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Circulatory > Exam 3 > Flashcards

Exam 3 Flashcards

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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
Adverse effects of nitroglycerin
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)
26
Nitroglycerin drug interactions
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
27
Calcium channel blocker subclasses
Dihydropyridines: nifedipine (1st generation) Heart rate lowering : verapamil
28
Calcium channel blocker mechanism of action
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
29
Dihydropyridines have greater _ actions on VSM than on myocardium (as compared to HRL CCBs)
Inhibitory
30
Dihydropyridines have less depression of
Myocardial contractibility, and minimal effects SA nodal automaticity and AV nodal conduction velocity
31
Extended release nifedipine or second generation, agents are preferred because
They are associated with fewer hypotension related side effects Immediate release nifedipine is NOT recommended
32
Dihydropyridines are metabolized by
CYP384 so grapefruit juice should be avoided
33
HRL CCBs are
less potent peripheral vasodilators than DHP’s, but more depressive in the myocardium
34
HRL CCB half life
Short- around four hours Must be administered several times per day
35
HRL CCBs are contraindicated in
Sick sinus syndrome, AV nodal block
36
HRL CCB use
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
37
Adverse effects of DHPs
Headache Facial flushing Peripheral edema Gingival hyperplasia
38
Adverse effects of HRL drugs
Bradyarrhythmia (decreased cardiac output) Constipation Gingival hyperplasia
39
Beta blocker prototype
Metoprolol
40
Metoprolol mechanism of action
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
41
Metoprolol use
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
Ranolazine mechanism of action
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
Ranolazine efficacy
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
Ranolazine is contraindicated
With other CYP3A4 substrates
45
Therapeutic approach to unstable angina
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
ED
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
Phosphodiesterase type 5 Inhibitors prototype drug
Sidenafil
48
Sildenafil mechanism of action
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
Sildenafil pharmacokinetics
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
Sildenafil metabolism
CYP3A4
51
Sildenafil other uses
Pulmonary arterial hypertension
52
Sildenafil adverse effects
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
Sidenafil drug interactions
Organic nitrates and alpha blockers
54
CHF pathophysiology
Insufficient CO leads to: Increase blood volume Edema Enlarged heart
55
CHF 5 year survival (50%). Patients die from…
Arrhythmias and heart failure
56
Feedback loops that maintain cardiac output
Autonomic feedback loop: increase heart rate, contractility, or venous tone to increase cardiac output Hormonal feedback loop: AngII increases BP and CO
57
Compensation failure CHF
Decreased cardiac output> increased after load> decreased cardiac output Cardiac remodeling
58
Cardiac remodeling
Increase volume leads to increased wall stress Stress and neurohumoral activation lead to remodeling (terminal decline in CHF)
59
CHF autonomic feedback loop
Reduced cardiac output> sympathetic, nervous system activation> vasoconstriction> further reduces cardiac output
60
Hormonal Feedback Loop
61
Sympathetic nervous system activation, Ang II, and aldosterone cause
Cardiac remodeling which leads to heart failure progression
62
CHR therapy goals
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
Diuretics reduce
Congestive symptoms Decrease intravascular volume> decrease pre-load after load Adema and ventricular wall stress
64
Negative of diuretics
Stimulate RASS (negates benefit of decreased wall stress) Decreased cardiac output
65
Diuretic dose
Should use lowest dose to decrease congestive symptoms with minimal decrease in cardiac output
66
People on diuretics should restrict
Salt intake
67
The efficacy of diuretics can be monitored by
Monitoring body weight
68
Diuretics do not
Reduce mortality
69
Loop diuretics
Widely used but potassium depleting
70
Diuretic resistance
Diuretics become less effective in later stages of CHF
71
Thiazides
Limited use diarrhetic Used to potentiate loop diuretics , greater potassium, depletion
72
Potassium sparing, diuretics
Aldosterone antagonists (spironolactone)
73
Aldosterone antagonists are
Potassium sparing Inhibit remodeling to decrease mortality
74
Negative of aldosterone antagonists
Hyperkalemia
75
RAAS antagonists
Stop release of Ang II (increases Na+ and water retention, increases catecholamine release, arrhythmogenic and myocardial remodeling)
76
ACE inhibitors mechanism
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
Angiotensin II type 1 receptor blockers
Block AT1 but not AT2 receptors (loses bradykinin benefit) Avoids Ang II escape Alternative for patients intolerant to ACE inhibitors Increases survival
78
Angiotensin receptor-Neprilysin Inhibitors
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
Nitro vasodilators (NO)
Venodilator Reduce preload Nitrate tolerance
80
Hydralazine
Vasodilator Reduces afterload Positive inotropic effect
81
Hydralazine _isosorbide dinitrate
Reduces mortality (esp in African Americans)
82
Beta androgenic receptor blockers
Long term use improve symptoms in survival and mild to moderate CHF
83
Beta blockers decrease
Contraction to reduce cardiac output
84
Beta androgenic receptor blockers mechanism
Reduce cardiac ischemia, arrhythmias, cardiac remodeling Decrease renin, secretion
85
Beta androgenic, receptor blocker drugs
Metoprolol Biosoprolol Carvedilol dosing: start low, go slow
86
Renin inhibitor Aliskiren
No beneficial effect on CHF survival
87
Cardiac glycosides (digoxin)
From Fox glove Narrow margin of safety, and does not increase survival (may decrease survival in women) + inotropy> increased contractile force> increased CO
88
Digoxin mechanism
Inhibits Na+/K+-ATPase to increase Ca++ release upon depolarization Increase force of contraction and cardiac output
89
Effect of K+ on Digoxin
Hyper kalemia: decrease digoxin binding Hypokalemia: increase digoxin binding> calcium overload> increased myocyte excitability> arrhythmia Potassium must be maintained at 3.5-5
90
Electrophysiological effects of digoxin
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
Digoxin pharmacokinetics
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
Digoxin use in CHF
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
Digoxin toxicity
Cardiac arrhythmias
94
Predisposing factors for arrhythmias with digoxin
Low potassium Hi digoxin Heart disease
95
Non-cardiac adverse effects of the Jackson
Nausea, vomiting, anorexia Fatigue, yellow, green, visual halos Reduce dose
96
Digoxin drug interactions
Diuretics increase digoxin affects Ace inhibitors/ Ang II type 1 repertory blocker decrease digoxin effects Anti-arrhythmics increase serum digoxin
97
Treatment in preserved ejection fraction HF
Treat, hypertension and volume overload (diuretics
98
Treatment of low ejection fraction HF
Hydralazine-isosorbide dinitrate combo ACE inhibitors Angiotensin II type 1 receptor antagonists Beta blockers
99
Drugs that only relieve symptoms of CHF
Diuretics (loop/thiazide Digoxin
100
Therapeutic strategy for CHF
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
Drugs, contraindicated in CHF
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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