygen supply in vasospastic angina

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29
Q

Dihydropyridines have greater _ actions on VSM than on myocardium (as compared to HRL CCBs)

A

Inhibitory

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30
Q

Dihydropyridines have less depression of

A

Myocardial contractibility, and minimal effects SA nodal automaticity and AV nodal conduction velocity

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31
Q

Extended release nifedipine or second generation, agents are preferred because

A

They are associated with fewer hypotension related side effects
Immediate release nifedipine is NOT recommended

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32
Q

Dihydropyridines are metabolized by

A

CYP384 so grapefruit juice should be avoided

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33
Q

HRL CCBs are

A

less potent peripheral vasodilators than DHP’s, but more depressive in the myocardium

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34
Q

HRL CCB half life

A

Short- around four hours
Must be administered several times per day

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35
Q

HRL CCBs are contraindicated in

A

Sick sinus syndrome, AV nodal block

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36
Q

HRL CCB use

A

Effective prophylaxis against angina attacks; reduce consumption of nitroglycerin
Hypertension: use alone or in combination with thiazide diuretic or ACE inhibitor/ARB
Cardiac arrhythmias-HRL CCBs

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37
Q

Adverse effects of DHPs

A

Headache
Facial flushing
Peripheral edema
Gingival hyperplasia

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38
Q

Adverse effects of HRL drugs

A

Bradyarrhythmia (decreased cardiac output)
Constipation
Gingival hyperplasia

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39
Q

Beta blocker prototype

A

Metoprolol

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40
Q

Metoprolol mechanism of action

A

Beta-1 selective androgenic receptor antagonist
Minimal affect on resting heart rate
Decrease HR/contractibility during exertion to decrease myocardial oxygen demand
Negative chronotropism increases perfusion during diastole, thus increasing oxygen supply
Antihypertensive effect reduces afterload

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41
Q

Metoprolol use

A

Call Nick stable angina
Call is to maintain resting heart rate of 55 BPM and limit peak HR during exertion to 110 BPM
Reduce severity and frequency of stable anginal attacks
Reduce mortality by decreasing incidence of sudden, cardiac death, especially in patients with silent ischemia
NOT useful for Viso spastic angina (may worsen condition due to unopposed alpha-1 arterial vasoconstriction)

42
Q

Ranolazine mechanism of action

A

Antianginal effects achieved without hemodynamic changes
Increased sodium in flux occurs in ischemic myocytes leading to calcium overload (Na+ Ca++ exchanger)
Ca++ overload impairs myocardial relaxation, decreases perfusion, and increases oxygen demand
Inhibits, late phase of sodium current in cardiac cycle, thereby blocking calcium overload and ischemic myocytes, reducing oxygen demand

43
Q

Ranolazine efficacy

A

Effective and prevention of anginal attacks
Anti-arrhythmic properties (K+ channel blocker)
Useful in patients who have uncontrolled angina (as mono therapy or in combination)
Reserved for refractory angina because it prolongs QT-interval

44
Q

Ranolazine is contraindicated

A

With other CYP3A4 substrates

45
Q

Therapeutic approach to unstable angina

A

Initial agent is cardioselective beta blocker, due to survival benefit
Sublingual nitroglycerin is prescribed for the rapid termination of anginal symptoms as needed
CCBs are effective alternatives to beta blockers as monotherapy (in asthma/COPD, vasospasm) usually as add-ons
combinations are effective, but should be avoided (beta blocker +HRL CCB can cause sever bradycardia)
Ranolazine can mitigate problems with combos, potentially safer to use with vasodilator drugs for ED

46
Q

ED

A

Age related disorder
Common in patients with untreated hypertension, CAD, and diabetes, along with those with a long history of smoking
Failure to achieve and maintain an erection despite arousal over 50% of the time indicates treatment is required
Therapeutic management includes lifestyle and drug therapy modifications

47
Q

Phosphodiesterase type 5 Inhibitors prototype drug

A

Sidenafil

48
Q

Sildenafil mechanism of action

A

Selective inhibitor of PDE-5 (highly expressed in VSM of corpora cavernous)
Prolongs the activity of endogenous cGMP
Relaxes corpora cavernosa smooth muscle allowing blood flow into penis at arterial pressure, producing an erection
No effect in the absence of sexual stimulation (parasympathetic NANC innervation must be intact)

49
Q

Sildenafil pharmacokinetics

A

Taken orally one hour before sexual activity
Onset is about 60 minutes and duration is 2 to 4 hours (related agents have longer durations of action)
Anza is delayed by a high fat meal

50
Q

Sildenafil metabolism

A

CYP3A4

51
Q

Sildenafil other uses

A

Pulmonary arterial hypertension

52
Q

Sildenafil adverse effects

A

Headache and flushing due to inhibition of major isoform in vasculature (PDE1)
Abnormal vision -blue color tinge, blurring, light sensitivity due to inhibition of the major isoform in the retina (PDE6)
Dyspepsia due to inappropriate relaxation of the lower esophageal sphincter muscle
Risk of sudden hearing loss
Priapism- treated with vasoconstrictors

53
Q

Sidenafil drug interactions

A

Organic nitrates and alpha blockers

54
Q

CHF pathophysiology

A

Insufficient CO leads to:
Increase blood volume
Edema
Enlarged heart

55
Q

CHF 5 year survival (50%). Patients die from…

A

Arrhythmias and heart failure

56
Q

Feedback loops that maintain cardiac output

A

Autonomic feedback loop: increase heart rate, contractility, or venous tone to increase cardiac output
Hormonal feedback loop: AngII increases BP and CO

57
Q

Compensation failure CHF

A

Decreased cardiac output> increased after load> decreased cardiac output
Cardiac remodeling

58
Q

Cardiac remodeling

A

Increase volume leads to increased wall stress
Stress and neurohumoral activation lead to remodeling (terminal decline in CHF)

59
Q

CHF autonomic feedback loop

A

Reduced cardiac output> sympathetic, nervous system activation> vasoconstriction> further reduces cardiac output

60
Q

Hormonal Feedback Loop

A
61
Q

Sympathetic nervous system activation, Ang II, and aldosterone cause

A

Cardiac remodeling which leads to heart failure progression

62
Q

CHR therapy goals

A

Reduce volume overload, congestion (diuretics)
Increase myocardial contraction (digoxin )
Reduce preload and afterload (vasodilators)
Slow disease progression by blocking neurohumoral activation of remodeling
Prevent arrhythmia S

63
Q

Diuretics reduce

A

Congestive symptoms
Decrease intravascular volume> decrease pre-load after load Adema and ventricular wall stress

64
Q

Negative of diuretics

A

Stimulate RASS (negates benefit of decreased wall stress)
Decreased cardiac output

65
Q

Diuretic dose

A

Should use lowest dose to decrease congestive symptoms with minimal decrease in cardiac output

66
Q

People on diuretics should restrict

A

Salt intake

67
Q

The efficacy of diuretics can be monitored by

A

Monitoring body weight

68
Q

Diuretics do not

A

Reduce mortality

69
Q

Loop diuretics

A

Widely used but potassium depleting

70
Q

Diuretic resistance

A

Diuretics become less effective in later stages of CHF

71
Q

Thiazides

A

Limited use diarrhetic
Used to potentiate loop diuretics , greater potassium, depletion

72
Q

Potassium sparing, diuretics

A

Aldosterone antagonists (spironolactone)

73
Q

Aldosterone antagonists are

A

Potassium sparing
Inhibit remodeling to decrease mortality

74
Q

Negative of aldosterone antagonists

A

Hyperkalemia

75
Q

RAAS antagonists

A

Stop release of Ang II (increases Na+ and water retention, increases catecholamine release, arrhythmogenic and myocardial remodeling)

76
Q

ACE inhibitors mechanism

A

Block angiotensin one conversion to angiotensin II (decrease vasoconstriction, decrease SNS, decreased remodeling)
Block bradykinin degradation (vasodilation, and decrease remodeling-also causes dry cough and angioedema)
Ang II escape
CAN increase survival in CHF

77
Q

Angiotensin II type 1 receptor blockers

A

Block AT1 but not AT2 receptors (loses bradykinin benefit)
Avoids Ang II escape
Alternative for patients intolerant to ACE inhibitors
Increases survival

78
Q

Angiotensin receptor-Neprilysin Inhibitors

A

Elevates B type natriuretic peptide- increased Na+ excretion
Sacubitril-valsartan combo
Alternative for ACE and single ARB if no history of angioedema and no hypotension risk
Improves survival

79
Q

Nitro vasodilators (NO)

A

Venodilator
Reduce preload
Nitrate tolerance

80
Q

Hydralazine

A

Vasodilator
Reduces afterload
Positive inotropic effect

81
Q

Hydralazine _isosorbide dinitrate

A

Reduces mortality (esp in African Americans)

82
Q

Beta androgenic receptor blockers

A

Long term use improve symptoms in survival and mild to moderate CHF

83
Q

Beta blockers decrease

A

Contraction to reduce cardiac output

84
Q

Beta androgenic receptor blockers mechanism

A

Reduce cardiac ischemia, arrhythmias, cardiac remodeling
Decrease renin, secretion

85
Q

Beta androgenic, receptor blocker drugs

A

Metoprolol
Biosoprolol
Carvedilol
dosing: start low, go slow

86
Q

Renin inhibitor Aliskiren

A

No beneficial effect on CHF survival

87
Q

Cardiac glycosides (digoxin)

A

From Fox glove
Narrow margin of safety, and does not increase survival (may decrease survival in women)
+ inotropy> increased contractile force> increased CO

88
Q

Digoxin mechanism

A

Inhibits Na+/K+-ATPase to increase Ca++ release upon depolarization
Increase force of contraction and cardiac output

89
Q

Effect of K+ on Digoxin

A

Hyper kalemia: decrease digoxin binding
Hypokalemia: increase digoxin binding> calcium overload> increased myocyte excitability> arrhythmia
Potassium must be maintained at 3.5-5

90
Q

Electrophysiological effects of digoxin

A

Increase parasympathetic tone which can cause bradycardia
Inhibit AV node to reduce ventricular rate in a fib with CHF
Toxic levels> increase sympathetic activity> proarrhythmic
Toxic levels : calcium overload, and arrhythmias

91
Q

Digoxin pharmacokinetics

A

36 to 48 hour half life
Eliminated by kidneys
E. Lentum eliminates digoxin
Distributed to muscles- dosed by lean body mass
Reduced clearance in elderly
Must monitor digoxin levels (<1st/ml)

92
Q

Digoxin use in CHF

A

No longer first line
Reduces hospitalizations, but not mortality
Use for LV systolic dysfunction and atrial fibrillation or in patients with CHF that are symptomatic, despite ACE inhibitors and beta blockers

93
Q

Digoxin toxicity

A

Cardiac arrhythmias

94
Q

Predisposing factors for arrhythmias with digoxin

A

Low potassium
Hi digoxin
Heart disease

95
Q

Non-cardiac adverse effects of the Jackson

A

Nausea, vomiting, anorexia
Fatigue, yellow, green, visual halos
Reduce dose

96
Q

Digoxin drug interactions

A

Diuretics increase digoxin affects
Ace inhibitors/ Ang II type 1 repertory blocker decrease digoxin effects
Anti-arrhythmics increase serum digoxin

97
Q

Treatment in preserved ejection fraction HF

A

Treat, hypertension and volume overload (diuretics

98
Q

Treatment of low ejection fraction HF

A

Hydralazine-isosorbide dinitrate combo
ACE inhibitors
Angiotensin II type 1 receptor antagonists
Beta blockers

99
Q

Drugs that only relieve symptoms of CHF

A

Diuretics (loop/thiazide
Digoxin

100
Q

Therapeutic strategy for CHF

A

Ace inhibitors (or angiotensin II type I receptor antagonist) and beta blockers to slow disease progression
Diuretics to control volume
Worsening CHF : aldosterone antagonist, nitrates, hydralazine
Digoxin is still symptomatic

101
Q

Drugs, contraindicated in CHF

A

NSAIDs- reduce diarrhetic and ace, inhibitor efficiency
Anti-arrhythmics - pro arrhythmic and cardio suppressive
Calcium channel blockers - cardio suppressive

Circulatory (2 decks)

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