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Nurp 423 Exam 1 > Week 3 > Flashcards

Week 3 Flashcards

1
Q

A constellation of symptoms that results from myocardial oxygen demand being greater than the supply.

A

Angina

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2
Q

Class 1 angina:

A

Proven CAD without symptoms

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3
Q

Class 2 angina:

A

Angina with unusually strenuous physical activity.

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4
Q

Class 3 angina:

A

Angina during the routine physical activity.

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5
Q

Class 4 angina:

A

Angina during minimal activity and rest.

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6
Q

MOA of an ACEI:

A

Inhibits the affect the enzyme responsible for converting angiotensin I to angiotensin II. Blocking the production of angiotensin II results in vasoconstriction and sodium and water retention, thus reducing preload, afterload, and increasing EF.

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7
Q

What to monitor with ACEI?

A

Renal function and serum potassium

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8
Q

Contraindications for ACEI:

A

Pregnancy, bilateral renal artery stenosis, renal insufficiency, hyperkalemia (k greater than 5.5), and sever hypotension

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9
Q

Adverse events of ACEI:

A

Hypotension (first-dose effect), worsening renal function, hyperkalemia, cough, angioadema, rash

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10
Q

Why are beta blockers effective in managing angina?

A

They are effective due to the reduction in the workload of the heart and the overall decrease in myocardial oxygen demand and consumption. They reduce heart rate and myocardial contractility at rest and during periods of normal exercise.

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11
Q

What drugs have complementary effects on myocardial oxygen supply and demand and are often used together?

A

Nitrates and beta-blockers

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12
Q

Types of beta-blockers:

A

1: cardioselective- block only beta1 receptors

2. Noncardioselective- block both beta1 and beta2 receptors

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13
Q

Contraindications for beta blockers:

A

Asthma (reactive airway disease), AV block (unless pacemaker), symptomatic hypotension/bradycardia

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14
Q

Adverse events of beta blockers:

A

Hypotension (first-dose effect), fluid retention/worsening of the failure, fatigue, bradycardia/heart block, can mask symptoms of hypoglycemia.

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15
Q

Teaching points of beta blockers:

A

Do not stop abruptly- reduce dose

Discontinue only in severe cases

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16
Q

Why are CCB effective in treatment of angina?

A

Due to vasodilators effects on the coronary and peripheral vessels. Depending on the agent they have the potential to depress cardiac contractility, heart rate, and conduction.

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17
Q

CCB have a positive or negative inotropic effect?

A

Negative inotrope- decreases contractility

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18
Q

CCB should NOT be used in what?

A

Heart failure

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19
Q

Because CCB do not cause substantial venous dilation they do no reduce what?

A

Preload

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20
Q

Types of CCB?

A
  1. Nondihydropyridines

2. Dihydropyridines

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21
Q

Which type of CCB reduce HR by slowing contraction through the SA and AV nodes and depress cardiac contractility?

A

Nondihydropyridines

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22
Q

These have more antianginal properties, used to treat arrhythmia, with minimal effect on BP.

A

Nondihydropyridines: verapamil and diltizem

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23
Q

Dihydropyridines have no effect on what?

A

HR

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24
Q

Nondihydropyridine CCB can cause what adverse events:

A

Constipation, edema

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25
Q

Adverse events of CCB:

A

Edema, fatigue, dizziness, HA, flushing, and gingival hyperplasia

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26
Q

Antiplatelet therapy includes:

A

ASA therapy

Thienopyridine (plavix-clopidogrel) therapy

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27
Q

ASA MOA:

A

Inhibits platelet activation through irreversible enzyme antagonism to block prostaglandin synthesis.

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28
Q

Thienopyridines MOA:

A

Reduced ADP-induced platelet activation. Works on receptors.

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29
Q

In patients with stable angina, the risk of MI can be lowered with:

A

Daily ASA therapy

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30
Q

Adverse events of ASA:

A

Dyspepsia, bruising, and bleeding

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31
Q

Plavix- clopidogrel is recommended for:

A

Prevention of MI in angina patients who have contraindications to ASA

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32
Q

Plavix has better what then ASA?

A

GI tolerance

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33
Q

This drug can be used alone or in combo with nitrates, BB, CCB, or ACEI.

A

Ranolazine

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34
Q

When to use Ranolazine?

A

Chronic treatment of angina only when all other modalities are tried.

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35
Q

MOA of ranolazine:

A

Thought to block late-phase sodium channels, which remain open during hypoxia or ischemic events. By blocking these it decreases calcium overload and breaks the cycle of ischemia.

36
Q

Adverse events of ranolazine:

A

QT prolongation, dose-related dizziness, HA, constipation, nausea, palpitations, vertigo, peripheral edema, hypotension. Less common: angioedema and renal failure

37
Q

Nitrates are used to:

A

Halt an acute angina attack, to prevent predictable episodes, and for chronic treatment to prevent episodes.

38
Q

MOA of nitrates:

A

Cause dilation throughout the vasculature- in the peripheral veins as well as coronary arteries. When dilated the veins return less blood to the heart, thereby decreasing LV filling and preload. This decreases workload of the heart.

39
Q

Nitrates do not affect the cardiac function but rather:

A

Decreases workload of the heart and increases myocardial oxygenation

40
Q

Can you develop tolerance with prolonged nitrate use?

A

Yes

41
Q

Nitrates are contraindicated in:

A

Anemic/volume depleted patients, head trauma, issues with hemorrhage

42
Q

Adverse events of nitrates?

A

Vasodilatory effects: HA, flushing, dizziness, weakness, and orthostatic hypotension. Reflex tachycardia: results as the heart compensates for the bp drop

43
Q

Examples of long and short-acting nitrates:

A

Long-acting: isordil, indur, NTG transdermal

Short-acting: NTG spray and tabs

44
Q

All patients with angina use:

A

Short-acting nitrate, ASA

45
Q

First-Line therapy in angina:

A

BB+ lifestyle+ ASA+ short-acting nitrate

46
Q

Second line therapy in angina:

A

CCB or combo therapy (CCB + BB or long-acting nitrate + BB)

47
Q

Third-line therapy for angina:

A

CCB + BB + long-acting nitrate

48
Q

Types of heart failure:

A

Systolic dysfunction- ventricular contraction/ejection- failure of the pump with low EF

Diastolic dysfunction- ventricular filling/relaxation- stiff ventricle/ inadequate SV

49
Q

In patients with a reduced EF what drugs should be used to prevent HF?

A

ACEI or ARBS

50
Q

In patients with MI and a reduced MI what drugs should be used to prevent HF:

A

BB with a statin

51
Q

Class I HF:

A

Patients may have symptoms of HF only at levels that would produce symptoms in normal people- no limitations

52
Q

Class II HF:

A

Patients may have symptoms of HF on ordinary exertion- slight limitations- comfortable at rest

53
Q

Class III HF:

A

Patients may have symptoms of HF on less than ordinary exertion- marked limitations

54
Q

Class IV HF:

A

Patients may have symptoms of HF at rest- severe limitations

55
Q

ACEI are used in HF for:

A

Patients with LV systolic dysfunction and an EF less than 35-40%.

First-line in HF

56
Q

ACEI reduce:

A

Preload and afterload

57
Q

What ARB is most studied in heart failure?

A

Losartan- decreases BP, SVR, pulmonary capillary wedge pressure, and heart rate. Raises cardiac index

58
Q

BB should be used in HF treatment:

A

After an MI- improves function

59
Q

What BB for HF?

A

Carvedilol- improves BP and cardiac output in stages B and C

Metoprolol

60
Q

Diuretics do what in HF?

A

Reduce preload by decreasing extracellular fluid volume that can be used to manage HTN, which will then reduce afterload

61
Q

Digitalis has a positive or negative inotropic effect?

A

Positive inotrope- increases contractility

62
Q

Digitalis is not good for what type of HF?

A

Diastolic HF with hypertrophic cardiomyopathy.

63
Q

Digitalis is good for this Hf:

A

A-fib induced HF due to its Na pump effect and subsequent rate control.

64
Q

What stage should dig be used in HF?

A

Stage C only

65
Q

Adverse events of digitalis?

A

Dig toxicity, anorexia, N/V, HA, fatigue, malaise, disorientation, confusion, delirium, seizure, and visual disturbances. Followed by cardiac symptoms manifested by arrhythmia.

66
Q

Contraindications for digitalis:

A

Dig toxicity, advanced A-V block without a pacemaker, bradycardia/ sick sinus with pacemaker, PVCs/VT, marker hypokalemia, WPW with a fib

67
Q

Spironolactone is an:

A

Aldosterone antagonist

68
Q

Spironolactone is used:

A

For stage C only and with recent or current symptoms despite ACEI, diuretics, digoxin, and BB

69
Q

Contraindications of spironolactone:

A

Hyperkalemia and renal insufficiency

70
Q

Nitrates are used in HF:

A

In stage C with hydralazine when intolerant to an ACEI

71
Q

Hydralazine is a:

A

Vasodilator that works directly on smooth muscle to dilate the blood vessel; very effective on arterioles; some NO donation, which has been shown to trigger vasodilation

72
Q

Hydralazine is used in HF:

A

In stage C with nitrates when intolerant to ACEI.

Not used alone

73
Q

Hydralazine should be with:

A

Diuretic and BB due to high incidence of fluid retention and elevated HR

74
Q

Medications that can exacerbate HF:

A 
NSAIDS
steroids
Hormones
Lithium 
Anti-hypertensives 
BB
Arrhythmics
TCA
CCB 
Cardiac toxins
75
Q

First line therapy in HF:

A

ACEI or ARB with or without diuretic

76
Q

Second line therapy in HF:

A

ACEI or ARB and BB with a diuretic

In patients with mild heart failure, use a potassium sparing diuretic when serum K is less than 4

77
Q

Third line therapy in HF:

A

ARB, BB, aldosterone antagonist, diuretic, and digoxin

78
Q

2 strategies for management of dysrhythmias:

A
  1. Rate control

2. Rhythm control

79
Q

Rate control consists of:

A 
Use of AV Nodal agents (class 2 and 4)
Primary strategy for patients over 65, with CAD, with contraindications to antiarrhythmic drugs, unsuitable for cardioversion, or without CHF.
80
Q

Rhythm control consists of:

A 
Use of antiarrhythmia meds (class 1 and 3)
Primary strategy for patients that are symptomatic, presenting for the first time with AF and can pinpoint the exact time the symptoms began within 48-72 hours, secondary to a treated/corrected precipitation, or with CHF
81
Q

Class I AAD drugs are:

A

Sodium channel blockers- membrane stabilizing agents

82
Q

Class II AAD drugs:

A

Beta-blockers

83
Q

Beta blockers are useful in treating what arrhythmia:

A

Supraventricular tachycardias

84
Q

Class III AADs:

A

K channel binders- prolongs depolarization

85
Q

Class IV AADs:

A

Calcium channel blockers

Used for a fib/a flutter

86
Q

Class V AADs:

A

Others:

Digoxin- excellent for a fib induced HF

Nurp 423 Exam 1 (3 decks)

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