Cardiology Flashcards

1
Q

On a lateral view CXR, extension of the heart border posteriorly and inferiorly indicates enlargement of which ventricle?

A

Extension of the heart border posteriorly and inferiorly on lateral view CXR indicates enlargement of the left ventricle.

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2
Q

On a lateral view CXR, extension of the cardiac shadow of the lower part of the anterior clear space behind the sternum indicates enlargement of which ventricle?

A

Extension of the heart shadow into the retrosternal airapsce indicates right ventricular enlargement.

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3
Q

What conditions is a TEE useful for evaluating?

A

TEE is useful for evaluating the left atrium (left atrial appendage), valvular disease, endocarditis, aortic dissection, cardiac masses, and intracardiac shunts.

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4
Q

What are absolute indications for terminating an ETT?

A

Absolute indications for terminating an ETT include: ST segment elevation>1mm in leads without Q waves, decrease in SBP >10mmHg, Moderate-to-severe angina, CNS symptoms, signs of poor perfusion, sustained 2nd or 3rd degree AV block, patient requests to stop, severe arrhythmias.

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5
Q

When are stress imaging studies done instead of an ETT?

A

Stress imaging is done when the patient is unable to exercise on the treadmill or has baseline ECG changes that would confound interpretation of the ECG.

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6
Q

When are exercise stress echo and MPI indicated instead of ETT?

A

Stress imaging is done when the patient is able to exercise on the treadmill or has baseline ECG changes that would confound interpretation of the ECG.

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7
Q

Which stress imaging tests are used in patients with LBBB? With paced ventricular rhythm?

A

A patient with LBBB needing stress imaging should do a vasodilator MPI or dobutamine stress echo. A patient with a pacemaker should have a vasodilator MPI as treadmill or dobutamine may not elevate heart rate in such patients.

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8
Q

Which patients may benefit from cardiopulmonary exercise testing?

A

Cardiopulmonary testing should be performed to evaluate patients with systolic heart failure, patients undergoing a pre-transplant evaluation, and for patients with unexplained dyspnea.

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9
Q

When is PCWP increased?

A

PCWP increased with LV systolic and diastolic failure, mitral stenosis, aortic and mitral insufficiency, tamponade, and constrictive pericarditis.

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10
Q

At which PCWP do you expect to see frank pulmonary edema?

A

The PCWP in a patient with frank pulmonary edema should be >35mmHg.

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11
Q

When is diastolic pressure equal in all 4 chambers?

A

Equalization of diastolic pressure in all 4 chambers is seen with pericardial tamponade and constrictive pericarditis.

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12
Q

Name 1 indication for doing endomyocardial biopsy.

A

Endomyocardial biopsy is usually used to monitor for heart transplant rejection. It is also used to evaluate the cause of a cardiomyopathy or myocarditis in patients where the diagnosis is uncertain and would change management.

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13
Q

True or false? Pulsus paradoxus can be seen in cardiac tamponade.

A

True,pulsus paradoxus is seen in cardiac tamponade. It can also be seen in constrictive pericarditis, asthma, and tension pneumothorax.

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14
Q

What is pulsus bisferiens? What does it indicate?

A

Pulsus bisferiens is a pulse with 2 systolic peaks per cardiac cycle. It is seen in aortic regurgitation and hypertrophic cardiomyopathy.

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15
Q

What does pulsus alternans indicate?

A

Pulsus alternans is a varying pulse pressure with regular pulse rate and is seen in severely depressed systolic function from any cause.

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16
Q

True or false? Sustained handgrip increases the murmur of mitral valve prolapse, but decreases the murmur of HCM.

A

True. Sustained handgrip increases systemic vascular resistance and decreases the murmurs of HCM and aortic stenosis while prolonging the murmur of MVP.

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17
Q

When is a persistently split S2 heard?

A

Persistent splitting of S2 is seen in pulmonic stenosis, acute pulmonary embolism, and rhythms arising in the left ventricle (due to pacemaker or RBBB).

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18
Q

What causes a paradoxically split S2?

A

Paradoxical splitting of S2 is seen with delay in aortic closure as is seen with LBBB and pacemaker beats originating in the right ventricle.

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19
Q

When is an S3 important?

A

S3 is common before age 40 years but is abnormal after that and often indicates LV systolic dysfunction with early filling of the LV.

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20
Q

When are large v waves seen on the left side? Right side?

A

Large v waves on the left side are seen with mitral regurgitation. Right sided large v waves are seen with tricuspid regurgitation.

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21
Q

When is rapid x and y descent seen?

A

Rapid x and y descents are seen in restrictive cardiomyopathy.

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22
Q

When is the y descent absent?

A

The y descent is slow or absent with tricuspid stenosis.

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23
Q

When are large, right-sided a waves seen?

A

Large, right sided a waves are seen in tricuspid stenosis, severe pulmonic stenosis, and severely noncompliant RV.

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24
Q

When are large, left-sided a waves seen?

A

Large, left sided a waves are seen in mitral stenosis.

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25
Q

When are “cannon” a waves seen?

A

“Cannon” a waves are seen with AV dissociation such as complete AV block, VT, and asynchronous ventricular pacing.

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26
Q

When does a slow y descent occur?

A

Slow y descent occurs in tricuspid stenosis.

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27
Q

In which patients should you suspect secondary HTN?

A

Suspect secondary HTN in patients who develop HTN before age 30, who have drug-resistant HTN, or who develop uncontrolled HTN that was previously controlled.

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28
Q

True or false? A systolic abdominal bruit without a diastolic bruit suggests renal vascular HTN.

A

True, a systolic abdominal bruit without diastolic bruit suggests renal vascular HTN.

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29
Q

What disorder should you think of if a patient presents with HTN, hypokalemia, and low renin?

A

Patients with HTN, hypokalemia, and low renin should be evaluated for primary hyperaldosteronism.

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30
Q

True or false? Digoxin prolongs survival.

A

False. Digoxin may improve symptoms and reduce hospitalizations in heart failure, but it does not improve survival in heart failure or post-MI.

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31
Q

Which medications have been shown to prolong survival both post-MI and for patients with heart failure?

A

Only beta-blockers, ACEIs, and ARBs have been shown to prolong survival in both post-MI and heart failure patients.

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32
Q

With which medication should a nitrate be paired to improve survival in heart failure patients?

A

Hydralazine paired with a nitrate has been shown to improve survival in African American heart failure patients.

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33
Q

What is the most common cause of acute coronary syndrome?

A

Plaque rupture or erosion with thrombosis is the most common cause of acute coronary syndrome.

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34
Q

What is the cause of Prinzmetal angina?

A

Prinzmetal angina is caused by spasm of a coronary artery.

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35
Q

What does ST-segment elevation suggest on an exercise ECG stress test?

A

ST-segment elevation in >3 leads on ETT suggest significant ischemia. It can also be seen in coronary vasospasm.

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36
Q

What causes resting ST-segment elevation?

A

Resting ST-segment elevation is caused by acute MI, coronary spasm, pericarditis, LV aneurysm, LBBB, LV pacing, LVH, and early repolarization.

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37
Q

Explain the similarities and differences between hibernating myocardium, reperfusion injury, and stunned myocardium.

A

Hibernating myocardium is chronically underperfused myocardium which has no irreversible injury. If reperfused it can return to normal function. Reperfusion injury is irreversible myocardial injury that occurs if reperfusion occurs after 1 hour. Stunned myocardium is the result of acute ischemia. From time of reperfusion it can take 7-10 days for ventricular function to return to normal.

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38
Q

What are the main drugs used to treat angina?

A

Beta-blockers and nitrates are the mainstays of antianginal therapy with calcium channel blockers also playing a role.

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39
Q

Which patients might benefit from ranolazine (Ranexa)?

A

Ranolazine can be used for antianginal effect in those on maximal standard therapy including beta-blockers or in those who cannot tolerate beta-blockers.

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40
Q

Which antianginal drugs decrease myocardial oxygen demand?

A

Beta-blockers, nitrates, and calcium channel blockers all decrease myocardial oxygen demand. Beta-blockers decrease myocardial oxygen demand by decreasing heart rate, blood pressure, and contractility.

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41
Q

Which antianginal drugs decrease afterload?

A

Calcium channel blockers predominantly reduce afterload.

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42
Q

Which antianginal drugs decrease preload?

A

Nitrates reduce preload and to a lesser extent afterload.

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43
Q

Which antianginal drug do you not give to a patient with RV infarct? Why?

A

Nitrates should not be used in RV infarct as they can reduce RV preload and lead to reduced cardiac output and hypotension.

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44
Q

Why should you determine the probability of CAD in a person with intermittent chest pain?

A

History and physical along with baseline ECG are the first steps to determine the pre-test probability of CAD.

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45
Q

What is the most important test for risk stratification in patients with stable ischemic heart disease?

A

Exercise treadmill testing is the most important test for risk stratification in patients with stable ischemic heart disease.

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46
Q

For which patient with chronic stable angina do you do an echocardiogram? Why?

A

Use echocardiogram to assess the patient with chronic stable angina if they have prior MI, pathologic Q waves, symptoms or signs of heart failure, arrhythmias, or heart murmur as this will help guide treatment.

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47
Q

A patient undergoing a workup for chronic stable angina is determined to be at high risk for death. What is the next step?

A

High risk patients with chronic stable angina should be referred for coronary angiography to determine coronary artery anatomy.

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48
Q

What is the goal for blood pressure management in a patient with stable ischemic heart disease?

A

Blood pressure should be kept <140/90 in patients with chronic stable angina.

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49
Q

Would you recommend aspirin in a healthy woman <65 years of age for primary prevention of MI?

A

There is no clear evidence of benefit of preventive aspirin in women <65 years of age.

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50
Q

What are the 2 major categories of ACS?

A

The two major categories of ACS are ST-segment elevation ACS and non-ST-segment elevation ACS.

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51
Q

How are troponin I and T used? How long do they stay elevated after an MI?

A

Troponins I and T are the gold standard for detection of myocardial necrosis. They start to elevate 4 hours after event, peak at 44 hours, and may remain elevated for 10-14 days.

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52
Q

What are the prehospital guidelines for chest pain?

A

Prehospital guidelines for chest pain include: call 911, take an aspirin 162-325mg chewed and swallowed, give a nitrate times up to three doses, in-field ECG by EMS, monitoring and preparing to manage ventricular arrhythmias.

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53
Q

What are the major things you should do in early risk stratification of a patient who presents with ACS in the emergency department?

A

ECG, aspirin, measuring of cardiac markers, and directed history and physical should be done early in management of patient with ACS. If initial ECG is non-diagnostic, this should be repeated q15-30 minutes to evaluate for changes.

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54
Q

Based on early stratification of ACS, to what groups can a patient be assigned?

A

Based on early stratification, patients should be assigned to 1) noncardiac chest pain, 2) possible ACS, and 3) definite ACS.

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55
Q

What anti-ischemic measures are done initially for all patients with ACS?

A

Initial anti-ischemic measures for all patients with ACS include: aspirin, nitrates, morphine is unrelieved by nitrates, and beta-blockers and ACEI if still hypertensive or evidence of LV dysfunction.

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56
Q

Which patients should receive a platelet GP IIb/IIIa inhibitor?

A

GP IIb/IIIa inhibitors should be considered in high risk ACS patients including those with elevated troponin, hemodynamic instability, or dynamic ECG changes. Since the advent of dual antiplatelet therapy, GP IIb/IIIa inhibitors are used less frequently.

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57
Q

Of those with ACS, what group gets considered for fibrinolytic therapy and what group definitely does not?

A

Fibrinolytic therapy should not be given to those without ST-segment elevation. Those with ST-segment elevation should be given fibrinolytic therapy if immediate PCI is not available and they do not have contraindications.

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58
Q

Which NSTE-ACS patients should be considered for an early invasive strategy?

A

Indications for an early invasive strategy include heart failure, hemodynamic instability, recurrent or refractory angina. Other indications for invasive therapy include: elevated cardiac markers, dynamic ST changes, diabetes, EF <40%, PCI within the last 6 months, prior MI, prior CABG, intermediate/high risk patients based on scoring such as TIMI scoring.

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59
Q

What are the reperfusion therapies you give to (or consider for) those with STEMI or new LBBB/ Who gets what?

A

All patients who present within 12 hours of symptom onset with STEMI or new LBBB should be considered for emergent reperfusion with PCI or fibrinolysis (if PCI is not available).

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60
Q

What are the absolute and relative contraindications to fibrinolytic therapy?

A

Absolute contraindications to fibrinolytic therapy include any prior cerebral hemorrhage, other cerebrovascular events within 1 year, intracranial neoplasm, active internal bleeding, or suspected aortic dissection. Relative contraindications include BP >180/110, remote nonhemorrhagic CVA >1 year ago, current use of anticoagulants with INR >2-3, bleeding diathesis, recent major trauma or surgical procedure (2-4 weeks), noncompressible vascular puncture, previous exposure to streptokinase/anistreplase, pregnancy, active peptic ulcer.

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61
Q

How does management of RVI differ from LV infarction?

A

RV infarcts are preload dependent. They should not receive nitrates. Fluid support is often needed to maintain preload in RV infarct.

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62
Q

Which patients with tachyarrhythmias after an MI get DC cardioversion?

A

Ventricular fibrillation and pulseless VT should be treated with unsynchronized DC cardioversion. Sustained VT with pulse but with hemodynamic instability is treated with synchronized DC cardioversion.

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63
Q

What are the medical options for hemodynamically stable MI patients with VT?

A

Amiodarone is the drug of choice for the hemodynamically stable MI patient with VT. Hypokalemia and hypomagnesemia should be corrected as well.

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64
Q

When do the major mechanical complications tend to occur after an MI? How do they present? What is the best initial test to diagnose such a complication?

A

Papillary muscle rupture presents 3-7 days after inferior MI and presents with rapid development of shock and pulmonary edema. Ventricular septal defect presents 3-7 days after anteroseptal MI and presents with shock and a loud holosystolic murmur. Both papillary muscle rupture and post-MI VSD are diagnosed by echocardiogram. Free wall rupture occurs 3-7 days after large, anterior MI and presents with sudden syncope, distended neck veins, tachycardia, pulsus paradoxus, and hypotensions. This complication almost always results in death.

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65
Q

When should a patient with STEMI be referred for consideration of an ICD?

A

ICD placement is indicated in STEMI patients with sustained VT or V-fib >48 hours after MI. It is also indicated in those patients with post-MI EF <30-35% when reevaluated by echo >40 days after MI.

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66
Q

What are the primary risk factors for CAD?

A

The primary risk factors for CAD are age, male gender, family history of early CAD, smoking, HTN, diabetes, elevated LDL, and low HDL.

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67
Q

What lab tests should general lipid screening include?

A

General lipid screening should include measurement of total cholesterol, HDL cholesterol, and triglyceride with a calculation of LDL cholesterol.

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68
Q

In what situations are LDL receptors down-regulated? Up-regulated?

A

LDL receptors are down-regulated when dietary cholesterol or saturated fats are high, with increasing age, and in patients with familial hypercholesterolemia (50% in heterozygotes, 0% in homozygotes). LDL receptors are up-regulated when diet is low in cholesterol and saturated fats, by estrogen, by thyroxine, by statins, by a decrease in bile acid uptake for the intestines (as with use of bile acid binding resins).

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69
Q

Which familial dyslipidemia is the most common? What lipoproteins are elevated?

A

Familial combined hyperlipidemia is the most common familial dyslipidemia. In FCHL there is increased production of both apoB100 and VLDL, and the increased VLDL stresses the pathway toward increased LDL production.

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70
Q

What lipid test results suggests the need to work up familial hypoalphalipoproteinemia?

A

Isolated low HDL should prompt consideration of familial hypoalphalipoproteinemia, an autosomal dominant condition resulting from a mutation in the gene for apoA1 or for the gens ABCA1 or LCAT. It is found in 6% of Japanese patients with low HDL.

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71
Q

What is the primary endpoint of lipid screening done for primary prevention of CHD?

A

The primary endpoint for lipid screening to prevent CHD is the LDL.

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72
Q

Explain the ATPIII treatment priority for lipid abnormalities?

A

The ATPIII priority levels for treatment of dyslipidemia are 1) lower elevated LDL, 2) treat elevated non-HDL, then 3) raise low HDL.

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73
Q

List the CHD-equivalent diseases.

A

CHD-equivalent diseases include diabetes, carotid artery disease, peripheral artery disease, TIA or stroke, AAA, chronic kidney disease, and 10 year risk of CHD >20% using Framingham risk calculator.

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74
Q

Per ATPIII what are the non-LDL risk factors for CHD that are considered when you stratify patients for primary prevention of CHD?

A

Per ATPIII the non-LDL risk factors to consider in risk stratification of patients include age, family history, smoking, HTN, and low HDL cholesterol.

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75
Q

Per ATPIII, at what LDL level if TLC started on a 38yo man with diabetes? At what level do you start drug therapy?

A

A 38yo man with diabetes has a CHD-equivalent, so TLC should be initiated with LDL >100 and drug therapy should be started if LDL > 130.

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76
Q

Per ACC/AHA ASCVD guidelines, name the 4 statins benefit groups.

A

The 4 statin benefit groups per ACC/AHA ASCVD guidelines are clinical atherosclerotic cardiovascular disease, LDL>190, diabetes 40-75 years of age with LDL 70-189 and no evidence of atherosclerotic CV disease, and those without atherosclerotic CV disease or diabetes with 10-year risk of CV disease >7.5%.

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77
Q

How is high-intensity statin defined? A moderate-intensity statin?

A

High intensity statin therapy reduces LDL >50%. Moderate intensity statin therapy reduces LDL 30-50%.

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78
Q

Which fats are the “good fats”? The “bad fats”?

A

Monounsaturated fats such as olive/peanut/canola oils and omega-3 fatty acids are considered good fats. Hydrogenated vegetable oils (“trans fats”), saturated fats, and polyunsaturated fats are considered “bad fats”.

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79
Q

What class of drugs is recommended 1st line to reduce LDL?

A

Statins are considered first line to reduce LDL.

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80
Q

What are the major side effects of statins?

A

Major side effects of statins include myalgias, elevated glucose, memory loss and confusion.

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81
Q

What are the side effects of colesevelam?

A

Colesevelam and the other bile acid binding resins may cause nausea, vomiting, constipation and bloating. They can also interfere with absorption of other medications, so other medicines should be given one hour before or 4 hours after bile acid binding resins.

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82
Q

What is the main action of the fibrate drugs?

A

The main action of fibrates is to increase the activity of LPL on VLDL thus increasing the rate of conversion of VLDL to IDL.

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83
Q

What are the relative contraindications to niacin?

A

Niacin may contribute to hyperuricemia and insulin resistance, so relative contraindications to niacin include gout and diabetes.

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84
Q

What activities increase HDL? Lower HDL?

A

Moderate alcohol intake, exercise, smoking cessation, weight loss if obese, and reducing intake of trans fats all increase HDL levels. Smoking, weight gain, diets high in trans fats or polyunsaturated fats all decrease HDL levels.

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85
Q

What happens to the lipid panel in ACS?

A

A recent MI or any serious illness can lower LDL and HDL cholesterol and variably affect triglycerides, so a lipid panel should be checked 8 weeks after illness to better determine patient’s lipid abnormalities.

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86
Q

Which patient groups definitely should get CABG?

A

Patients with significant left main CAD and patients with significant stenoses in 3 major coronary arteries or with proximal LAD artery plus 1 other major coronary artery stenosis are best treated with CABG to improve survival. Diabetics with multivessel CAD also have improved survival with CABG.

87
Q

Which patient groups could get either PCI or CABG?

A

PCI or CABG are reasonable alternatives in patients with 1 or more significant coronary artery stenoses amenable to revascularization and unacceptable angina despite medical therapy, patients with presumed ischemia-mediated VT caused by stenosis of a major coronary artery, or in patients with left main CAD with low risk of PCI complications and significantly increase surgical morbidity/mortality.

88
Q

In 3 vessel disease, what is the benefit or CABG - survival, symptoms, or both?

A

Both can be improved with CABG. However, survival is only improved in the presence of 3 vessel disease with significant LV dysfunction, left main or left main-equivalent disease, or in diabetes.

89
Q

Why is dual antiplatelet therapy so important after stent placement?

A

DAPT is essential after stent placement to prevent stent thrombosis. THis is needed for one month after placement of a bare metal stent and for at least one year after placement of a drug-eluting stent.

90
Q

What are the causes of arteriosclerotic PAD?

A

The two major risk factors for PAD are diabetes and smoking. Other modifiable risk factors are hyperhomocysteinemia, hyperlipidemia, and HTN.

91
Q

What is Buerger disease?

A

Beurger disease is also known as thromboangiitis obliterans. It involves small and medium arteries, especially in male smokers >30 years of age.

92
Q

What is the difference between claudication and pseudoclaudication?

A

Claudication occurs with walking and resolves with stopping, whether the patient remains standing or not. Pseudoclaudication due to lumbar spinal disease occurs with walking, especially downhill, and requires one to sit down to resolve.

93
Q

What is the first test to establish the diagnosis of lower extremity PAD? What result is considered abnormal?

A

The first test to diagnose PAD is the resting ABI. An ABI <0.9 is considered abnormal.

94
Q

What antiplatelet therapy is recommended for patients with PAD?

A

Aspirin 75-325mg daily or clopidogrel 75mg daily is recommended for PAD. Warfarin is not beneficial.

95
Q

In which patients is cilostazol contraindicated?

A

Cilostazol is contraindicated in patients with class 3 or 4 systolic heart failure.

96
Q

Atherosclerotic disease of the carotid artery results in more risk for which of these: MI, stroke, or TIA?

A

Patients with atherosclerotic disease of the carotid artery are at higher risk for MI than for cerebrovascular events.

97
Q

When is carotid endarterectomy indicated?

A

Symptomatic patients with stroke or TIA within six months should be considered for carotid endarterectomy if they have >70% carotid narrowing by noninvasive studies or >50% narrowing by catheter angiography and they have <6% risk of perioperative morbidity/mortality.

98
Q

How might spontaneous dissection of the internal carotid artery present clinically? What is the prognosis?

A

Spontaneous dissection of the internal carotid artery presents clinically as unilateral headache along with either TIA or dilated pupil. Spontaneous dissection of the internal carotid artery typically resolves without treatment and has an excellent recovery.

99
Q

What is the most common cause of cerebral embolic events?

A

The most common cause of cerebral embolic events is atrial fibrillation.

100
Q

What are the procedures of choice for diagnosing dissecting aortic aneurysm?

A

Transesophageal echocardiogram is the procedure of choice for diagnosing proximal thoracic aortic dissection. For all others, chest or cardiac CT or MRI are the procedures of choice.

101
Q

At what size is surgery indicated for a thoracic aortic aneurysm?

A

Surgery is indicated for ascending aortic aneurysms >5.5cm (>5cm in Marfan syndrome) and for descending thoracic aortic aneurysms >6cm.

102
Q

At what size is surgery indicated for an abdominal aortic aneurysm?

A

AAA should be operated on if >5.5cm, symptomatic, or if they expand >0.5cm over 6 months.

103
Q

With which common clinical symptoms do patients with aortic valve stenosis present?

A

The clinical symptoms of aortic valve stenosis include angina, heart failure, or syncope.

104
Q

When should valve replacement occur for aortic valve stenosis?

A

Valve replacement should be done for AS in all patients with symptoms (stage D) and in asymptomatic patients with a gradient >40 mmHg, velocity >4.0 m/s, or valve area <1cm2. It should also be done in patients with severe asymptomatic AS with EF <50% or who need to undergo CABG.

105
Q

Name 2 conditions that cause chronic aortic valve regurgitation.

A

Valve deformity (ie. bicuspid valve, rheumatic fever, endocarditis, or degenerative valve disease) and aortic root dilation (Marfan syndrome, senile aortic disease, giant cell arteritis, relapsing polychondritis, or syphilis) cause chronic aortic regurgitation.

106
Q

What is the usual treatment for acute aortic valve regurgitation with associated heart failure?

A

Patients with acute aortic regurgitation with heart failure need immediate aortic valve replacement.

107
Q

When the mitral stenosis is more severe, is the S2-OS interval smaller or larger?

A

The more severe the MS, the smaller the S2-OS interval.

108
Q

Which type of murmur occurs in mitral stenosis?

A

The murmur of mitral stenosis is a diastolic rumble.

109
Q

Hemoptysis is seem with which mitral lesion?

A

Hemoptysis occurs in mitral stenosis due to rupture of pulmonary bronchial vessels distended by pulmonary venous hypertension.

110
Q

Describe the murmur sometimes heard with MVP. Does that murmur’s intensity decrease or increase with standing? With Valsalva maneuver?

A

The murmur of MVP is a mid-to-late systolic murmur that follows a midsystolic click. Both standing and Valsalva maneuver cause the murmur of MVP to become louder and move earlier into systole because they decrease preload and hence LV volume.

111
Q

Carcinoid usually presents with what type of tricuspid murmur?

A

Carcinoid is associated with a combination of tricuspid stenosis and tricuspid regurgitation.

112
Q

On physical exam, in patients with tricuspid regurgitation, what large waves are noted on the jugular waveform?

A

Tricuspid regurgitation is associated with large jugular v waves.

113
Q

True or false? Pulmonic stenosis is virtually always acquired.

A

False. Pulmonic stenosis is almost always congenital.

114
Q

Ebstein anomaly is occasionally seen with which structural and electrical abnormalities?

A

Ebstein anomaly is occasionally seen with ASD or WPW.

115
Q

Are blood cultures more frequently positive in right-sided or left-sided endocarditis?

A

Blood cultures are positive equally frequently in right-sided and left-sided endocarditis (95%).

116
Q

Which type of ASD requires antibiotic prophylaxis before a dental procedure?

A

The only ASDs that require dental prophylaxis are those that are unrepaired and cyanotic or those that are repaired with residual defect.

117
Q

Which of these require antibiotic prophylaxis: previous CABG? VSD? Mitral valve prolapse without murmur? Mitral valve prolapse with murmur? Prosthetic valve?

A

Previous CABG, VSD, MVP with or without murmur do not require antibiotic prophylaxis. Prosthetic valves do require antibiotic prophylaxis.

118
Q

Following acute rheumatic fever, how many years on average does it take for valvular dysfunction to occur?

A

Symptoms of valvular dysfunction generally take 20 years to occur after acute rheumatic fever.

119
Q

What are the major prognostic factors after valve surgery?

A

The major prognostic factors after valve surgery are ejection fraction, degree of symptoms, and type of valve surgery (valve repair is better than replacement).

120
Q

Describe the abnormal heart sounds found in AS, chronic AR, and MS.

A

Aortic stenosis presents with systolic murmur with possible thrill at suprasternal notch and paradoxically split S2. Chronic aortic regurgitation has an early diastolic, blowing, decrescendo murmur at the 3rd intercostal space with the patient leaning forward and exhaling. AR may also be accompanied by a low-pitched, late diastolic rumble (Austin Flint murmur). Mitral stenosis is associated with an opening snap and a low-pitched diastolic murmur at the apex.

121
Q

What is the treatment sequence for atrial flutter?

A

The most effective treatment for atrial flutter is DC cardioversion. If patient is unstable always shock. If patient repeatedly reverts back to atrial flutter do not continue to shock. IV ibutilide is most effective for nonemergent medical cardioversion. Procainamide, flecainide, and propafenone can also be used. Radiofrequency ablation can cure most types of atrial flutter.

122
Q

What procedure can cure the most common types of atrial flutter with 85-95% success rate?

A

Radiofrequency ablation can cure most types of atrial flutter with 85-95% success.

123
Q

In what circumstances is immediate DC cardioversion indicated for A-fib?

A

Patients with A-fib with hemodynamic instability, ongoing myocardial ischemia, symptomatic hypotension, or heart failure should undergo immediate DC cardioversion.

124
Q

What can happen after DC cardioversion to the patient who has A-fib with a slow rate? What intervention prevents this complication?

A

A patient with slow A-fib may have sinus node dysfunction and may develop asystole after DC cardioversion. To prevent this insertion of a temporary pacemaker should be done before cardioversion.

125
Q

According to the 2013 guidelines, what HR is an acceptable target for patients with A-fib and stable ventricular function? For others, how is strict control of heart rate defined?

A

An acceptable heart rate target for atrial fibrillation is <110 bpm. Strict control of heart rate is defined as 80-110bpm.

126
Q

What medication should you use to prevent postoperative A-fib in patients undergoing cardiac surgery?

A

For patients undergoing cardiac surgery a beta-blocker may be used to prevent postoperative A-fib.

127
Q

How is the CHA2DS2-VASc score calculated? At what score should you treat with warfarin/NOACs (unless contraindicated)?

A

CHA2D2-VASc is calculated based on CHF, HTN, age (>75yo = 2 pts.), diabetes, prior stroke (2 pts.), vascular disease, age (65-74 = 1 pt.), and sex. A score of 2 points or greater is an indication for anticoagulation.

128
Q

In what patient group is MAT found?

A

MAT is most commonly found in patients with chronic pulmonary disease.

129
Q

What is the treatment for acute A-fib in WPW?

A

Verapamil and digoxin must be avoided in acute A-fib in WPW patients. Instead they should receive IV procainamide, ibutilide, or amiodarone.

130
Q

On an ECG, PVCs are often followed by what type of pause?

A

PVCs are followed by a compensatory pause because they do not reset the SA node.

131
Q

Ventricular tachycardia is defined as >3 sequential PVCs occurring at what bpm?

A

VT is >3 sequential PVCs occuring at a rate of >100 bpm.

132
Q

List the ECG criteria consistent with VT.

A

The ECG criteria for VT are: AV dissociation, fusion and capture beats, northwest axis, positive or negative concordance in the precordial leads, QRS width of >140 msec with RBBB, and QRS width of >160 with LBBB.

133
Q

With what type of tachycardia should you never use verapamil?

A

Never use verapamil for any wide complex tachycardia in the emergency setting as 30% of those with VT will rapidly deteriorate.

134
Q

ICDs are recommended for primary prevention in what situations with ischemic and nonischemic cardiomyopathy patients?

A

ICD placement is indicated for survivors of cardiac arrest due to VT/V-fib, structural heart disease and spontaneous, sustained VT (>30 sec) whether hemodynamically stable or unstable, syncope patients with sustained VT or V-fib induced at electrophysiology study, post-MI patients with EF <35% more than 40 days after MI, patients with nonischemic cardiomyopathy with EF <35% who are in the NYHA functional class II or III, or patients with nonsustained VT due to prior MI, LVEF <40% and inducible VF or sustained VT at EP study.

135
Q

Which antiarrhythmic drugs prolong the QT interval?

A

Class Ia (quinidine, procainamide, and disopyramide) and class III antiarrhythmics (sotalol, dofetilide, and amiodarone) can cause QT prolongation.

136
Q

What is the treatment for torsades de pointe?

A

Treat torsades de pointes with DC cardioversion, magnesium sulfate 2-4 grams IV over 10-15 minutes, correction of hypokalemia, and correction of bradycardia. Never use class Ia or class III antiarrhythmics to treat torsades de pointes.

137
Q

Under what conditions is permanent pacing recommended?

A

In the absence of symptoms, permanent pacing is recommended for complete heart block and advanced (not Wenckebach) second degree AV block.

138
Q

How long do you have to wait for an antiarrhythmic to reach steady-state therapeutic levels?

A

It can take an antiarrhythmic drug 4-5 half-lifes to achieve steady-state therapeutic levels.

139
Q

When is it okay to use verapamil; when is it not okay

A

Verapamil can be used to control ventricular response in A-fib or atrial flutter, in MAT, for SVT, and for HTN. Verapemil should not be used in A-fib/atrial flutter with WPW, wide complex tachycardias, and with beta-blockers.

140
Q

Which antiarrhythmic drug can cause lupus?

A

Procainamide can cause drug-induced lupus.

141
Q

Name the side effects seen with amiodarone.

A

Amiodarone has many potential side effects owing to its high iodine concentration. These include hyper-/hypothyroidism, corneal deposits (seen in 98% of patients), pulmonary fibrosis, grey skin, and sun sensitivity.

142
Q

What determines a toxic level of digoxin?

A

Digoxin toxicity causes generalized symptoms including confusion, nausea, vomiting, vague abdominal pain, and visual changes. Digoxin toxicity is determined by ECG changes rather than serum levels.

143
Q

For what condition is the treatment of choice radiofrequency ablation?

A

Radiofrequency ablation is the treatment of choice for WPW syndrome.

144
Q

What is the most common cause of syncope?

A

Vasovagal syncope, the common faint, is the most common cause of syncope.

145
Q

Explain how you approach the diagnostic workup in a patient with probable neurocardiogenic (vasovagal) syncope.

A

If the history is typical for vasovagal syncope, and it is the first episode in a young patient with no suspected heart disease, the patient can be reassured and sent home.

146
Q

What are the tests used to workup high-risk patients with syncope?

A

Patients with high-risk syncope should be admitted for possible coronary angiography and EP study.

147
Q

What are the risk factors for sudden death in patients with HCM?

A

Risk factors for sudden death in patients with HCM include septal thickness >30 mm, personal history of syncope, family history of sudden death in 1st degree relative, NSVT on Holter monitor, failure to augment systolic BP on exercise tolerance testing.

148
Q

What are the 3 main medications used in the treatment of HCM?

A

The 3 main medications used to treat HCM are beta-blockers, disopyramide, and IV phenylephrine (to treat HCM patients with hypotension who do not respond to fluids).

149
Q

What auscultatory finding is pathognomonic for constrictive pericarditis?

A

A pericardial knock in early diastole is pathognomonic for constrictive pericarditis.

150
Q

What are some causes of restrictive cardiomyopathy?

A

Causes of restrictive cardiomyopathy include amyloidosis, sarcoidosis, hemochromatosis, and lipid storage diseases.

151
Q

List some of the etiologies of dilated cardiomyopathy.

A

Causes of dilated cardiomyopathy include familial cardiomyopathies (noncompaction), idiopathic (mostly viral), obesity, diabetes, hyperthyroidism, acromegaly, alcohol, cocaine, cancer chemotherapy, ephedra, tachycardia-induced, amphetamines, and anabolic steroids.

152
Q

In the 2013 ACC/AHA guidelines, what are the newly defined 2 major subdivisions of heart failure?

A

In the 2013 ACC/AHA guidelines the categories of HFrEF and HFpEF were introduced.

153
Q

Define stage A through stage D heart failure (ACC/AHA classification). What are the goals of therapy at each of these stages?

A

Stage A heart failure includes patients with risk factors for HF but no structural heart disease or symptoms of HF; goal is to treat the conditions the lead to HF. Stage B patients have structural heart disease but no signs/symptoms of HF; goal is prevention of HF symptoms and further cardiac remodeling. Stage C have structural heart disease and present or prior symptoms of HF; goals are to control symptoms, patient education, improved quality of life, and prevention of hospitalizations and mortality. Stage D patients have marked symptoms at rest; goals are reduced symptoms, reduced hospitalizations, improved quality of life, and establishment of goals of care.

154
Q

What is the sequence of drugs to treat HF based on ACC/AHA stages?

A

For stage B HF use ACEIs/ARBs and beta-blockers. For stage C loop diuretics, aldosterone inhibitors, and hydralazine/nitrates are used.

155
Q

What are the most common causes of low output HF?

A

The most common causes of HFrEF are coronary artery disease (40-60%), dilated cardiomyopathy (30%), valvular disease (15%), and HTN (10%).

156
Q

What factors result in poor prognosis in HF?

A

Factors that correspond to a worse prognosis in HF include: low EF, low sodium, CKD, anemia, elevated troponin, high BNP, increased width of QRS, persistent sinus tachycardia, poor functional capacity, and high norepinephrine and catecholamine levels.

157
Q

What is the sequence of events that worsens HF?

A

Low CO leads to low renal perfusion leads to high renin leads to high angiotensin I leads to high angiotensin II leads to high aldosterone leads to retention of sodium leads to retention of water leads to high filling pressure leads to exacerbation of HF.

158
Q

When are beta-blockers started in the treatment of HF?

A

Current guidelines recommend addition of a beta-blocker at any stage of HF once adequate diuresis has been achieved and IV diuretics have been discontinued.

159
Q

With what type of HF do aldosterone antagonists prolong survival?

A

Aldosterone antagonists reduce morbidity and prolong survival in HFrEF and NYHA class II-IV.

160
Q

True or false? Digoxin can be beneficial in HFrEF patients to decrease hospitalizations for HF.

A

True, digoxin can be beneficial in HFrEF patients to reduce hospitalizations, but it does not improve survival.

161
Q

True or false? Ivabradine can be beneficial in stable HF patients to decrease hospitalizations for HF.

A

True, ivabradine can reduce hospitalizations, but it has not been shown to improve survival.

162
Q

In what population is hydralazine + isosorbide dinitrate beneficial?

A

Hydralazine + isosorbide has been shown to reduce morbidity and mortality in African Americans with HFrEF in NYHA class III-IV.

163
Q

Which patients with chronic HF should receive anticoagulation?

A

Anticoagulation is recommended for HF patients with A-fib and one other risk factor as well as those with a cardioembolic source (history of embolism or mobile left ventricular thrombus).

164
Q

CRT is indicated for which HF patients?

A

CRT is indicated for patients with EF <35%, sinus rhythm, LBBB with QRS duration >150 msec, and NYHA class II-III or ambulatory patients with NYHA class IV.

165
Q

Know all drugs for emergency treatment of severe HF.

A

Options for emergency treatment of severe HF include: dobutamine, milrinone, dopamine, mechanical circulatory support, and revascularization.

166
Q

What does dopamine do at low doses (<2 mcg/kg/min)? At doses 2-5 mcg/kg/min?

A

Low dose dopamine stimulates dopaminergic receptors and causes mesenteric dilation. At doses of 2-5 mcg/kg/min, dopamine has a predominantly beta-agonist effect leading to positive inotropy and increased renal perfusion. At doses >10 mcg/kg/min it has alpha-agonist effects and causes vasoconstriction.

167
Q

True or false? Mechanical circulatory support is beneficial in selected patients with stage D HFrEF in whom definitive management (cardiac transplantation) or cardiac recovery is anticipated or planned.

A

True, MCS is beneficial in selected stage D HF patients who are expected to recover or are candidates for definitive management.

168
Q

What are some causes of nonconstrictive pericarditis? What ECG changes can you see?

A

Causes of nonconstrictive pericarditis include idiopathic (90%, mostly viral), connective tissue diseases, sepsis, renal failure, cancer, postradiation, hypothyroidism, MI, open heart surgery, and certain drugs (procainamide and hydralazine).

169
Q

What are the 2 clinical hallmarks of constrictive pericarditis?

A

Two clinical hallmarks of constrictive pericarditis are 1) Kussmaul sign (lack of normal decrease in JVD with inspiration) and 2) large right sided x and y descents of jugular veins.

170
Q

When is the measured diastolic pressure in all four chambers equal?

A

Equalization of diastolic pressure in all four chambers is seen in both cardiac tamponade and constrictive pericarditis.

171
Q

How is BNP used to differentiate constrictive pericarditis for restrictive cardiomyopathy?

A

BNP is elevated in restrictive cardiomyopathy but not in constrictive pericarditis.

172
Q

What treatments can be helpful in recurrent pericarditis?

A

Colchicine and NSAIDs can be used to treat recurrent pericarditis. Steroids should not be used as they increase morbidity and recurrence rates.

173
Q

Name the 3 hallmarks of cardiac tamponade.

A

Three hallmarks of cardiac tamponade are: 1) hypotension and muffled heart sounds, 2) pulsus paradoxus, and 3) jugular venous distension with no collapse during diastole.

174
Q

What is the most common congenital abnormality found initially in adults?

A

Ostium secundum ASD is the most common congenital heart abnormality found initially in adults.

175
Q

True or false? Ostium secundum ASD often has right axis deviation and/or RBBB on ECG.

A

True, ostium secundum ASD presents with RBBB and RAD.

176
Q

When should surgery be performed for a secundum ASD?

A

Closure of ASD should be done when there is >2:1 left-to-right shunt as this will lead to increased pulmonary vascular resistance and complications.

177
Q

What type of cyanosis would you expect to see in someone with a PDA?

A

Differential cyanosis with clubbed toes but normal fingers may be seen in PDA.

178
Q

What is the most common congenital defect in children?

A

VSD is the most common congenital heart defect diagnosed in children.

179
Q

What are the 2 most common causes of sudden cardiac death in an exercising young person? What 3rd cause do you consider in young women?

A

The most common cause of sudden cardiac death in an exercising young person is hypertrophic cardiomyopathy with anomalous coronary anatomy being the second most common cause.

180
Q

What is the only effective treatment for Eisenmenger syndrome?

A

Heart-lung transplant is the only effective treatment for Eisenmenger syndrome.

181
Q

What are the 2 cardiac-related absolute contraindications to pregnancy?

A

The two cardiac absolute contraindications to pregnancy are pulmonary hypertension and Eisenmenger syndrome.

182
Q

True or false? Warfarin is not contraindicated at any time during pregnancy.

A

False, warfarin is contraindicated in the 1st trimester of pregnancy.

183
Q

Does a positive deflection on ECG tracing indicate the depolarization wave is moving toward or away from the lead?

A

A positive deflection on ECG means that the impulse is moving toward the lead.

184
Q

How do you very quickly evaluate the QRS axis on ECG?

A

QRS axis is best assessed by looking at leads I and aVF.

185
Q

What are the causes of left axis deviation?

A

Left axis deviation is usually due to LAFB and, therefore, a marker for CAD.

186
Q

What are the causes of right axis deviation?

A

Causes of right axis deviation include left posterior hemiblock, RVH, acute or chronic RV overload syndromes, and pulmonic stenosis.

187
Q

Does RAD always warrant additional workup in an adult?

A

RAD can be normal in children, but in adults it should prompt further workup.

188
Q

Describe one way to determine heart rate from a 12-lead ECG.

A

The heart rate can be calculating using 300/number of large boxes between QRS complexes. Alternatively, one can calculate it using 1500/RR interval.

189
Q

Name all of the causes of prolonged QT intervals.

A

Prolonged QT can be caused by genetic syndromes, tricyclic overdose, hypocalcemia, hypomagnesemia, hypokalemia, starvation, CNS insult, hypothermia, type Ia and III antiarrhythmics.

190
Q

What are the P wave findings for RAH? For LAH?

A

RAH leads to peaked P waves in II and large positive P wave in V1. LAH causes a widened, notched P wave in II and a biphasic P wave in V1.

191
Q

What are the 5 causes of an R wave in lead I?

A

R wave in I may be caused by RBBB, RVH, WPW pattern, prior RV infarct, and Duschenne muscular dystrophy.

192
Q

What does failure of R waves to progress across the precordial leads indicate?

A

Failure of R waves to progress across precordium is indicative of prior anterior MI.

193
Q

When are peaked T waves seen?

A

Peaked T waves are seen in hyperkalemia, hyperacute MI, intracerebral hemorrhage, and in leads V1-V2 in evolving posterior MI.

194
Q

When are focal flipped T waves seen?

A

Focal flipped T waves are seen in ischemia, in V1-V2 with RBBB, RVH, and RV HTN, V1-V2 with LVH, lateral leads with LBBB, precordial leads with LVH with strain.

195
Q

U waves indicate a predisposition to what serious condition?

A

A predominant U wave suggests a predisposition to torsades de pointes.

196
Q

What is the significance of a negative U wave?

A

Negative U waves, even with otherwise normal ECG, are caused by ischemia, HTN, AV valve disease, and RVH.

197
Q

What are the common causes of U waves?

A

Common causes of U waves are hypokalemia, bradycardia, digitalis, and amiodarone.

198
Q

What are the 3 main common causes of ST-segment elevation?

A

The 3 main causes of ST-segment elevation are acute MI, Prinzmetal angina, and pericarditis.

199
Q

What are the causes of ST-segment depression?

A

ST-segment depression occurs with subendocardial ischemia, in V1-V2 with posterior MI, LVH with strain, isolated RV infarct, RVH, digitalis toxicity, and hypokalemia.

200
Q

What are the ECG criteria for LVH? RVH?

A

One commonly used criteria for LVH is “S in V1 + the R in V5 is >35mm. If there is left axis deviation, use S in III >15mm.

201
Q

What ECG changes would you expect to see in the presence of a large pulmonary embolism causing acute cor pulmonale?

A

A large PE causing acute cor pulmonale leads to S1Q3T3.

202
Q

In LBBB, the left side of the septum depends on what to depolarize?

A

In LBBB the left side of the septum depends on myocardial conduction to depolarize.

203
Q

What do you see on an ECG in LBBB? RBBB?

A

LBBB leads to wide QRS with SS’ in V1 and RR’ in V6. In RBBB there is RSR’ in V1 and wide terminal S wave in V6.

204
Q

What is so serious about a recent MI and the development of a bifascicular block?

A

A recent MI with development of a bifascicular block portends a high risk of development of complete AV block.

205
Q

What is the difference between an ectopic beat and an escape beat?

A

An ectopic beat comes early and an escape beat comes late.

206
Q

What are the ECG findings with A-fib?

A

ECG findings of A-fib are absence of P waves and variable RR intervals (“irregularly irregular”).

207
Q

What are the ECG findings with MAT?

A

MAT is an irregularly, irregular rhythm with rate 100-130 and varying P waves.

208
Q

What are the ECG findings with PVC?

A

A PVC is a QRS complex that occurs earlier than expects, is wider than normal, and is higher amplitude than normal. It obscures the P wave and leads to a compensatory pause. THe T wave is also inverted.

209
Q

Describe the sequence of ECG changes with the different phases of an MI.

A

The sequence of ECG changes in acute MI are: 1) T wave changes, 2) ST-segment changes, then 3) development of Q waves.

210
Q

What ECG changes occur with a septal MI? Anterior? Lateral?

A

Septal MI leads to ECG changes in V1-V2. Anterior MI has ECG changes in V3-V4. Lateral MI has ECG changes in V5-V6 and I and aVL.

211
Q

What conditions can cause diffuse inverted T waves?

A

Diffuse inverted T waves signify ischemia, pericarditis, drugs, metabolic abnormalities, or CNS insult.

212
Q

What conditions can cause a prolonged QT?

A

Prolonged QT is caused by drug effect, hypocalcemia, hypomagnesemia, and CNS insult.

213
Q

AV node dysfunction is seen in which type of MI? What about bifascicular block?

A

AV node dysfunction is seen with inferior MI or with digitalis and verapamil toxicity.

214
Q

What conditions cause resting ST elevation?

A

Resting ST-segment elevation is due to acute MI, spontaneous spasm of coronary artery, and pericarditis.