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PANCE-Flashcards > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the first line therapy for Cardiogenic shock?

A

Dobutamine (Beta Agonist) is first line therapy

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2
Q

What is the most common organism involved in Acute pericarditis?

A

Coxsackie B Virus, Hep B, and CMV

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3
Q

What ECG signs are seen with acute pericarditis?

A

ST elevations, PR depression in most leads

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4
Q

WHat is Pulsus Paradoxus?

A

Classic finding in pericardial effusion

Abnormally large decrease in systolic BP (>10 mmHg) and pulse wave amplitude during inspiration

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5
Q

What CXR finding do you see with Acute pericarditis?

A

Water bottle heart, cardiomegaly

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6
Q

What is the gold standard for diagnosing Pericardial effusion? what confirms the dx?

A

Echo-shows fluid between layers of pericardium

Pericardiocentesis: confirms dx

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7
Q

What is cardiac tamponade? what is a common cause?

A

Emergency! Occurs when large pericardial effusion compresses the heart, or greatly reduces CO

common cause: Penetrating trauma to the heart

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8
Q

What are the s/s of cardiac tamponade?

A

Sharp, stabbing CP (worsened by deep breathing or coughing), dyspnea, nonproductive cough

PE: Beck’s Triad-JVD, Arterial hypotension, muffled heart sounds

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9
Q

What is the gold standard for diagnosing Cardiac tamponade?tx?

A

ECHO

Tx: urgen pericardiocentesis!! (by echo guidance)

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10
Q

What is COnstrictive pericarditis? What are the common causes?

A

Diffuse thickening of the pericardium with possible calcifications

Associated with TB, radiation therapy, cardiac surgery, or following viral pericarditis

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11
Q

What are the S/S of constrictive pericarditis? how is it tx?

A

Slowly progressive dyspnea and fatigue, weakness

PE: LE edema, Ascites, elevated JVP, pericardial Knock, + kussmaul sign (evidence of Rt heart failure)

Tx: NSAID, Corticosteroids, Colchicine, Pericardiectomy

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12
Q

What is Dressler syndrome?

A

Postmyocardial infarction Pericarditis

Occurs 2-5 days after infarction due to inflammatory rxn to transmural myocardial necrosis

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13
Q

What are the s/S of infective endocarditis?

A

New systolic murmur, Roth spots, osler nodes, Janeway lesions, splinter hemorrhages

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14
Q

How do you dx Infective endocarditis?

A

Transesophageal Echocardiogram (TEE)-may show vegetations on valves

Blood cultures: 3 sets at least 1 hour apart

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15
Q

What are the most common valves affected in infected endocarditis?

A

Mitral valve most commonly affected

Tricuspid valve most common in IV drug users

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16
Q

What are the most common organisms involved in infective endocarditis?

A

Native valves + IV drug users: Staph aureus

Prosthetic valves: Staph epidermidids

Subacute endocarditis: Streptococcus viridans

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17
Q

Enfective endocarditis: What abx are given while Blood culture is pending? If prosthetic valve? native valve, community? If MRSA?

A
  • Vancomycin + gentamycin
  • Prosthetic valve=Vanco + gentamycin + Rifampin
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18
Q

When does rheumatic fever occur and what are the most common valves involved?

A

Occurs 2-3 weeks following a beta-hemolytic Strep phargyngitis

  • Mitral valve-most common
  • Aortic valve
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19
Q

What are the signs and symptoms of Rheumatic fever?

A
  • Subcutaneous nodues on extensor surfaces
  • Sydenham’s chorea: involuntary movements
  • Erythema marginatum: painless pink rash with well defined edges; central clearing
  • PE: new murmur–mitral regurgitation
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20
Q

HOw do you diagnose Rheumatic fever? How to you treat?

A

Dx: + Antistreptolysin O (90%)

Tx: NSAIDs, beta-lactams, corticosterois

prophylaxis: Benzathine penicillin G q 4 weeks

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21
Q

What is the most appropriate initial diagnostic test in the evaluation of a patient with signs and symptoms consistent with stable angina? Tx?

A

Nuclear stress test

Tx: Sublingual nitroglycerin

(Will reduce effects of GERD and esophageal spasm as well)

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22
Q

What is Printzmetal angina?

A

Occurs in younger patients at rest; Squeezing CP, 2-5 minutes

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23
Q

What leads show an inferior wall MI? what artery is involved?

A

ST elevation in lead II, III, and aVF

Right coronary artery

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24
Q

What leads show a lateral wall MI? What artery is involved?

A

I, AVL, V5 and V6

LAD, LCA, and CFX

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25
Q

What leads show an anterior wall MI? artery?

A

V1-V4

LAD

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26
Q

What leads and arteries are involved in posterior wall MI?

A

V1 and V2

RCA, CFX

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27
Q

What leads and artery are involved in anterolateral MI?

A

V4-V6

CFX

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28
Q

What leads and artery are involved in Anteroseptal MI?

A

V1 and V2

LAD

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29
Q

What medications should you avoid in Long QT syndrome?

A

Macrolides and Fluoroquinolones (may prolong QT interval)

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30
Q

What med is used to treat HTN in pregancy?

A

Hydralazine

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31
Q

What are the common causes of secondary HTN?

A

Most common cause: Renal Parenchymal Disease

CHAPS

  • Cushings
  • Hyperaldosteronism (primary)
  • Coarctation of the Aorta
  • Pheochromocytoma
  • Renal artery stenosis
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32
Q

What is the clinical defn of renal artery stenosis? what med is contraindicated?

A

HTN that is resistant to 3 or more medications

Renal artery bruit on exam

ACE Inhibitors are C/I!!

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33
Q

What are the symptoms of pheochromocytoma? how is it dx?

A

Paroxysms of HA, flushing, sweating, palpitations, and fluctuating BP

  • Dx: elevated urinary vanilyl mandelic acid (VMA)
    • A metabolite of catecholamines
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34
Q

What is Hypertensive emergency? HOw is it tx?

A

Diastolic >130; Situation that requires RAPID (within 1 hour) lowering of BP

Increased risk of target organ damage

Tx: Nitroprusside sodium IV or IV esmolol

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35
Q

What is Hypertensive urgency? How is it tx?

A

Should be corrected within 24 hours of presentation

Systolic >180, Diastolic >120

Not associated with target organ damage–>main diff between urgency and emergency

Tx: Oral clonidine

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36
Q

What is malignant HTN and how is it tx?

A

Life threatning secondary to elevated BP resulting in Grade IV hypertensive retinopathy, papilledema, cardiovascular or renal compromise and encephalopathy

>220/140

TOC: IV nitroprusside if HTN encephalopathy; oral labetolol if papilledema without encephalopathy

Papilledema indicates End organ damage!

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37
Q

How do you screen for Abdominal Aortic aneurysm? How do you monitor?

How do you dx thoracic aneurysms?

A

AAA–>US for screening; MOnitor changes with CT scan\

Thoracic: CT with contrast, Aortography

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38
Q

How do you treat Aortic aneurysms?

A

Tx: Monitor with periodic US if <5 cm

AAA> 5.5 cm or undergone rapid expansion (>5 mm in 6 months)–>Surgery

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39
Q

How do you distinguish Stanford A aortic dissections from Standford B dissections?

A
  • Standford A–Ascending Aorta
  • Tx: Surgical emergency! IV Labetolol and IV nitroprusside
  • stanford B–>Distal to Left subclavian
  • Treat with beta blocker and conservative tx
  • Followed by serial CT scans every 6 months
40
Q

What are the sxs of Aortic dissection? How do you dx?

A

Severe chest/flank/back pain-described as “tearing, ripping, or sharp”

Presence of unexplained syncope in male pt >60 y/o should raise possibility

PE: variation in BP >20 mmHg difference between arms

Dx: TEE (unstable) or thoracic MRI (stable)

CXR: widened mediastinum with enlarged aortic knob

41
Q

What is Giant cell Arteritis? Sxs?

A

50% also have polymyalgia rheumatica (PMR)

Sxs: acute onset of HA, jaw pain, exacerbated by chewing, monocular blindness, visual abnormalities (Amaurosis fugax)

PE: enlarged temporal artery, pulseless

42
Q

What is the gold standard of dx Giant cell arteritis? What is the tx?

A

Gold standard: Superficial temporal artery Bx

Elevated ESR (90%)

Complication: Blindness seconary to occlusion of central retinal artery

Tx: high dose prednisone (60 mg/day) and low dose ASA

43
Q

What is the medical tx and pt ed for peripheral artery dz?

A

Cilostazol (phophodiesterase Inhibitors): Increases claudication distance by 40-60%

Walking recommended because it increases angiogenesis

44
Q

What is the difference in ulcers in Chronic venous insufficiency and Chronic arterial insufficiency?

A

Chronic venous insufficiency: Painless ulcers most commonly located at the medial malleolus; pigmentation

Chronic arterial insufficiency: Painful “punched out” ulcers on pale, necrotic base; Intermittent claudication more common

45
Q

What are the values of Ankle-brachial index?

A
  • 1.0 normal, <0.9 indicates dz
  • <1.0 chronic occlusive dz
  • <0.7 claudication
  • <0.3 pain at rest
46
Q

How do you treat a coronary artery spasm?

A

Calcium channel blockers (Nifedipine)

47
Q

What are the different classes of Heart failure?

A
  1. Class I: Asymptomatic
  2. Class II: Symptomatic with angina with exertion, but no paint at rest
  3. Class III: Symptomatic with minimal exertion (ordinary activities cause angina or pain)
  4. class IV: Symptomatic at rest
48
Q

What is the most common cardiomyopathy?

A

Dilated cardiomyopathy

49
Q

What is dilated cardiomyopathy? what is the most common cause?

A

Impaired contractability; systolic dysfunction

Most common cause: chronic alcohol abuse

50
Q

What are the signs of dilated cardiomyopathy? dx? How do you tx?

A

Signs of LEFT congestive heart failure, S3 gallop

Systolic dysfunction and LV dilations are essential for dx

dx: Transthoracic Echo

Treat CHF; abstinence from alcohol is essential

51
Q

Who does Tako Tsbuo cardiomyopathy commonly affect? What is seen on Echo?

A

Commonly seen in postmenopausal women after a major discharge of catecholamines

ECHO: Left ventricle apical ballooning

52
Q

What is Hypertrophic cardiomyopathy (HOCM)?

A

Massive hypertrophy of the septum; Impaired relaxation of LV (impaired diastolic filling–>pulmonary congestion)

Most common cause of sudden death in young athletes; exclusively genetic

53
Q

Hypertrophic cardiomyopathy: what are the common signs? How is it dx?

A

PE: systolic murmur that increases with valsalva maneuver, decreses with squatting (only other murmur that does this besides MVP); JVP with A wave

Dx: Echo-interventricular septal hypertrophy

CXR- boot shaped heart; ECG: Long QT syndrome is the first sign in children; Abnormal Deep Narrow Qs

54
Q

How is HOCM tx?

A

First line: Beta blockers

Second line: CCB

May eventually need ablation of hypertrophic septum, or dual chamber pacing

55
Q

What is restrictive Cardiomyopathy? what is the most common cause?

A

Impaired diastolic filling; Impaired Elasticity

Fibrosis–>stiffness and inabiity of chambers to fill

Most common cause: Amyloidosis

56
Q

What are teh s/S of restrictive cardiomyopathy? What is the key to diagnosing restrictive cardiomyopathy? Tx?

A

sxs of Right sided heart failure

Echo is key to diagnosis: Small thickened LV

may need endomyocardial biopsy

Tx: diuretics

57
Q

What is a common SE from ACE inhibitors?

A

Angioedema

58
Q

Distinguish the sxs of RHF from LHF

A
  • RHF: Elevated JVP and ankle edema; Dependent edema, hepatomegaly
  • LHF: Dry cough, exertional dyspnea, Hypotension, perivascular and interstitial edeam, 3-pillow orthopnea, S3 heart sound
59
Q

What are the most common C/I of exercise stress test?

A
  • Aortic stenosis
  • Unstable angina
60
Q

What are common causes of heart block?

A
  • Hyperkalemia
  • Lyme dz
  • MI
  • Lithium
61
Q

What is first degree AV block?

A

ECG: prolonged PR>0.2 seconds, Constant

Asymptomatic, no Tx necessary

62
Q

What is Wenckebach AV block?

A

second degree AV block–Mobitz II

ECG: PR intervals progressively lengthen until skipped QRS

Tx: no tx unless symtomatic bradycardia–>pacemaker

63
Q

What is a Mobitz II heart block?

A

Secondary AV block

ECG: randomly skipped QRS without change in PR interval

Tx: Permanent dual chamber pacemaker insertion

64
Q

What is a third degree block?

A

Complete block

Occurs when atria and ventricles are controlled by different pacemakers

ECG: no relationship btwn P waves and QRS

Ventrical rate (QRS) slower than atrial rate (P waves)

Tx: Ventricular pacemaker (initially a temporary pacemaker can be inserted until a permanent one can be implanted

65
Q

What is Wolff-Parkinson-White syndrome (WPW)? what drugs are C/I?

A

Young males, palpitations, SOB, lightheadedness

ECG: delta wave in LEad II; Short PR interval

Tx: Radiofrequency ablation

C/I: digoxin and CCB

66
Q

Who is Paroxysmal supraventricular tachycardia commonly seen in? How is it tx?

A

Young patients with healthy hearts

Tx: DOC: IV adenosine

Recurrent episodes: Radiofrequency ablation

Prevention: betablocker or verapamil, or diltiazem

67
Q

What is seen in both RBBB and LBBB

A

Prolonged QRS duration (>.12 sec)

68
Q

What does this show?

A

Right BBB

69
Q

What is this?

A

Left BBB

70
Q

What is the most common cause of sudden cardiac death?

A

V. fib

71
Q

What is this? How is it treated?

A

V. Fib

totally erratic tracing, no P waves or QRS

Tx: CPR, immediate cardioversion

72
Q

What is this? How is it treated?

A
  • V. Tach
  • 3+ PVCs in a row
  • Regular, wide QRS complexes independent of P waves
  • Dx: Holter monitor
  • Tx: Electrical cardioversion follwed by antiarrhythmic meds (Flecainide)–>Can quickly deteriorate to V fib.
  • To prevent recurrent VT: Sotalol and Amiodarone
73
Q

What can cause Torsades de Pointes?

A

Can occur spontaneously, with hypokalemia or hypomagnesemia, or drug induced

Drugs: TCA, erythromycin, haloperidol, Ibutilide

74
Q

How do you tx Torsades de Pointes?

A

Magnesium, beta blockers

75
Q

What is the most common chronic arrhythmia?

A

A fib

76
Q

What is this? How do you treat?

A

A. fib

  • Synchronized cardioversion
    • A min INR of 1.8 (x 3 weeks) is rec. before cardioversion
    • Anticoagulate with warfarin
  • Betablocker and Amiodarone should also be used
77
Q

What it is this? How is it tx?

A

Atrial Flutter

Rate control with CCB, BB

Long term tx: amiodarone

78
Q

Most common cyanotic congenital Heart disease? what are it’s characteristics?

A

Tetralogy of Fallot

  • (P.O.S.H)
  • Pulmonary stenosis, Overriding Aorta, Septal defect (VSD), RVH
  • R to left shunt
  • crescendo-decrescendo holosystolic
79
Q

What are TET spells and were are they seen?

A

Hypercyanotic episodes, seen with Tetralogy of Fallet

A medical emergency followed by syncope

80
Q

What is the most common congenital heart disease?

A

Ventricular Septal Defect (VSD)

Harsh, holosystolic murmur; no murmur at birth but appears a few weeks later

L to R shunt

81
Q

What is the most common type of Atrial septal defect?

A

Ostium Secundum

82
Q

What is an important characteristic of ASD? ECG finding? What does the patient need to know about changing altitudes?

A

Wide Fixed Split S2

ECG: RAD

More susceptible to O2 desaturation at high altitudes and decompression sickness during deep sea diving

83
Q

What is the characteristic murmur for PDA? How is it treated?

A

Continuous, rough, machinery pansystolic murmur

Tx: Indomethacin is routinely adminstered to help close a PDA

84
Q

WHat is the main PE finding found with Coarctation of the Aorta?

A

HTN in the UE and normal or low BP in the LE

Weak femoral pulses, exaggerated radial pulses

Seen in Turner’s syndrome

CXR: rib notching and cardiomegaly

ECG: LVH

85
Q

What is Mitral stenosis?

A

Mid-diastolic murmur with an opening snap

heard best at apex

Echo: Fish mouth

Jugular A wave

86
Q

What is mitral regurgitation?

A

Blowing holosystolic murmur

87
Q

What is the murmur of MVP?

A

Mid to late systolic murmur; midsystolic click

Increased with standing/valsalva

Decreased with squatting

Thin females with minor chest wall deformities

88
Q

What is the murmur of Aortic stenosis?

A
  • Harsh, midsystolic decrescendo crescendo
  • Right sternal border, radiates to neck
  • Narrow pulse pressures
  • +thready carotids, + thrill
  • Increases with leaning forward
89
Q

What is Aortic Regurgitation?

A
  • blowing decrescendo diastolic murmur
  • Widened pulse pressures; Bounding “water hammer” pulses
  • Chronic: Austin flint murmur
  • Increases with leaning forward
  • Tx: Nitroprusside
90
Q

What is the most common Valve disorder of the elderly?

A

Aortic stenosis

91
Q

What is orthostatic hypotension?

A

drop in systolic BP (of at least 20 mmhg or >10 mmHg of diastolic) immediately upon arising from the sitting to standing position

If rise in pulse is >15 bpm: Depleted volume is most likely cause

92
Q

How does Hypercalcemia and hypocalcemia show on ECG?

A

Hypercalcemia: Shortend QT

Hypocalcemia: prolonged QT

“Too much too soon, too little too late”

93
Q

What is this?

A

RVH

R wave>Swave in V1

94
Q

What is this?

A

Left Ventricular Hypertrophy

S wave in V1 + R wave in V5=More than 35 mm

95
Q

What BP meds are best for AA?

A

CCB or Thiazides

ACE Inhibitors tend to not be effective, and AA have higher risk for Angioedema

PANCE-Flashcards (11 decks)

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