Cardiovascular Flashcards

1
Q

What is normal blood pressure?

A

120/80 mm Hg

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2
Q

What is stage I hypertension?

A

140-159/ 90 - 99

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3
Q

What is stage II hypertension?

A

160-179/100-109

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4
Q

What is stage III hypertension?

A

180-209/110-119

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5
Q

What is pre-hypertension?

A

120-139/80-89

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6
Q

What is isolated systolic hypertension?

A

> 140/80

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7
Q

What are the 7 risk factors for hypertension?

A
  • Blood relatives with hypertension
  • Men over the age of 55
  • Post-menopausal women
  • Obesity
  • Smoking
  • Diabetes
  • High blood cholesterol
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8
Q

What are 6 complications of hypertension?

A
  • Cerebrovascular hemorrhage
  • Stroke
  • Renal failure
  • Heart failure
  • Myocardial infarction
  • Retinal damage
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9
Q

What % of hyper tension is primary? What % is secondary?

A

95 % primary

5 % secondary

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10
Q

What is meant by primary hypertension?

A
  • Idiopathic
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11
Q

What are 3 possible contributors to primary hypertension?

A
  • High sodium in diet/ sodium retention
  • Enhanced sympathetic nerve activity
  • Pertubations in renin-angiotensin-aldosterone system
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12
Q

What are the 4 common precipitating events of secondary hypertension?

A
  • Chronic renal disease/ Diabetic neuropathy
  • Pheochromocytoma
  • Stress
  • Aortic coarctation
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13
Q

What type of heart failure is left-sided heart failure?

A

Congestive heart failure

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14
Q

What type of loading will occur on the right side in CHF?

A

Volume loading

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15
Q

What 3 main factors affect blood pressure?

A
  • Vascular resistance
  • Blood volume
  • Cardiac output
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16
Q

*** See slide 7… maybe… **

A

** See slide 7… maybe… **

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17
Q

What are 2 examples of loop diuretics?

A
  • Furosemide/ Lasix

- Bumetanide/ Bumex

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18
Q

What is the mechanism of action of loop diuretics?

A
  • Inhibition of Na+, K+, and Cl- reabsorption in the loop of henle resulting in electrolyte and fluid excretion
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19
Q

What are the 2 indications for loop diuretics?

A
  • Acute pulmonary edema

- Congestive heart failure

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20
Q

What type of adverse effects typically result from loop diuretics?

A

Electrolyte imbalances such as:

  • Hyponatremia
  • Hypokalemia
  • Reactive increase in renin levels
  • Alkalosis
  • Hyperuricemia
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21
Q

How much sodium chloride resorption is the loop of henle responsible for?

A

50 - 75 %

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22
Q

What are 3 thiazide/ thiazide-like diuretics?

A
  • Chlorothiazide/ Diuril
  • Hydrochlorothiazide/ Hyodrodiuril
  • Metolazone/ Zaroxolyn
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23
Q

What is the mechanism of action of thiazide and thiazide-like diuretics?

A

Inhibition of Na+, Cl-, and resorption in distal convoluted tubulue

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24
Q

What are the 2 indications for thiazide and thiazide-like diuretics?

A
  • Hypertension

- CHF

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25
Q

What is the advantage of a thiazide/ thiazide-like diuretic over lasix?

A
  • Do not develop tolerance
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26
Q

What type of adverse effects result from thiazide and thiazide-like diuretics?

A
  • Electrolyte imbalances
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27
Q

What class of drug is a K+ sparing diuretic?

A

Mineralocorticoid receptor antagonist

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28
Q

What is the chemical/ brand name of the most common K+ sparing diuretic?

A

Spironolactone/ Aldactone

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29
Q

From what is aldosterone secreted?

A

The adrenal cortex

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30
Q

What structure does aldosterone work on? What the effect?

A
  • The collecting ducts

- Enhance exchange of Na+ and K+

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31
Q

What is Spironolactone/ Aldactone’s mechanism of action?

A
  • Competitive blocker of aldosterone receptors in collecting duct
  • Decreases exchange of Na+ and K+
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32
Q

What is the indication for use of K+ sparing diuretics?

A
  • In conjunction with thiazides or loop diuretics in treatment of hypertension and CHF
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33
Q

What are 6 adverse effects of K+ sparing diuretics?

A
  • Life-threatening hyperkalemia
  • Gynecomastia
  • Impotence
  • Decreased libido
  • Acidosis
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34
Q

Retention of what electrolyte is promoted by the aldosterone? Which is lost?

A
  • Na+ maintained

- K+ lost

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35
Q

What are 2 common adverse effects of potassium sparing diuretics?

A
  • Hyperkalemia

- Acidosis

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36
Q

What are 2 combination therapies that include K+ sparing diuretics?

A
  • Amiloride and Hydrocholorothiazide (Moduretic)

- Spironolactone and isobutylhydrocholorthiazide (Aldazide)

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37
Q

What are 2 methods of controlling hyperkalemia?

A
  • IV injection of insulin and dextrose

- Echange resin (Sodium polystyrene, Kayexalate)

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38
Q

Describe the renin-angiotensin II-aldosterone system.

A
  • Renin secreted by renal cells
  • Rening convers angiotensin to angiotensin I
  • Angiotensin I converted to Angiotensin II by Angiotensin converting enzyme (ACE)
  • Angiotensin II increases levels of aldosterone, and constricts vascular smooth muscle
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39
Q

What 3 effects does aldosterone have?

A
  • Increase blood volume
  • Increase sodium levels
  • Decrease potassium levels
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40
Q

What is the counter-therapeutic effect of loop and thiazide diuretics?

A
  • When blood volume is lost, the kidneys increase renin production to compensate
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41
Q

What type of drug can prevent the counter-therapeutic effects of loop and thiazide diuretics?

A

ACE inhibitors

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42
Q

What are 4 ACE-inhibitors?

A
  • Captopril/ Capoten
  • Enlapril/ Vasotec
  • Lisinopril/ Prinivil
  • Quinapril/ Accupril
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43
Q

What is the mechanism of action of ACE-inhibitors?

A
  • Inhibition of angiotensin converting enzyme
  • Reduces levels of vasoconstriction by Angiotensin II
  • Reduces level of aldosterone by inhibiting angiotensin II
  • Increases levels of vasodilator bradykinin
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44
Q

What are 2 indications for ACE-inhibitors?

A
  • Diabetic hypertensive populations (slow development of diabetic neuropathy)
  • Hypertensive populations with left ventricular hypertrophy (reverses/ slows down hypertrophy)
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45
Q

What are 5 adverse effects of ACE-inhibitors?

A
  • Cough
  • Dizziness
  • Angioedema due to bradykinin
  • Hyperkalemia
  • Renal insufficiency
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46
Q

What are 3 angiotensin-receptor blockers?

A
  • Losatran/ Cozaar
  • Valsartan/ Diovan
  • Candesartan/ Atacand
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47
Q

What is the mechanism of action of ARBs?

A
  • Competitive inhibition of AT-1 receptor in vascular smooth muscle
  • Relaxation of smooth muscle and decreased vascular resistance
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48
Q

What are 2 indications for ARBs?

A
  • Diabetic hypertensive populations

- Hypertensive populations with left ventricular hypertrophy

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49
Q

What is 1 adverse effect of angiotensin-receptor blockers?

A
  • Hypotension
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50
Q

When should ARBs be discontinued? Why?

A

In 2nd and 3rd trimesters. Fetal circulation is affected

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51
Q

What are 3 beta-1 blockers used for the treatment of hypertension?

A
  • Metropolol/ Lopressor
  • Atenolol/ Tenormin
  • Esmolol/ Breibloc
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52
Q

What is a non-selective beta blocker used to treat hypertension?

A
  • Propranolol/ Inderal
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53
Q

What is the mechanism of action of beta-blockers?

A
  • Blocks renin production in kidneys

- Decrease in myocardial contractility

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54
Q

What is the indication for beta-blockers in cardiac patients?

A
  • Hypetensive patients with angina following heart attack
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55
Q

In whom should beta-blockers be avoided? Why?

A
  • Should be avoided in diabetics

- Masks hypoglycemic tachycardia

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56
Q

What are 3 alpha-1 blockers used to treat hypertension?

A
  • Prazocin/ Minipress
  • Doxazocin/ Cardura
  • Terazocin/ Hytrin
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57
Q

What is the mechanism of action of an alpha-1 blocker?

A
  • Blocks effect of NE (at sympathetic neurons) or epinephrine to active alpha receptors on vascular smooth muscle, decreasing vasoconstriction and growth-promoting actions
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58
Q

What is the indication for alpha-1 blocker?

A
  • Combination therapy with diuretics, and beta-1 blockers for hypertension
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59
Q

Why shouldn’t alpha blockers be used alone?

A
  • Increased risk of CHF
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60
Q

What is the adverse effect of alpha-1 blockers?

A
  • First-dose phenomenon

- Orthostatic hypotension in 50 % of patients

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61
Q

What are 4 common calcium channel blockers?

A
  • Verpamil/ Isoptin
  • Nifedpine/ Adalat
  • Dilitiazem/ Cardiazem
  • Amlodipine/ Norvasc
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62
Q

What is the mechanism of action of calcium channel blockers?

A
  • Block Ca++ channels in arteriolar smooth muscles
  • Flow Ca++ in cell blocked
  • Prevents/ decreases contraction
  • Decreases peripheral resistance
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63
Q

What is the indication for Ca++ channel blocker?

A
  • Elderly populations with low circulating renin levels
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64
Q

What are 2 direct-acting vasodilators used to treat outpatients?

A
  • Hydralazine/ Apresoline

- Minoxidil/ Loniten

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65
Q

What are 2 vasodilator used in an emergency situation?

A
  • Sodium nitroprusside

- Diazoxide/ Hyperstat IV

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66
Q

What is the mechanism of action of a direct-acting vasodilator?

A
  • Direct relaxation of vascular smooth muscles

- Decreased peripheral resistance

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67
Q

What are 4 adverse effects of direct-acting vasodilators?

A
  • Reflex tachycardia- Hypotension
  • Fluid retention
  • Hypertrichosis (Minoxidil)
  • Methemoglobinemia (Sodium nitroprusside_
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68
Q

What are the 2 major centrally acting sympatholytic agents for the treatment of hypertension?

A
  • Clonidine/ Catapress

- Reserpine

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69
Q

What is the mechanism of action of Clonidine?

A
  • Agonist of alpha-2 receptor in brainstem

- Reduces sympathetic outflow

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70
Q

What is the mechanism of action of Reserpine?

A
  • Inhibit vascular storage of norepinephrine and dopamine in central adrenergic neurons
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71
Q

What is the major adverse effect of Reserpine?

A
  • Depression
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72
Q

What is congestive heart failure?

A

Inability of the heart to maintain adequate blood flow to meet the demands of peripheral tissues and itself

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73
Q

What is the most common form of CHF?

A
  • Systolic failure because of decreased pressure and volume loads on right and left ventricles
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74
Q

What are 3 causes of CHF?

A
  • Uncontrolled hypertension
  • Coronary artery diseases
  • Idiopathic cardiomyopathy
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75
Q

What are 7 symptoms of CHF?

A
  • Orthopnea
  • Paroxymal Nocturnal Dyspnea
  • Tachypnea
  • Peripheral edema
  • Ankle swelling
  • Weight gain
  • Hepatomegaly
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76
Q

Describe the pathogenesis of CHF as it relates to sympathetic nerve activity and kidney perfusion.

A

Increased sympathetic activity:

  • Tachycardia
  • Vasoconstriction
  • Increased vascular resistance

Decreased kidney perfusion:

  • Increased renin release
  • Increased angiotensin II release (which increases vascular resistance)
  • Decreased urine output (which leads to edema)
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77
Q

What are the 3 therapy objectives for a patient with CHF?

A
  • Increase CO
  • Decrease ventricular filling volume
  • Slow pathological remodeling of ventricles
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78
Q

What 3 drugs are used in CHF, and what is the basic function of each?

A
  • Diuretics (gets rid of fluid)
  • Vasodilatorys (decrease resistance problems due to sympathetic activation)
  • Inotropic agents (heart stimulation)
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79
Q

What loop diuretics are typically used in CHF?

A
  • Furosemide

- Bumetanide

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80
Q

What problem may occur when using loop diuretics for CHF?

A
  • Resistance to the actions of the loop diuretic when the drug is used chronically
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81
Q

How can the problems with resistance to loop diuretics be overcome?

A

Paired with a thiazide diuretic

82
Q

What type of diuretic may be used in mild CHF?

A
  • Thiazides
83
Q

What type of diuretic has beneficial effects in advanced CHF, and can be used in combination therapy?

A
  • Spironolactone
84
Q

What vasodilators are used in the treatment of CHF?

A
  • ACE-inhibitors

- ARBs

85
Q

Which type of vasodilator is a first line therapy in the treatment of CHF?

A
  • ACE-inhibitors
86
Q

What is are the 2 types of nitrovasodilators used in CHF?

A
  • Sodium nitroprusside

- Organic nitrates (isosorbide, dinitrate, nitroglycerin)

87
Q

What is the mechanism of action of nitrovasodilators?

A
  • Release of nitric oxide –> potent vasodilator
88
Q

What is a second-line option for vasodilation in treatment of CHF?

A
  • Ca++ Channel Blockers
89
Q

What is the major benefit of beta blockers in the treatment of CHF?

A

Retards pathological remodelling of ventricles by neutralizing NE abd epinephrinr

90
Q

What are 2 cardiac glycosides (inotropic drugs used in CHF?

A
  • Digoxin/ Lanoxin

- Digitoxin/ Crystodigin

91
Q

What is the mechanism of action of Cardiac Glycosides?

A
  • Inhibition of Na+/K+ ATPase pump in ventricular myocytes leading to elevation of intracellular Ca++ and increased myocardial contractility
  • Potentiation of vagal nerve effects on heart
92
Q

Why does it take a long time for cardiac glycosides to be eliminated from the body?

A
  • Long half-lives
93
Q

What is a problem with cardiac glycoside use?

A

Narrow therapeutic index

  • Cardiac arrhythmia due to inhibition of Na+/K+ pump
  • Atrial arrhythmia (A-fib, sinus brachycardia)
  • Ventricular arrhythmia (angina, MI)
94
Q

The level of what electrolyte is specifically related to digoxin toxicity?

A
  • Potassium
95
Q

What are the negative and positive effects of cardiac glycosides?

A
Negative:
- Decreases heart rate
Positive:
- Increased CO
- Increased Kidney perfusion
- Increased urine output
96
Q

What 2 drugs are indicated for short-term support of circulation in advanced CHF?

A
  • Dopamine

- Dobutamine/ Dobutrex

97
Q

What is the mechanism of action of dopamine and dobutamine?

A
  • Positive inotropic effects

- Vasodilation

98
Q

What is the mechanism of action of inamirnone/ inocor and milirnone/ primacor?

A
  • Inhibit phosphodiesterase enzyme
  • Stimulates myocardial contractility
  • Accelerates myocardial relaxation
  • Decreases vascular resistance
99
Q

What stages of HF put patients at risk for development of HF?

A

A and B

100
Q

What stages of HF are symptomatic?

A

C and D

101
Q

In what stage of HF is structural heart disease present, but there are no symptoms?

A

B

102
Q

What stage of HF is end-stage?

A

D

103
Q

What stage of HF puts a patient at high risk for HF, but patients show no structural heart disease?

A

A

104
Q

What stage of HF would a patient that demonstrates past or current symptoms of be classified as?

A

C

105
Q

Can a patient revert back to an earlier stage of HF?

A

No

106
Q

What are 4 non-pharamacological management techniques of HF?

A
  • Daily weight monitoring
  • Exercise as tolerated
  • Sodium restriction
  • Fluid restriction
107
Q

What should a patient with HF’s sodium intake be limited to?

A

< 2 gm/ day

108
Q

What should a patient with HF’s fluid intake be limited to?

A

< 1.5 L/ day

109
Q

What are the 3 aspects of pharamcologic management of HF?

A
  • Appropriately manage and treat co-morbid illness
  • D/C drugs that may contribute to HF
  • Recommend treatment options based on ACC/AHA staging
110
Q

What is the purpose of drugs in stage A HF, and what are they?

A
  • Slow disease progression
  • ACE-I
  • ARB
111
Q

What is the most common adverse effect of ACE inhibitors?

A
  • Dry cough in 7 - 15 % of patients
112
Q

What is the contraindication for ACE inhibitors?

A
  • Angioedema
113
Q

What 2 parameters should be monitored in patients taking ACE inhibitors?

A
  • Renal function (SCr)

- K+

114
Q

What is the most common adverse effect of ARBs?

A
  • Dry cough, but less common than in ACE-I
115
Q

What are the 2 contraindications for ARBs?

A
  • Bilateral renal artery stenosis

- Pregnancy in 2nd and 3rd trimesters

116
Q

What 2 parameters should be monitored in patients taking ARBs?

A
  • Renal function (SCr)

- K+

117
Q

What is the drug therapy for stage B HF?

A
  • ACE-I or ARB
    PLUS
  • Beta blocker
118
Q

What is the mechanism of action of bisoprolol?

A

Beta-1 blocker

119
Q

What is the mechanism of action of Carvedilol?

A

Non-selective beta and alpha receptor blocker

120
Q

What is the mechanism of action of metoprolol succinate?

A

Beta-1 receptor blocker

121
Q

What are 4 common adverse effects of beta-blockers?

A
  • Hypotension
  • Bradycardia
  • Fluid retention
  • Fatigue
122
Q

What are 2 relative contraindications for beta-blockers?

A
  • HR < 60 bpm

- SBP <100 mmHg

123
Q

What are 2 co-morbidities that are precautions for beta-blockers?

A
  • Asthma/ COPD

- Peripheral vascular disease

124
Q

What 2 paraemeters should be monitored in patients using beta-blockers?

A
  • HR

- Blood pressure

125
Q

What is the drug therapy for all patients in stage C HF?

A
  • Diuretics
  • ACE-I or ARB
  • Beta blockers
126
Q

What are 3 drug therapies for selected patients in stage C HF?

A
  • Aldosterone antagonist
  • Digitalis
  • Hydralazine/ nitrates
127
Q

What are 2 devices for selected patients in stage C HF?

A
  • Biventricular pacing (BivP)

- Implantable cardioverter difibrillator (ICD)

128
Q

Are loop or thiazide diuretics more potent?

A

Loop

129
Q

Are loop or thiazide diuretics longer acting?

A

Thiazides

130
Q

Are loops an adjunct to thiazides, or are thiazides an adjunct to loops?

A

Thiazides adjunct to loops

131
Q

Are loops or thiazides more appropriate for treatment of renal dysfunction?

A

Loop

132
Q

What thiazide is the only one appropriate for renal dysfunction?

A

Metolazone

133
Q

What is the half-life of furosemide?

A

4 - 6 hours

134
Q

What type of diuretic is most appropriate for CHF?

A

Loop

135
Q

Where do loop diuretics prevent reabsorption of sodium and chloride?

A

Ascending loop of henle AND distal renal tubule

136
Q

Where do thiazide diuretics prevent reabsorption of sodium?

A

Distal renal tunule only

137
Q

What is 1 common adverse effect of diuretics?

A

Urinary frequency

138
Q

What are 2 contraindications for diuretics?

A
  • Anuria

- Renal decompensation

139
Q

What 3 parameters should be monitored in patients taking diuretics?

A
  • Electrolytes
  • Renal function
  • Weight
140
Q

What are 2 common aldosterone antagonists?

A
  • Spironolactone

- Eplerenone

141
Q

What is a common adverse effect of an aldosterone antagonist?

A

Gynomastia (benign enlargement of breast tissue in males)

142
Q

What is the contraindication for the use of aldosterone antagonists?

A
  • Hyperkalemia
143
Q

What 3 parameters should be monitored in patients taking aldosterone antagonists?

A
  • Renal fxn (ScR)
  • K+
  • BP
144
Q

What is the half-life of digitalis?

A

40 hours

145
Q

What is the usualy dose of digitalis?

A

0.125 to 0.25 mg

146
Q

What should the serum levels of digitalis be?

A

0.5 - 0.8 ng/mL

147
Q

How is digitalis expelled from the body?

A

The kidneys

148
Q

Above what serum level will arrythmia result in digitalis?

A

< 1.2 ng/mL

149
Q

What 5 drugs is toxicity enhanced by?

A
  • Quinidine
  • Amiodarone
  • Low K+
  • Low Mg
  • High Ca+
150
Q

What is the mechanism of action of Digoxin?

A
  • Inhibits the Na/ K+ ATPase
  • Increases Na/Ca exchange
  • Increases in intracellular calcium
  • Increased myocardial contractility (arrythmias)
151
Q

What are 6 side effects of Digoxin?

A
  • Visual disturbance
  • Myocardial Infarction
  • Vomiting
  • Nausea
  • Vomiting
  • Dizziness
152
Q

What should be always kept in mind when administering Digoxin?

A

Narrow TI

153
Q

What parameters should be monitored in a patient taking Digoxin?

A
  • Serum concentrations
154
Q

What is the mechanism of action of Hydralazine? What load is affected by Hydralazine?

A
  • Direct vasodilation of arterial smooth muscle

- Reduced afterload

155
Q

What is the mechanism of action of long-acting nitrates?

A
  • Vasodilation

- Decreased cardiac oxygen consumption by increase of intracellular cyclic-GMP

156
Q

What are 4 side effects of Hydralazine?

A
  • Reflex tachycardia
  • Lupus
  • Headache
  • Flushing
157
Q

What is the side effect of nitrates?

A
  • Headache
158
Q

What are 3 contraindications for Nitrates?

A
  • PDE-5 inhibitors
  • Head trauma
  • Cerebral hemorrhage
159
Q

What parameter should be monitored in patients taking Hydralazine/ Nitrates?

A
  • Orthostasis
160
Q

What are 2 treatments for stage D HF?

A
  • Hospice care

- Heart transplant

161
Q

What is a self-care strategy for medication adherence?

A

Pill organizer

162
Q

What is a self-care strategy for dietary adherence?

A
  • Fluid restriction

- Sodium restriction

163
Q

What is a self-care strategy for monitoring of daily weight?

A
  • Purchase scale

- Log book

164
Q

What is myocardial ischemia?

A
  • Insufficient blood flow through coronary arteries leadings to imbalance between O2 supply and demand
165
Q

What is angina pectoris?

A

Choking, squeezing pain in chest produced by ischemia

166
Q

What is myocardial infarction?

A

Extreme ischemia, leading to cardiac tissue damage and cell death

167
Q

What is stable angina?

A
  • Exertional angina
  • Blockage of coronary arteries by artherosclerotic lesions
  • Pain and discomfort following exercise or stress
168
Q

What is unstable angina?

A
  • Caused by artherosclerotic lesion and/or clot that can occlude smaller coronary vesels
  • Most common cause of MI
169
Q

What is prinzmetal angina?

A
  • Variant/ vasospastic

- Spasmso f coronary arteries that are sudden and unpredictable

170
Q

What 2 factors contribute to myocardial oxygen demand?

A
  • Heart rate

- Preload/ Afterload

171
Q

What 2 factors contribute to coronary blood flow?

A
  • Coronary vascular resistance

- Aortic pressure

172
Q

What does coronary blood flow affect?

A

Myocardial oxygen supply

173
Q

What is an example of an organic nitrate (that will be on the exam)?

A

Isosorbide dinitrate

174
Q

What effect greatly decreases organic nitrates efficacy when taken PO?

A
  • First-pass effect
175
Q

What other effect decreases organic nitrate therapy over time?

A
  • Tolerance
176
Q

What side effect should be monitored when using organic nitrates?

A
  • Severe drops in BP
177
Q

What is the half life of nitrogylcerin?

A

3 minutes

178
Q

What is the half life of isosorbide dinitrate?

A

45 minutes

179
Q

What formulation of organic nitrates provide immediate relief of angina symptoms within 1 - 2 minutes?

A
  • Sublingual tablets

- Inhalation spray

180
Q

What formulation of organic nitrates is used for prophylaxis in patients having more than one angina attack?

A

Oral nitrate

181
Q

What formulation of organic nitrates is used for short-term prophylaxis in anticipation of an angina attack?

A
  • Transmucosal

- Buccal

182
Q

What type of nitrate is used in acute management of unstable angina?

A

Nitroglycerin

183
Q

Describe the process of a nerve signal conducting through the heart including relevant nodes and structures.

A
  • Signal generated form SA node (pacemaker) under control of sympathetic and parsympathetic systems
  • Signal travels to AV node contracting atria
  • Signel enters ventrivles through bundle of His and Purkinje fibers causing ventricular contraction
184
Q

What is the P wave?

A

Atrial depolarization

185
Q

What is the QRS complex?

A

Ventricular depolarization

186
Q

What is the T wave?

A

Ventricular repolarization

187
Q

What are 2 examples of abnormal heart rhythms?

A
  • Atrial fibrillation

- Ventricular tachycardia

188
Q

What is a class 1 antiarrhythmic drug?

A

Na+ channel blockers

189
Q

What is a class 2 antiarrhythmic drug?

A

Beta blocker

190
Q

What is a class 3 antiarrhythmic drug?

A

K + channel blocker

191
Q

What is a class 4 antiarrhythmic drug?

A

Ca++ channel blocker

192
Q

What are 3 examples of class 1 antiarrhythmic drugs?

A
  • Quindine
  • Lidocaine
  • Procainamide
193
Q

What are 2 examples of class 2 antiarrhythmic drugs?

A
  • Metoprolol

- Propanolol

194
Q

What is 1 example of class 3 antiarrhythmic drugs?

A
  • Amiodarone
195
Q

What are 2 examples of class 2 antiarrhythmic drugs?

A
  • Verapamil

- Diltiazem

196
Q

What class of drugs antagonize sympathetic nerve activity, decreasing SA automaticity and causing a negative iontropic effect?

A
  • Class II (Beta-blockers)
197
Q

What class of drugs extend the duration of action potentials through the heart?

A

Class III/ K+ channel blockers

198
Q

What class of drugs decrease conduction velocity through the heart?

A

Class I/ Na+ channel blockers

199
Q

What class of drugs antagonize sympathetic nerve activity on the SA and AV nodes?

A

Class IV/ Ca++ channel blockers

200
Q

What are 2 common cardiac glycosides?

A
  • Digoxin

- Digitoxin

201
Q

What is the mechanism of action of cardiac glycosides?

A
  • Enhance effects of vagus nerve on heart
  • Slows SA node
  • Slows conduction through AV node
202
Q

What type of arrythnmias are cardiac glycosides used to treat?

A

Artrial arrhythmia associated with tachycardia