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Pharmacology II > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

What is ischemic heart disease also known as?

A

Coronary artery disease

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2
Q

What does the prevalance of ischemic heart disease increase with in men and women?

A

Age

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3
Q

What causes ischemic heart disesae?

A
  • -Imbalance between oxygen supply and demand  ischemia
  • -Mostly caused by atherosclerotic narrowing of coronary arteries
  • -Atherosclerotic vessels do not dilate in response to normal stimuli
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4
Q

What is the presenting manifestation in women for ischemic heart disease?

A

Angina

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5
Q

What is the presenting manifestation in men for ischemic heart disease?

A

MI is usually initial event

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6
Q

What is the cardinal sx for ischemic heart disease?

A

Chest pain (Angina)

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7
Q

What are the four major factors that determine myocardial work and therefore myocardial oxygen demand?

A
  • -Heart rate
  • -SBP (clinical marker of afterload)
  • -Myocardial wall tension or stress (product of ventricular end-diastolic volume or preload and myocardial muscle mass)
  • -Myocardial contractility
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8
Q

How can you increase O2 delivery?

A

Most tissues can increase O2 extraction with demand
Heart extracts near maximal amount of O2 at rest
Therefore can only increase O2 delivery by increasing coronary blood flow

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9
Q

What are the types of ischemic heart disease?

A 
Angina pectoris
Chronic stable angina
Unstable angina
Vasospastic (Prinzmetals angina)
Myocardial Infarction (MI)
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10
Q

What is angina pectoris?

A

Caused by ischmia
Angina characterized by paroxysmal chest “squeezing” or pressure, often accompanied by sensation of smothering and fear of impending death

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11
Q

what is angina characterized by paroxysmal chest “squeezing” or pressure, often accompanied by sensation of smothering and fear of impending death?

A

Angina pectoris

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12
Q

What is angina Exacerbated by physical activity and relieved by rest or sublingual nitroglycerin?

A

Chronic stable angina

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13
Q

What is angina characterized by Increasing pattern of pain in previously stable patient
Less responsive to medications, lasts longer, and occurs at rest or with less exertion?

A

Unstable angina

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14
Q

What is vasospastic (prinzmetal’s angina)?

A
  • -Occurs in patient with or without coronary heart disease and is due to a spasm of the coronary artery that decreases myocardial blood flow
  • -More likely to experience pain at rest and in early morning hours
  • -Pain not usually brought on by exertion or emotional stress or relieved by rest
  • -Occurs most often in smokers, young patients, with illicit drug use (esp. cocaine) and with alcohol withdrawal
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15
Q

What is the quality of angina pectoris?

A
  • Sensation of pressure or heavy weight on chest
  • Burning sensation
  • Feeling of tightness
  • Shortness of breath with feeling of constriction around throat
  • Visceral quality (deep, heavy, squeezing, aching)
  • Gradual increase in intensity followed by gradual fading away
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16
Q

What is the location of angina pectoris?

A
  • -Over sternum or very near to it
  • -Anywhere between epigastrium and pharynx
  • -Occasionally limited to left shoulder and left arm
  • -Rarely limited to right arm
  • -Limited to lower jaw
  • -Lower cervical or upper thoracic spine
  • -Left interscapular or suprascapular area
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17
Q

What is the radiation of angina pectoris?

A

Medial aspect of left arm; left shoulder; jaw; occasionally right arm

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18
Q

What is the duration of angina pectoris?

A

0.5-30 minutes (unstable angina typically lasts 10-20 minutes)

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19
Q

What are the precipitating factors of angina pectoris?

A
  • Relationship to exercise
  • Effort that involves use of arms above head
  • Cold environment
  • Walking against the wind
  • Walking after large meal
  • Emotional factors- Fright, anger
  • Coitus
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20
Q

Is there nitroglucerin relief with angina pectoris?

A

Relief of pain occurring within 45 sec. to 5 min. of taking NTG

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21
Q

What are the risk factors for CHD?

A

Hypertension, hypercholesterolemia, smoking, a family history of premature CHD, and diabetes mellitus

22
Q

What are the coronary risk factors for ischemic heart disease?

A
  • Age — relative risk 1.63 per six year increase
  • Serum cholesterol — relative risk 1.92 per 40 mg/dL [1.04 mmol/L] increase
  • Systolic blood pressure — relative risk 1.32 per 20 mmHg increase
  • Cigarette smoking — relative risk 1.36 per 10 cigarette/day increase
  • Obesity appears to be an independent risk factor for coronary atherosclerosis, at least in young men
23
Q

What do guidelines recommend that most patients with suspected stable ischemic heart disease undergo? and why?

A

A stress testing to secure the diagnosis and to gain prognostic information
These patients are at risk for having an MI and ischemic stroke in the future so we need to identify these patients

24
Q

What are the drugs used in the management of angina?

A

–Nitrates
–Calcium channel blockers
–Beta-blockers
–All decrease myocardial O2 demand
–Nitrates increase myocardial O2 delivery by reversing coronary spasm
DOC for spastic

25
Q

What are the treatment mechanisms for angina?

A

–Relaxation of resistance vessels (small arteries and arteriol (decrease TPR- decrease BP-decrease afterload)

–Relaxation of capacitance vessels (veins and venules) Decrease venous return- decrease heart size- decrease preload

–Blockade or attenuation of sympathatic influence on heart- decrease contractility- decrease HR- decrease Oxygen demand

–Coronary dilation- important for relieving vasospastic angina- increase oxygen supply

26
Q

What are used for relaxation of resistance vessels in angina?

A

Nitrates, CCB, BB

27
Q

What are used for relaxation of capacitance vessels in angina?

A

Nitrates, CCB

28
Q

What are used for blockade or attenuation of sympathatic influence on heart in angina?

A

BB

29
Q

What are used for coronary dilation in angina?

A

Nitrates

30
Q

Nitrates nitroglycerin (prototype)- MOA

A

–Denitrated in smooth muscle cells NO activation of guanylate cyclasecGMP  increased Ca++ uptake by SR
–All segments of the vascular system relax (veins > arteries)
Resultant pooling of blood in veins decreased preload and work
Dilate coronary vasculature increased blood supply (O2) to heart
–Decreases platelet aggregation (beneficial in patients with atherosclerotic plaques)

31
Q

Nitrates- Pharamacokinetics

A

SIGNIFICANT 1ST PASS EFFECT IN LIVERTRANSDERMAL OR SUBLINGUAL

32
Q

Nitrates- Acute adverse effects

A

HA (30-60%), Orthostatic hypotension, facial flushing, tachycardia
Tolerance occurs rapidly
Tachyphylaxis (drug doesn’t work as well the body works against it) with increased duration of exposure
More common with long-acting or transdermal preparations
Patients should be given 8hrs off per day

33
Q

Nitrates- drug interaction

A

Sildenafil (Viagra)

34
Q

Nitroglycerine- formulations available

A 
Sublingual–mainstay for immediate relief
Loses potency when stored for long periods – especially in plastic
Buccal 
Oral spray 
Topical: ointment ; Transdermal patch 
IV
35
Q

What do beta blockers do?

A
  • -Decrease myocardial O2 demand at rest and during exercise by decreasing HR and contractility, decreased CO (blocks B1 receptors)
  • -Decrease sympathetic outflow from CNS; Inhibits release of renin from kidneys thus decreasing formation of angiotensin II and secretion of aldosterone  decreased BP  decreased afterload; decreased preload
36
Q

Beta blockers- uses

A

Angina, post MI, HTN, anxiety

37
Q

Beta blockers- contraindication

A

in asthma/COPD, CHF, PVD;

CONTRAINDICATED IN VARIANT ANGINA

38
Q

Beta blockers- Adverse effects

A

Adverse effects – sexual dysfunction, fatigue, insomnia, bradycardia, alter HLD and TG, rebound HTN with abrupt W/D
Patients who continue to smoke have reduced antianginal efficacy of B-Blockers

39
Q

What are the calcium channel blockers?

A 
Verapamil
Diltiazem 
Nifedipine
Nicardipine
Bepridil
40
Q

Calcium channel blockers- Use

A

Well documented efficacy in angina (vasospastic and classic), HTN, supraventricular arrhythmias
Migraine, Raynauds

Verapamil (myocardium), diltiazem (intermediate), nifedipine, amlodipine, nicardipine (peripheral vascular smooth muscle)

41
Q

Calcium channel blockers- contraindications

A

Contraindicated in patients with unstable angina

42
Q

Calcium channel blockers- MOA

A

Block inward movement of Ca++ by binding to L-type calcium channelsdecreased TPR; decreased afterload (also increased coronary flow)

43
Q

Calcium channel blockers- Organ effects

A 
Smooth Muscle 
Vascular > other smooth muscle
Arterioles > Veins
Cardiac Muscle
SA and AV node = slow potentials
Cardiac contractility
44
Q

What are the two CCB useful for CAD?

A

Dihydropyridine – Nifedipine

Diltiazem/Verapamil

45
Q

What are the mechanisms of clinical effects of calcium channel blockers?

A
  • Decrase myocardial contractile force - decrease oxygen demand
  • Decrease arteriolar tone and PVR-decreases ventricular wall stress
  • Increase myocardial O2 supply
  • Relieve and prevent vasospasm
46
Q

Calcium channel blockers- adverse effects

A
  • Hypotension
  • Effects related to vasodilation (dizziness, flushing HA)
  • Gingival hyperplasia
  • Myocardial depression with verapamil and diltiazem
  • Constipation, especially with verapamil (tx with stool softner)
  • Tachycardia with nifedipine and nicardipine
  • Worsen CHF (verapamil-negative inotropic effects)
  • Arrhythmias and agranulocytosis with bepridil
47
Q

Ranolazine

A

late calcium channel blocker
Used in place of BB or in addition to a BB
High potential for interactions: Ranolazine is primarily metabolized by CYP3A; use is contraindicated with inducers and strong inhibitors of CYP3A.

Newer therapy

48
Q

What might nitrates cause?

A

Reflex increase and HR and/or contractility

CCBs and Beta blockers prevent this

49
Q

What do beta blockers and CCBs increase?

A

LVEDV (work)

Nitrates decreased LVEDV

50
Q

What is the treatment for angina pectoris according to the national guideline recommendation unless contraindicated?

A
  • Aspirin (daily)
  • B-Blockers- with prior MI
  • ACEI- with CAD and diabetes or LV systolic dysfunction
  • LDL lowering therapy- with CAD and LDL > 100mg/dL
  • SL nitroglycerin- for immediate relief
  • CCB or long-acting nitrates when B-Blockers contraindicated or in combination with B-Blockers if B-Blocker therapy not successful
51
Q

When should aspirin be used?

A

Aspirin should be used routinely to all patients with acute and chronic ischemic heart disease in the absence of contraindications

52
Q

What does aspirin do?

A
  • -ASA exerts an anti-thrombotic effect (inh COX and thromboxane A2)
  • -Patients with stable angina reduces risk of adverse cardiovascular events by 33%
  • -With unstable angina decreases short and long term risk of MI

Pharmacology II (23 decks)

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