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Clin Med, Path, Pharm > cardiology > Flashcards

cardiology Flashcards

1
Q

Atrial contraction squeezes last bit out into the ventricles, 10% of EDV

A

Atrial kick

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2
Q

What is S1 from?

A

Tricuspid and mitral valve closure during systole

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3
Q

What is S2 from?

A

Pulmonic and Aortic valves close during diastole

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4
Q

Division of the aortic root that supplies the septum and anterior ventricular wall (left coronary circulation)

A

Left Anterior Descending Artery

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5
Q

Division of the aortic root that supplies the left ventricular wall (left coronary circulation)

A

Left circumflex artery

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6
Q

Division of the aortic root hat supplies the right ventricle (right coronary circulation)

A

Marginal Branch

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7
Q

Division of the aortic root that supplies the posterior and inferior left ventricle (right coronary circulation)

A

Posterior descending

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8
Q

What % of people have a posterior descending artery from the RCA?

A

80%, right dominance

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9
Q

The ability of cardiac cells to independently and repeatedly depolarize

A

automaticity

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10
Q

How do you find CO?

A

CO = SV x HR

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11
Q

How do you find SV?

A

EDV - ESV = SV

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12
Q

Cardiac muscle stretch at the start of systole

A

Preload

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13
Q

Pressure that the ventricles contract against during systole (aortic pressure)

A

Afterload

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14
Q

What affects preload?

A 
Blood volume
Distribution of BV
Atrial contraction
Heart Rate
Ventricular complicance
(BDAHV)
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15
Q

T or F: Aortic pressure = ventricular pressure = Systolic BP

A

True

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16
Q

T or F: As BP rises, there is more SV

A

False. More resistance, less SV

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17
Q

What affects afterload?

A 
Vascular resistance (systemic)
Elasticity of the aorta
Arterial blood volume
Ventricular wall tension
Aortic Valve stenosis
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18
Q

What could affect stroke volume on both preload and afterload curve?

A

Contractility

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19
Q

What affects contracility?

A 
Calcium (intramyocardial)
Ischemia/Necrosis
Rate
Fibrosis or ventricular compliance
Ventricular remodeling
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20
Q

How do you find mean arterial pressure?

A

MAP = 1/3 systolic BP + 2/3 diastolic BP

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21
Q

What are the three layers of arteries and veins?

A

Intima
Media
Adventitia

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22
Q

Which structure has elastic tissue between intima and media?

A

Aorta

“vasa vasorum”

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23
Q

Myocardial contraction

A

Inotropy

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24
Q

Myocardial relaxation

A

Lusitropy

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25
Q

SA node firing

A

Chronotropy

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26
Q

AV node conduction velocity

A

Dromotropy

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27
Q

P wave on EKG

A

Atrial systole

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28
Q

How are mitral and tricuspid valves during atrial systole?

A

OPEN

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29
Q

What is S4 from?

A

Extra heart sound during atrial systole from forceful atrial contraction against a stiff ventricle

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30
Q

QRS on EKG

A

Isovolemic contraction

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31
Q

Ventricular pressure > atrial pressure

A

Ventricular contraction, aka Isovolemic contraction

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32
Q

How are mitral and tricuspid valves during isovolemic contraction?

A

Closed (S1)

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33
Q

Ventricular emptying. Ventricular pressure > Aortic pressure

A

Rapid ejection

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34
Q

ST segment and T wave on EKG

A

Rapid ejection

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35
Q

How are aortic and pulmonary valves during rapid ejection?

A

Open

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36
Q

Closure of the cycle, Aortic pressure > Ventricular pressure.

A

Isovolemic relaxation

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37
Q

What heart sound is associated with isovolemic relaxation?

A

Aortic and pulmonary valves closing (S2)

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38
Q

What is S3 from?

A

Extra heart sound in which you can hear rapid filling of ventricles

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39
Q

How are mitral and tricuspid valves during rapid filling?

A

OPEN

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40
Q

Peak pressure in the arteries near the end of systole

A

SBP

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41
Q

resting pressure in the arteries during diastole

A

DBP

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42
Q

Why worry about HTN?

A 
It DOUBLES the risk of:
CAD
PAD
CHF
Stroke
Renal failure
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43
Q

How does BP change over time?

A

SBP: men higher than women until 60, then women are higher
DBP: increase until 55, then decrease

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44
Q

If you’re over 60, there’s a _____% chance of having HTN

A

60

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45
Q

What are the signal pathways through which the ANS regulates BP?

A

Pressure
Volume
Chemoreceptors

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46
Q

Receptor Alpha 1: Location, effect?

A

Vascular smooth muscle

Vasoconstricts

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47
Q

Receptor Alpha 2: Location, effect?

A

neurotransmitter (epi or NE) synthesizing nerves

Inhibits NT release

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48
Q

Receptor Beta 1: Location, effect?

A

Cardiac cells

Increases rate and contractility

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49
Q

Receptor Beta 2: Location, effect?

A

Vascular smooth muscle

Vasodilation

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50
Q

Stretch or pressure sensor in aortic arch and carotids

A

Baroreceptors

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51
Q

With an increase in pressure, and therefore increased stretch, signals are released that cause what?

A

Decrease in sympathetic output

Decrease in HR and pressure

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52
Q

With a decrease in pressure and a decrease in stretch, signals are released that cause what?

A

Increase in sympathetic output

Increase in HR and Pressure

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53
Q

An alpha 1 antagonist would cause what?

A

lower BP

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54
Q

An alpha 1 agonist would cause what?

A

Higher BP

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55
Q

An alpha 2 antagonist would cause what?

A

higher BP

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56
Q

An alpha 2 agonist would cause what?

A

Lower BP

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57
Q

A beta 1 agonist would cause what?

A

higher BP

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58
Q

A beta 1 antagonist would cause what?

A

lower BP

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59
Q

A beta 2 antagonist would cause what?

A

higher BP

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60
Q

A beta 2 agonist would cause what?

A

lower BP

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61
Q

What effect does norepinephrine have at arteriole level?

A

Vasoconstricts

Main source of afterload

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62
Q

What will the kidneys release renin in response to?

A

Low BP
Low sodium
NE stimulation (Sympathetic signaling)

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63
Q

Where is angiotensin formed?

64
Q

How does angiotensin become fully activated angiotensin II?

A

Anigotensin (made by liver) is cleaved by renin (made by kidneys) into angiotensin 1. Angiotensin 1 is cleaved by ACE in the lungs and vasculature to angiotensin II.

65
Q

How does Angiotensin II work in its different locations?

A

Vascular: triggers smooth muscle contriction
Kidneys: triggers water resorption
Pituitary: Triggers ADH release
Adrenals: triggers Aldosterone release (renal sodium resorption)

66
Q

What else does ACE do besides convert angiotensin 1 to II?

A

Make bradykinin (vasodilater) inactive

67
Q

What happens to large vessels from remodeling?

A

Increased intima and media thickness

68
Q

What happens to small vessels from remodeling?

A

Decreased lumen diameter

69
Q

What is metabolic syndrome?

A

Constellation of insulin resistance, abdominal obesity, HTN, dyslipidemia

70
Q

What is the most common cause of secondary hypertension?

A

primary renal disease

71
Q

How can HTN and the kidneys be involved in a vicious cycle?

A

HTN causes renal cell death
Renal cell death leads to a loss of auto-regulation
Loss of auto-regulation leads to HTN
This repeats until kidney failure :(

72
Q

What is considered HTN?

A

Anything over 140/90

73
Q

Cardiovascular disease DOUBLES for every ____ above 115 SBP and ____ above 75 DBP

A

20 mmHg

10mmHg

74
Q

How do you diagnose HTN?

A

2 recordings at 2 or more different office visits.

75
Q

BP cuff bladder width should be _____% the arm circumference. Bladder length should be _____% the arm circumference.

76
Q

Someone with BP of 135/90 would be in what stage?

77
Q

Someone with BP of 138/85 would be in what stage?

78
Q

Someone with a BP of 160/96 would be in what stage?

79
Q

Refractory HTN associated with insulin resistance and hypokalemia. Increased salt as well.

A

Primary aldosteronism. Aldosterone increases independent of RAAS.

80
Q

Excess Cortisol prouction, excess ACTH secretion.

A

Cushing’s syndrome

81
Q

Catecholamine (epi) secreting tumor of the adrenal medulla. Rare, treatment is surgical.

A

Pheochromocytoma

82
Q

What is the most common congenital cardiovascular cause of HTN?

A

Coarctation of the aorta (narrowing of the aorta)

83
Q

A drop of 10 lbs can result in BP drop of ___ mmHg systolic and ____ 3 mmHg diastolic.

A

6 SBP

3 DBP

84
Q

If your patient is hypertensive, what salt recommendation should you give them to lower BP?

A

4.4-7.4 g/day

85
Q

How much does a decrease in salt lower BP?

A

4 mmHg systolic

1 mmHg diastolic

86
Q

What can reduce risk of CVA by 35-40% in 5 years?

A

Reduction of 10-12 mmHg SBP and 5-6 mmHg DBP

87
Q

What can reduce risk of CAD by 12-16% in 5 years?

A

Reduction of 10-12 mmHg SBP and 5-6 mmHg DBP

88
Q

On average, how much do most meds drop BP by?

A

Systolic: 7-13 mmHg
Diastolic: 7-8 mmHg

89
Q

Inhibits the Na/Cl pump in the distal convoluted tubule

90
Q

First line antihypertensive

A

Hydrochlorothiazide (diuretic)

91
Q

Block sodium channels in the distal nephron

A

K+ sparing diuretics

92
Q

First line antihypertensive that is potassium sparing with once daily dosing

A

Amiloride (Midamor)

93
Q

Potassium sparing antihypertensive with BID dosing

A

Triamterne (Dyrenium)

94
Q

The “-semides”

A

Loop diuretics

95
Q

Block Na/K/Cl transporter in loop of Henle causing decreased Na resorption (and thus less water resorption).

A

Loop diuretics

96
Q

Diuretic used in pts with CHF

A

Loop diuretic

97
Q

Best for pressure and volume reduction in a CHF patient. Dosed BID

A

Furosemide (Lasix) loop diuretic

98
Q

Best for pressure and volume reduction in a CHF patient with daily dosing.

A

Torsemide (Demandex)

99
Q

The “-prils”

100
Q

Decreases Angiotensin II production, increases bradykinin levels, decreases sympathetic activity.

101
Q

Best for first line antihypertensives for patients with renal disease

A 
ACEI: 
Lisinopril (Prinvil)  OR
Enalapril (Vasotec)
ARBs:
Valsartan (Diovan) OR
Losartan (COZAAR)
102
Q

What are SE for ACEIs?

A

Cough, angioedema

103
Q

The “-sartans”

104
Q

Works by blocking the angiotensin receptors

105
Q

Receptor antagonist that decreases Na resorption, thereby decreasing water resorption and increasing potassium.

A

Aldosterone antagonists

106
Q

Second line aldosterone antagonist taken daily or BID

A

spironolactone (aldactone)

107
Q

What are SE of spironolactone?

A

Binds to androgen receptors, decreasing testosterone and increasing estradiol.
Gynecomastia, impotence, menstrual abnormalities

108
Q

The “-olols”

A

Beta blocker

109
Q

How do beta blockers work?

A

Competitive inhibition of beta 1 receptor.

Decreases heart and contractility, thereby lowering cardiac output

110
Q

Beta blocker that is best for patients with a history of MI?

50-100 mg PO

A

Metoprolol (lopressor)

111
Q

Who would metoprolol NOT be indicated for?

A

Asthma/COPD patients

112
Q

Beta blocker that is best for patients with history of MI that also has Alpha 1 inhibition?

A

Labetalol (trandate)

113
Q

The “-azosins”

A

Alpha blockers (alpha-1 receptor blockers)

114
Q

Used in prostatic hypertrophy, not as effective as other meds for HTN

A

alpha blockers:
Doxazosin (Cardua)
Terazosin (Hytrin) taken QHS

115
Q

Alpha-2 receptor agonists that decrease sympathetic outflow and decrease peripheral vascular resistance by depleting NE

A

Sympatholytic Agents

116
Q

What are SE of Clonidine (Catapress)?

A

Sympatholytic Agents

Rebound HTN, sexual dysfunction, helps with heroin withdrawal

117
Q

How do CCBs reduce HTN?

A

Block calcium channels, reducing intracellular calcium and reduces vasoconstriction

118
Q

What do nondihydrophyridines focus on?

A

CCB that causes:
Decreased force of contraction
Vasodilation
Decreased conduction through SA and AV node

119
Q

What do dihydrophyridines focus on?

A

CCB that causes:
Decrease SVR and arterial pressure
Can have REFLEX tachy
Doesn’t affect AV node conduction

120
Q

Which CCB is first line?

A

Dihydros
Amlodipine (NORVASC)
Nifedipine (PROCARDIA)

121
Q

When would you prescribe diltiazem (cardiazem)?

A

First line CCB for patients with conduction issues, like A. Fib.
It is Nondihydro

122
Q

SE of Dilitazem?

A

Peripheral edema

123
Q

If your patient is younger, they MAY do better with what?

A

Beta or ACEI

124
Q

If your patient is over 50, they MAY do better with what?

A

diuretic or CCB

125
Q

What’s average Joe with HTN’s target BP?

A

<135-140/80-85

126
Q

What’s someone with CAD and DM’s target BP?

127
Q

What’s someone with proteinurea’s target BP?

A

<120 systolic

128
Q

What’s someone with CHF’s target BP?

A

no set number

129
Q

What is considered resistant hypertension?

A

BP >140/90 while on 3 antihypertensive agents

130
Q

What are the main causes of resistant HTN?

A

Non-adherence
Obesity
Drugs or alcohol

131
Q

What is the initial lab work up of someone with resistant HTN?

A

BUN/Cr (renal function)
Electrolytes
Urinalysis (proteinuria, renal dz)
Fasting glucose and cholesterol (metabolic syndrome?)

132
Q

According to JNC 8, a pt with DM or CKD between ages 30-59 should shoot for what DBP?

A

<90

Same as someone without those diseases in any age group

133
Q

According to JNC 8, what treatment method was eliminated?

A

Beta blockers

134
Q

According to JNC 8, what should you use to treat African Americans?

A

CCB or Thiazide

135
Q

According to JNC 8, what should you use for someone with CKD?

A

Add ACE or ARB to improve renal outcomes

136
Q

What were differences with JNC 7 and JNC 8?

A

JNC 7: thought SBP >140 was more important than any DBP.
Initial treatment with Thiazide, then add any other class.
WIth DM and CKD, goal BP 130/80

137
Q

Why aren’t beta blockers being used as much anymore?

A

More cardiovascular events when compared to ARBs

138
Q

In the general nonblack population, including those with DM, initial antihypertensive treatment should include anything but what?

A

Alpha and beta blockers

Use thiazide diuretic, CCB, ACEI, or ARB

139
Q

Initial treatment for African Americans should be what?

A

thiazide or CCB

140
Q

T or F: Beta blockers have been shown to cause depression.

141
Q

What antihypertensive would you put someone on with A. fib?

A

Diltiazem

nondihydro that slows conduction

142
Q

> 180/100 mmHg with end organ damage

A

Hypertensive Emergency

That pressure without organ damage would be hypertensive URGENCY

143
Q

What organs are involved in hypertensive end organ damage?

A 
Eye (retinal hemorrhage)
Brain (stroke, seizure, encephalopathy)
Heart (MI, CHF, aortic dissection)
Lung (pulmonary edema from CHF)
Kidney (acute renal failure)
144
Q

Sudden HTN in a previously normotensive pt

Sudden spike in known HTN patient

A

Malignant hypertension

145
Q

What is malignant HTN associated with?

A

Diffuse necrotizing vasculitis
Arteriolar thrombi
Fibrin deposition in arteriolar wall
Fibrin necrosis of arterioles of brain, retina, and kidney

146
Q

What is the treatment goal of malignant HTN?

A

Lower BP to 160/110-100 OR

NO more than 25% reduction in MAP in first 2 hours

147
Q

What meds are used for malignant hypertension?

A

Beta Blockers

CCBs

148
Q

Continuous IV that blocks beta-1 and alpha-1

A

Labetalol (trandate)

149
Q

Continous IV CCB for malignant HTN

A

Nicardapine (cardene)

150
Q

What med is best for hypertensive encephalopathy?

A

Nitroprusside (nitropress)

Vasodilation via action on vessel smooth muscle

151
Q

What are SE of Nitroprusside?

A

Cyanide toxicity, drug is photosensitive

152
Q

What are situations besides malignant HTN where BP management is crucial?

A 
Hypertensive encephalopathy
Stroke
MI
Aortic Dissection
Eclampsia
153
Q

What is generally used in an MI?

A

Nitroglycerine

154
Q

What two things do you want to control in an aortic dissection?

A
  1. Control shearing forces with a reduction in rate and contractility (beta blocker)
  2. Control hypertension (Nitroprusside)
155
Q

What med is best for a pregnant hypertensive pt?

A

Hydralazine
Arterial vasodilator.
SE: rebound HTN

156
Q

What are all the med options for a hypertensive pregnant woman?

A

Hydralazine, labetalol, nicardipine.

Magnesium used too, but not for BP control

Clin Med, Path, Pharm (12 decks)

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