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EOR - Internal Med > Internal Med - Cardio > Flashcards

Internal Med - Cardio Flashcards

1
Q

Stable angina sx

A

Stable angina is a clinical syndrome of precordial discomfort or pressure due to transient myocardial ischemia predictably (versus unstable angina which doesn’t follow a pattern) exacerbated by physical activity and relieved by rest or sublingual nitroglycerin

Myocardial ischemia is often experienced as a sensation of discomfort lasting 5-15 minutes, described as dull, aching or pressure

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2
Q

Stable angina workup

A

> 70 % stenosis
Normal troponin and CK-MB
Resting ECG is normal
During anginal episode abnormal ECG with greater than 1 mm ST depression +/- T wave

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3
Q

Stable angina tx

A

Treatment may include aspirin, nitrates, β-blockers, Ca channel blockers, ACE inhibitors, statins, and coronary angioplasty or coronary artery bypass graft surgery

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4
Q

Unstable angina sx

A
  • Angina at rest (most common)
  • New onset of angina symptoms
  • Increasing pattern of pain in previously stable patient

Unstable angina is suspected when the pain is less responsive to NTG, lasts longer, and occurs at rest or with less exertion than previous episodes of angina. Such changes are termed unstable angina and require prompt evaluation and treatment

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5
Q

Unstable angina dx

A

Gold std= Angio

EKG - Can be normal

Stress test - If a patient has a normal resting ECG and can exercise, exercise stress testing with ECG is done

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6
Q

Angina tx

A

Modification of risk factors (smoking, BP, lipids)

  • Antiplatelet drugs (aspirin and/or clopidogrel or ticagrelor)
  • β-Blockers
  • Nitroglycerin and Ca channel blockers for symptom control
  • Revascularization if symptoms persist despite medical therapy
  • ACE inhibitors and statins
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7
Q

Prinzmetal variant angina

A

Cardiac chest pain (angina), that occurs at rest and usually happens at night or early morning hours

  • Prinzmetal variant angina: Transient coronary artery vasospasms within normal coronary anatomy or at site of atherosclerotic plaque
  • Variant angina is characterized by a transient, abrupt, marked reduction in the luminal diameter of a coronary artery which leads to symptomatic myocardial ischemia
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8
Q

Biggest RF of prinzmetal angina

A

Smoking #1, substance abuse, cocaine

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9
Q

Dx of prinzmetal anginga

A

Angiography

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10
Q

Tx of Prinzmetal Variant Angina

A

itrates and calcium channel blockers.

  • Calcium channel blockers are effective prophylactically to treat coronary vasospasm associated with variant or Prinzmetal’s angina.

Use of a beta-blocker such as propranolol is contraindicated in Prinzmetal’s angina

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11
Q

Afib presents as

A

low-amplitude fibrillatory waves without discrete P waves and an irregularly irregular pattern of narrow QRS complexes.

Palpitations

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12
Q

Aflutter presents as

A

Regular,sawtooth pattern, atrial rate 250-350 BPM, narrow QRS complex

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13
Q

Tx of Afib

A

Rate control - below 110 beats per minute

Calcium channel blocker (diltiazem, verapamil) or beta-blocker (metoprolol)

Rhythm control

Duration of Afib < 48 hours- cardioversion, amiodarone (obtain transesophageal echo (TEE) to determine if a clot is present prior to cardioversion)

  • Duration > 48 hours - anticoagulate for 21 days prior to cardioversion
  • Unstable Patient with rapid ventricular rate = synchronized cardioversion

Anticoagulation is determined by CHA2DS2-VASc

Direct oral anticoagulants or DOAC (eg, dabigatran, rivaroxaban, apixaban, or edoxaban) rather than warfarin for most patients in whom oral anticoagulant therapy is chosen

  • Warfarin for mechanical heart valves, mitral stenosis, unacceptable increase in cost, EGFR < 30 ml/min, on certain medications (phenytoin or certain antiretroviral therapy)
  • Adjusted-dose warfarin target INR is 2.5 (range 2–3)
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14
Q

Sx of sick sinus syndrome

A

dysfunction in the sinus node’s automaticity and impulse generation

  1. Sinus bradycardia: Sinus rhythm with a resting heart rate of < 60 bpm in adults, or below the normal range for age in children
  2. Sinus pause: pause
  3. Sinus arrest: pause > 3 seconds
  4. Tachy-Brady Syndrome: Episodes of alternating sinus tachycardia and bradycardia
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15
Q

MCC of sick sinus syndrome

A

Idiopathic SA node fibrosis ; Other causes → Drugs or inflammatory/infiltrative disorders

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15
Q

MCC of sick sinus syndrome

A

Idiopathic SA node fibrosis ; Other causes → Drugs or inflammatory/infiltrative disorders

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16
Q

Tx of Sick Sinus Syndrome

A

Pacemaker

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17
Q

MC type of cardiomyopathy

A

Dilated

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18
Q

What heart sound is associated with dilated cardiomyopathy?

A

S3

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19
Q

MCC of dilated cardiomyopathy

A
  • Causes include viral infections, genetic abnormalities (25% to 30%), hypertension, excessive alcohol consumption, postpartum state, chemotherapy toxicity, endocrinopathies, and myocarditis; it may also be idiopathic
    • Dilated cardiomyopathy is characterized by a reduced strength of contraction and systolic dysfunction. The result is right and/or left ventricular enlargement and progressive heart failure with increased risk for sudden cardiac death
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20
Q

Dx of dilated cardiomyopathy

A

Echo = Most definitive

EKG = nonspecific ST/T wave changes

CXR = Balloon - like heart, cardiomegaly, pulmonary congestion

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21
Q

Tx of dilated cardiomyopathy

A

Tx like systolic heart failure → Bblockers + Ace + Loop Diuretic

*Add Digitalis to increase contractility

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22
Q

What will increase murmur intensity associated with HCOM?

A

The murmur associated with HCM is worsened by conditions that cause reduced ventricular volumes such as the Valsalva maneuver, sudden standing, and tachycardia

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23
Q

MCC of HCOM

A

Hypertrophic cardiomyopathy (HCM) is a congenital or acquired disorder characterized by marked ventricular hypertrophy with diastolic dysfunction

  • Myocardium gets sick, heavy, and hypercontractile
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24
Q

MC sudden death in young athletes

A

HCOM

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25
Q

What heart sound and what kind of murmur is heart with HCOM

A

S4 gallop and apical lift with a thick, stiff left ventricle

medium-pitched, mid-systolic crescendo-decrescendo murmur that decreases with squatting and increases with standing or Valsalva

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26
Q

How do you dx HCOM

A

Echo or MRI; EKG will show left ventricular hypertrophy

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27
Q

Tx for HCOM

A

β-blockers (metoprolol) and/or rate-limiting Ca channel blockers (usually verapamil) to decrease myocardial contractility and slow the heart rate and thus prolong diastolic filling and decrease outflow obstruction

  • Avoid nitrates and other drugs that decrease preload (eg, diuretics, ACE inhibitors, angiotensin II receptor blockers) because these decrease LV size and worsen LV function
  • Digoxin is contraindicated since it increases the force of contraction which can increase the obstruction
  • Consider an implantable cardioverter-defibrillator for patients with syncope or sudden cardiac arrest
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28
Q

MCC of Restrictive cardiomyopathy

A

History of an infiltrative process ⇒ caused by deposition into or between myocardial cells ⇒ amyloidosis, hemochromatosis, sarcoidosis, scleroderma, fibrosis, radiation and chemotherapy

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29
Q

What heart sounds are heart with restrictive cardiomyopathy?

A
  • Think diastolic heart failure: S4 and thick stiff ventricle
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30
Q

Dx of restrictive cardiomyopathy

A

Echo + cardio cath

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31
Q

Tx of restrictive cardiomyopathy

A

Tx underlying cause

Diuretics ; ACE/ARB;CCB

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32
Q

NY heart failure classification for congestive heart failure

A
  • Class 1: no limitation of physical activity
  • Class 2: slight limitation physical activity; comfortable at rest
  • Class 3: marked physical limitation; comfortable at rest
  • Class 4: can’t carry on physical activity; anginal syndrome at rest
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33
Q

MCC of congestive heart failure

A

MC cause: CAD, HTN, MI, DM – LV remodeling ⇒ dilation, thinning, mitral valve incompetence, RV remodeling

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34
Q

Sx of congestive heart failure

A
  • exertional dyspnea ⇒ rest, chronic nonproductive cough, fatigue, orthopnea, nocturnal dyspnea, nocturia
  • Signs: Cheyne-stokes breathing, edema, rales, S4 (diastolic HF, preserved EF); S3 (systolic; reduced EF); JVD >8cm, cyanosis, hepatomegaly, jaundice
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35
Q

Dx of CHF

A

ECHO → Most useful imaging (EF determines prognosis)

CXR → Kerley B lines, cardiomegaly, pleural effusion, pulmonary edema

BNP>100 = CHF is likely

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36
Q

Tx of CHF

A

Systolic left heart failure: Treat with Ace Inhibitor + βblocker + Loop Diuretic

Diastolic heart failure: Ace inhibitor + βblocker or CCB (do not use diuretics in stable chronic diastolic failure)

ACEI need to be used ASAP /decrease comorbidity and mortality

Three specific beta-1 selective drugs in reducing mortality from heart failure:

  • bisoprolol
  • carvedilol
  • metoprolol succinate
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37
Q

1 killer in the US and worldwide

A

Coronary artery dz (Stemi + Nstemi)

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38
Q

Most sensitive and specific cardiac marker

A

TROPONIN; Appears at 4-8hours peaks 12-24 hours and lasts for 7-10 days

  • CK/CK-MB appears at 4-6 hours, peaks at 12-24 hours and lasts for 3-4 days
  • Myoglobin (Mb): appears at 1-4 hours, the peak is 12 hours, and returns to baseline levels within 24 hours.
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39
Q

Tx of NSTEMI

A

Obtain EKG within first 10 minutes

  1. Morphine (IV iw pain not relieved by NTG)
  2. Oxygen (4L/min)
  3. Nitroglycerine (sublingual)
  4. Aspirin (160-325 mg)
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40
Q

Tx of STEMI

A

Reperfusion therapy is the mainstay of treatment in STEMI especially within 12 hours of symptom onset

  1. PCI (Percutaneous Coronary Intervention) GOLD STANDARD - best if within 3 hours of sx onset (especially 90 minutes) PCI is superior to thrombolytics
  2. Thrombolytic therapy - Done if no access to cath lab or surgery is contraindicated
    1. TPA
      1. Streptokinase
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41
Q

Primary prevention of CAD

A

Smoking cessation, lifestyle (BP, LDL/HDL, obesity)

  • Primary prevention = platelet inhibitors (Aspirin, etc.) = cornerstone
  • Secondary prevention = aspirin, β-blockers, ACE-I/ARB, statins; nitro if symptomatic
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42
Q

What is the MOA for atherosclerotic dz

A
  • Foam cells are macrophages that gobble up lipids in the wall; it then dies off and stays there and becomes a foam cell; when it dies it releases cytokines that attract more macrophages to the area ⇒ plaque clot
  • Fibrous plaque forms over lipid core: Complete clot – ST-elevation MI; Incomplete clot – unstable angina/NSTEMI
    • Vulnerable plaque is easy to rupture; thick plaque is stable
    • Adhesion, activation, aggregation, propagation of clot, platelet adherence
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43
Q

What are the bugs associated with Acute, Subacute, IVDU, and Prosthetic valve endocarditis

A

Acute bacterial endocarditis: Infection of normal valves with a virulent organism (S. aureus)

Subacute bacterial endocarditis: Indolent infection of abnormal valves with less virulent organisms (S. viridans)

Endocarditis with intravenous drug users - Staphylococcus aureus

Prosthetic valve endocarditis - Staphylococcus epidermidis

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44
Q

MC bug of endocarditits

A

Strep Viridans

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45
Q

Sx of endocarditis

A
  • Splinter hemorrhages in fingernail beds
  • Osler nodes painful lesions on fleshy portions of extremities
  • “Roth spots” retinal hemorrhages
  • Janeway lesions (cutaneous evidence of septic emboli)
  • Palatal or conjunctival petechiae
  • Splenomegaly
    • hematuria (due to emboli or glomerulonephritis)
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46
Q

Dx of endocarditis

A

Duke Criteria - Major = 2 positive blood cultures, positive echo (will show vegetations), new murmur (valve regurge)

Duke Criteria - Minor = Fever, predisposing heart condition, vascular phenomena, immunological phenomena

TEE = Gold Standard

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47
Q

Tx of Endocarditis

A
  • Empiric treatment: IV vancomycin or ampicillin/sulbactam PLUS aminoglycoside
  • Prosthetic valve: Add rifampin
  • High-Risk patients prophylaxis for procedures: Amoxicillin - 2 g 30-60 minutes before the procedure
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48
Q

Diastolic Heart Murmurs

A

Ass rim, pussy rim, makes sexy tits sweat

Aortic Rergurg

Pulmonic Regurg

`Mitral Stenosis

Tricupsid stenosis

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49
Q

harsh systolic ejection crescendo-decrescendo at the right upper sternal border with radiation to neck and apex

A

Aortic Stenosis

50
Q

blowing holosystolic murmur at the apex with split S2 radiating to the left axilla

A

Mitral regurgitation

51
Q

midsystolic ejection click heard best at the apex

A

Mitral Valve Prolapse

52
Q

Four groups most likely to benefit from Statin therapy

A
  • Patients with any form of clinical atherosclerotic cardiovascular disease (ASCVD)
  • Patients with primary LDL-C levels of 190 mg per dL or greater
  • Patients WITH diabetes mellitus, 40 to 75 years of age, with LDL-C levels of 70 to 189 mg per dL
    • Patients WITHOUT diabetes, 40 to 75 years of age, with an estimated 10-year ASCVD risk ≥ 7.5%
53
Q

Optimal lipid goals

A

LDL < 100 optimal

TOTAL< 200 desirable

HDL> 60 protective

54
Q

Primary HTN is defined as

A

rimary hypertension is defined as a resting systolic BP ≥ 130 or diastolic BP ≥ 80 on at least two readings on at least two separate visits with no identifiable cause

55
Q

What is the target BP for pts with comorbities

A
  • Targets for patients with comorbidities: < 130/80
56
Q

For NON-BLACK patients, including those with diabetes: Initial treatment should be with either:

A
  • ACE inhibitor or ARB
  • Long-acting calcium channel blockers (most often a dihydropyridine such as amlodipine)
  • or a thiazide-like diuretic (chlorthalidone or indapamide)

For stage 2 HTN: the recommendation → 2 BP-lowering medications of different classes

57
Q

For BLACK adults 2 or more medications are recommended to achieve a target of less than 130/80 mm Hg

A

Thiazide-type diuretics and/or calcium channel blockers are more effective in black adults at lowering BP alone or in multidrug regimens

58
Q

Amlodipine is what class of antihypertensive?

A

CCB

59
Q

Which CCB are used for rate control?

A

erapamil and diltiazem

60
Q

Which CCB are used for rate control?

A

erapamil and diltiazem

61
Q

Which class of antihypertensive is used for HTN and BPH?

A

a-blockers (-zosin drugs)

62
Q

What classifies htn urgency vs emergency?

A

Hypertensive emergency:

  • BP usually >180/120 WITH impending or progressing end-organ damage

Hypertensive Urgency:

  • BP usually > 180/120 WITHOUT signs of end-organ damage
63
Q

Tx of htn emergency

A

sodium nitroprusside (drug of choice)

64
Q

Tx of htn urgency

A

clonidine (drug of choice)

65
Q

MCC of myocarditis

A

viral infection → etiologies: bacterial, parasitic, cardiotoxin, systemic disorders, radiation, hypersensitivity

66
Q

Sx of myocarditis

A

Symptoms include fatigue, fever, chest discomfort, dyspnea, palpitations, tachycardia disproportionate to fever or discomfort

** A severe case can weaken the heart, which can lead to heart failure, abnormal heartbeat, and sudden death

67
Q

Dx of myocarditis

A

endomyocardial biopsy = gold standard; clinical presentation, cardiovascular MRI; echo = decreased ventricular EF with hypokinesis

68
Q

Tx of myocarditis

A

supportive, heart failure treatment prn, antidysrhythmic prn

69
Q

MCC of pericarditis

A

SLE, uremia, coxsackievirus, TB, RA, neoplasm, drug, radiation, scleroderma, MI, open-heart surgery, radiotherapy

70
Q

MOA of pericarditis

A

inflammation of pericardial sac; often ⇒ pericardial effusion

71
Q

Sx of pericarditis

A
  • Chest pain that is relieved by sitting and/or leaning forward
  • A pericardial friction rub is heard best with patient upright and leaning forward:
    • Worse when the patient is supine and during inspiration
    • Alleviated when the patient leans forward
72
Q

What is Dresslers syndrome?

A

pericarditis 2-5 days after an acute myocardial infarctions

73
Q

Which virus is MCC of pericarditis

A

Coxsackie virsu

74
Q

Dx of pericarditis

A

EKG will demonstrate diffuse, ST-segment elevations in the precordial leads

  • Echo may show pericardial effusion/tamponade
75
Q

Tx of pericarditis

A

Tx underlying dz

  • NSAIDs 7-14 days; steroids if sx > 48 hrs; abx to treat bacterial endocarditis; pericardiocentesis; head at 45 degrees
  • Dressler’s syndrome: pericarditis 2-5 days after acute MI
76
Q

6 Ps of peripheral vascular dz

A

pain, pulselessness, pallor, paresthesias, poikilothermia (inability to regulate temperature), paralysis

Caused by acute arterial embolism

77
Q

Ulcers from arterial insufficiency are painless or painful?

A

Painful

78
Q

Peripheral artery dz sx

A
  • Lower extremity atherosclerotic PAD is initially asymptomatic but typically progresses to claudication, ischemia, and pain with exercise
79
Q

Sx of peripheral artery disease

A
  • Femoral and distal pulses will be weak or absent; an aortic, iliac, or femoral bruit may be present.
  • Skin changes to the lower extremity include loss of hair, shiny atrophic skin, and pallor with dependent rubor
  • Severe, chronic disease results in numbness, tingling, and ischemic ulcerations, which may lead to gangrene.
  • Acute arterial occlusion threatens limb viability and results in the “6 Ps”: pain, pallor, pulselessness, paresthesias, poikilothermia, and paralysis
80
Q

Dx of intermittent claudication

A

An ankle-brachial index (ABI), which uses Doppler measurements to compare the BP in the upper and lower extremities, is a highly sensitive and specific test

** An ABI of ≤ 0.9 indicates significant disease

Angiography remains the gold standard study

81
Q

Tx of intermittent claudication

A

Stop smoking first line

Graduated exercise - walk to point of claudication, rest, then continue walking

Control HTN, DM, weight

ASA + clopidogrel (plavix → blood thinner)

Cilostazol → Vasodilator via platelet inhibition

Surgery → Angioplasty; Bypass grafting

82
Q

PE sign with phlebitis

A

Homan’s sign (calf pain w foot dorsiflexion)

83
Q

MCC rheumatic fever

A

Inflammatory reaction to strep throat infection

inflammatory immune response to Group A Strep, with the formation of antistreptolysin antibodies which react with proteins on the synovium, heart muscle, and heart valves

84
Q

Dx of rheumatic fever

A

2 major criteria or 1 major and 2 minor Jones criteria are required, along with evidence of preceding GAS infection

MAJOR:

Carditis

Chorea

Erythema marginatum

Polyarthritis

Subcutaneous nodules

MINOR:

Arthralgia

Elevated ESR or C-reactive protein

Fever

Prolonged PR interval (on ECG)

85
Q

Major vs Minor Jones criteria for Rheumatic Fever

A

Major = Carditis, chorea, erythema marginatum, polyarthritis, subcutaneous nodules

Minor = Arthralgia, elevated ESR/CRP, fever, prolonged PR on ECG

86
Q

Rheumatic fever MC affects which valve

A

Mitral valve

87
Q

Major: J♥NES

A

J oints - polyarthritis; ♥ - carditis; N odules (subcutaneous); E rythema marginatum; S ydenham’s chorea

88
Q

Tx of Rheumatic fever

A
  • Aspirin or another NSAID
  • Sometimes corticosteroids
  • Antibiotics
89
Q

Prophy against recurrent strep A infections

A

Pen G; alternatives → Pen V, Sulfadiazine; Erythromycin for PCN allergies

90
Q

Etiology of rheumatic heart disease

A

consequence of rheumatic fever characterized by inflammation and scarring of the heart valves

  • Most commonly affects the mitral valve > aortic valve > tricuspid valve
  • Etiology → at least 1 episode of acute rheumatic fever from group A streptococci
91
Q

Dx of rheumatic heart dz

A
  • Echocardiography → valvular abnormalities, including regurgitation or stenosis
  • Labs: ↑ anti-streptolysin O (ASO) titers
  • Histology: Aschoff bodies (granulomas with giant cells) on heart valves
92
Q

Tx of rheumatic heart dz

A
  • All patients with rheumatic heart disease should undergo prophylaxis with penicillin for the specified time period below
    • No evidence of carditis ⇒ 5 years or until age 21 (whichever is longer)
    • Evidence of carditis without valvular abnormalities ⇒ 10 years or until age 21 (whichever is longer)
    • Evidence of carditis and valvular abnormalities ⇒ 10 years or until age 40 (whichever is longer)
93
Q

Tx of aortic aneurysm

A

immediate surgical repair if >5.5cm or expands >0.5cm per year;

monitor annual if >3cm, q6mo >4cm; beta-blocker

94
Q

Tx of aortic dissection

A

ascending aorta = surgical emergency; descending: beta-blocker

95
Q

spontaneous / after trauma or IV/PICC lines – dull pain, erythema, induration of vein, palpable cord

A

Phlebitis/thrombitis

96
Q
A

Sx of Endocarditis

97
Q

PE findings in restrictive cardiomyopathy

A

Increased JVP, pericardial knock, Kussmaul sign, pulsus paradoxsus

98
Q

JNC 8 recommendations for BP goals for pts < 60 years or those with diabetes

A

Age < 60 years or those with diabetes: 140/90 mm Hg

99
Q

Ankle-brachial index (ABI) of <0.4 indicates

A

Ischemia

<0.9 indicates 50% stenosis

Hanging the foot over the side of the bed relieves pain in individuals with PAD because they are increasing the amount of blood flow and pressure to their lower legs by means of gravity.

100
Q

PE shows ↓ breath sounds + dull percussion + ↓ tactile fremitus

A

Pleural effusion

CXR will show blunting of the costophrenic angle

  • Can also use CT or US to diagnose
  • Most common causes
    • Transudate: heart failure
    • Exudate: infection > malignancy, PE
101
Q

MCC of pleural effusions

A
  • Most common causes
    • Transudate: heart failure
    • Exudate: infection > malignancy, PE
102
Q

How is orthostatic hypotension diagnosed?

A
  • Decrease in systolic blood pressure of 20 mm Hg
  • Decrease in diastolic blood pressure of 10 mm Hg
  • Inadequate physiologic response to postural changes
103
Q

Dx of Sarcoidoisis

A
  • Labs will show hypercalcemia and elevated serum ACE
  • CXR will show bilateral hilar adenopathy
  • Biopsy will show noncaseating granulomas
104
Q

Anterior vs Lateral MI locations

A

Anterior wall myocardial infarction is characterized by ST elevation in leads V1–V4, with reciprocal changes in the inferior leads (III and aVF)

105
Q

Polymorphic ventricular tachycardia is dx by

A

Prolonged QT interval → QTc interval > 480 ms with a syncopal episode, or > 500 ms in the absence of symptoms

106
Q

Cardiac electrical conduction system (how electricity goes through the heart)

A

SA node → AV node → bundle of His → bundle branches → Purkinje fibers

107
Q

At what age is statin therapy recommended if family hx of premature ASCVD

A
  • Age 20–39
    • Estimate lifetime risk to encourage lifestyle to reduce ASCVD risk
    • Consider statin if family Hx of premature ASCVD and LDL-C ≥ 160 mg/dL
108
Q

ECG findings in Wolff-Parkinson White Syndrome

A

ECG will show short PR, delta wave, wide QRS

109
Q

Definitive tx of WPW syndrome

A

Radiofrequency ablation

110
Q

MCC of WPW syndrome

A

Accessory pathway (bundle of kent) connecting atria to ventricles, bypassing AV node

111
Q

PE findings of constrictive pericarditis

A

pericardial knock, kussmaul sign, pulsus paradoxus

112
Q

Sx of Aortic stenosis

A

RF: Advancing age, DM, HTN

Sx → Dyspnea, chest pain, syncope

113
Q

PE findings of Aortic Stenosis

A

PE: Cresendo-decresendo systolic mumur radiating to carotids paradoxically split s2, s4 gallop; Murmur decreases with Valsava

114
Q

Soft S1 and a loud blowing holosystolic murmur

A

Mitral Valve Regurge

115
Q

The PR interval is longer than 0.2 seconds or one block on EKG.

A

First Degree AV Block

116
Q

progressive lengthening of PR interval then missed QRS complex

A

Type I Second Degree (Wenckebach)

117
Q

fixed PR interval with occasional dropped QRS complexes

A

Type II Second Degree (Mobitz)

118
Q

R and R’ (upward bunny ears) in V4-V6

A

Left bundle branch block

119
Q

R and R’ (upward bunny ears) in V1-V3

A

Right bundle branch block

120
Q

Heart unable to pump normally → blood flow through chambers obstructed → cardiac output decreases → hypotension → lower tissue perfusion → heart rate increase

A

Cardiac tamponade

121
Q

2 main causes of cardiac tamponade

A
  • Acute onset: trauma, myocardial infarction, aortic dissection, pericardial effusion
  • Slow onset: cancer, chronic inflammation, uremic pericarditis, hypothyroidism, connective tissue disease
122
Q

3 D’s in Becks Triad

A

Cardiac Tamponade

The 3 D’s: D istant heart sounds, D istended jugular veins, and D ecreased arterial pressure = Beck’s triad

Beck’s triad:

  1. Hypotension
  2. muffled heart sounds
  3. elevated neck veins (JVD)

EOR - Internal Med (9 decks)

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