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Clin Med 2 > HTN, CAD, and Valvular Heart Disease > Flashcards

HTN, CAD, and Valvular Heart Disease Flashcards

1
Q

Elevated SDP as defined without an etiology; onset 25-50 years old

A

Primary (essential) hypertension

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2
Q

Elevated BP where the cause of the high BP can be identified and sometimes treated

A

Secondary HTN

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3
Q

BP uncontrolled despite adherence to an appropriate 3-drug regimen, in which all drugs are dosed at >50% of recommended dose

A

Resistant HTN

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4
Q

Patient with resistant HTN who cannot be controlled >4 medications

A

Refractory HTN

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5
Q

What is white coat syndrome?

A

BP that are high in the clinic or office but normal elsewhere

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6
Q

What is masked HTN?

A

BP that is consistently elevated out-of-office measurements but does not meet criteria for HTN upon office readings

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7
Q

What is a hypertensive urgency?

A

Severe HTN >120 DBP in asymptomatic patient

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8
Q

What is a hypertensive emergency?

A

Sever HTEN >120 DBP with acute end-organ damage

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9
Q

Blood Pressure = ?

A

Cardiac output x Vascular resistance (SVR)

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10
Q

What are the 3 factors affecting BP?

A
  1. Sympathetic nervous system
  2. Renin-angiotensin-aldosterone system
  3. Plasma volume (mediated by kidneys)
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11
Q

What is the average pressure in the arterial system?

A

Mean arterial pressure

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12
Q

MAP (mean arterial pressure) = ?

A

[(2xdiastolic) + systolic]/3

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13
Q

What is the normal range of mean arterial pressure?

A

70-110

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14
Q

<50% of people with HTN have it adequately controlled, why?

A

Poor access to healthcare, lack of adherence to long-term asymptomatic condition, therapeutic inertia

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15
Q

What is HTN a risk factor for?

A

Heart attack, stroke, CVD, kidney disease

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16
Q

When does the risk of major CV and stroke events double?

A

Above 115/75, for each increase of 20 mm Hg in systolic BP or 10 mmHg in diastolic BP

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17
Q

Who has an earlier age onset and worst outcomes of HTN?

A

Blacks

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18
Q

What are the benefits of lowering BP?

A

Stroke incidence decrease 35-40%
MI decrease 20-25%
Heart failure decrease 50%

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19
Q

What are some risk factors for primary HTN?

A

exact etiology is unknown age, obesity, family hx, race, high-sodium diet, excess alcohol consumption, physical inactivity, diabetes and dyslipidemia, hostile/angry/depression

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20
Q

What are the common etiologies for secondary HTN?

A

Chronic kidney disease renovascular disease/renal artery stenosis, mineralocorticoid excess, sleep breathing disorder, medications

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21
Q

What are the uncommon etiologies for secondary HTN?

A

Pheochromocytoma, endocrine disorders, coarctation of aorta

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22
Q

What is the most common cause of renovascular HTN in older patients?

A

Atherosclerosis

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23
Q

What is the most common cause of renovascular HTN in young patients (especially females)?

A

Fibromuscular dysplasia

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24
Q

Other causes of renovascular HTN?

A

Aortic/renal dissection, Takayasu’s arteritis, thrombotic/cholesterol emboli, CVD, post transplantation stenosis, post radiation

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25
Q

Brain complications of uncontrolled HTN?

A

Ischemic stroke, intracerebral hemorrhage, cerebral atrophy and dementia

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26
Q

Eye complications of uncontrolled HTN?

A

Retinopathy, retinal hemorrhages, vitreous hemorrhage, retinal detachment, impaired vision/blindness

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27
Q

Kidney complications of uncontrolled HTN?

A

CKD, ESRD

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28
Q

Cardiac complications of uncontrolled HTN?

A

Coronary heart disease, ischemic heart disease, LVH, HF, acute aortic dissection, arterial aneurysm, HTN emergency

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29
Q

What are the 4 stages of hypertensive retinopathy?

A

Stage 1: Narrowing
Stage 2: AV Nicking
Stage 3: Hemorrhages, cotton wool spots and exudates
Stage 4: Papilledema

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30
Q

What is the screening technique for 18-39YO (HTN) <130/80

A

Every 3-5 years

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31
Q

What is the screening technique for 18-39 YO with risk factors or >130-139/85-89 BP

A

Screen annually

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32
Q

What is the screening technique for someone >40YO (HTN)

A

Annually

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33
Q

Normal BP is considered what?

A

<120 / <80

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34
Q

PreHTN is considered what?

A

120-39 / 80-89

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35
Q

Stage 1 HTN is considered what?

A

140-159 / 90-99

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36
Q

Stage 2 HTN is considered what?

A

> 160 / >100

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37
Q

Isolated systolic HTN is what?

A

> 140

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38
Q

Isolated diastolic HTN is what?

A

> 90

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39
Q

What do you need in order to diagnose HTN?

A

BP readings >two separate office visits*
Average of 2 or more properly measured readings/visit
Weeks-months apart

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40
Q

HTN diagnosis

A

Home BP >130/80

24 hour ambulatory monitoring: daytime <135/85 nighttime: 120/70

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41
Q

What are some initial symptoms seen with HTN?

A

HA, dizziness, weakness, vision changes, SOB, orthopnea, chest pain, claudication, palpitations, sweating, fatigue, daytime sleepiness, weight gain

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42
Q

Secondary HTN hx clues

A

Onset at age <30 years, unresponsive to treatment, episodic, HA and chest pain/palpation (pheochromocytoma, thyroid dysfunction), morbid obesity with history of snoring and daytime sleepiness (sleep disorders)

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43
Q

Secondary HTN PE clues

A

Pallor, edema, other signs of renal disease, abdominal bruit especially with a diastolic component (renovascular), truncal obesity, purple striae, buffalo hump (hyercortisolism)

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44
Q

Labs for HTN

A

BMP, LFTs or CMP, Lipids (fasting), hemoglobin/hematocrit, Urinalysis, EKG

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45
Q

Lipids tested for HTN

A

HDL, LDL, triglycerides

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46
Q

What are some things that may trigger a clinician to investigate secondary causes of HTN?

A

New onset @ younger age, pts presenting with Stage 2 HTN, abrupt onset in previously normal, resistant HTN, abdominal bruits, hypokalemia

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47
Q

What are some non-pharmacologic treatments for preHTN and HTN?

A

Weight reduction, adopt DASH eating plan, dietary sodium reduction, physical activity, moderation of alcohol consumption

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48
Q

What is the DASH eating plan?

A

Diet rich in fruits, veggies, and low-fat dairy products with a reduced content of saturated and total fat

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49
Q

What type of physical activity is good for HTN and preHTN?

A

Regular aerobic activity such as brisk walking (at least 30 minutes per day, most days of the week)

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50
Q

What are the recommended pharmacologic treatments for HTN and preHTN?

A

Diuretics: HCTZ, Chlorthalidone
CCB: Amlodipine, Dihydropyridine preferred
ACE: Lisinopril, benazapril
ARB: Losartan

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51
Q

According to the JNC 8, what are the recommended treatments for HTN?

A

All therapy includes lifestyle modifications

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52
Q

What are the JNC recommendations for preHTN?

A

Non-pharmacological therapy only

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53
Q

CKD>?

A

CKD>Race>Comorbidities according to the JNC 8 for HTN recommendations

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54
Q

What is the proper treatment for someone with CKD?

A

Any age or race, ACE inhibitor or ARB

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55
Q

What is the proper treatment for someone who is >18YO and black?

A

Thiazide or CCB

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56
Q

What is the proper treatment for someone who is >18YO non black and non CKD?

A

Thiazide, CCB, ACE inhibitor, ARB

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57
Q

Most patient with HTN will require what?

A

More than one BP medication to reach the goal

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58
Q

When should a new drug be added to HTN regimen?

A

Increase or add new drug at 2-4 week intervals

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59
Q

After 5 years how many patients will require dual or triple therapy for HTN?

A

40-43%

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60
Q

Follow-up and monitoring for HTN

A

PreHTN: non-pharm management and f/u annually

Stage 1: non pharm-management 1-6mo f/u

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61
Q

Patients on pharmacological therapy should be monitored how often?

A

Re-evaluated every 2-4weeks until BP is achieved

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62
Q

Thiazide monitoring

A

Check K 3 weeks after each adjustment

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63
Q

After BP goal is stable, how often should they be monitored?

A

3-6 month intervals, most should reach the regimen within 6-8 weeks

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64
Q

Serum potassium and creatinine should be monitored how often?

A

1-2 times per year

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65
Q

Things to consider if BP therapy isnt working

A

Inaccurate BP measurement, poor adherence to meds, poor adherence to lifestyle and dietary approaches, suboptimal antihypertensive therapy, white coat syndrome, resistant HTN

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66
Q

How do you treat resistant HTN?

A

Refer to HTN specialist. Consider: lifestyle, diet or medications that interfere

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67
Q

Resistant HTN treatment

A

Add ons to the 3 original medications: Potassium-sparing diuretics Spironolactone, Eplerenone, Amiloride
BB Labetolol Carvedilol
Alpha-1 blocker Clonidine
Others: vasodilator like Hydralazine

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68
Q

What are the 3 original medications that should be used for resistant HTN?

A

Thiazide, CCB, ACE/ARB

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69
Q

HTN urgency si/sx

A

Systolic >180
Diastolic >120
Asymptomatic, no evidence of organ damage, no benefit in rapid reduction, slow reduction over days

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70
Q

HTN emergency si/sxi

A

Systolic >180
Diastolic >120
Symptomatic: HA, blindness, chest pain, dizziness

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71
Q

What end organ signs will be seen with HTN emergency?

A

Hypertensive encephalopathy, acute left ventricular failure with pulmonary edema, acute MI or unstable angina pectoris, dissecting aortic aneurysm

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72
Q

What is the management for hypertensive urgency?

A

Lower BP over a period of hours to days, goal is <160/<100 or no more than 25-30% baseline

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73
Q

Medication options for hypertensive urgency management

A

Furosemide: if not volume depleted

Oral clonidine or oral captopril: if not volume overload

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74
Q

Hypertensive emergency management

A

Immediate but careful reduction in BP is indicated, excessive hypotension may lead to ischemic complications

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75
Q

Parenteral agents for hypertensive emergency

A

Nitroprusside, Nitroglycerin, Nicardipine, Labetolol, Esmolol, Hydralazine

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76
Q

Pathophys of coronary artery disease

A

Atherosclerosis causes: Thickening of the arterial vessel wall, leading to deposits of cholesterol and other substances

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77
Q

Increased vascular resistance leads to what?

A

Increase vascular resistance -> progressive -> complete occlusion (ruptured clot) -> myocardial infarction

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78
Q

The Framingham Heart study

A

Began in 1948 with 5,209 adults. Much of “common knowledge” about heart disease has been learned through this study

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79
Q

Framingham study taught us what?

A

Risk factors: HTN, high cholesterol, cigarette smoking, healthy diet (good), weight, regular exercise (good)

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80
Q

What is the framingham risk score?

A

It estimates the 10 year cardiovascular risk of an individual

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81
Q

What does the risk score not include?

A

Diabetes or Family Hx, so it may underestimate the risk

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82
Q

Risk factors for CAD

A

> 65YO, M>F until menopause, smoking, dyslipidemia, HTN, DM, abdominal obesity, family Hx of 1st degree relative with premature MI (men <55 women <65), cocaine use

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83
Q

Stroke risk factors (also found in framingham study)

A

HTN and LVH

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84
Q

HF risk factors (found in framingham study)

A

HTN

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85
Q

Metabolic syndrome is three or more of the following

A
  1. Abdominal obesity
  2. Triglycerides >150mg/dL
  3. HDL <40 for men and <50 for women
  4. Fasting glucose >110
  5. HTN
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86
Q

Primary prevention of CAD involves what?

A

Maintaining or achieving ideal weight, physical activity, eat healthy diet, refrain from cigarette smoking, maintain BP at goal, maintain normal “bad” cholesterol, glycemic control in diabetes, high risk: take aspirin, small amount of alcohol consumption

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87
Q

What type of diet will help with primary prevention of CAD?

A

Fruits, veggies, fiber, low glycemic index, unsaturated fats, omega-3 fatty acids (Mediterranean diet)

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88
Q

Chest “pain” attributable to myocardial ischemia (oxygen supply/demand mismatch)

A

Angina pectoris

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89
Q

What is anginal equivalent?

A

Symptoms other than chest discomfort attributable to myocardial ischemia (SOB, dizziness, nausea, fatigue)

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90
Q

What are the 4 main factors that affect oxygen demand in angina pectoris?

A
  1. Heart Rate
  2. Systolic BP
  3. Myocardial wall tension or stress
  4. Myocardial contractility
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91
Q

What are the symptoms of chronic stable angina pectoris?

A

Chest discomfort or dyspnea WITH EXERTION lasting 5-15 mins, relieved by rest and/or nitro, typically located central or slightly left side of chest, lightheadedness, fatigue

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92
Q

Stable angina pectoris description of discomfort?

A

Tightness, squeezing, burning, gas, indigestion or ill characterized

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93
Q

Differential diagnosis of chest pain

A

Cardiac ischemia or infarction, aortic dissection, pulmonary embolism

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94
Q

Most patients with stable CAD will have what?

A

Fairly normal physical exam

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95
Q

What is the PE of someone with stable CAD?

A

General appearance: Central obesity, sweaty, SOB with minimal exertion
Vitals: High BP
Diminished peripheral pulses (peripheral artery disease)
Bruits of arteries: carotid, renal, aorta, femoral

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96
Q

Possible EKG findings in patients with CAD

A

Pathologic Q waves, non-specific ST-T wave abnormalities, LVH, ST depressions, ST elevations during STEMI

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97
Q

What does a pathologic Q wave suggest?

A

Previous infarction

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98
Q

What does a non-specific ST-T wave abnormality suggest?

A

Suggests previous or active ischemia or infarction

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99
Q

What does LVH on an EKG suggest?

A

Long standing HTN

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100
Q

What does ST depressions suggest on an EKG?

A

During active ischemia; when supply is less than demand

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101
Q

Stable angina

A

Patient is asymptomatic at rest, symptoms are provoked by predictable amount of exertion (or stress, high BP, etc.)

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102
Q

Unstable angina

A

Symptoms at rest or with less exertion than prior baseline

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103
Q

What is stress testing?

A

The method of diagnosing CAD in conjunction with the rest of the clinical assessment, non-invasive, appropriate for stable angina

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104
Q

What is stress testing C/I in?

A

Unstable angina

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105
Q

What is the “gold standard” for diagnosing CAD?

A

Coronary angiography, but not used as primary modality due to limitations (invasive, costly, does not yield physiologic information)

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106
Q

What are the 3 categories of chest pain?

A
  1. Classic (typical) angina
  2. Probably or atypical angina
  3. Nonanginal or nonischemic chest pain
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107
Q

What is classic (typical) angina?

A

Substernal chest discomfort, typical in quality and duration, provoked by exertion or stress & relieved by rest or NTG

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108
Q

What is probably or atypical angina?

A

Chest pain with 2/3 of the following characteristics:
Substernal chest discomfort, typical in quality and duration, provoked by exertion or stress & relieved by rest or NTG

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109
Q

What is nonanginal or nonischemic chest pain?

A

Chest pain with one or non of the following characteristics:
Substernal chest discomfort, typical in quality and duration, provoked by exertion or stress & relieved by rest or NTG

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110
Q

What are the indications for stress testing?

A

Patients with symptoms suggesting stable angina with intermediate pretest probability or disease
Pre-op risk assessment for non-cardiac surgery
Pts with significant change in cardiac symptoms
After resolution of acute chest pain
Prior to angiography to localize lesion

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111
Q

What can happen with the pretest probability?

A

High pretest probability will have some false negative rate of tests, while low pretest probability will have some false positive tests

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112
Q

What are some factors to consider when choosing the type of stress test?

A

Pts ability to exercise, pts resting EKG, the clinical indication for performing the test, pts body habitus, hx of prior re-evaluation

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113
Q

What are the 4 types of stress tests?

A
  1. Exercise tolerance testing (ETT) uses treadmill and EKG
    Imaging Tests
  2. Echocardiography (exercise or pharmacologic)
  3. Radionuclide myocardial perfusion imaging (exercise or pharmacologic)
  4. Positron emission tomography (PET) almost always pharmacologic
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114
Q

What type of stress test is first line for most patients?

A

ETT (exercise tolerance testing)

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115
Q

In order to do the ETT, what must the resting EKG be without? (exclusion criteria)

A

ST abnormalities, LVH, LBBB, vent-paced, WPW (CAD risk low to moderate)

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116
Q

ETT criteria

A

Patient must be able to exercise, simple and inexpensive!

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117
Q

False positives with ETT

A

Women have more than men, but its still first line for them

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118
Q

What test looks for stress induced regional wall motion abnormalities?

A

Stress echocardiogram

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119
Q

Stress Echocardiogram

A 
Exercise or pharmacologic, echo at rest, then after stress
Operator dependent (sensitivity relates to technician experience)
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120
Q

What are other names for the radionuclide myocardial perfusion imaging?

A

Stress myoview, stress MIBI (Sestamibi)

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121
Q

Radionuclide myocardial perfusion

A

Inject radioactive nucleotide, poorly perfused areas of the heart do not take up color, localize lesion to coronary artery

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122
Q

Nuclear medicine PET CT stress test

A

Very sensitive, very expensive, best test for obese patients, not readily available

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123
Q

Which test is best used for obese patients?

A

Nuclear medicine PET CT stress test

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124
Q

Acute Coronary Syndrome (ACS)

A
  1. Unstable angina
  2. Non-STEMI
  3. STEMI (most serious)
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125
Q

Classic presentation of ACS

A

Early am, substernal chest pressure “an elephant sitting on my chest,” severe, sense of impending doom, radiates to L arm, both arms or jaw, associated SOB, nausea, diaphoresis, light-headed, lasts >20min but <1hour

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126
Q

Unstable Angina

A

Ischemic symptoms suggestive of ACS and no elevation of cardiac biomarkers (Troponin)
Unstable plaque without plaque rupture
May or may not have ST depression or non-specific changes

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127
Q

NSTEMI

A

Potentially same manifestations as US but DO have elevated cardiac biomarkers (Troponin) suggestive of myocardial tissue death
Unstable plaque +/- rupture with complete occlusion

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128
Q

STEMI

A

More likely have “classic” presentation

Plaque rupture with complete occlusion

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129
Q

Diagnosing ACS

A

Story trumps all! EKG: look for changes compared to prior EKG
Cardiac biomarkers: CK, CKMB, Troponin, can show evidence of myocardial infarction
Women and diabetics are more likely to present with atypical symptoms

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130
Q

What are the CK isoenzymes?

A

Skeletal muscle: CK-MM 98%, CKMB 1%
Myocardium: CK-MM 70%, CKMB 25-30%\
Troponin: TnC skeletal muscle, TnI and T specific to cardiac muscle

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131
Q

Out of the cardiac isoenzymes, which are more specific to the heart and should be measured?

A

CKMB (mostly just in heart, not so much in skeletal muscle)

Troponin TnI and TnT

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132
Q

Initial ER assessment and management of chest pain

A

MONA

133
Q

What does MONA stand for?

A

Morphine, oxygen, nitrates, aspirin

134
Q

Assessment and management of chest pain

A

Vitals, 12 lead EKG, cardiac monitor, oxygen, IV access and blood work, CXR, Hx and PE, aspirin (324 or 325mg), nitrates and morphine

135
Q

When do you use oxygen?

A

If sat is <90%, dont want to cause oxygen toxicity

136
Q

Chest pain NTG

A

Sublingual Nitroglycerin 0.4mg q5min for chest pain X3

137
Q

What is morphine used for?

A

Severe chest pain 2mg IV q5-15min

138
Q

What beta-blockers can be used for chest pain in ER?

A

Metoprolol (Lopressor), it improves the outcomes

139
Q

What High dose statin can be used for chest pain in ER?

A

Atorvastatin (Lipitor), 80mg PO nightly, also improves outcomes with its anti-inflammatory properties

140
Q

LMNOP + hep + statin eventually

A

Treatment of UA and NSTEMI

141
Q

What else is used to treat UA and NSTEMI in ER?

A

Anticoagulation (IV heparin), potassium and magnesium

142
Q

What does the TIMI score estimate?

A

14 day mortality for patient with UA/NSTEMI

143
Q

Low risk with a TIMI score is what?

A

Score of 0-2

144
Q

Intermediate risk for TIMI is what?

A

Score of 3-4

145
Q

High risk of TIMI is what?

A

Score 5-7

146
Q

What is taken into consideration with the TIMI score?

A

Age >65yrs, >3 risk factors for CAD, prior coronary stenosis >50%, presence of ST segment deviation, >2 anginal episodes in last 24 hours, elevated serum cardiac biomarkers, use of aspirin in last 7 days

147
Q

Which UA and NSTEMI pts need urgent angiography and revascularization?

A

Hemodynamic instability or cardiogenic shock, severe LV dysfunction or HF, recurrent or persistent rest angina despite intensive medical therapy, new or worsening mitral regurg, sustained ventricular arrhythmias

148
Q

What happens to the coronary blood flow in a STEMI?

A

Flow decreases abruptly after a thrombotic occlusion or coronary artery (acute plaque rupture has occurred)

149
Q

> 2mm ST elevation in 2 contiguous precordial leads OR >1mm ST elevation in 2 contiguous other leads is what?

A

STEMI

150
Q

What is an MI until proven otherwise?

A

New LBBB in setting of acute CP

151
Q

You can often see reciprocal changes in opposite leads in what?

A

STEMI

152
Q

Anterior STEMI occurs in which leads?

A

V2, V3, V4

153
Q

An anterior STEMI effects which coronary artery?

A

Left anterior descending artery (LAD)

154
Q

Left lateral STEMI occurs in which leads?

A

I, aVL, V5, V6

155
Q

Left lateral STEMI effects which coronary artery?

A

Left circumflex artery (Lcx)

156
Q

Right ventricular STEMI occurs in which leads?

A

aVR, V1

157
Q

Right ventricular STEMI effects which coronary artery?

A

Right coronary artery (RCA)

158
Q

Posterior STEMI occurs in which leads?

A

ST depressions in V2-V4

159
Q

Posterior STEMI effects which coronary artery?

A

Right coronary artery (RCA)

160
Q

What are some goals of therapy for a STEMI?

A

Pain relief, vital signs, initiation of reperfusion therapy within 90 MINS, or fibrinolysis if PCI unavailable

161
Q

What is the time limit for reperfusion therapy for STEMI?

A

90 mins from door to balloon

162
Q

What is the other option for STEMI therapy if a balloon cannot be put in?

A

Fibrinolysis- Alteplase, Reteplase, Stretokinase

163
Q

What drugs can be used for antithrombotic therapy for STEMI?

A

Prevents re-thrombosis or acute stent thrombosis, used Clopidogrel, Plavix or Prasugrel (Effient)

164
Q

Why is beta-blocker therapy important for STEMI?

A

Prevents recurrent ischemia and life-threatening ventricular arryhthmias

165
Q

Management of pts with acute STEMI

A

Activate cardiac cath lab, IV heparin bolus then continuous infusion, MONA (morphine, oxygen, nitrates, aspirin)

166
Q

Acute triage for acute STEMIs

A

Check responsiveness, airway, breathing, circulation, check for evidence of hypoperfusion/cardiogenic shock, CHF, ventricular arrythmias

167
Q

When do you give oxygen for a pt with an acute STEMI?

A

If there arterial O2 is <90% or if in respiratory distress

168
Q

What should be given prior to reperfusion procedure with acute STEMI?

A

Clopidogrel (Plavix)

169
Q

What else can be considered for acute STEMI management?

A

Glycoprotein 2b/3a inhibitors (Eptifibatide)

170
Q

What yields the highest rates of survival if reperfusion is done within 90 mins?

A

Percutaneous coronary intervention (PCI)

171
Q

If patient is found to have severe 3 vessel disease during PCI ->

A

Will need coronary artery bypass graft surgery (CABG)

172
Q

What is “Prinzmetal angina” or “variant angina”

A

Angina symptoms at rest, often between midnight and early morning, associated with transient (15 min) ST segment elevation, generally in the absence of high grade coronary artery stenosis

173
Q

What is variant angina triggered by?

A

Coronary artery vasospasm

174
Q

What is the patho behind variant angina?

A

Vascular smooth muscle hyper-reactivity, focal spasms of a major coronary artery, transient myocardial ischemia, occasionally myocardial infarction

175
Q

Can variant angina happen in just diseased vessels?

A

No, can also happen in normal vessels

176
Q

When do the spasms occur in variant angina?

A

Spasms occur in the absence of oxygen supply/demand mismatch

177
Q

What are some risk factors for variant angina?

A

Cigarette smoking, genetic factors, insulin resistance

178
Q

What are some triggers for variant angina?

A

Changes in autonomic activity (HR variability), Drugs, Magnesium deficiency

179
Q

What drugs are triggers for variant angina?

A

Ephedrine, Cocaine, Marijuana, Alcohol, Amphetamines

180
Q

How can you differentiate variant angina from a true STEMI?

A

Pts are usually younger, family hx of variant angina, few if any CV risks, drug use, repeat EKG after 15 min with total resolution of ST segments

181
Q

What are some complications of variant angina?

A

MI and arrhythmias

182
Q

How can you manage variant angina?

A

Sublingual NTG, stop smoking, long acting nitrates, CCBs, Statins (fluvastatin), magnesium, PCI with stent

183
Q

What promotes vasoconstriction and vasodilation of coronary arteries?

A

Long acting NTG, CCBs

184
Q

How many leaflets are in the tricuspid valve?

A

Three

185
Q

What is the tricuspid valve in between?

A

Right atrium and right ventricle

186
Q

How many leaflets does the mitral valve have?

A

Two

187
Q

What is the mitral valve between?

A

Left atrium and left ventricle

188
Q

How many leaflets does the aortic valve have?

A

Three

189
Q

What is the aortic valve between?

A

The left ventricle and the aorta

190
Q

How many leaflets does the pulmonic valve have?

A

Three

191
Q

What is the pulmonic valve in between?

A

The right ventricle and pulmonary artery

192
Q

What are normal heart sounds?

A

S1: Lub
S2: Dub

193
Q

What is the S1?

A

Closure of the AV valves (systole)

194
Q

What is the S2 heart sound?

A

Closure of aortic and pulmonary valves (diastole)

195
Q

What is the dominant cause of valvular heart disease in developing countries?

A

Rheumatic fever

196
Q

Valvular disease in developed countries is now dominated by what?

A

Degenerative or inflammatory processes that lead to valve thickening, calcification, and dysfunction

197
Q

Does the prevalence of valvular heart disease increase with age?

A

Yes

198
Q

What is a marker for further cardiovascular events with valvular heart disease?

A

Aortic sclerosis

199
Q

What is a more frequent cause of acute valvular regurgitation?

A

Infective endocarditis

200
Q

Valvular disease is what

A

Abnormal function of any one or more of the cardiac valves

201
Q

The valves of the heart have two functions:

A
  1. When open: to allow the forward passage of blood flow

2. When closed, to retain the blood in the chamber and prevent backflow

202
Q

Term for a valve in which blood cant move through properly as a result of thickened, stiff of fused leaflets

A

Stenosis

203
Q

Stenosis of valves causes what?

A

Failure of valve to open completely, impedes forward flow and leads to PRESSURE OVERLOAD

204
Q

A term for incompetent, insufficient, and leaking heart valves

A

Regurgitation

205
Q

Regurgitation causes

A
  • Blood flows back through the valve as leaflets are closing OR blood leaks through leaflets when they should be completely closed
  • leads to VOLUME OVERLOAD as a results of reversal of flow
206
Q

What is a compensatory mechanism to increase load, typically discussed in relation to left ventricle although an occur in right ventricle?

A

Ventricular remodeling (in valvular heart disease)

207
Q

What happens in the stenotic lesions of valvular heart disease?

A

Increased afterload to the left ventricle results in CONCENTRIC LEFT VENTRICULAR HYPERTROPHY

208
Q

What happens in concentric left ventricular hypertrophy?

A

Ventricle is capable of generating greater forces and higher pressures, it will become thicker and stiff.
Similar pathology as seen in LVH due to HTN

209
Q

What happens in pure regurgitation lesions?

A

Increased volume overload to the left ventricle results in eccentric hypertrophy

210
Q

What happens in eccentric hypertrophy?

A

Compensatory mechanism that maintains ventricular compliance as the heart muscle wall thickens.
Ventricle wall thickness increases in proportion to increase in chamber radius

211
Q

What is the most common symptom associated with severe valve regurgitation or stenosis is?

A

Dyspnea with exertion

212
Q

What is the hallmark of valvular dysfunction on PE?

A

Heart murmur

213
Q

What else can be found on a hx and PE for valvular disease?

A

Enlarged or displaced apical impulse, abnormal peripheral pulses, and timing and intensity of heart sounds (including extra heart sounds such as an S3 or S4 or a systolic ejection click)

214
Q

What types of imaging are used for valvular heart disease?

A

Transthoracic echocardiography (TTE), electrocardiography, B-type natriuretic peptide (BNP)

215
Q

What is the primary test for diagnosis of valvular heart disease?

A

TTE

216
Q

What does TTE allow for?

A

Evaluation of valve morphology, LV mass and function, and atrial and ventricular chamber sizes

217
Q

What can an electrocardiography evaluate for valvular heart disease?

A

Evaluate for adverse effects of valvular lesions, like LVH, ischemia, AFIB, but is insensitive for evaluation of ventricular fxn

218
Q

BNP is associated with what?

A

The presence and severity of symptoms (dyspnea)

219
Q

What is the “gold standard” for imaging valve morphology and motion?

A

2D echocardiography

220
Q

What can a 2D echocardiogram assess in valvular heart disease?

A

Leaflet thickness and mobility, valve calcification, and the appearance of valve structures

221
Q

How is valvular stenosis diagnosed?

A

By the thickening and decreased mobility of the valve

222
Q

Diagnosis of valvular regurgitation must be made by what?

A

Doppler echocardiography, but 2D is valuable for determining the etiology of the regurgitation and its effects on ventricular dimensions, shape, and fxn

223
Q

What determines the timing of intervention for valvular heart disease?

A

Cardiopulmonary symptoms

224
Q

When the symptoms develop (valvular HD), intervention is indicated regardless of what?

A

Regardless of preserved ventricular systolic fxn because of a significantly increased risk of adverse outcomes after symptom onset

225
Q

What is indicated in severe valvular dysfunction with symptoms or abnormal ventricular dysfunction?

A

Surgical valve repair or replacement, its the only definitive intervention for it

226
Q

Acute valvular regurgitation is what?

A

A medical emergency, regardless of the cause

227
Q

Most patient usually presumed to have underlying rheumatic heart disease in what?

A

Mitral stenosis

228
Q

Rheumatic mitral stenosis results in what?

A

Thickening of the leaflets, fusion of mitral commissaries and retraction thicken and fusion of the chordae

229
Q

The murmur will be diastolic in what?

A

Mitral stenosis, blood flows through stenotic valve from LA to LV during diastole

230
Q

What are some symptoms seen with mitral stenosis?

A

Insidious onset cough, new dyspnea on exertion, orthopedic, palpitations, fatigue
-can be precipitated by pregnancy as CO increased, symptoms emerge

231
Q

What can be seen on a PE for mitral stenosis?

A 
Diastolic murmur (low pitch, rumbling) best heard at APEX in left lateral position
OPENING SNAP following S2
232
Q

What are some initial tests to run for mitral stenosis?

A

TTE, EKG looking for: left atrial enlargement, RVH, AFIB, CXR, BNP

233
Q

What can be seen in a hx of mitral stenosis?

A

Rheumatic fever, pregnant pt, immigrant, prior untreated GABHS infection, AFIB

234
Q

The symptoms that indicate treatment for mitral stenosis are..

A

Episode of pulmonary edema, decline in exercise capacity, diagnosis of pulmonary HTN

235
Q

What is the procedure of choice for mitral stenosis?

A

Percutaneous Mitral balloon valvuloplasty (PMBV)

Very low mortality rate of <0.5%

236
Q

When is replacement of the valve indicated for mitral stenosis?

A

When combined stenosis and regurgitation are present or when the mitral valve echo score is >8-10

237
Q

What procedure can be done at the same time as a PMBV?

A

A Maze procedure can be done at the same time to reduce recurrent atrial arrhythmias
(Mitral stenosis treatment)

238
Q

Patients with mitral stenosis usually are not symptomatic until the mitral valve area is what?

A

<1.0 cm2 or the valve stenosis is moderate with associated tachycardia

239
Q

Symptoms of MS include

A

DOE, chest pain, palpitations, fatigue, and ca be precipitated by changes in HR or volume status such as AFIB, emotional stress, pregnancy, fever, or exercise

240
Q

What is the most common finding on PE for MS?

A

An irregular pulse due to AFIB is most common finding

241
Q

What happens during diastole?

A

Blood fills the left atrium

242
Q

When the left atrium pressure exceeds that of the LV, what valve opens?

A

The mitral valve opens and allows passive flow of blood into LV

243
Q

When the LA contracts, what closes?

A

Mitral valve closes and ends diastole

244
Q

What happens during ventricular contraction?

A

The papillary muscles contract, pulling the valve leaflets toward each other

245
Q

Organic Mitral Regurgitation

A

Primary abnormality in one or more of the vale apparatus

246
Q

What are some examples of organic mitral regurgitation?

A

Degenerative mitral valve disease (mitral valve prolapse)= most common cause
Rheumatic heart disease, infective endocarditis, trauma, mitral annular calcification

247
Q

Functional Mitral Regurgitation

A

Also known as secondary causes

248
Q

Examples of functional mitral regurgitation

A

CAD #1 cause -> ischemia or infarction leading to LV dilation
LV dilation causes mitral annular dilation and leaflet immobility

249
Q

What causes the primary symptoms/severe symptoms of mitral regurg?

A

Left ventricular dilation

250
Q

What does left ventricular dilation cause in mitral regurg?

A

Significant CHF symptoms: dyspnea, fatigue, othopnea, pulmonary edema, S3 on auscultation, displaced apical impulse

251
Q

What type of murmur will be heard in mitral regurg?

A

Systolic (blood flows regurgitate back through incompetent valve during systole)
Specifically HOLOSYSTOLIC/PANSYSTOLIC MURMUR

252
Q

What is an acute cause of mitral regurg?

A

Rupture of chordae tendinae/papillary muscles apparatus

253
Q

Acute cause of mitral regurg si/sx

A

Post-MI pts, sudden rapid onset of dyspnea resulting from marked pulmonary edema
Stat echo and cardiac surgery consult

254
Q

Hx taking for mitral regurgitation

A

Previous MI, ischemia, infarction, CHF, h/o infective endocarditis, cardiomyopathy

255
Q

Symptoms for chronic mitral regurgitation

A

Dyspnea, SOB, orthopedic, pulmonary edema, progressive LVD develops within 6-10 yrs

256
Q

Symptoms of a cute mitral regurgitation

A

Heart failure, cardiogenic shock b/c LA cannot tolerate increased volumes f blood, severe pulmonary edema ensues

257
Q

PE findings of mitral regurgitation

A

Pan-systolic murmur best heard at apex with RADIATION TO AXILLA, S3 heart sound, rales, wheeze, rhonchi, JVD

258
Q

Initial tests done for mitral regurgitation?

A

Echocardiogram; also need EKG and CXR

259
Q

What can be seen in an EKG for a pt with mitral regurgitation?

A

LA abnormalities (double hump)

260
Q

How if the prognosis of mitral regurgitation?

A

Degree of LV enlargement reflects severity and chronicity

261
Q

What does severe LV volume overload lead to in mitral regurgitation?

A

Leads to LV failure and reduced cardiac output

262
Q

Echocardiographic findings of mitral regurg?

A

Left atrial size, pulmonary pressures, LV dimensions can be used to determine progression of disease

263
Q

When is surgery necessary for mitral regurg?

A

When symptoms develop or when there is evidence of LV dysfunction

264
Q

Early surgery for mitral regurg is indicated when?

A

Even in asymptomatic pts with an ejection fraction <60% or marked LV dilation with reduced contractility

265
Q

Development of pulmonary HTN with mitral regurg suggests what?

A

Severe mitral regurg, needs prompt intervention!!

266
Q

What is the most common congenital valve lesion?

A

Mitral valve prolapse

267
Q

What is usually asymptomatic, but if present; chest pain, palpitations, fatigue and panic

A

Mitral valve prolapse

268
Q

What type of murmur is heard for mitral valve prolapse?

A

Mid-systolic click (single of multiple), often an incidental finding
-worse with Valsalva’s maneuver, improves with leg elevation

269
Q

How can you diagnose mitral valve prolapse?

A

Echocardiogram

270
Q

What is the treatment for mitral valve prolapse?

A

BBs is symptoms of chest pain, palpitations, panic present

MV repair/replacement only with development of severe MR

271
Q

A disease of the aortic valve that causes obstruction to the ejection of blood from the LV to aorta

A

Aortic stenosis

272
Q

Two common clinical scenarios result in aortic stenosis:

A
  1. Congenitally abnormally unicuspid or bicuspid valve

2. Pathologic process such as valve degeneration or calcific aortic stenosis

273
Q

A congenital abnormalities resulting in a unicuspid or bicuspid valve that is often asymptomatic until middle or old age

A

Congenital aortic stenosis

274
Q

Coarctation of aorta is also seen in many pts with what?

A

Congenital aortic stenosis

275
Q

What is thought to be related to calcium deposition due to processes similar to atherosclerotic disease?

A

Degenerative or calcific aortic stenosis

276
Q

Up to 20% of pts with degenerative or calcific aortic stenosis can progress to what?

A

Hemodynamically significant AS

277
Q

What is the most common surgical valve lesion in developed countries?

A

Degenerative or calcific aortic stenosis

278
Q

What are the risk factors for degenerative or calcific aortic stenosis?

A

HTN, HLD, smoking

279
Q

The most common presentation of aortic stenosis:

A

CHF like symptoms; dyspnea, fatigue, orthopnea, can present with chest pain, syncope with severe obstruction of blood flow into aorta
All tend to occur and worsen with exertion

280
Q

What type of murmur will be heard with aortic stenosis?

A

Systolic ejection murmur; blood flows though stenotic valve during systole
Crescendo-decrescendo murmur-BEST heard over aortic area, radiating to neck

281
Q

What PE findings are seen with aortic stenosis?

A

Paradoxical S2 split, can also have a LV heave or thrill with severe AS

282
Q

What are the key factors that lead to aortic valve repair, implantation, or replacement

A

The onset of sx and LV dysfunction

Once symptoms of HF, angina, or syncope occur: Average survival of only 2-3years

283
Q

What happens in aortic stenosis?

A

Hypertrophied heart muscles requires more blood flow than normal heart muscle during exercise and may exhibit areas of relatively ischemic heart muscles

284
Q

What is severe stenosis?

A

An aortic valve area of <1.0cm2 is severe

285
Q

Nonrheumatic causes of aortic regurgitation

A

Congenitally bicuspid valves, infective endocarditis, HTN, Aortic root disease such as connective tissue disease (Marfan syndrome, Ehler’s Danlos)

286
Q

What is the most common presentation of aortic regurg?

A

SOB and dyspnea

287
Q

What type of murmur will be heard with aortic regurgitation?

A

Diastolic-decrescendo (blood regurgitates back through aortic valve during ventricular diastole/relaxing)

288
Q

Chronically high LV preload in aortic regurg causes what?

A

Increased LVEDP, increase in pressure causes LVH and LV dysfunction, resulting in CHF

289
Q

What is Quincke’s pulse and what is it found in?

A

Nail bed change colors from normal to pale along with pulses- found in aortic regurg

290
Q

What is Watson’s waterhammer pulse and what is it found in?

A

“Bounding” pulses found in aortic regurg

291
Q

What is De Musset’s sign and what is it found in?

A

Head bobbing along with pulse, found in aortic regurg

292
Q

What is Duroziez’s sign and what is it found in?

A

Diastolic murmur heard on auscultation of femoral artery, found in aortic regurg

293
Q

What is the Austin Flint murmur and what is it found in?

A

Diastolic rumbling murmur heard at cardiac apex associated with regurg blood and afterload blood colliding- found in aortic regurg

294
Q

What will be found in the Hx for someone with aortic regurg?

A

Pt with HTN, connective tissue disorder, trauma, h/o CAD

295
Q

What symptoms can be seen with acute aortic regurg?

A

Sudden onset of pulmonary edema, hypotension or cardiogenic shock

296
Q

What symptoms can be seen with chronic aortic regurg?

A

Dyspnea, SOB (CHF-like), palpitations

297
Q

What will the PE show if someone has aortic regurg?

A

Wide pulse pressure on BP, diastolic murmur best heard at right eternal border, and various pathognomonic signs associated with wide pulse pressure

298
Q

What is the initial test of choice for aortic regurg?

A

Echocardiogram

299
Q

What is the treatment for aortic regurg?

A

Timing aortic valve repair/replacement BEFORE irreversible myocardial dysfunction
Medical therapy

300
Q

What medical therapy can be used for aortic regurg?

A

Vasodilators (Hydralazine, Nifedipine, and ACE inhibitors)

301
Q

Acute severe aortic regurg often needs what?

A

Often is a surgical emergency

302
Q

Surgery should be done for aortic regurg before what?

A

Before LVEF <50% and/or before LVESD >55 mm

303
Q

In aortic regurg, timing aortic valve repair/replacement can lead to what?

A

If done before irreversible myocardial damage, can lead to reversal of left ventricular dilation and improvement in EF

304
Q

Which treatment is the ONLY therapy with proven survival benefit for aortic regurg?

A

Surgical aortic valve replacement

305
Q

Are there percutaneous approaches to aortic regurg?

A

No

306
Q

Does medical therapy with vasodilators improve mortality for aortic regurg?

A

No

307
Q

What are some causes of tricuspid stenosis?

A

Rheumatic fever, carcinoid syndrome, infective endocarditis, trauma

308
Q

What are some symptoms for tricuspid stenosis?

A

RA enlargement (seen on EKG), R sided HF symptoms (Hepatomegaly, ascites, LE pitting edema)

309
Q

What is the treatment for tricuspid stenosis?

A

Definitive -> bio prosthetic TVR

Preferred surgical approach -> tricuspid valve replacement

310
Q

Why is mechanical tricuspid valve replacement rarely done?

A

The low flow predisposes to thrombosis and b/c the mechanical valve cannot be crossed should the need arise for right heart catheterization or pacemaker implantation.

311
Q

What type of valve is preferred for tricuspid stenosis?

A

Bioprosthetic

312
Q

What are some causes of tricuspid regurg?

A

RV dilation, R sided HF (Pulmonary HTN, Chronic PE, severe COPD)

313
Q

What is the treatment for tricuspid regurgitation?

A

Treat the underlying cause of RV dilation

314
Q

What other symptoms can occur with severe tricuspid regurg?

A

Symptoms of right-sided congestive heart failure (painful hepatosplenomegaly, ascites, and peripheral edema) and a sensation of pulsation in the neck (from distended and pulsating jugular veins) may occur

315
Q

What are the causes of pulmonic valve regurgitation divided into?

A

High-pressure causes and low-pressure causes

316
Q

What are the high-pressure causes of pulmonic valve regurgitation?

A

Pulmonary HTN

317
Q

What are the low-pressure causes of pulmonic valve regurg?

A

Usually due to a dilated pulmonary annulus, bicuspid or dysplastic pulmonary valve, or to plaque

318
Q

What are the symptoms for pulmonic valve regurg?

A

R sided HF symptoms, loud P2 followed by a rapidly attenuating early diastolic murmur

319
Q

What is the treatment for pulmonic valve regurgitation?

A

Correct the underlying cause

320
Q

What are current bio prosthetic valves made of?

A

Porcine or bovine pericardial tissue and require reoperation 10-20 yrs after implantation.

321
Q

Do bioprosthetic valves require long-term anticoagulation?

A

No

322
Q

Mechanical valves

A

Not prone to degeneration but patients are exposed to risks of lifelong anticoagulation

323
Q

After implantation of either a biologic or mechanical valve, what is recommended for atleast 3 months?

A

Anticoagulation with Warfarin, aspirin should be continued indefinitely

324
Q

All pts with prosthetic valves are at an increased risk for what?

A

Infective endocarditis, and Abx prophylaxis is recommended for dental procedures

325
Q

Abx prophylaxis is NOT recommended for pts with what?

A

Native valvular lesions, including mitral valve prolapse with regurg, bicuspid aortic valve, or rheumatic valve dx, UNLESS there is a history of previous endocarditis

326
Q

Abx prophylaxis for for dental procedures

A

Indicated for patients after valve replacement

327
Q

The American heart association recommends infective endocarditis prophylaxis for pts with

A

A prosthetic cardiac valve, a hx of infective endocarditis, certain types of congenital heart dx, or those who are cardiac transplantation recipients

328
Q

Which leads are effected in an inferior STEMI?

A

II, III, aVF

329
Q

Which coronary artery is effected in an inferior STEMI?

A

Right coronary artery (RCA)

Clin Med 2 (4 decks)

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