Cardiac Part I- Intro Flashcards

1
Q

Classic cardiac sx

A
CP or discomfort
Palpitations
Arrhythmias
Dyspnea
Syncope
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2
Q

Other cardiac sx

A
Fatigue (rule out the following:)
-Anemia, hypothyroid, depression
-Vit D deficiency, dehydration, DI
-Addison's, fibromyalgia
Swelling in hands or feet
Tooth pain
Reflux
Asymptomatic
Shoulder pain
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3
Q

Major independent risk factors

A
HTN
Tobacco use
DM
Elevated serum total (and LDL) cholesterol
Low serum HDL cholesterol
Advancing age
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4
Q

Major risk factors

A

Obesity/abdominal obesity

Physical inactivity

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5
Q

Gender for risk factors

A

Men > pre-menopausal women

Once past menopause, risk is similar

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6
Q

Risk factors- FHx

A

First-degree blood relative with coronary heart disease or stroke before 55 yo (male) or 65 yo (females)

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7
Q

6 vital signs

A
  1. Temperature and location
  2. Pulse and regular or irregular
  3. BP and location
  4. Respirations and labored or unlabored
  5. Pulse ox and on how much oxygen
  6. Pain (out of 10) and when last took pain medication
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8
Q

BP

A
After pt rests for at least 5 min with both feet on the ground
No recent stimulants
Auscultatory
-Sphygmomanometer (Korotkoff sound)
Palpation
-Systolic number only
-70/80/90 rule
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9
Q

What does central cyanosis indicate?

A

Significant right-to-left shunting

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10
Q

What does peripheral cyanosis indicate?

A

Small vessel constriction (heart failure, shock, PVD)

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11
Q

What does jaundice indicate?

A

Advanced right heart failure (cardiac cirrhosis)

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12
Q

What do subcutaneous xanthomas (tendon sheaths) indicate?

A

Various lipid disorders

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13
Q

What does a high-arched palate indicate?

A

Marfan’s syndrome

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14
Q

What do blue sclerae indicate?

A

Osteogenesis imperfecta

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15
Q

In head and neck, what does dusky and slightly cyanotic with elevated venous pressure indicate?

A

SVC syndrome

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16
Q

What can be found in advanced obstructive lung disease?

A

PMI may be in the epigastrium

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17
Q

What does liver enlargement indicate?

A

Chronic heart failure

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18
Q

Marfan syndrome

A

Arachnodactyly

Positive “wrist” or “thumb” sign

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19
Q

Endocarditis

A

Osler’s nodes
Janeway lesions
Splinter hemorrhages

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20
Q

What can lower extremity edema indicate?

A

Chronic heart failure or constrictive pericarditis

Lymphatic or venous obstruction (insufficiency)

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21
Q

What is nl JVP?

A

<4 cms elevation above the sternal angle

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22
Q

What is HTN a major contributing factor to?

A
CAD
CVA
CHF
Chronic renal failure
Atherosclerosis
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23
Q

When should one suspect secondary HTN?

A

Onset <30 or >50
Sudden onset of HTN
Sudden change in chronic HTN
Multi-drug resistance

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24
Q

Primary vs secondary HTN

A

Primary- 95%
-Genetic and/or idiopathic
Secondary- 5%

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25
Q

Renal causes of secondary HTN

A

Renal artery stenosis (atherosclerosis > fibromuscular dysplasia)
Renal parenchymal diseases (most common), DM

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26
Q

Adrenal causes of secondary HTN

A

Cushing’s syndrome
Pheochromocytoma (intermittent sx)
Hyperaldosteronism

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27
Q

Medications/drugs causing secondary HTN

A
OCPs
Ephedrine
MAOIs
Cocaine
Adderall
EPO
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28
Q

Other causes of secondary HTN

A
Pregnancy
Coarctation of aorta
OSA (obstructive sleep apnea)
Thyroid disease
Hypercalcemia
Increased ICP
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29
Q

Physical exam of HtN

A
Evaluate for signs of end-organ damage
-Claudication
-Bruits
-LVH
-Angina
-MI
-HF
-CVA
-PAD
-Retinopathy
-Renal disease
Evidence of potential causes of secondary HTN
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30
Q

Labs for HTN

A
Electrolytes (sodium) and serum creatinine
Fasting glucose or A1C
UA
CBC (Hgb) and lipid profile
Uric acid
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31
Q

HTN meds for general nonblack population (including diabetics)

A

Thiazide diuretic
Calcium channel blocker
ACE-inhibitor
Angiotensin receptor blocker

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32
Q

HTN meds for general black population (including diabetics)

A

Thiazide diuretic

Calcium channel blocker

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33
Q

Thiazide diuretics MOA

A

Inhibits sodium reabsorption in distal renal tubules, resulting in increased excretion of water and of Na, K, and H ions

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34
Q

Main indications for thiazide diuretics

A

HTN and edema

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35
Q

Caution in thiazide diuretics

A
Fluid or electrolyte balance
Hypercholesterolemia
Hyperuricemia or gout
Hypercalcemia
Hypotension
SLE
Liver or renal disease
Hypokalemia
Parathyroid disease
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36
Q

Calcium channel blockers MOA

A

Inhibits transmembrane influx of extracellular calcium that inhibits cardiac and vascular smooth muscle contraction

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37
Q

Main indications for calcium channel blockers

A

HTN
Chronic stable angina and CAD (not 1st line therapy)
Vasospastic angina

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38
Q

Adverse effects of calcium channel blockers

A

Edema
HA
Heart block
Constipation

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39
Q

Cautions for calcium channel blockers

A

CHF
Symptomatic hypotension possible, particularly with severe aortic stenosis
Worsening of angina and acute MI, particularly with severe obstructive CAD

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40
Q

Considerations for HTN in elderly

A

Poorest rates of control, usually require multi-drug therapy

Start low and slow

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41
Q

HTN considerations in children/adolescents

A

Consider secondary causes (renal diseases, coarctation)

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42
Q

Secondary prevention of hyperlipidemia

A

In pts with known CVD or at similar risk who can tolerate statin therapy, treat with an intensive dose of a statin (e.g, atorvastatin 40-80 mg; rosuvastatin 20-40 mg) independent of the baseline LDL-C

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43
Q

Therapeutic lifestyle changes for hyperlipidemia

A
Reduce saturated and trans-fats
Restrict dietary cholesterol to <200 mg/d
Increase soluble fiber
Fish oil supplements
Weight reduction
Increase physical activity
Increase fruits/vegetables
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44
Q

Non-cholesterol drug therapy for hyperlipidemia

A

ASA prophylaxis 81 mg daily
Antihypertensives
Smoking meds

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45
Q

Pectus carinatum

A

Pigeon chest

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46
Q

Pectus excavatum

A

Funnel chest

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47
Q

What does a barrel chest indicate?

A

Obstructive lung disease

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48
Q

What can ankylosing spondylitis indicate?

A

Aortic regurgitation

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49
Q

What does straight back syndrome indicate?

A

Mitral valve prolapse

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50
Q

What can hepatomegaly indicate?

A

Chronic heart failure

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51
Q

What can liver systolic pulsations indicate?

A

Severe tricuspid regurg

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52
Q

What can splenomegaly indicate?

A

Infective endocarditis

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53
Q

What can ascites indicate?

A

Atherosclerotic disease

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54
Q

What can muscular atrophy or absence of hair indicate?

A

Severe arterial insufficiency

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55
Q

What is JVP a reflection of?

A

Right atrial pressure

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56
Q

What should the order be when auscultating carotid arteries

A

Auscultate first for bruits before ever palpating the neck

57
Q

What should you look for when evaluating extremities?

A
Pulses, cap refill, pallor
Shiny skin, absence of hair
Edema
-Pitting vs nonpitting
Warm, erythema, tenderness
Wounds-healing or nonhealing
Ankle-branchial index (ABI)
Allen test
58
Q

What should one look for in cardiac inspection and palpation?

A

Chest deformities (pectus carinatum or excavatum)
Apical impulse or point of maximal impulse (PMI)
-Left ventricular hypertrophy- tangential light
-May require left lateral decubitus position
Central precordial heave (lift)- palpable lifting sensation that suggest severe RV hypertrophy
Thrills- felt murmurs in your MCP joint

59
Q

What sound occurs with close of AV valves and carotid pulse with the onset of ventricular contraction?

A

Lub sound (S1)

60
Q

What causes the S2 sound?

A

Closing of semilunar valves

61
Q

S3

A

Low-pitched sound occurring in mid-diastole

Usually associated with heart failure or cardiomyopathy (rarely heard in >40 healthy individuals)

62
Q

S4

A

Occurs late in diastole and is generated by forceful atrial contraction
It indicates an abnormally increased resistance to ventricular filling

63
Q

HR

A

Normally 60-100 bpm

Max HR is 220 - age

64
Q

Stroke volume

A

Volume of blood pumped from one ventricle of the heart with each beat
Nl SV for a 70-kg person is approximately 70 mL

65
Q

Cardiac output (CO)

A
Volume of blood being pumped by the heart in one minute
CO= HR x SV
Nl value:
Males 5.6 L/min
Females 4.9 L/min
66
Q

Cardiac index (CI)

A

Parameter that relates cardiac output to body surface area
CI= CO/BSA
Nl range is 2.2-4.2 L/min per square meter
Cardiogenic shock can occur if the pt has a low CI

67
Q

Central venous pressure (CVP)

A

AKA Right atrial pressure (RAP)

Nl is 2-8 mmHg

68
Q

Right ventricular pressure

A

Systolic: 15-30 mmHg
Diastolic: 3-8 mmHg

69
Q

Pulmonary artery pressure (PAP)

A

Systolic: 15-30 mmHg
Diastolic: 4-12 mmHg

70
Q

Pulmonary capillary wedge pressure (PCWP)

A

Nl: 2-15 mmHg

71
Q

Left ventricular pressure

A

Systolic: 100-140 mmHg
Diastolic: 3-12 mmHg

72
Q

Mean Arterial Pressure (MAP)

A

Average BP over a cardiac cycle

MAP= DBP + 1/3 (SBP - DBP)

73
Q

Vascular resistance

A

Resistance to flow that must be overcome to push blood through the circulatory system

74
Q

Systemic vascular resistance (SVR)

A

Nl: 700-1600
Vasoconstriction increases SVR
Vasodilation decreases SVR

75
Q

HTN risk factors

A
Increasing age
Obesity
Physical inactivity
Ethnicity
EtOH
Smoking
DM
76
Q

Optimal BP

A

<120/80

77
Q

Prehypertension

A

120-139/80-89

78
Q

Stage 1 HTN

A

140-159/90-99

79
Q

Stage 2 HTN

A

Greater than or equal to 160/100

80
Q

How to take an accurate BP

A

Pt seated for 5 mins, feet flat on the floor, arm supported at heart level
Appropriate-sized cuff
At least 2 readings…both arms
1/2 hour after eating, drinking, or smoking

81
Q

Complications of HTN

A
Coronary heart disease
Heart failure
Ischemic and hemorrhagic stroke
Chronic kidney disease
End-stage renal disease
Acute hypertensive emergencies
82
Q

HTN tx goals

A

General <60 yrs, DM, and CKD = <140/90
60+ years = <150/90
Long-term reduction in cardiovascular morbidity and mortality, renal disease, cerebrovascular disease

83
Q

HTN meds in pts greater than or equal to 18 with CKD

A

ACE-inhibitors or ARBs

84
Q

When should the initial HTN med dose increase or add a second drug?

A

One month after BP goal is not reached

85
Q

What are the main classes of HTN meds

A

Thiazide diuretics
Calcium channel blockers
Angiotensinogen-converting enzyme (ACE) inhibitors
Angiotensin II receptor blockers (ARBs)

86
Q

ACE-inhibitors (ARBs) MOA

A

Prevents the conversion of angiotensin I to angiotensin II (potent vasoconstrictor) through competitive inhibition of angiotensin-converting enzyme and in part by decreasing renin activity, and decreased aldosterone secretion
Also increases renal blood flow

87
Q

Adverse effects of ACE-inhibitors (ARBs)

A

Dizziness

Cough

88
Q

Monitoring for ACE-inhibitors (ARBs)

A

Evaluate creatinine and potassium within 7-10 days of starting ACE-inhibitors

89
Q

Black box warning for ACE-inhibitors (ARBs)

A

Contraindicated in pregnancy

90
Q

Beta blocker MOA

A

Blocks response to beta-adrenergic stimulation; cardioselective (beta1 receptors) or noncardioselective (beta2 receptors)

91
Q

Main indications for beta blockers

A

HTN
Myocardial ischemia and infarction
CHF

92
Q

Black box warning for beta blockers

A

When long-term beta blocker therapy is d/c-ed, dosage should be gradually reduced over 1-2 weeks with careful monitoring

93
Q

Side effects of thiazide diuretics

A

Hypokalemia
Hyperglycemia
Gout

94
Q

Side effects of ACE-inhibitors

A

Angioedema
Cough
Hyperkalemia

95
Q

Side effects of ARBs

A

Hyperkalemia

96
Q

Side effects of calcium channel blockers

A

Constipation
Edema
Heart block

97
Q

Side effects of beta blockers

A

Fatigue
Bradycardia
Reactive airway disease/COPD (beta-2), heart block

98
Q

Side effect of methyldopa

A

Liver disease

99
Q

Contraindications for thiazide diuretics

A

None

100
Q

Contraindications for ACE-inhibitors or ARBs

A

Pregnancy

101
Q

Contraindications for calcium channel blockers

A
Bradycardia
Hypotension
2nd or 3rd degree heart block
Wolff-Parkinson-White syndrome
Ventricular tachycardia
102
Q

Contraindications for beta blockers

A

Bradycardia
Hypotension
2nd or 3rd degree heart block

103
Q

Contraindications for methyldopa

A

Active hepatic disease

MAOI use

104
Q

HTN considerations for left ventricular hypertrophy

A

Independent risk factor for CVD

Regression may occur with aggressive therapy leads to BP control, weight loss, Na+ reduction, Rx therapy

105
Q

HTN considerations with racial disparity

A

Native and Mexican Americans= lower rates of control
African Americans
-Increased prevalence, increased severity, increased morbidity and mortality
-Reduced effectiveness of ACEI and BB. First line is generally CCB or thiazide-type diuretic
-Increased angioedema

106
Q

HTN considerations in women

A

Increased risk with OCPs

Worse with longer duration, must consider non-hormonal alternative. Not with post-menopausal HRT

107
Q

HTN considerations in pregnancy

A

No ACEI/ARB

Methyldopa, BB, or hydralazine

108
Q

Possible causes of resistant HTN

A
Improper BP measurement
Excess sodium intake
Inadequate diuretic therapy
Drug nonadherence
Drug inadequate doses
Cocaine
Amphetamines
Oral contraceptives
Licorice
Obesity
Excess alcohol intake
109
Q

Hypertensive urgency

A
Severe HTN without severe end organ damage
Systolic >180 mmHg
Diastolic >110 mmHg
Generally treat as an outpatient
Goal: reduce BP within a few hours
110
Q

Hypertensive emergency

A

Acute, severe elevation of BP with evidence of end organ damage (usually DBP >130)

111
Q

CNS end organ damage

A
ICH, stroke- presenting disease
HA
Focal neuro deficits
Seizures
AMS
Visual disturbances
112
Q

CVS end organ damage

A
Diseases: 
-Angina
-MI
-Dissection
-CHF
Sx: pulmonary edema, chest/back pain
113
Q

Renal end organ damage

A

Acute renal failure

Sx: hematuria, oliguria, proteinuria

114
Q

Eyes end organ damage

A

Hypertensive encephalopathy

Sx: Papilledema, retinal hemorrhage

115
Q

Tx of hypertensive emergency

A
Hospital admission
Decrease MAP by 25% over 1-4 hrs (24 hrs in stroke)
IV meds
-Labetalol
-Sodium nitroprusside
-Nicardipine
-Esmolol
116
Q

LDL ranges

A
<100 optimal
100-129: above optimal
130-159: borderline high
160-189: high
>190: very high
117
Q

HDL ranges

A

<40: low

>60: high

118
Q

Total cholesterol ranges

A

<200: desirable
200-239: borderline high
>240: high

119
Q

Triglycerides

A

<150: nl
150-199: borderline high
200-499: high
>500: high

120
Q

Major drug classes- hyperlipidemia

A
Statins
Niacin
Fibrates
Bile acid sequestrants
Cholesterol absoprtion inhibitor: Ezetimib
Fish oil: OTC, Lovaza, Vascepa
121
Q

Effects of statin

A
Lipid-lowering activity
Improves endothelial function
Modulate inflammatory responses
Maintains plaque stability
Prevents thrombus formation
122
Q

Statin contraindications

A

Pregnancy

Liver disease

123
Q

Side effects of statins

A
Heptatotoxicity
Myalgia
Myopathy
Myositis
Decrease dose iwth Amiodarone
124
Q

F/u with statins

A

Monitor LFTs at 3 mos, 6 mos, then every year

Check CPK if myalgias

125
Q

Contraindications of Niacin

A

Active liver disease

126
Q

Side effects of Niacin

A

Flushing (minimize with ASA/NSAIDs and titrate slowly)
Peptid Ulcer Disease
Gout Hyperglycemia
Hepatotoxicity

127
Q

F/u with Niacin

A

LFTs +/- CPKs

128
Q

Severe Vit B3 deficiency

A
Pellagra
Diarrhea
Dermatitis
Dementia
Digestive disturbances
Delirium
Depression 
Death
129
Q

Fibrates examples

A

Gemfibrozil

130
Q

Contraindications of fibrates

A

Hepatic or severe renal dysfunction
Primary biliary cirrhosis
Use with simvastatin

131
Q

Major effects of statins

A

Increase HDL
Decrease LDL
Decrease triglycerides

132
Q

Major effects of niacin

A

Increase HDL
Decrease triglycerides
Decrease LDL

133
Q

Major effect of fibrates

A

Major class used if triglycerides >400

134
Q

Side effects of fibrates

A

Cholelithiasis
Myositis
Hepatotoxicity

135
Q

Bile acid sequestrants examples

A

Cholestyramine
Colesevelam
Colestipol

136
Q

Contraindications for bile acid sequestrants

A

Bowel obstruction and hypertriglyceridemia

137
Q

Side effects of bile acid sequestrants

A

GI sx
Flatulence and constipation
Decreased absorption of other drugs
Safest lipid class to use in pregnancy

138
Q

Major side effects of Ezetimibe

A

Back pain/arthralgias
Abdominal pain
Diarrhea

139
Q

F/u for Ezetimibe

A

CK for myalgias (esp with statins)

LFTs (esp with statins)