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CVPR > CVPR Week 4: Pharmacology of ischemic heart disease > Flashcards

CVPR Week 4: Pharmacology of ischemic heart disease Flashcards

1
Q

Objectives

A
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2
Q

Strategies to manage ischemic heart disease

2 listed

A
  • ↓ Oxygen demand
  • ↑ Oxygen delivery to the myocardium
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3
Q

Drug classes to treat angina pectoris

3 listed

A
  • Vasodilators
  • cardiac depressants
  • other drugs (metabolic modifiers, rate inhibitors)
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4
Q

Examples of vasodilators used to treat angina pectoris

A
  • Nitrates
  • Ca2+ channel blockers (verapamil)
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5
Q

Examples of cardiac depressants used to treat angina pectoris

A
  • Ca2+ channel blockers (verapamil)
  • Beta blockers (propranolol)
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6
Q

Propranolol drug class

A

β blockers

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7
Q

Verapamil drug class

A

Ca2+ blockers

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8
Q

Explain the balance of myocardial O2 supply and demand

A
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9
Q

Explain the factors of myocardial O2 supply

3 listed

A
  • Heart rate (reduces supply due to reduced diastolic time)
  • O2 content of the blood
  • Coronary perfusion
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10
Q

Explain the factors of myocardial O2 demand

4 listed

A
  • ↑ HR
  • ↑ contractility
  • ↑ ventricular wall tension (↑ afterload and ↑ preload)
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11
Q

O2 supply and demand modifiers

A
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12
Q

Epidemiology of Chronic Coronary artery disease

A
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13
Q

Coronary atherosclerosis evolves into

A

angina

then

heart failure

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14
Q

Angina semantic definition

A

Greek meaning to strangle, throttle or choke

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15
Q

Angina pectoris pain characteristics

A

deep visceral pressure or squeezing sensation rather than sharp or stabbing or pinprick-like pain

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16
Q

Angina pectoris location

A
  • The pain almost always has a substernal component although some patients complain of pain only on the right or left side of the chest, upper back or epigastrum
  • The pain may radiate from the thorax to the jaw, neck or arm
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17
Q

Angina pectoris precipitating factors

A

Angina is usually precipitated by exertion, emotional upset or other events that obviously increase myocardial oxygen demand such as rapid tachyarrhythmias or extreme elevations in blood pressure

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18
Q

Angina pectoris duration

A
  • is transient usually lasting between 2 and 30 minutes
  • It is relieved by cessation of the precipitating event such as exercise or by the administration of treatment such as sublingual nitroglycerin
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19
Q

Types of angina

3 listed

A
  • Stable (classic or effort)
  • Vasospastic or variant (Prinzmetal)
  • Unstable (medical emergency)
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20
Q

Prinzmetal angina is what?

A
  • Vasospastic or variant angina which has localized spasms associated with atheroma
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21
Q

Vasospastic angina AKA

A

Variant

or

Prinzmetal

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22
Q

Description of vasospastic angina

A

Localized spasms associated with atheroma

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23
Q

Description of unstable angina

A

angina when at rest or when it becomes longer or more frequent

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24
Q

Goals of managing stable angina

2 listed

A
  • Reduce symptoms and ischemia
  • Prevent MI and death
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25
Q

Methods of managing stable angina

5 listed

A
  • Treat associated conditions that can increase oxygen demand or limit oxygen supply
  • Manage risk factors (obesity, hyperlipidemia, smoking, etc.)
  • Utilize antiplatelet agents (aspirin or clopidogrel)
  • Coronary revascularization
  • USe pharmacological agents
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26
Q

Risk factors for angina

A
  • Advancing age
  • Smoking
  • DM
  • Dyslipidemia (statins are very beneficial)
  • Hypertension
  • Obesity
  • Family Hx of premature heart disease
  • Physical inactivity
  • Psychosocial factors
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27
Q

Factors that can aggravate myocardial ischemia: Increasing oxygen demand

6 listed

A
  • Tachycardia
  • Hypertension
  • Hyperthyroidism
  • Heart failure
  • Valvular heart disease
  • Catecholamine analogs (bronchodialators, TCAs)
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28
Q

Factors that can aggravate myocardial ischemia: Reducing oxygen supply

A
  • Tachycardia
  • Anemia
  • Hypoxia
  • Hypotension
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29
Q

Explain methods of coronary revascularization

A
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30
Q

Pharmacological agents to treat stable angina

5 listed

A
  • Nitrates
  • β blockers
  • Ca2+ channel antagonists
  • Ranolazine
  • Ivabradine
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31
Q

Examples of nitrates

4 listed

A
  • Trinitrotoluene (TNT) NOT A MEDICATION
  • Nitroglycerine (glyceryl trinitrate)
  • Isosorbide dinitrate
  • Isosorbide mononitrate
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32
Q

Metabolism of nitrates

A

Organic nitrate reductase in the liver removes nitrate groups in a step-wise fashion which results in a short half-life

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33
Q

Oral bioavailability of nitroglycerin

A

<10-20%

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34
Q

Oral bioavailability of Isosorbide dinitrate

A

< 10 - 20%

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35
Q

Oral bioavailability of isosorbide mononitrate

A

100 %

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36
Q

Nitroglycerin routes of administration

6 listed

A
  • Sublingual
  • Buccal
  • Parenteral
  • Transdermal
  • Topical
  • Oral sustained release
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37
Q

Isosorbide dinitrate routes of administration

3 listed

A
  • Sublingual
  • oral chewable
  • oral sustained release
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38
Q

Isosorbide mononitrate routes of administration

2 listed

A
  • Oral
  • Oral sustained release
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39
Q

Nitrovasodilators MOA

A

Aldehyde dehydrogenase takes NO2- off of nitrates

NO2- is broke ndown into NO

NO activates Guanylyl cyclase to form cGMP

cGMP activates cGMP-dependent kinase (PKG)

cGMP-dependent kinase (PKG) has various effects on vasculature such as

  1. Potentiates K+ channels leading to smooth muscle relaxation
  2. Decreases cytoplasmic [Ca2+] leading to smooth muscle relaxation
  3. Activates myosin-light chain phosphotase (MLCP) leading to smooth muscle relaxation
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40
Q

cGMP-dependent kinase (PKG) has various effects on vasculature such as

3 listed

A
  1. Potentiates K+ channels leading to smooth muscle relaxation
  2. Decreases cytoplasmic [Ca2+] leading to smooth muscle relaxation
  3. Activates myosin-light chain phosphotase (MLCP) leading to smooth muscle relaxation
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41
Q

PKG AKA

A

cGMP-dependent kinase (PKG)

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42
Q

Riociguat MOA

A

activates guanylyl cyclase to produce more cGMP to promote more vasodilation and smooth muscle relaxation

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43
Q

Sildenafil AKA

A

Viagra

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44
Q

Sildenafil MOA

A

Inhibits PDE5 preventing the breakdown of cGMP to GMP thereby increasing smooth muscle relaxation and vasodilation

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45
Q

PDE5 AKA

A

Phosphodiesterase Type 5

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46
Q

PDE5 function

A

Breaks down cGMP into GMP

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47
Q

The formation of nitric oxide from nitrates is dependent upon?

A

ALDH2 (Mitochondrial aldehyde dehydrogenase)

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48
Q

ALDH2 AKA

A

Mitochondrial aldehyde dehydrogenase

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49
Q

ALDH2 MOA

A

takes nitrates into NO2- which can be further processed into NO

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50
Q

NO AKA

A

Nitric oxide

51
Q

NO2- AKA

52
Q

Polymorphisms in ALDH2 can cause

A

reduced effectiveness for treatment of angina with nitrates

because they can’t be broken down into NO

53
Q

Nitrovasodilator organ system effects

7 listed

A
  • Relax veins > arteries
  • Increase venous capacitance
  • Decrease preload
  • Decrease pulmonary vascular pressure
  • Heart size is decreased
  • Decreased cardiac output
  • Dilate epicardial coronaries
54
Q

Identify

55
Q

Beneficial effects and the result of angina treatment with nitrates

5 listed

56
Q

Describe coronary steal

A
  • if no drug in someone with CAD
  • showing how the fully dilated arterioles cant fill
  • Dipyridamole well dilate the healthy artery and will steal away blood from the affected side making the ischemia worse (base for pharmacological induction of ischemia in the stress test)
  • nitrates dilate the collaterals instead of the main arteries which don’t produce the steal effect phenomenon
57
Q

Additional beneficial effects of nitrates

58
Q

Adverse effects of nitrates

A

Reflex tachycardia - increase mycardial oxygen demand and reduce coronary perfusion

Reflex increase in contractility which will further increase the myocardial oxygen requirements

59
Q

Amyl Nitrite caveat

A
  • induce the conversion of hemoglobin into Methemoglobin (ferric iron-lower O2 affinity)
  • so causes methhemoglobinemia
  • Treatment is methylene blue
60
Q

Nitrites and cyanide poisoning

A

The bond between cyanide and cytochrome oxidase is weaker than that between cyanide and methemoglobin which leads to the transfer of cyanide from mitochondria to the circulation

61
Q

The treatment of choice for cyanide poisoning

A

Hydroxycobalamin (form of vitamin B12) with high cyanide affinity

62
Q

Nitrovasodilators adverse effects List

8 Listed

might have to do some combining of flashcards

A
  • Orthostatic hypotension (due to increased venous capacitance)
  • syncope (due to a decrease in arterial pressure)
  • reflex tachycardia (due to decreased atrial pressure)
  • throbbing headache (due to the dilation of meningeal arteries)
  • Increase in intracranial pressure (be careful in patients with trauma)
  • Use without interruption will result in tachyphylaxis (tolerance to nitrates)
  • Common with long-acting preparations or continuous IV infusions (Monday disease in explosive manufacturing)
  • sudden termination from long-acting preparations can have a rebound effect and can worsen angina
63
Q

Monday disease description

A

Common with long-acting preparations or continuous IV infusions (Monday disease in explosive manufacturing) tolerance to nitrates over week, lose tolerance over the weekend and are sick again on monday

64
Q

Nitrovasodilators drug interactions

A
  • Sildenafil (excessive effect)
  • Riociguat (excessive effect)
  • Anti-hypertensive meds
  • Morphine (decreases sympathetic efferent discharge)
  • Anesthetics
  • CNS depressants
65
Q

Other uses of nitrovasodilators

2 listed

A
  1. Hypertensive emergencies (Na+ Nitroprusside)
  2. Congestive heart failure (Isosorbide dinitrate + hydralazine)
66
Q

Na+ Nitroprusside description

A

A complex of cyanide, ironn and nitroso moiety

Does not need enzymatic denitration!

67
Q

Na+ Nitroprusside caveat

A

does not require enzymatic degradation

68
Q

Na+ Nitroprusside uses

A

used for hypertensive emergencies and severe heart failure

69
Q

Na+ Nitroprusside effects

A

Dilates both veins and arteries

Decreases peripheral resistance, or ↓ Cardiac output (RESEARCH THIS IDK WHAT VALENZUELA SAID) the effect on preload sometimes offsets the increase in cardiac output that is normally seen with an arterial vasodilator

70
Q

Na+ Nitroprusside metabolism

A
  • Rapidly metabolized in the RBCs
  • Cyanide is metabolized by rhodanase combined to less toxic thiocyanate in the presence of a sulfur donor (thiosulfate)
  • Thiocyanate is slowly eliminated by the kidneys
71
Q

Cyanide is metabolized by?

72
Q

Na+ Nitroprusside side effects

3 listed

A
  • an excessive decrease in blood pressure
  • Cyanide toxicity (to decrease risk co-administer sodium thiosulfate or hydroxocobalamin)
  • Thiocyanide toxicity in patients with renal failure can cause (Psychosis and seizures)
73
Q

Isosorbide dinitrate + hydralazine AKA

A

BiDil because Bi = Two and Dil = dilators

74
Q

Hydralazine indications ORAL

2 listed

A
  • Advanced?refractory heart failure (with nitrates), particularly in African-Americans
  • Used for severe hypertension NEVER USED ALONE Usually combined with a β blocker to prevent reflex tachycardia, a diuretic must also be used to prevent fluid retention (Triple Therapy)
75
Q

Hydralazine indications IV

A

Indicated in some cases of eclampsia

76
Q

Hydralazine MOA

A
  • ↑ NO release
  • reduction of superoxide
77
Q

Hydralazine adverse effects

4 listed

A
  • Tachycardia
  • fluid retention
  • aggravation of angina
  • lupus-like syndrome
78
Q

Drugs that cause Lupus-like-Syndrome

A
  • Hydralazine
  • Isoniazide
  • Procainamide
  • Phenytoin

It is not HIPP to have lupus

79
Q

β blockers antianginal MOA

A

↓ Hr and Contractility

↓ CO

Additionally

↓ Renin secretion

80
Q

β blockers antianginal Pros

A

↓ O2 consumption

↑ Diastolic coronary perfusion time

81
Q

β blockers antianginal Cons

2 listed

A

↑ End diastolic volume

↑ Ejection time

These can be mitigated by coadministration with a nitrate

82
Q

β blockers antianginal selectivity considerations

A

Avoid non-selective agents to avoid complicated peripheral vascular disease etc. and partial agonists with intrinsic sympathomimetic activity such as Pindolol (non-selective agonist) or Acebutolol (β1 selective agonist)

83
Q

Pindolol drug class

A

non-selective β agonist

84
Q

Acebutolol drug class

A

β1 selective agonist

85
Q

How should β blockers be used in angina

A

recommended that β blockers be used as a first-line therapy in the treatment of chronic stable angina

86
Q

Selectivity in β-blockers for angina

A

cardioselective β blockers offer the potential advantage of not interfering with bronchodilation or peripheral vasodilation and are equally effective in reducing anginal attacks and increasing exercise capacity

87
Q

β blockers effectiveness for angina

A

β blockers decrease angina frequency and threshold but have nevere been shownn to decrease mortality, cardiovascular events or improve survival in patients with stable angina

88
Q

β blockers post acute MI

A

β blockers do reduce short-term complications and improve long-term survival in patients after an acute MI with or without revascularization

89
Q

Ca2+ channel antagonists types for angina

2 Listed

A

Cardiac > Vascular

Vascular > Cardiac

EXCEPT for immediate-release dehydropyridines

90
Q

Ca2+ channel antagonists for angina with Cardiac > Vascular

A
  • Verapamil
  • Diltiazem
91
Q

Ca2+ channel antagonists for angina with Vascular > Cardiac

A
  • Dihydropyridines such as Nifedipine except for immediate release
  • commonly used Amlodipine
  • used in hypertensive emergencies Clevidipine
92
Q

Ca2+ channel antagonists used in emergent situations

A

Clevidipine

93
Q

Clevidipine drug class

A

Dihydropyridines: Ca2+ channel antagonist with Vascular > Cardiac selectivity

94
Q

Ca2+ channel antagonists MOA for antianginal action for Cardiac selective (non-dihydropyridines

A

↓ contractility (Verapamil-Diltiazem)

↓CO (Verapamil-Diltiazem)

95
Q

Ca2+ channel antagonists MOA for antianginal action for Vascular Selective (Dihydropyridines)

A

↓ Peripheral resistance (Dihydropyridines)

↓ Coronary tone (Dihydropyridines) (Useful in variant angina)

96
Q

Ca2+ channel antagonists antiangina treatment pros

A
  • ↓O2 consumption
  • ↑ Diastolic coronary perfusion time
  • Dilate coronaries (only class of drugs that does this and is a particularly helpful action for angina)
97
Q

Amlodipine drug class

A

Long-acting dihydropyridine

98
Q

Ca2+ channel antagonists antiangina treatment Cons

A

↑ HR (Dihydropyridines)

↓ BP (Dihydropyridines) (can be massive)

99
Q

Amlodipine benefits

A
  • A slow smooth onset of action
  • long half-life (once a day administration)
  • Antiatherogenic action (hyperlipidemia increases Ca2+ influx to smooth muscle?)
  • Decreased progression of carotid atherosclerosis (but not coronary)
  • Reduce the risk of major cardiovascular events
  • Minimal negative ionotropic effects (useful in patients with LV dysfunction)
100
Q

Ca2+ channel antagonist that can be used in patients with LV dysfunction

A

Amlodipine, because of its minimal negative ionotropic effect

101
Q

Effects of nitrates alone and with β-blockers or Ca2+ channel blockers for treating Angina

Know this table

A

Table 12-1 Katzung Pharm review

102
Q

Nitrates effect on HR

A

undesirable increase in HR due to reflex tachycardia

103
Q

Nitrates effect on contractility

A

undesirable increase

104
Q

Nitrates effect on ejection time

A

Decreases as a result of the baroreceptor reflex

105
Q

Ranolazine MOA

A

blocks late INa+ which is enhanced in ischemia and facilitates Ca2+ intake via NCX

blocks late sodium currents in the context of lidocaine and perhaps its how lidocaine shortens the action potential duration

Late INa are essentially coupled with Na+ /Ca2+ exchanger

by blocking this channel reducing Ca2+ influx from NCX which decreases diastolic tension, cardiac contractility and improves blood through coronary arteries

106
Q

Ivabradine MOA

A

blocks the funny current directly reducing HR and O2 consumption

107
Q

Vasospastic angina common causes

3 listed

A
  • Smoking
  • excessive alcohol consumption
  • stress
108
Q

Know this whole table

109
Q

Vasospastic Treatment of angina

A
  • statins
  • low dose aspirin (high dose aspirin will block the production of prostacyclin which has vasodilatory actions)
  • Avoid using sumatriptan (a 5-HT1D receptor agonist) for migraines
  • Ca2+ channel blockers and nitrates are effective (but not β-blockers, particularly non-selective agents which can aggravate vasospasm due to antagonism of β2 coronary artery dilatory actions
110
Q

Unstable Angina Non-STEMI and normal enzymes: Relief of ischemic pain

5 listed

A
  • O2 if saturation < 90%
  • Nitroglycerin (except with right ventricular infarction
  • Severe aortic stenosis
  • or Sildenafil use within 24hrs
  • morphine only if pain control is unacceptable
111
Q

Unstable Angina Non-STEMI and normal enzymes: Assess hemodynamic status and correction of abnormalities

A
  • Hypertension and tachycardia both of which will markedly increase myocardial oxygen consumption requirements may be managed with β-blockers and IV nitroglycerin
112
Q

Unstable Angina Non-STEMI and normal enzymes: Estimation of risk and choice of a management strategy

A
  • ie an early invasive strategy (percutaneous coronary intervention or coronary artery bypass graft surgery; examples of indications
  • hemodynamic instability, sustained ventricular arrhythmias, etc) versus a conservative strategy with medical therapy
113
Q

Unstable Angina STEMI: Relief of ischemic pain

A
  • O2 if saturation < 90%
  • Nitroglycerin (except with right ventricular infarction
  • Severe aortic stenosis
  • or Sildenafil use within 24hrs
  • morphine only if pain control is unacceptable
  • same as NON-STEMI
114
Q

Unstable Angina STEMI: Assessment of the patients hemodynamic status and correction of abnormalities

A

Hypertension and tachycardia both of which will markedly increase myocardial oxygen consumption requirements may be managed with β-blockers and IV nitroglycerin

same as non-STEMI

115
Q

Unstable Angina STEMI: Initiation of reperfusion therapy

A

Initiation of reperfusion therapy with primary percutaneous coronary intervention (PCl- should be accomplished in < 90 min from onset)

or if this isn’t possible

fibrinolysis (should be accomplished in < 30 min from onset)

116
Q

Unstable Angina STEMI: Antithrombotic therapy

A

to prevent rethrombosis or acute stent thrombosis (aspirin and heparin)

117
Q

Unstable Angina STEMI: β-blocker therapy

A

to prevent recurrent ischemia and life-threatening ventricular arrhythmias (metoprolol or atenolol)

Same as non-STEMI

118
Q

Unstable Angina Non-STEMI and normal enzymes: Initiation of antithrombotic therapy

A

(including antiplatelet and anticoagulant therapies) to prevent further thrombosis of or embolism from an ulcerated plaque

119
Q

Unstable Angina Non-STEMI and normal enzymes: β-blocker therapy

A

to prevent recurrent ischemia and life-threatening ventricular arrhythmias (metoprolol or atenolol)

120
Q

Overview of clinical management of unstable angina

121
Q

Long term care of unstable angina

122
Q

READ and Know it

A

this can also happen with patients that have aortic stenosis

123
Q

MI involving the Right Ventricle

124
Q

inferior myocardial infarctions

A

β-blockers can trigger bradycardia and AV block

CVPR (93 decks)

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