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Cardiology - MTB Flashcards

0
Q

A 48 y.o woman comes to the office wth chest pain that has been occuring for the past several weeks. Not reliably related to exertion. She is comfortable now. Pain sometimes associated with nausea. No SOB. and pain does not radiate beyonf chest. She has no PMH. What is most likely diagnosis?

A

GERD

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1
Q

Coronary artery disease

A
  • aka atherosclerotic disease

- ischemic heart disease

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2
Q

Risk factors for CAD

A
  • Diabetes mellitus
  • Tobacco smoking
  • HTN
  • Hyperlipidemia
  • Family hx of premature coronary arery disease
  • Age above 45 in men and above 55 in women
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3
Q

Worst risk factor for CAD

A

Diabetes mellitus

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4
Q

Premature coronary heart disease

A
  • male relative under 55

- female relative under 65

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5
Q

Postmenopausal woman develops chest pain immediately on hearing news of her son’s death in war. She develops acute chest pain , dyspnea, ST segment elevation in V2 - V4 on ECG. Elevated levels of troponin confirm an acute MI. Coronary angiography is normal including absence of vasospasm with provocative testing. ECG reveals apical LV “ballooning”. Mechanism of this disorder?

A
  • massive catecholamine discharge
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6
Q

Tako-Tsubo cardiomyopathy

A
  • often occurs in postmenopausal women s/p emotionally stressful event
  • manage w/ Beta blockers and ACE inhibitors
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7
Q

Most dangerous risk factors in terms of risk or CAD?

A

Elevated LDL

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8
Q

Correcting which risk factor for CAD will result in the most immediate benefit for the patient?

A

Smoking cessation

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9
Q

Chest pain described as dull / “sore” and/or squeezing or pressure-like

A

ischemic pain

  • sharp (“knifelike”) or pointlike
  • lasts for a few seconds
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10
Q

Chest pain that excludes ischemic pain

A
  1. changes with respiration (pleuritic)
  2. changes with position of the body
  3. changes with touch of the chest wall (tenderness)

** if patient answers yes to the previous questions, likely NOT ischemic

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11
Q

Most common cause of chest pain

A

Gastrointestinal disorders

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12
Q

Patient describes chest wall tenderness. Most likely diagnosis?

A

Costochrondritis

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13
Q

Most accurate test for costochondritis

A

Physical exam

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14
Q

Patient describes chest pain that radiates to the back, unequal blood pressure between arms. Most likely diagnosis?

A

Aortic dissection

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15
Q

Most accurate test for aortic dissection

A

CXR
w/ widened mediastinum
- chest CT, MRI, or TEE confirms the disease

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16
Q

Young Pt (< 40) c/o chest pain worse with lying flat, better when sitting up. Likely diagnosis?

A

Pericarditis

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17
Q

Most accurate test for pericarditis

A

Electrocardiogram with ST elevation every where

PR depression

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18
Q

Pt describes epigastric discomfort, pain better when eating. Likely diagnosis?

A

Duodenal ulcer disease

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19
Q

Most accurate test for chest pain

A

Endoscopy

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20
Q

Pt describes chest pain with bad tatse, cough, hoarsness

A

Gastroesophageal reflux

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21
Q

Most accurate test for GERD

A

Response to PPIs;

  • alumnium hydroxide and magnesium hydroxide
  • viscous lidocaine
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22
Q

Pt describes chest pain with cough, sputum, and hemoptysis. Likely diagnosis?

A

Pneumonia

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23
Q

Most accurate test for pneumonia

A

CXR

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24
Q

Patient describes chest pain with sudden onset SOB, tacycardia, and hypoxia.

A

Pulmonary embolus

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25
Q

Most accurate test for pulmonary embolus

A
  • spiral CT

- V/Q scan

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26
Q

Pt complains chest pain with sharp, pleuritic pain, and tracheal deviation. Likely diagnosis?

A

Pneumothorax

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27
Q

Most accurate test for pneumothorax

A

Chest X-ray

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28
Q

Worst prognostic significance for chest pain

A

Shortness of breath

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29
Q

Best initial test for chest pain

A

Electrocardiogram (EKG)`

- in office setting, the EKG is normal most of time but cannot progress to other testing without this test

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30
Q

If patient has acute chest pain in an office/ambulatory setting, what is the next best step to evaluate chest pain?

A

Transfer to ER

- DON’T ANSWER CARDIAC ENZYMES!!

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31
Q

If patient has chest pain in office/clinic for days to weeks, are cardiac enzymes appropriate?

A

No enzymes

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32
Q

If patient has chest pain in emergency department for minutes to hours, are cardiac enzymes appropriate?

A

Yes enzymes,

after an EKG is performed

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33
Q

When the etiology of chest pain is not clear, what is the best tool for evaluation of chest pain?

A

Exercise tolerance testing (ETT)

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34
Q

What are the two best factors for ETT

A
  1. You can read the EKG

2. The patient can exercise (gets heart rate > 85% of maximum)

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35
Q

Maximum heart rate

A

220 - age of patient

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36
Q

Best way to detect ischemia on EKG

A

ST segment depression

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37
Q

If you cannot read EKG because of baseline EKG abnormality, what are the 2 best ways to detect ischemia w/o EKG?

A
  • Nuclear isotope uptake: thallium or sestamibi

- Echocardiographic detection of wall abnormalities

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38
Q

Reasons for baseline EKG abnormalities

A
  • Left bundle branch block
  • Left ventricular hypertrophy
  • Pacemaker use
  • Effect of digoxin
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39
Q

Thallium testing for detection of cardiac ischemia

A

Normal myocardium will pick up thallium

  • if myocardium is alive and perfused, thallium will be picked by Na/K ATPase
  • if myocardium is abnormal, thallium has decreased uptake
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40
Q

Echocardiogram for detection of cardiac ischemia

A

Normal myocardium will move on contraction

- abnormal heart has decreased wall motion (dyskinesis, akinesis, or hypokinesis)

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41
Q

Ischemia vs infarction

A

ischemia: decreased perfusion that is detected by REVERSAL of thallium uptake or wall motion that returns to normal after rest period

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42
Q

If patient is unable to exercise to detect cardiac ischemia with exercise tolerance testing, what is the best method of detecting cardiac ischemia?

A

Pharm testing

  • Persantine (dipyramidole) or adenosine in combination with thallium or nuclear isotopes
  • Dobutamine in combination with echocardiogram
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43
Q

How does dobutamine work to detect cardiac ischemia

A

Dobutamine will increase myocardial oxygen consumption and provoke ischemia detected as wall motion abnormalities on ech

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44
Q

Coronary Angiography

A
  • used to detect anatomic location of coronary artery disease
  • use to determine whether narrowing should be best dealt with by surgery, angiography, or methods of revascularization
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45
Q

Most accurate test for detecting coronary artery disease

A

Angiography

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46
Q

Arterial stenosis

A
  • insignificant when less than 50%

- surgically correctable when > 70%

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47
Q

Holter monitoring

A
  • continuous ambulatory EKG monitor that records rhythm
  • used for 24 - 72 hrs
  • mainly detects rhythm disorders (a-fib, a-glutter, PVCs)
  • does not detect ischemia and not for evaluating ST segment
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48
Q

48 y.o woman comes to office w/ chest pain that has been occurring over the last several weeks. The pain is not reliably related to exertion. She is comfortable now. The location of pain is retrosternal. She has no hypertension and the EKG is normal. What is the next best step?

A

Exercise tolerance testing

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49
Q

Medications that lower mortality in setting of chronic angina

A
  • Aspirin
  • Beta blockers
  • Nitroglycerin
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50
Q

Route of nitroglycerin in chronic angina

A

Orally or a transdermal patch

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51
Q

Route of nitroglycerin in acute coronary syndromes

A

Sublingual, paste, and IV forms of nitroglycerine

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52
Q

Clopidogrel

A
  • aspirin intolerance (e.g. allergy)
  • recent angioplasty with stenting
  • rarely used with TTP
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53
Q

Prasugrel

A
  • thienopyridine medication in same clas as clopidogrel and ticlopidine
  • antiplatelet medication best used for angioplasty ad stenting
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54
Q

Ticlopidine

A
  • antiplatelet med in rare patient intolerant of both aspirin and clopidogrel
  • should not be used if aspirin/clopidogrel intolerance is bleeding
  • can cause neutropenia and TTP
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55
Q

Ranolazine

A
  • additional therapy for angina refractory or persistent through treatment
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56
Q

ACE inhibitors / ARBS: Indications

A
  • low systolic ejection raction/ systolic dysfunction (best mortality beneift)
  • regurgitant valvular disease
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57
Q

Most common side effect of ACE inhibitors

A

Cough

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58
Q

64 y/o man is placed on lisinopril as part of managing CAD in association with ejection fraction of 24% and symptoms of breathlessness. Although he sometimes has rales on lung exam, the patient is asymptomatic today. PE should minimal edema of lower extremities. Blood tests reveal an elevated level of K that is present on a repeat measurement. EKG is unchanged. What’s the best way to manage this patient

A

Switch from lisinopril to hydralazine and nitrates

  • Lisinopril also cause hyperkalemia due to inhibition of aldosterone
  • hydralazine will decrease afterload a arterial vasodilator
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59
Q

Why should hydralazine be used with nitrates in systolic dysfunction?

A

Hydralazine in an arterial vasodilator that decreases afterload
- used w/ nitrates to dilate coronary arteries so that blood isn’t stolen away from coronary perfusion when afterload is decreased w/ hydrazalines

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60
Q

Lipid Management in CAD

A

Patients use statins w/ CAD with an LDL above 100 mg/dL

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61
Q

Aside from CAD, other conditions in which lipids should be controlled to < 100 mg/dL

A
  • Peripheral artery disease (PAD)
  • Carotid disease (not stroke)
  • Aortic disease ( the artery, not the valve)
  • Diabetes mellitus
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62
Q

Most common adverse effect of statins

A

Liver dysfunction

- elevation of transaminases

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63
Q

Why are statins considered to have some mortality benefit?

A

Statins have antioxidant effect on endothelial lining of coronary arteries

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64
Q

Niacin

A
  • used to lower lipid levels
  • associated w/ glucose intolerance, elevation of uric avid level and itchiness due histalimine rlease
  • excellent ADDITION to statins if full lipid control not achieved with statins alone
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65
Q

Gemfibrozil

A
  • fibric acids lower triglyceride levels more than statins however, less mortality benefit than statins
  • caution using with statins due to increased risk of myositis
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66
Q

Cholestyramine

A
  • bile acid sequestrant but often has interactions with other drugs in gut by blocking their absorption
  • associated with uncomfortabe GI complaints such as constipation and flatus
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67
Q

Ezetimibe

A
  • lowers LDL level w/o any evidence of actual benefit to patient
  • no better than placebo in terms of endpoints (e.g. MI, stroke or death)
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68
Q

Statin: adverse effect

A
  • elevations of transaminases (liver fxn tests)

- myositis

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69
Q

Niacin: adverse effect

A
  • elevation in glucose and uric acid level

- pruritis

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70
Q

Fibric acid derivatives: adverse effect

A
  • increased risk of myositis when combined with statins
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71
Q

Cholestyramine: adverse effect

A

Flatus and abdominal discomfort

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72
Q

Ezetimibe: adverse effect

A
  • well tolerated and nearly useless
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73
Q

Dihydropyridine calcium channel blockers

A
  • Nifedipine
  • Nitrenipine
  • Nicardipine
  • Nimodipine
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74
Q

Dihydropyridine calciums affect mortality of CAD patients in which way?

A

They INCREASE mortality in patients with CAD b/c they raise heart rate
- the increased HR will increase myocardial oxygen consumption

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75
Q

Which calcium channel blockers are used in CAD?

A

Verapamil

Diltiazem

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76
Q

Indications for use of CCB in CAD

A
  • Severe asthma precluding use of B-blockers
  • Prinzmetal variant angina
  • Cocaine induced chest pain (B-blockers are contraindicated)
  • Inability to control pain w/ maximal medical therapy
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77
Q

Calcium channel blockers: Adverse effects

A
  • Edema
  • Constipation (verapamil most often)
  • Heart block (rare)
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78
Q

Which diagnostic test is best to evaluate patient for revascularization?

A
  • Angiography to determine whether patient needs CABG or angioplasty
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79
Q

Indications for coronary artery bypass grafting (CABG)

A
  • Three vessels > 70% stenosis in each vessel
  • Left main coronary artery occlusion
  • Two-vessel disease in a patient with diabetes
  • Persistent symptoms despite maximal medical therapy
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80
Q

Pts that benefit the most from CABG

A
  • patients with EF < 35%
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81
Q

Which grafted veins are used for CABG

A
  • Internal mammary artery grafts last 10 yrs before occlusion
  • Saphenous vein grafts remain patent reliably for 5 years
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82
Q

Percutanous coronary intevention

A
  • aka angioplasty
  • best therapy for acute coronary syndromes esp those with ST segment elevation
  • does not provide clear mortality benefit for stable CAD patients
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83
Q

Maximal medical therapy in stable CAD

A
  • ASpirin
  • Beta Blockers
  • ACEis / ARBs
  • Statin
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84
Q

70 y.o F comes to ED w/ crushing substernal chest pain for the last hr. The pain radiates to her left artm and is associated with anxiety, diaphoresis, and nausea. She describes the pain as “sore” and “dull” and clenches her fist in front of her chest/ She has a hx of hyperension What is most likely to be found in this patient?

A

S4 gallop b/c ishemia leading to noncompliance of left ventricle

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85
Q

Kussmaul sign

A
  • increase in JVP on inhalation
  • often associated with constrictive pericarditis or restrictive cardiomyopathy
  • “scratchy” sound in pericardial friction rub
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86
Q

Dressler synrome

A
  • complication of myocardial infarction that occurs several days after MI and is much rarer than simpler ventricular iscemia
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87
Q

Patent ductus arteriosus (PDA)

A
  • continuous “machinery” murmur t
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88
Q

Displaced point of maximal impulse (PMI)

A
  • characteristic of left ventricular hypertrophy as well as dilated cardiomyopathy
  • anatomic abnormality that can’t occur with an acute coronary syndrome
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89
Q

70 y.o F comes to the emergency department w/ crushing substernal chest pain for the last hr. Which of the following EKG findings would be associated with the prognosis?

A

ST elevations in V2 - V4

  • corresponds to the anterior wall of the left ventricle
  • signifies an acute myocardial infarction
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90
Q

Premature ventricular complexes (PVCS)

A
  • should not be treated
  • associated with an acute infarction
  • treatment of PVCs only worsens outcome
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91
Q

70 y/o F comes to the emergency department w/ crushing substernal chest pain for the last hour. An EKG shows ST segment elevation in V-2. What is the most appropriate next step of management in this patient?

A

Aspirin

  • lowers mortality and important to administer as quickly as possible
  • initiate therapy before moving patien to the ICU
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92
Q

70 y/o F comes to the emergency department w/ crushing substernal chest pain for the last hr. An EKG shows ST segment elevation in leads V2 - V4. Aspirin has been given to the patient to chew. What is the most appropriate next step in management?

A

Angioplasty is associated with greatest mortality benefit

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93
Q

Pt c/o chest pain, when to do an EKG

A
  • immediately at onset of pain

- ST elevation progresses to Q waves over several days to a week

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94
Q

Myoglobin

A
  • becomes abnormal 1-4 hrs

- duration of myoglobin elevation is 1-2 days

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95
Q

CK-MB

A
  • becomes abnormal 4-6 hrs

- duration of elevated CK-MB for 1-2 days

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96
Q

Troponin

A
  • becomes abnormal in 4-6 hrs

- duration of elevated troponin is 10-14 hrs

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97
Q

Difficulty of using troponin levels in detection of myocardial infarctions

A
  • Troponin can’t distinguish btwn reinfarction occurring several days after 1st event
  • Renal insufficiency can result in false positive tests since troponin is excreted via kidneys
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98
Q

If pt c/o of new chest pain within a few days of first cardiac event, how do you manage this condition?

A

Concern for reinfarction

  1. Perform an EKG to detect NEW ST segment abnormalities
  2. Check CK-MB levels
    * * after two days, the CK-MB levels should have returned to normal
  3. Transfer to ICU if new infarction
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99
Q

Most common cause of death in first several days of MI

A

Ventricular arrhythmia (v-tach, v-fib)

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100
Q

ST segment elevation myocardial infarction (STEMI)

A
  • best initially managed with aspirin (orally or chewed).

- clopidogrel can be used an alternative to aspirin if there is an allergy

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101
Q

Angioplasty vs Thromobolytics

A

Angioplasty is superior to thrombolytics b/c

  • Survival and mortality benefit
  • Fewer hemorrhagic complications
  • Likelihood of developing MI complicatins (less arrhythmia, less CHF, fewer septal ruptures, few episodes of tampanade)
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102
Q

PCI

A
  • standard of care is expected to be performed within 90 minutes of patient arriving in ED with chest pain
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103
Q

Complications of PCI

A
  • Rupture of coronary artery on inflation of the balloon
  • Restenosis (thrombosis) of the vessel after angioplasty
  • Hematoma at the site of entry into artery
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104
Q

Which of the following is most important in decreasing the risk of restenosis of the coronary artery after PCI?

A

Placement of drug eluting stent (paclitazel, siroliums)

- inhibit the local T cell response which reduces rate of sternosis

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105
Q

Absolute contraindications to thrombolytics

A
  • Major bleeding into the bowel (melena) or brain (any type of CNS bleeding)
  • Recent surgery (within the last 2 weeks)
  • Severe hypertension (above 180/110)
  • Nonhemorrhagic stroke within the last 6 months
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106
Q

Pt comes to a small rural hospital w/o catherization lab. The patient has chest pain and ST segment elevation. What is the most appropriate next step in the management of the patient?

A

Administer thrombolytics now

  • better than angioplasty delayed by several hrs
  • mortality benefit of thombolytics extend to 12 hrs
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107
Q

Best initial therapy for acute coronary syndrome?

A

Asprin

- best used for everyone

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108
Q

Indication for clopidogrel in ACS

A
  • when aspirin not tolerated, those undergoing angioplasty and stenting
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109
Q

Indication for Beta blockers in ACS

A
  • used in everyone

- effect is not dependent on time - starting anytime during admission

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110
Q

Indication for ACE inhibitors and ARB in ACS

A
  • used in everyone

- benefits those with ejection fraction < 35%

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111
Q

Indication for statins in ACS

A
  • used in everyone

- benefits those with LDL > 100 mg/ dL

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112
Q

Indication for oxygen and nitrates in ACS

A
  • used everyone

- no clear mortality benefit

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113
Q

Indication for heparin in ACS

A
  • after thrombolytics / PCI to prevent restenosis

initial therapy with ST depression and other non- STEMI events (unstable angina)

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114
Q

Indication for calcium channel blockers in ACS

A
  • when beta blockers can’t be used
  • cocaine induced pain
  • Prinzmetal variant or vasospastic variant angina
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115
Q

Most dangerous risk factors in terms of risk or CAD?

A

Elevated LDL

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116
Q

Man comes to the emergency department w/ chest pain for the last hr that is crushing in quality and does not change w/ respiration or position of his body. EKG shows ST segment depression in leads V2 - V4. Aspirin has been given. What is the most appropriate next step in management?

A

Heparin

  • heparin will prevent clot formation in coronary arteries but does not dissolve already formed clots
  • there is no ST ELEVATION, no benefit of thrombolytics
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117
Q

Glycoprotein IIb/IIIa Inhibitors (Abciximab, Tirofiban, Eptifibitide)

A
  • used in ACS in those are to undergo angioplasty and stenting
  • inhibit the aggregation of plateletss.
  • led to reduction in mortality in those w/ ST depression, particularly in patients whose troponin or CK-MB levels
  • not useful in acute STEMIs separate from angioplasty and stenting
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118
Q

tPA (thrombolytics) best used in which patients?

A
  • ST elevation MI patients
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119
Q

Heparin is best used in which patients?

A
  • non-STEMI patients
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120
Q

Glycoprotein IIa/IIIb inhibitors are best in used in which patients?

A

non-STEMO patients and those undergoing angioplasty and stenting

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121
Q

If in non-STEMI ACS, when all meds have been given, and patient has persistent pain, S3 gallop or CHF develop, worse EKG changes or SVT, rising troponin levels. Next step?

A

Urgent angiography and possible angioplasty

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122
Q

Complications of acute MI

A
  • Bradycardia
  • Tachycardia
  • Tamponade/Free wall rupture
  • Ventricular tachycardia/ventricular fibrillation
  • Valve/septal rupture
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123
Q

Sinus bradycardia in setting of MI

A
  • common w/ MI if vascular insufficiency of the SA node
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124
Q

3rd degree (complete) AV block

A
  • will have CANNON A WAVES

- obtain EKG to distinguish 3rd degree AV block vs sinus bradycardia

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125
Q

Cannon A waves

A
  • produced by atrial systole against closed tricuspid valve
  • tricuspid valve is closed b/c essence of 3rd degree block is that atria and valves are contracting separate
  • JVD is bouncing up into the neck
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126
Q

Right ventricular infarction

A
  • associated w/ new inferior wall MI and clear lungs

- diagnosed by flipping EKG from usual left side to right side of chest

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127
Q

R coronary artery supplies

A
  • RV
  • AV node
  • inferior wall of heart
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128
Q

R ventricular infarction: treatment

A
  • High volume fluid replacement

- avoid nitroglycerin to RV infarctions which markedly worsen cardiac filling

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129
Q

Tamponade/free wall rupture s/p MI

A
  • takes several days s/p infarction for wall to scar and weakens enough to rupture
  • look for sudden loss of pulse
  • lungs are clear and is cause of pulseless electrical activity
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130
Q

Tamponade/Free Wall Rupture: Diagnosis

A
  • emergency echocardiography
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131
Q

Ventricular Tachycardia/Ventricular Fibrillation s/p MI

A
  • can cause sudden
  • must use EKG to distinguish v-tachycardia and v-fibrillaiotn
  • both treated w/ cardiovarsion/defibrillation
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132
Q

Septal rupture/Valve rupture s/p MI

A
  • new onset of murmur and pulmonary congestion
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133
Q

Ventricular septal rupture best heard where?

A
  • can be seen s/p MI

- best heart at LLSB

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134
Q

Mitral regurgitation

A
  • can occur s/p MI

- best heard at apex w/ radiation to axilla

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135
Q

Most accurate test to detect valve rupture and septal rupture

A
  • Echocardiogram
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136
Q

Septal rupture

A
  • look for increase in oxygen saturation as you go from right atrium to right ventricle
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137
Q

Intraaortic balloon pump

A
  • used when there is acute pump failure from anatomic problem that can be fixed in OR
  • contracts and relazes w/ natural heartbeat
  • helps give a “push forward to the blood”
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138
Q

Reinfarction or extension of infarction

A
  • patient often presents w/ either inferior or anterior infarction
  • look for reoccurrence of pain, new rales on exam, bump up CK-MB and even suddent onset of pulmonary edema
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139
Q

Reinfarction or extension of infarction

A
  • repeat EKG
  • retreat w/ angioplasty and sometimes thrombolytics in addition to usual meds (aspirin, metoprolol, nitrates, ACE, statins)
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140
Q

Aneurysm/ Mural Thrombus

A
  • detected with echocadiogramy

- treated w/ heparin followed by warfarin

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141
Q

Pt s/p MI presents w bradycardia and cannon A waves. Likely dx?

A

3rd degree AV block

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142
Q

Pt s/p MI presents w/ bradycardia. No cannon A waves on EKG. Likely dx?

A

Sinus bradycardia

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143
Q

Pt s/p MI w/ PMH of inferior wall MI, clear lungs, tachycardia, hypotension w/ nitroglycerin. Likely dx?

A

RV infarction

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144
Q

Pt s/p MI with new murmur, rales/congestion. Likely dx?

A

Valve rupture

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145
Q

Pt s/p MI with new murmur, increase in oxygen saturation on entering the right ventricle. Likely dx?

A

Septal rupture

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146
Q

Pt s/p MI with loss of pulse, need EKG to answer question. Likely diagnosis

A

Ventricular fibrillation

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147
Q

Before patient w/ MI is discharged. Which test should be done?

A

Stress test

  • to determine if angiography is needed
  • angiogrpay determines need for revascularization
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148
Q

Meds needed for postinfarction patients

A

Every MI patient should go home:

  • Aspirin
  • Beta blockers (metoprolol)
  • Statins
  • ACE inhibitors
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149
Q

ACE inhibitors are best used for which type of MI patients?

A

Anterior wall infarctions b/c of high likelihood of developing systolic dysfunction

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150
Q

Clopidogrel

A
  • used for those intolerant of aspirin or post-stenting
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151
Q

ARBS

A
  • used for MI patients with cough on ACE inhibitor
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152
Q

Prophylactic antiarrhythmic medications

A
  • don’t use amiodarone, flecainide or any rhythm controlleing med to prevent development of v-tach
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153
Q

Sexual issues postinfarction

A
  1. Don’t combine nitrates w/ sildenafil
  2. Erectile dysfunction (usually from anxiety)
  3. Pt doesn’t have to wait after an MI to begin sexual activity
  4. If post-MI stress test is normal, pt can engage in exercise program
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154
Q

Congestive Heart Failure

A
  • dysfunction of heart as pump of blood
  • dyspnea is most common function
  • can be due to either systolic or diastolic dysfunction
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155
Q

Diastolic dysfunction

A
  • inability of heart to “relax” and receive blood

- ejection fraction is preserved and sometimes even above normal

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156
Q

Most common causes of systolic dysfunction (3)

A
  1. Infarction
  2. Cardiomyopathy (2/2 HTN)
  3. Valve disease
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157
Q

Less common causes of systolic dysfunction

A
  • Alcohol
  • post viral myocarditis
  • Doxorubicin use
  • Chagas disease
  • Hemochromatosis
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158
Q

CHF: presentation

A
  • dyspnea
  • pulmonary edema, in worst form
  • orthopnea (worse when lying flat, relieved when sitting up)
  • Rales on lung exam
  • JVD
  • paroxysmal nocturnal dyspnea (sudden worsening at night)
  • S3 gallop
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159
Q

Pt presents with sudden onset dyspnea with clear lungs. Likely dx?

A

Pulmonary embolus

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160
Q

Pt presents w/ sudden onset dyspnea, wheexing, increased expiratory phase. Likely dx?

A

Asthma

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161
Q

Pt presents w/ slower onset dyspnea, sputum, unilateral rales/rhonci

A

Pneumonia

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162
Q

Pt presents w/ dyspnea, circumoral numbness, caffeine use, hx of anxiety. Likely dx?

A

Panic attack

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163
Q

Pt presents w/ pallor, gradual onset dyspnea over days to weeks. Likely dx?

A

Anemia

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164
Q

Pt presents w/ dyspnea, pulsus paradoxus, decreased heart sounds, JVD. Likely dx?

A

Tamponade

165
Q

Pt presents w/ dyspnea, palpitations, syncope. Likely dx?

A

Arrhythmia of almost any kind

166
Q

Pt presents w/ dyspnea, dullness to percussion at bases. Likely dx?

A

Pleural effusion

167
Q

Pt presents w/ dyspnea, long smoking hx, barrel chest. Likely dx?

A

COPD

168
Q

Pt presents w/ dyspnea, recent anesthetic use, brown blood not improved w. oxygen, clear lungs on auscultation, cyanosis. Likely dx?

A

Methemoglobinemia

169
Q

Pt presents w/ dyspnea, burning building or car, wood burning stove in winder, suicide attempt. Likely dx?

A

Carbon monoxide poisoning

170
Q

Most important test in CHF

A

Echocardiography

171
Q

Best initial test to evaluate ejection fraction

A

Transthoracic echo

172
Q

Most accurate test to evaluate ejection fraction

A

MUGA or nuclear vetriculography

173
Q

When is nuclear ventriculography used to evaluate ejection fraction

A
  • necessary when precision is needed

- example if giving doxorubicin for chemo but need to ensure maximum treatment w/o cardiomyopathy

174
Q

BNP level is used t evaluate

A
  • acute SOB with unclear etiology

- normal BNP excludes CHG

175
Q

Best test to detemine CHF 2/2 MI or heart block

A

EKG

176
Q

Best test to determine CHF 2/2 dilated cardiomyopathy

A

CXR

177
Q

Best test to determine CHF 2/2 paroxysmal arrhythmias

A

Holter monitoring

178
Q

Best test to determine precise valve diameter

A

Cardiac catherization

179
Q

Best test to determine CHF 2/2 abnormal thyroid levels (high or low)

A

Thyrid function tests (T4/TSH)

180
Q

Best test that distinguishes CHF from ARDS

A

Swan Ganz right heart catherization

181
Q

Systolic Dysfunction (Low Ejection Fraction): Test

A
  • ACE inhibitors
  • Beta Blockers
  • Spironolactone
  • Diuretics
  • Digoxin
182
Q

Specific B-blockers beneficial in systolic dysfunction

A
  • Metoprolol (specific B-1 antagonists)
  • Bisoprolol (specific B-1 antagonists)
  • Carvedilol (nonspecific B-blocker w/ alpha blocker)
183
Q

Why B-blockers (carvedilol, metoprolol, bisoprolol) are beneficial in systolic dysfunction

A
  • Antiischemic effect
  • Decrease in HR leading to decreased oxygen consumption
  • antiarrhythmic effect
184
Q

Most common cause of death from CHF

A
  • Arrhythmia/sudden death
185
Q

Spironolactone

A
  • beneficial b/c it inhibits effects of aldosterone

- effective in later stages of CHF (stages III and IV)

186
Q

Spironolactone: adverse effects

A
  • Hyperkalemia

- Gynecomastia

187
Q

Eplerone

A
  • alternative to spironolactone
  • inhibits aldosterone
  • doesnt have antiandrogen effects that leads to gynecomastia
188
Q

Pt w/ CHF who develops gynecomastia?

A

Switch from spironolactone to eplerone

189
Q

Indications for diuretics in CHF

A
  • initial therapy in CHF w/ low ejection fraction

- often loop diuretic with ACEi/ARB

190
Q

Digoxin

A
  • doesn’t lower mortality in CHF

- used to control symptoms of dyspnea and will decrease frequency of hospitalixations

191
Q

74 y/o A-A man w/ hx of dilatered cardiomyopathy 2/2 o MI in past is seen in office. He is asymptomatic and is maintained on lisinopril, furosemide, metoprolol aspirin, and digoxin. Lab tests reveal elevated K level. EKG is unchanged. Best management?

A

Switch from lisinopril to hydralazine and nitroglycerin

192
Q

Non pharm treatments that have mortality benefit in CHF

A
  1. Implantable defribrillator: used in for EF < 35% and ischemic cardiomyopathy
  2. Biventricular pacemaker: used in dilated cardiomopathy and ejection fraction < 35% and a wide QRS > 120ms
193
Q

Drugs w/ mortality benefit in CHF

A
  • ACEi/ARBS
  • Spironolactone or eplerone
  • Beta blockers
  • Hydralazine/nitrates
  • Implantable defibrillator
194
Q

Diastolic Dysfunction (CHF w/ preserved EF)

A
  • B-blockers are beneficial

- Diuretics are used to control symptoms of fluid overload

195
Q

HOCM (hypertrophic obstructive cardiomyopathy)

A
  • congenital disease w/ asymmetrically enlarged (hypertrophic) septum leading to an obstruction of LV outflow tract
  • diuretics are contraindicated b/c they increase obstruction**
196
Q

Pulmonary edema

A
  • most severe form ofCHF

- rapid onset of fluid accumulating in lungs

197
Q

Pulmonary edema: presentation

A
  • Rales
  • JVD
  • S3 gallop
  • Edema
  • Orthopnea
198
Q

Pulmonary edema: diagnostic tests

A
  • BNP is etiology of dyspnea is unclear
  • CXR shows vascular congestion with filling of blood vessels towards the head
  • Respiratory alkalosis on ABG
  • EKG
  • Echo
199
Q

Best test to do in acute pulmonary edema

A

EKG

** if pt has arrhythmia (a-fib, a-flutter, or v-tach) best thing to do is rapid cardioversion

200
Q

Correcting which risk factor for CAD will result in the most immediate benefit for the patient?

A

Smoking cessation

201
Q

Chest pain described as dull / “sore” and/or squeezing or pressure-like

A

ischemic pain

  • sharp (“knifelike”) or pointlike
  • lasts for a few seconds
202
Q

Chest pain that excludes ischemic pain

A
  1. changes with respiration (pleuritic)
  2. changes with position of the body
  3. changes with touch of the chest wall (tenderness)

** if patient answers yes to the previous questions, likely NOT ischemic

203
Q

Most common cause of chest pain

A

Gastrointestinal disorders

204
Q

Patient describes chest wall tenderness. Most likely diagnosis?

A

Costochrondritis

205
Q

Most accurate test for costochondritis

A

Physical exam

206
Q

Patient describes chest pain that radiates to the back, unequal blood pressure between arms. Most likely diagnosis?

A

Aortic dissection

207
Q

Most accurate test for aortic dissection

A

CXR
w/ widened mediastinum
- chest CT, MRI, or TEE confirms the disease

208
Q

Young Pt (< 40) c/o chest pain worse with lying flat, better when sitting up. Likely diagnosis?

A

Pericarditis

209
Q

Most accurate test for pericarditis

A

Electrocardiogram with ST elevation every where

PR depression

210
Q

Pt describes epigastric discomfort, pain better when eating. Likely diagnosis?

A

Duodenal ulcer disease

211
Q

Most accurate test for chest pain

A

Endoscopy

212
Q

Pt describes chest pain with bad tatse, cough, hoarsness

A

Gastroesophageal reflux

213
Q

Most accurate test for GERD

A

Response to PPIs;

  • alumnium hydroxide and magnesium hydroxide
  • viscous lidocaine
214
Q

Pt describes chest pain with cough, sputum, and hemoptysis. Likely diagnosis?

A

Pneumonia

215
Q

Most accurate test for pneumonia

A

CXR

216
Q

Patient describes chest pain with sudden onset SOB, tacycardia, and hypoxia.

A

Pulmonary embolus

217
Q

Most accurate test for pulmonary embolus

A
  • spiral CT

- V/Q scan

218
Q

Pt complains chest pain with sharp, pleuritic pain, and tracheal deviation. Likely diagnosis?

A

Pneumothorax

219
Q

Most accurate test for pneumothorax

A

Chest X-ray

220
Q

Worst prognostic significance for chest pain

A

Shortness of breath

221
Q

Best initial test for chest pain

A

Electrocardiogram (EKG)`

- in office setting, the EKG is normal most of time but cannot progress to other testing without this test

222
Q

If patient has acute chest pain in an office/ambulatory setting, what is the next best step to evaluate chest pain?

A

Transfer to ER

- DON’T ANSWER CARDIAC ENZYMES!!

223
Q

If patient has chest pain in office/clinic for days to weeks, are cardiac enzymes appropriate?

A

No enzymes

224
Q

If patient has chest pain in emergency department for minutes to hours, are cardiac enzymes appropriate?

A

Yes enzymes,

after an EKG is performed

225
Q

When the etiology of chest pain is not clear, what is the best tool for evaluation of chest pain?

A

Exercise tolerance testing (ETT)

226
Q

What are the two best factors for ETT

A
  1. You can read the EKG

2. The patient can exercise (gets heart rate > 85% of maximum)

227
Q

Maximum heart rate

A

220 - age of patient

228
Q

Best way to detect ischemia on EKG

A

ST segment depression

229
Q

If you cannot read EKG because of baseline EKG abnormality, what are the 2 best ways to detect ischemia w/o EKG?

A
  • Nuclear isotope uptake: thallium or sestamibi

- Echocardiographic detection of wall abnormalities

230
Q

Reasons for baseline EKG abnormalities

A
  • Left bundle branch block
  • Left ventricular hypertrophy
  • Pacemaker use
  • Effect of digoxin
231
Q

Thallium testing for detection of cardiac ischemia

A

Normal myocardium will pick up thallium

  • if myocardium is alive and perfused, thallium will be picked by Na/K ATPase
  • if myocardium is abnormal, thallium has decreased uptake
232
Q

Echocardiogram for detection of cardiac ischemia

A

Normal myocardium will move on contraction

- abnormal heart has decreased wall motion (dyskinesis, akinesis, or hypokinesis)

233
Q

Ischemia vs infarction

A

ischemia: decreased perfusion that is detected by REVERSAL of thallium uptake or wall motion that returns to normal after rest period

234
Q

If patient is unable to exercise to detect cardiac ischemia with exercise tolerance testing, what is the best method of detecting cardiac ischemia?

A

Pharm testing

  • Persantine (dipyramidole) or adenosine in combination with thallium or nuclear isotopes
  • Dobutamine in combination with echocardiogram
235
Q

How does dobutamine work to detect cardiac ischemia

A

Dobutamine will increase myocardial oxygen consumption and provoke ischemia detected as wall motion abnormalities on ech

236
Q

Coronary Angiography

A
  • used to detect anatomic location of coronary artery disease
  • use to determine whether narrowing should be best dealt with by surgery, angiography, or methods of revascularization
237
Q

Most accurate test for detecting coronary artery disease

A

Angiography

238
Q

Arterial stenosis

A
  • insignificant when less than 50%

- surgically correctable when > 70%

239
Q

Holter monitoring

A
  • continuous ambulatory EKG monitor that records rhythm
  • used for 24 - 72 hrs
  • mainly detects rhythm disorders (a-fib, a-glutter, PVCs)
  • does not detect ischemia and not for evaluating ST segment
240
Q

48 y.o woman comes to office w/ chest pain that has been occurring over the last several weeks. The pain is not reliably related to exertion. She is comfortable now. The location of pain is retrosternal. She has no hypertension and the EKG is normal. What is the next best step?

A

Exercise tolerance testing

241
Q

Medications that lower mortality in setting of chronic angina

A
  • Aspirin
  • Beta blockers
  • Nitroglycerin
242
Q

Route of nitroglycerin in chronic angina

A

Orally or a transdermal patch

243
Q

Route of nitroglycerin in acute coronary syndromes

A

Sublingual, paste, and IV forms of nitroglycerine

244
Q

Clopidogrel

A
  • aspirin intolerance (e.g. allergy)
  • recent angioplasty with stenting
  • rarely used with TTP
245
Q

Prasugrel

A
  • thienopyridine medication in same clas as clopidogrel and ticlopidine
  • antiplatelet medication best used for angioplasty ad stenting
246
Q

Ticlopidine

A
  • antiplatelet med in rare patient intolerant of both aspirin and clopidogrel
  • should not be used if aspirin/clopidogrel intolerance is bleeding
  • can cause neutropenia and TTP
247
Q

Ranolazine

A
  • additional therapy for angina refractory or persistent through treatment
248
Q

ACE inhibitors / ARBS: Indications

A
  • low systolic ejection raction/ systolic dysfunction (best mortality beneift)
  • regurgitant valvular disease
249
Q

Most common side effect of ACE inhibitors

A

Cough

250
Q

64 y/o man is placed on lisinopril as part of managing CAD in association with ejection fraction of 24% and symptoms of breathlessness. Although he sometimes has rales on lung exam, the patient is asymptomatic today. PE should minimal edema of lower extremities. Blood tests reveal an elevated level of K that is present on a repeat measurement. EKG is unchanged. What’s the best way to manage this patient

A

Switch from lisinopril to hydralazine and nitrates

  • Lisinopril also cause hyperkalemia due to inhibition of aldosterone
  • hydralazine will decrease afterload a arterial vasodilator
251
Q

Why should hydralazine be used with nitrates in systolic dysfunction?

A

Hydralazine in an arterial vasodilator that decreases afterload
- used w/ nitrates to dilate coronary arteries so that blood isn’t stolen away from coronary perfusion when afterload is decreased w/ hydrazalines

252
Q

Lipid Management in CAD

A

Patients use statins w/ CAD with an LDL above 100 mg/dL

253
Q

Aside from CAD, other conditions in which lipids should be controlled to < 100 mg/dL

A
  • Peripheral artery disease (PAD)
  • Carotid disease (not stroke)
  • Aortic disease ( the artery, not the valve)
  • Diabetes mellitus
254
Q

Most common adverse effect of statins

A

Liver dysfunction

- elevation of transaminases

255
Q

Why are statins considered to have some mortality benefit?

A

Statins have antioxidant effect on endothelial lining of coronary arteries

256
Q

Niacin

A
  • used to lower lipid levels
  • associated w/ glucose intolerance, elevation of uric avid level and itchiness due histalimine rlease
  • excellent ADDITION to statins if full lipid control not achieved with statins alone
257
Q

Gemfibrozil

A
  • fibric acids lower triglyceride levels more than statins however, less mortality benefit than statins
  • caution using with statins due to increased risk of myositis
258
Q

Cholestyramine

A
  • bile acid sequestrant but often has interactions with other drugs in gut by blocking their absorption
  • associated with uncomfortabe GI complaints such as constipation and flatus
259
Q

Ezetimibe

A
  • lowers LDL level w/o any evidence of actual benefit to patient
  • no better than placebo in terms of endpoints (e.g. MI, stroke or death)
260
Q

Statin: adverse effect

A
  • elevations of transaminases (liver fxn tests)

- myositis

261
Q

Niacin: adverse effect

A
  • elevation in glucose and uric acid level

- pruritis

262
Q

Fibric acid derivatives: adverse effect

A
  • increased risk of myositis when combined with statins
263
Q

Cholestyramine: adverse effect

A

Flatus and abdominal discomfort

264
Q

Ezetimibe: adverse effect

A
  • well tolerated and nearly useless
265
Q

Dihydropyridine calcium channel blockers

A
  • Nifedipine
  • Nitrenipine
  • Nicardipine
  • Nimodipine
266
Q

Dihydropyridine calciums affect mortality of CAD patients in which way?

A

They INCREASE mortality in patients with CAD b/c they raise heart rate
- the increased HR will increase myocardial oxygen consumption

267
Q

Which calcium channel blockers are used in CAD?

A

Verapamil

Diltiazem

268
Q

Indications for use of CCB in CAD

A
  • Severe asthma precluding use of B-blockers
  • Prinzmetal variant angina
  • Cocaine induced chest pain (B-blockers are contraindicated)
  • Inability to control pain w/ maximal medical therapy
269
Q

Calcium channel blockers: Adverse effects

A
  • Edema
  • Constipation (verapamil most often)
  • Heart block (rare)
270
Q

Which diagnostic test is best to evaluate patient for revascularization?

A
  • Angiography to determine whether patient needs CABG or angioplasty
271
Q

Indications for coronary artery bypass grafting (CABG)

A
  • Three vessels > 70% stenosis in each vessel
  • Left main coronary artery occlusion
  • Two-vessel disease in a patient with diabetes
  • Persistent symptoms despite maximal medical therapy
272
Q

Pts that benefit the most from CABG

A
  • patients with EF < 35%
273
Q

Which grafted veins are used for CABG

A
  • Internal mammary artery grafts last 10 yrs before occlusion
  • Saphenous vein grafts remain patent reliably for 5 years
274
Q

Percutanous coronary intevention

A
  • aka angioplasty
  • best therapy for acute coronary syndromes esp those with ST segment elevation
  • does not provide clear mortality benefit for stable CAD patients
275
Q

Maximal medical therapy in stable CAD

A
  • ASpirin
  • Beta Blockers
  • ACEis / ARBs
  • Statin
276
Q

70 y.o F comes to ED w/ crushing substernal chest pain for the last hr. The pain radiates to her left artm and is associated with anxiety, diaphoresis, and nausea. She describes the pain as “sore” and “dull” and clenches her fist in front of her chest/ She has a hx of hyperension What is most likely to be found in this patient?

A

S4 gallop b/c ishemia leading to noncompliance of left ventricle

277
Q

Kussmaul sign

A
  • increase in JVP on inhalation
  • often associated with constrictive pericarditis or restrictive cardiomyopathy
  • “scratchy” sound in pericardial friction rub
278
Q

Dressler synrome

A
  • complication of myocardial infarction that occurs several days after MI and is much rarer than simpler ventricular iscemia
279
Q

Patent ductus arteriosus (PDA)

A
  • continuous “machinery” murmur t
280
Q

Displaced point of maximal impulse (PMI)

A
  • characteristic of left ventricular hypertrophy as well as dilated cardiomyopathy
  • anatomic abnormality that can’t occur with an acute coronary syndrome
281
Q

70 y.o F comes to the emergency department w/ crushing substernal chest pain for the last hr. Which of the following EKG findings would be associated with the prognosis?

A

ST elevations in V2 - V4

  • corresponds to the anterior wall of the left ventricle
  • signifies an acute myocardial infarction
282
Q

Premature ventricular complexes (PVCS)

A
  • should not be treated
  • associated with an acute infarction
  • treatment of PVCs only worsens outcome
283
Q

70 y/o F comes to the emergency department w/ crushing substernal chest pain for the last hour. An EKG shows ST segment elevation in V-2. What is the most appropriate next step of management in this patient?

A

Aspirin

  • lowers mortality and important to administer as quickly as possible
  • initiate therapy before moving patien to the ICU
284
Q

70 y/o F comes to the emergency department w/ crushing substernal chest pain for the last hr. An EKG shows ST segment elevation in leads V2 - V4. Aspirin has been given to the patient to chew. What is the most appropriate next step in management?

A

Angioplasty is associated with greatest mortality benefit

285
Q

Pt c/o chest pain, when to do an EKG

A
  • immediately at onset of pain

- ST elevation progresses to Q waves over several days to a week

286
Q

Myoglobin

A
  • becomes abnormal 1-4 hrs

- duration of myoglobin elevation is 1-2 days

287
Q

CK-MB

A
  • becomes abnormal 4-6 hrs

- duration of elevated CK-MB for 1-2 days

288
Q

Troponin

A
  • becomes abnormal in 4-6 hrs

- duration of elevated troponin is 10-14 hrs

289
Q

Difficulty of using troponin levels in detection of myocardial infarctions

A
  • Troponin can’t distinguish btwn reinfarction occurring several days after 1st event
  • Renal insufficiency can result in false positive tests since troponin is excreted via kidneys
290
Q

If pt c/o of new chest pain within a few days of first cardiac event, how do you manage this condition?

A

Concern for reinfarction

  1. Perform an EKG to detect NEW ST segment abnormalities
  2. Check CK-MB levels
    * * after two days, the CK-MB levels should have returned to normal
  3. Transfer to ICU if new infarction
291
Q

Most common cause of death in first several days of MI

A

Ventricular arrhythmia (v-tach, v-fib)

292
Q

ST segment elevation myocardial infarction (STEMI)

A
  • best initially managed with aspirin (orally or chewed).

- clopidogrel can be used an alternative to aspirin if there is an allergy

293
Q

Angioplasty vs Thromobolytics

A

Angioplasty is superior to thrombolytics b/c

  • Survival and mortality benefit
  • Fewer hemorrhagic complications
  • Likelihood of developing MI complicatins (less arrhythmia, less CHF, fewer septal ruptures, few episodes of tampanade)
294
Q

PCI

A
  • standard of care is expected to be performed within 90 minutes of patient arriving in ED with chest pain
295
Q

Complications of PCI

A
  • Rupture of coronary artery on inflation of the balloon
  • Restenosis (thrombosis) of the vessel after angioplasty
  • Hematoma at the site of entry into artery
296
Q

Which of the following is most important in decreasing the risk of restenosis of the coronary artery after PCI?

A

Placement of drug eluting stent (paclitazel, siroliums)

- inhibit the local T cell response which reduces rate of sternosis

297
Q

Absolute contraindications to thrombolytics

A
  • Major bleeding into the bowel (melena) or brain (any type of CNS bleeding)
  • Recent surgery (within the last 2 weeks)
  • Severe hypertension (above 180/110)
  • Nonhemorrhagic stroke within the last 6 months
298
Q

Pt comes to a small rural hospital w/o catherization lab. The patient has chest pain and ST segment elevation. What is the most appropriate next step in the management of the patient?

A

Administer thrombolytics now

  • better than angioplasty delayed by several hrs
  • mortality benefit of thombolytics extend to 12 hrs
299
Q

Best initial therapy for acute coronary syndrome?

A

Asprin

- best used for everyone

300
Q

Indication for clopidogrel in ACS

A
  • when aspirin not tolerated, those undergoing angioplasty and stenting
301
Q

Indication for Beta blockers in ACS

A
  • used in everyone

- effect is not dependent on time - starting anytime during admission

302
Q

Indication for ACE inhibitors and ARB in ACS

A
  • used in everyone

- benefits those with ejection fraction < 35%

303
Q

Indication for statins in ACS

A
  • used in everyone

- benefits those with LDL > 100 mg/ dL

304
Q

Indication for oxygen and nitrates in ACS

A
  • used everyone

- no clear mortality benefit

305
Q

Indication for heparin in ACS

A
  • after thrombolytics / PCI to prevent restenosis

initial therapy with ST depression and other non- STEMI events (unstable angina)

306
Q

Indication for calcium channel blockers in ACS

A
  • when beta blockers can’t be used
  • cocaine induced pain
  • Prinzmetal variant or vasospastic variant angina
308
Q

Man comes to the emergency department w/ chest pain for the last hr that is crushing in quality and does not change w/ respiration or position of his body. EKG shows ST segment depression in leads V2 - V4. Aspirin has been given. What is the most appropriate next step in management?

A

Heparin

  • heparin will prevent clot formation in coronary arteries but does not dissolve already formed clots
  • there is no ST ELEVATION, no benefit of thrombolytics
309
Q

Glycoprotein IIb/IIIa Inhibitors (Abciximab, Tirofiban, Eptifibitide)

A
  • used in ACS in those are to undergo angioplasty and stenting
  • inhibit the aggregation of plateletss.
  • led to reduction in mortality in those w/ ST depression, particularly in patients whose troponin or CK-MB levels
  • not useful in acute STEMIs separate from angioplasty and stenting
310
Q

tPA (thrombolytics) best used in which patients?

A
  • ST elevation MI patients
311
Q

Heparin is best used in which patients?

A
  • non-STEMI patients
312
Q

Glycoprotein IIa/IIIb inhibitors are best in used in which patients?

A

non-STEMO patients and those undergoing angioplasty and stenting

313
Q

If in non-STEMI ACS, when all meds have been given, and patient has persistent pain, S3 gallop or CHF develop, worse EKG changes or SVT, rising troponin levels. Next step?

A

Urgent angiography and possible angioplasty

314
Q

Complications of acute MI

A
  • Bradycardia
  • Tachycardia
  • Tamponade/Free wall rupture
  • Ventricular tachycardia/ventricular fibrillation
  • Valve/septal rupture
315
Q

Sinus bradycardia in setting of MI

A
  • common w/ MI if vascular insufficiency of the SA node
316
Q

3rd degree (complete) AV block

A
  • will have CANNON A WAVES

- obtain EKG to distinguish 3rd degree AV block vs sinus bradycardia

317
Q

Cannon A waves

A
  • produced by atrial systole against closed tricuspid valve
  • tricuspid valve is closed b/c essence of 3rd degree block is that atria and valves are contracting separate
  • JVD is bouncing up into the neck
318
Q

Right ventricular infarction

A
  • associated w/ new inferior wall MI and clear lungs

- diagnosed by flipping EKG from usual left side to right side of chest

319
Q

R coronary artery supplies

A
  • RV
  • AV node
  • inferior wall of heart
320
Q

R ventricular infarction: treatment

A
  • High volume fluid replacement

- avoid nitroglycerin to RV infarctions which markedly worsen cardiac filling

321
Q

Tamponade/free wall rupture s/p MI

A
  • takes several days s/p infarction for wall to scar and weakens enough to rupture
  • look for sudden loss of pulse
  • lungs are clear and is cause of pulseless electrical activity
322
Q

Tamponade/Free Wall Rupture: Diagnosis

A
  • emergency echocardiography
323
Q

Ventricular Tachycardia/Ventricular Fibrillation s/p MI

A
  • can cause sudden
  • must use EKG to distinguish v-tachycardia and v-fibrillaiotn
  • both treated w/ cardiovarsion/defibrillation
324
Q

Septal rupture/Valve rupture s/p MI

A
  • new onset of murmur and pulmonary congestion
325
Q

Ventricular septal rupture best heard where?

A
  • can be seen s/p MI

- best heart at LLSB

326
Q

Mitral regurgitation

A
  • can occur s/p MI

- best heard at apex w/ radiation to axilla

327
Q

Most accurate test to detect valve rupture and septal rupture

A
  • Echocardiogram
328
Q

Septal rupture

A
  • look for increase in oxygen saturation as you go from right atrium to right ventricle
329
Q

Intraaortic balloon pump

A
  • used when there is acute pump failure from anatomic problem that can be fixed in OR
  • contracts and relazes w/ natural heartbeat
  • helps give a “push forward to the blood”
330
Q

Reinfarction or extension of infarction

A
  • patient often presents w/ either inferior or anterior infarction
  • look for reoccurrence of pain, new rales on exam, bump up CK-MB and even suddent onset of pulmonary edema
331
Q

Reinfarction or extension of infarction

A
  • repeat EKG
  • retreat w/ angioplasty and sometimes thrombolytics in addition to usual meds (aspirin, metoprolol, nitrates, ACE, statins)
332
Q

Aneurysm/ Mural Thrombus

A
  • detected with echocadiogramy

- treated w/ heparin followed by warfarin

333
Q

Pt s/p MI presents w bradycardia and cannon A waves. Likely dx?

A

3rd degree AV block

334
Q

Pt s/p MI presents w/ bradycardia. No cannon A waves on EKG. Likely dx?

A

Sinus bradycardia

335
Q

Pt s/p MI w/ PMH of inferior wall MI, clear lungs, tachycardia, hypotension w/ nitroglycerin. Likely dx?

A

RV infarction

336
Q

Pt s/p MI with new murmur, rales/congestion. Likely dx?

A

Valve rupture

337
Q

Pt s/p MI with new murmur, increase in oxygen saturation on entering the right ventricle. Likely dx?

A

Septal rupture

338
Q

Pt s/p MI with loss of pulse, need EKG to answer question. Likely diagnosis

A

Ventricular fibrillation

339
Q

Before patient w/ MI is discharged. Which test should be done?

A

Stress test

  • to determine if angiography is needed
  • angiogrpay determines need for revascularization
340
Q

Meds needed for postinfarction patients

A

Every MI patient should go home:

  • Aspirin
  • Beta blockers (metoprolol)
  • Statins
  • ACE inhibitors
341
Q

ACE inhibitors are best used for which type of MI patients?

A

Anterior wall infarctions b/c of high likelihood of developing systolic dysfunction

342
Q

Clopidogrel

A
  • used for those intolerant of aspirin or post-stenting
343
Q

ARBS

A
  • used for MI patients with cough on ACE inhibitor
344
Q

Prophylactic antiarrhythmic medications

A
  • don’t use amiodarone, flecainide or any rhythm controlleing med to prevent development of v-tach
345
Q

Sexual issues postinfarction

A
  1. Don’t combine nitrates w/ sildenafil
  2. Erectile dysfunction (usually from anxiety)
  3. Pt doesn’t have to wait after an MI to begin sexual activity
  4. If post-MI stress test is normal, pt can engage in exercise program
346
Q

Congestive Heart Failure

A
  • dysfunction of heart as pump of blood
  • dyspnea is most common function
  • can be due to either systolic or diastolic dysfunction
347
Q

Diastolic dysfunction

A
  • inability of heart to “relax” and receive blood

- ejection fraction is preserved and sometimes even above normal

348
Q

Most common causes of systolic dysfunction (3)

A
  1. Infarction
  2. Cardiomyopathy (2/2 HTN)
  3. Valve disease
349
Q

Less common causes of systolic dysfunction

A
  • Alcohol
  • post viral myocarditis
  • Doxorubicin use
  • Chagas disease
  • Hemochromatosis
350
Q

CHF: presentation

A
  • dyspnea
  • pulmonary edema, in worst form
  • orthopnea (worse when lying flat, relieved when sitting up)
  • Rales on lung exam
  • JVD
  • paroxysmal nocturnal dyspnea (sudden worsening at night)
  • S3 gallop
351
Q

Pt presents with sudden onset dyspnea with clear lungs. Likely dx?

A

Pulmonary embolus

352
Q

Pt presents w/ sudden onset dyspnea, wheexing, increased expiratory phase. Likely dx?

A

Asthma

353
Q

Pt presents w/ slower onset dyspnea, sputum, unilateral rales/rhonci

A

Pneumonia

354
Q

Pt presents w/ dyspnea, circumoral numbness, caffeine use, hx of anxiety. Likely dx?

A

Panic attack

355
Q

Pt presents w/ pallor, gradual onset dyspnea over days to weeks. Likely dx?

A

Anemia

356
Q

Pt presents w/ dyspnea, pulsus paradoxus, decreased heart sounds, JVD. Likely dx?

A

Tamponade

357
Q

Pt presents w/ dyspnea, palpitations, syncope. Likely dx?

A

Arrhythmia of almost any kind

358
Q

Pt presents w/ dyspnea, dullness to percussion at bases. Likely dx?

A

Pleural effusion

359
Q

Pt presents w/ dyspnea, long smoking hx, barrel chest. Likely dx?

A

COPD

360
Q

Pt presents w/ dyspnea, recent anesthetic use, brown blood not improved w. oxygen, clear lungs on auscultation, cyanosis. Likely dx?

A

Methemoglobinemia

361
Q

Pt presents w/ dyspnea, burning building or car, wood burning stove in winder, suicide attempt. Likely dx?

A

Carbon monoxide poisoning

362
Q

Most important test in CHF

A

Echocardiography

363
Q

Best initial test to evaluate ejection fraction

A

Transthoracic echo

364
Q

Most accurate test to evaluate ejection fraction

A

MUGA or nuclear vetriculography

365
Q

When is nuclear ventriculography used to evaluate ejection fraction

A
  • necessary when precision is needed

- example if giving doxorubicin for chemo but need to ensure maximum treatment w/o cardiomyopathy

366
Q

BNP level is used t evaluate

A
  • acute SOB with unclear etiology

- normal BNP excludes CHG

367
Q

Best test to detemine CHF 2/2 MI or heart block

A

EKG

368
Q

Best test to determine CHF 2/2 dilated cardiomyopathy

A

CXR

369
Q

Best test to determine CHF 2/2 paroxysmal arrhythmias

A

Holter monitoring

370
Q

Best test to determine precise valve diameter

A

Cardiac catherization

371
Q

Best test to determine CHF 2/2 abnormal thyroid levels (high or low)

A

Thyrid function tests (T4/TSH)

372
Q

Best test that distinguishes CHF from ARDS

A

Swan Ganz right heart catherization

373
Q

Systolic Dysfunction (Low Ejection Fraction): Test

A
  • ACE inhibitors
  • Beta Blockers
  • Spironolactone
  • Diuretics
  • Digoxin
374
Q

Specific B-blockers beneficial in systolic dysfunction

A
  • Metoprolol (specific B-1 antagonists)
  • Bisoprolol (specific B-1 antagonists)
  • Carvedilol (nonspecific B-blocker w/ alpha blocker)
375
Q

Why B-blockers (carvedilol, metoprolol, bisoprolol) are beneficial in systolic dysfunction

A
  • Antiischemic effect
  • Decrease in HR leading to decreased oxygen consumption
  • antiarrhythmic effect
376
Q

Most common cause of death from CHF

A
  • Arrhythmia/sudden death
377
Q

Spironolactone

A
  • beneficial b/c it inhibits effects of aldosterone

- effective in later stages of CHF (stages III and IV)

378
Q

Spironolactone: adverse effects

A
  • Hyperkalemia

- Gynecomastia

379
Q

Eplerone

A
  • alternative to spironolactone
  • inhibits aldosterone
  • doesnt have antiandrogen effects that leads to gynecomastia
380
Q

Pt w/ CHF who develops gynecomastia?

A

Switch from spironolactone to eplerone

381
Q

Indications for diuretics in CHF

A
  • initial therapy in CHF w/ low ejection fraction

- often loop diuretic with ACEi/ARB

382
Q

Digoxin

A
  • doesn’t lower mortality in CHF

- used to control symptoms of dyspnea and will decrease frequency of hospitalixations

383
Q

74 y/o A-A man w/ hx of dilatered cardiomyopathy 2/2 o MI in past is seen in office. He is asymptomatic and is maintained on lisinopril, furosemide, metoprolol aspirin, and digoxin. Lab tests reveal elevated K level. EKG is unchanged. Best management?

A

Switch from lisinopril to hydralazine and nitroglycerin

384
Q

Non pharm treatments that have mortality benefit in CHF

A
  1. Implantable defribrillator: used in for EF < 35% and ischemic cardiomyopathy
  2. Biventricular pacemaker: used in dilated cardiomopathy and ejection fraction < 35% and a wide QRS > 120ms
385
Q

Drugs w/ mortality benefit in CHF

A
  • ACEi/ARBS
  • Spironolactone or eplerone
  • Beta blockers
  • Hydralazine/nitrates
  • Implantable defibrillator
386
Q

Diastolic Dysfunction (CHF w/ preserved EF)

A
  • B-blockers are beneficial

- Diuretics are used to control symptoms of fluid overload

387
Q

HOCM (hypertrophic obstructive cardiomyopathy)

A
  • congenital disease w/ asymmetrically enlarged (hypertrophic) septum leading to an obstruction of LV outflow tract
  • diuretics are contraindicated b/c they increase obstruction**
388
Q

Pulmonary edema

A
  • most severe form ofCHF

- rapid onset of fluid accumulating in lungs

389
Q

Pulmonary edema: presentation

A
  • Rales
  • JVD
  • S3 gallop
  • Edema
  • Orthopnea
390
Q

Pulmonary edema: diagnostic tests

A
  • BNP is etiology of dyspnea is unclear
  • CXR shows vascular congestion with filling of blood vessels towards the head
  • Respiratory alkalosis on ABG
  • EKG
  • Echo
391
Q

Best test to do in acute pulmonary edema

A

EKG

** if pt has arrhythmia (a-fib, a-flutter, or v-tach) best thing to do is rapid cardioversion

392
Q

74 y.o F comes to the ED w/ acute onset SOB, RR of 38 bpm, S3 gallop, and JVD. What’s the best initial step?

A

IV furosemide

- acute management to remove large amts of fluid

393
Q

CHF: Treatment

A

Initial therapy of pulmonary edema w/

  • Oxygen
  • Loop diuretics (e.g. furosemide or bumetanide)
  • Morphine
  • Nitrates
394
Q

CHF: Treatment options

A
  • Preload reduction ( w/ furosemide or bumetanide)
  • Positive inotropic agents (e.g dobutamide)
  • Afterload reduction (w/ ACEis / ARBs)
395
Q

Positive ionotropes in setting of CHF

A
  • Dobutamine

- Amrinone and milrinone - phosphodiesterase inhibitors increase contractility and decrease afterload

396
Q

Digoxin

A

positive ionotrope that increases contractility but does not have effect for several weeks

397
Q

Afterload reduction in CHF

A
  • Long term setting: ACEis/ ARBs

- Acute setting: nitroprusside and IV hydralazine

398
Q

Rheumatic fever

A
  • associated with any form of valve disease

- mitral stenosis is most common

399
Q

Regurgitant valvular disease

A
  • associated w. hypertension and ischemic heart disease

- infarction automatically leads to regurgitation which leads to dilation

400
Q

Right heart sided lesions: heart sounds

A
  • tricuspid and pulmonic valves increase in intensity or loudness w/ inhalation
  • inhalation will increase venous return to the heart
401
Q

Left sided lesions (mitral valve and aortic valve): presentation

A
  • increase w/ exhalation

- exhalation will “squeeze” blood out of the lungs and into the left side of the heart

402
Q

Best initial test for all valvular heart disease

A

Echocardiogram

- TEE is most sensitive and specific than TTE

403
Q

Most accurate test for valvular heart disease

A

Catherization

- allows for precise measurement of valve diameter as well as exact pressure gradient across the valve

404
Q

Mitral stenosis: treatment

A
  • dilated w. a ballooon
405
Q

Aortic stenosis: treatment

A

Surgical replacement of aortic valve

406
Q

Regurgitant lesions: treatment

A
  • respond best to vasodilator therapy w/ ACEi, ARBs, nifedipine, or hydralazine
  • ** surgical replacement of regurgitant valves must be done before valve dilates too much **
407
Q

Mitral stenosis

A
  • often caused by rheumatic fever

- critical narrowing by 1 cm ˆ2

408
Q

Why should we worried about pregnant patients who emigrated from country w. high prevalence of rheumatic fever?

A

Pregnancy increases plasma by 50% which now must traverse narrow valve which can lead to pregnancy induced cardiomyopathy

409
Q

Mitral stenosis: presentation

A
  • dyspnea and CHF
  • dysphagia (from dilated LA pressing on esophagus)
  • hoarseness (LA pressing on laryngeal nerve)
  • atrial fibrillation and stroke (from enlarged LA)
  • hemoptysis
410
Q

Mitral stenosis: physical findings

A

diastolic murmur (

First AId 2CK (22 decks)

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