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Adult Clinical Medicine > Cardiac Section > Flashcards

Cardiac Section Flashcards

1
Q

symptoms of arrhythmias

A 
Asymptomatic
Palpitations
Dizziness: vertigo, disequilibrium, or pre-syncope
Chest pain
Dyspnea: trouble breathing
Weakness
Anxiety
Note: sxs may be due to underlying heart disease (e.g. HF, ischemia)
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2
Q

sinus bradycardia: causes

A

normal (athletes), SA node dysfunction (called sick sinus syndrome if sxs), metabolic (including hyper or hypo-kalemia, hypercalcemia, and hyper- or hypothyroidism), drugs (beta-blockers, calcium-channel blockers, and lithium), neurogenic (vagal stimulation), cardiac ischemia (AMI), OSA, infection, inc. ICP

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3
Q

sinus bradycardia: treatment

A

stop meds causing slow HR; pacemaker

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4
Q

sinus tachycardia: causes

A

fever, sepsis, anemia, hypotention/shock, acute coronary ischemia/MI, heart failure, chronic pulm disease, hypoxia, pulm embolism, stimulants/illicit drugs, (nicotine, caffeine, OTC decongestants, cocaine), anxiety, pheochromocytoma

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5
Q

sinus tachycardia: treatment

A

target underlying disease

beta-blockers if not obvious dz

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6
Q

Guidelines for prevention of thromboembolism in A-Fib - moderate and high risk factors

A

moderate: > 75y/o, HTN, HF, DM

High: CVA, TIA, embolism, prosthetic valve

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7
Q

LBBB on EKG with ACS sxs

A

cannot R/O infarction - this is a STEMI (unless so elevation in cardiac markers)

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8
Q

variant (Prizmetal’s) angina: treatment

A

CCBs are 1st line
long-acting nitrates

Note: beta blockers are contraindicated

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9
Q

chronic stable angina: risk factor modification

A

LDL < 100 mg/dL
TG < 200 mg/dL
HDL > 40 mg/dL
BP < 130/85

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10
Q

chronic stable angina: life-style modifications

A

smoking, diet, activity, cholesterol, BP (salt intake)

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11
Q

chronic stable angina: medications

A

Beta-blockers (dec. oxygen demand)

Ca++ channel blockers (dec. afterload / demand)

Nitrates (inc. oxygen supply and dec demand)

Aspirin (ASA) (dec. vasoconstriction and platelet activity; 75-325mg/day) → reduced mortality

Statins (stabilize plaques): all pts w/ angina should be on statins regardless of LDL

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12
Q

suspect ACS: evaluation

A

Immediate EKG

MONA:

  • Morphine sulfate: 2-4 mg IV, then 2-8mg every 5-15 min (Fentanyl)
  • Oxygen
  • Nitrates: SL nitroglycerin 0.4 mg q 5 minutes x 3
  • ASA: 160-325 mg chewed

cardiac serum markers, CXR

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13
Q

NSTEMI management: low risk of progression to STEMI

A 
Beta-blocker
IV nitroglycerine (if pain persists)
Heparin, low molecular weight = Enoxaparin (Lovenox): anti-thrombin effect
Clopidogrel (Plavix): platelet inhibitor
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14
Q

NSTEMI management: high risk of progression to STEMI

*ST depression, persistent pain, unstable

A

Angiogram: diagnostic coronary arteriography (determines whether PCI is needed)

GP IIb/IIIa inhibitor: Abciximab (Reopro): platelet inhibitor, used prior to PCI

Percutaneous Coronary Intervention (PCI)

PTCA (Percutaneous Transluminal Coronary Angioplasty):“Balloon Angioplasty”

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15
Q

STEMI management

A

Beta-blocker
IV nitroglycerine (if pain persists)
IV Heparin
Clopidogrel (Plavix) (platelet inhibitor)

Primary PCI: goal less than 90 minutes
Thrombolysis with t-PA (tissue plasminogen activator): goal less than 30 minutes (if no PCI)

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16
Q

ACS: long-term risk factor modifications

A 
smoking cessation
weight, diet, exercise
lipid lowering therapy (statin)
fibrate or niacin if HDL<40
HTN control <130/80
control of hyperglycemia in DM
Also medications: see below
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17
Q

ACS: long-term risk factor modifications - medications

A

Aspirin 75-325 mg daily
Clopidogrel (75 mg daily) when ASA is not tolerated (hypersensitivity, GI intolerance)
• Note: combined ASA + clopidogrel for 9 months after NSTEMI

Beta blockers unless contraindicated

ACE-I for pts with CHF, LV dysfunction (EF <40%), HTN, or DM

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18
Q

gold standard for coronary heart disease evaluation

A

coronary angiogram

  • invasive and costly
  • can consider stress test
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19
Q

cardiac stress testing

A

non-invasive approach involving stressing the heart (via exercise or meds) and measuring changes in response to stressors (via EKG or imaging - thallium or echo)

use for both diagnostic and prognostic assessment

indicated if pretest probability of CHD is INTERMEDIATE

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20
Q

poor R-wave progression on EKG: causes

A

Old infarct (previous MI)
Emphysema
COPD (heart sits lower)
Dextrocardia: heart on right

Note: R waves get progressively taller from V1 - V6

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21
Q

normal sinus rhythm: definition

A

P wave b/f every QRS and QRS after every P
Rate 60-100
P wave directions:
- Upright in II (current heading towards positive pool)
- Negative (inverted) in aVR (current heads towards negative pool)
- AVL is pretty flat (current directly 90 degrees from positive pool)

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22
Q

sign of junctional rhythm

A

P-waves negative in II, III, and aVF and upright in aVR

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23
Q

signs of ischemia on EKG

*ischemia: restriction of blood flow causing low oxygen to cells

A

flipped T waves
ST segment depression

Note: this is reversible

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24
Q

signs of myocardial injury (infarct)

A

ST segment elevation

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25
Q

signs of myocardial necrosis (death)

A

significant Q waves (wider than 1 small box; >1/3 size of QRS)

Note: q waves are usually very small

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26
Q

EKG sign of posterior STEMI

A

ST segment depression in leads V2, V3, V4 (since this would be elevation if leads were on patient’s back)

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27
Q

EKG clues to pulmonary embolism (PE)

A

tachycardia, RAD, inc. R’ over rt ventricle (aVR) = RBBB, T-wave inversion in anterior and inferior leads

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28
Q

EKG clues to pericardial tamponade

A

Low voltage EKG (often with low BP), SOB, tachypnea. Tachycardia

Electrical alterans: QRS in rhythm strip is higher and lower, higher and lower

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29
Q

EKG clues to myocarditis

*infection of heart muscle - much more serious than pericarditis

A

Low voltage in limb leads (I, II, III, aVR, aVL, aVF), tachycardia

Can also get positive Trop levels since cell death releases troponin

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30
Q

EKG clues to pericarditis

*infection in sac around heart; can be due to virus

A

GLOBAL ST segment elevation (all chest and limb leads)

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31
Q

syncope

A

transient loss of consciousness (T-LOC) due to transient global cerebral hypo-perfusion characterized by rapid onset, short duration (20-30 sec, <5min), and spontaneous complete recovery

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32
Q

4 types of neurally-mediated (reflex) syncope

A

vaso-vagal
situational
carotid sinus
atypical

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33
Q

prodromal sxs of vasovagal syncope

A

sweating, pallor, nausea

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34
Q

orthostatic hypotension (OH) syncope: causes

A

DAAD:

Drugs: vasodilators, vol. depletion, BP meds, diuretics, TCAs

Autonomic insufficiency: Parkinson’s, DM, adrenal insufficiency

Alcohol

Dehydration

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35
Q

cardiovascular syncope: causes

A

arrhythmias (bradycardia or tachycardia)

structural disease: valvular dz, AMI, HCM, masses, pericardial dz, prosthetic valve dysfunction

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36
Q

syncope on exertion or supine

A

WORRISOME for cardiac origin

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37
Q

syncope: basic work-up

A

History/Physical including orthostatic BPs
Medication Review
EKG
Carotid Sinus Massage (if age >40)

Note: all pts then risk stratified (high or low risk of short-term cardiac event)

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38
Q

Carotid Sinus Massage: what indicates a positive test for cause of syncope

A

bradycardia, hypotension, transient pause/asystole, or prodrome symptoms w/ massage

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39
Q

syncope: high-rise for ST cardiac event

A

Evidence of heart disease (heart failure (fluid), low LVEF, structural abnormality, previous MI)

Clinical: palpitations, syncope on exertion or supine

FH of sudden cardiac death or non sustained ventricular tachycardia

Hypotension (systolic <90 mmHg)

EKG features suggesting arrhythmia or abnormal

Comorbidities such as severe anemia or electrolyte disturbance

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40
Q

diagnosing essential / primary HTN

A

SBP ≥ 140 mmHg OR DBP ≥ 90 mmHg (2 or more readings spaced at least 2 wks apart)

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41
Q

secondary HNT: causes

A

hints: severe, resistant to tx, sudden onset, young age (w/ no FH or obesity)

OSA: #1 cause tied w/ meds

meds: OCPs, NSAIDS, simulants, Calcineurin inhibitors, antidepressant (venlafaxine)

Heavy EtOH use

renal: renal vascular or primary renal dx

rare dz: pheo, primary aldosteronism, Cushings, coarctation, hyper- or hypothyroidism, primary hyperparathyroidism

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42
Q

hypothyroidism - signs

A

fatigue, unintentional weight gain, cold intolerance, constipation

43
Q

5 P’s of pheochromocytoma

A 
palpitations
perspiration
pallor
pounding HA
inc. BP
44
Q

labs to R/O secondary causes of HTN

A 
electrolytes (Na, K, Ca)
 - hyperaldosteronism, hyperparathyroidism 
creatinine
 - renal dz
TSH
 - hypo/hyperthyroidism
45
Q

HTN evaluation: target organ damage

A

neuro: HA, neurologic sx
ophthalmology: cotton-wool spots, AV nicking
CV: CP on exertion, dyspnea, claudication, dec. pulses
Pulm: rales, fluid (HF)

46
Q

HTN evaluation: risk stratification

A

Assess other CV disease risks:

  • Smoking, Type 2 Diabetes (T2DM)
  • Hyperlipidemia
  • Known vascular disease history

Labs:

  • lipid panal
  • EKG: LVH
47
Q

HTN management: lifestyle modifications

A

Weight maintenance/loss: ↓10kg = ↓BP 5-20 mm Hg

30 minutes exercise/day: ↓BP 4-9 mm Hg

Sodium <2400 mg/day: ↓BP 2-8 mm Hg

Restrict EtOH (1/day W or 2/day M): ↓BP 2-4 mm Hg

48
Q

HTN management: medications

A

JNC8 first-line agents

  • Thiazide-type diuretic
  • ACE-I OR ARB
  • CCB

JNC 8 second-line agents

  • Beta Blocker (BB)
  • Aldosterone antagonist (e.g. spironolactone)
49
Q

thiazide and loop diuretics: actions and side effects

A

decrease total body salt and water

dehydration
hypokalemia
worsens insulin resistance i
increases uric acid (gout)

Contraindicated in pregnancy

50
Q

ACE-I: actions and side effects

A

Inhibits activation of RAAS - leads to dec salt/water retention by kidney and dec peripheral vascular resistance

hyperkalemia
cough
urticaria/angioedema

Contraindicated in pregnancy
Decreases incidence of DM in hypertensive individuals

51
Q

ARBs: actions and side effects

A

inhibits RAAS one step later than ACE-I

hyperkalemia
urticaria/angioedema

Decreases incidence of DM in hypertensive individuals

52
Q

Calcium channel blockers: actions and side effects

A

Dipines (DHP): vasodilate peripheral blood vessels

Cardiac (non-DHP): lower heart rate

Edema
Bradycardia (non-DHP)
CHF exacerbation (non-DHP)

53
Q

Beta blockers: actions and side effects

A

lowers heart rate and decreases peripheral vascular resistance mediated by SNS

Bradycardia
CHF exacerbation

Masks signs of hypoglycemia in DM; some inc. insulin resistance

Contraindicated in asthma

54
Q

aldosterone antagonists

A

competes with aldosterone at distal renal tubule, conserves potassium and excretes sodium/water (diuretic)

hyperkalemia
dehydration

55
Q

chronic kidney disease: best HTN drug

A

ACE-I or ARB

56
Q

DM: best HTN drug

A

ACE-I or ARB preferred (avoid beta-blockers since mask hypoglycemia)

57
Q

Black: best HTN drug

A

diuretic or CCB

58
Q

All races (other than black): best HTN drug

A

diuretic or ACE-I/ARB or CCB preferred

59
Q

pregnancy: best HTN drug

A

1st-line: Methyldopa (long track record)

2nd-line: Labetalol (beta-blocker)

Additional options:

  • nifedipine
  • hydralazine
60
Q

chronic kidney disease: parameters

A

GFR < 60 ml/min
OR
microalbuminuria > 30mg / gram creatinine

61
Q

hypertensive urgency: treatment

A

decrease BP <160/100 over 3-6 hours

- usually use a diuretic

62
Q

hypertensive emergency: assessing for end organ damage

A

Neuro/optho: reversible encephalopathy, hemorrhagic stroke, retinal exudates/ hemorrhages, papilledema

CV: unstable angina/MI, HF (pulm edema), aortic dissection

Renal: proteinuria, hematuria, acute renal failure

Pregnancy only: preeclampsia/eclampsia

63
Q

hypertensive emergency: treatment

A

ADMIT: ED/ICU

Lower DBP by MAX of 25% in 2-6 hours

Goal DBP 100-105 mm Hg within minutes to 2 hours

use vasodilators, beta-blockers, dopamine-1 agonist
-nitroprusside, labetalol, fenoldopam, hydralaine

64
Q

3 determinants of stroke volume

A

preload
afterload
contractility

65
Q

cor pulmonale

A

isolated rt sided heart failure (not caused by left-sided)

66
Q

CHF: 3 ways patients usually present

A

asymptomatic (cardiac enlargement)

dec. exercise tolerance (inc. fatigue)

sxs of fluid retention (lungs, periphery)

67
Q

right-sided heart failure: what you see on PE

A

JVD, peripheral edema (bilateral), RUQ tenderness / hepatomegaly

68
Q

left-sided heart failure: what you see on PE

A

tachycardia, tachypnea, dyspnea (nocturnal), orthopnea, nocturnal cough, pulmonary rales, pneumonia, S3 gallop

69
Q

CHF: risk factors (call can cause remodeling)

A 
HTN
Valvular Disease
Diabetes
Myocardial infarction
Atherosclerosis
Cardiomyopathy
Arrhythmias/LBBB
COPD
Cardiotoxic drugs (smoking, alcohol, cocaine, ephedra, long-term NSAIDs use)
70
Q

CHF: diagnostic imaging

A

Echocardiogram

  • most important test (establishes baseline, help when change of sxs)
  • tells EF, LVH, structural abnormalities

EKG: LBBB, LVH, atrial fibrillation (evidence of prior MI or arrhythmia)

CXR: cardiomegaly, pulmonary infiltrate

71
Q

CHF: laboratory testing

A

BMP and CBC are standard

UA (kidney)
A1C: DM can lead to vascular dx
Lipid Panel: dyslipidemia can lead to vascular dx
Hepatic Function (ALT/AST)
Thyroid Function 
Transferretin: iron
HIV
72
Q

heart failure: stages

A

Stage A: people at risk for HF (see risk factors)

Stage B: begin to have structural heart disease (valve changes, EF), but no signs of systemic symptoms

Stage C: begin to have systemic symptoms

Stage D: end-stage disease

73
Q

heart failure: tx based on stage

A

stages A and B:

  • ACE-I / ARB
  • Beta-blockers (esp. if post MI)

stages C and D:

  • optimize ACE-I/ARB and beta-blocker
  • begin diuretics (loop, HCTZ)
  • aldosterone antagonists
  • digoxin

stage A: treat risk factors
stage D: palliative care, heart replacement

74
Q

heart failure: meds to avoid

A 
NSAIDS: cardiologists hate 
Cold meds containing pseudo ephedrine (Sudafed)
Na containing antacids: alka-seltzer
Anti-arrhythmic agents
CCBs
75
Q

heart failure: when to refer to cardiologist / work with cardiologist

A 
stage c = symptomatic
conduction abnormality
suspect prior/unknown MI
suspect CAD 
evidence of pulmonary HTN
76
Q

heart failure: acute exacerbation

A

presents as acute pulmonary edema

LMNOP:

  • lasix
  • morphine
  • nitrate
  • oxygen
  • pressors (vasoconstrict)
77
Q

heart failure: home monitoring

A

Patient and family education:

  • warning signs of worsening
  • weight monitored daily (fluid)
  • medication regimen
  • diet adjust (salt restrict)
  • moderate physical activity

Vaccinations:

  • pneumovac
  • influenza
78
Q

bacterial endocarditis: definition and types

A

infection of the endothelial lining of the heart (including, but not limited to the valves)

  • Acute Bacterial Endocarditis (ABE)
  • Subacute Bacterial Endocarditis (SBE)
79
Q

Acute Bacterial Endocarditis (ABE): sxs

A

infection of normal or abnormal valves with a virulent organism (e.g., Staph Aureus);

  • Abrupt onset: high fever, chills, night sweats
  • Prominent leukocytosis
  • Rapid, severe valve destruction
  • Apical heart murmur (not always in R-sided)
  • Often complicated by heart failure
80
Q

Subacute Bacterial Endocarditis (SBE): sxs

A

indolent infection of abnormal valves with a less virulent organism (e.g., Strep Viridans)

  • Indolent onset (wks-mos): fever, night sweats, weight loss
  • Apical heart murmur (not always in R-sided)
  • Minor endocardial damage
  • Leukocytosis often minimal or not present
81
Q

bacterial endocarditis: high risk groups

A

Abnormal cardiac structure (anatomy or “foreign bodies)

  • congenital heart disease (VSD, PAD, etc.)
  • abnormal cardiac valves (prosthetic valves, mitral or aortic valve regurgitation)

Abnormal risk of bacteremia (IV drugs or IV access)

Age > 60

Immune compromised

82
Q

abnormal risks of bacteremia

A 
IV drug use (IVDU)
Indwelling central venous catheter
Chronic hemodialysis
Poor dentition/dental caries
Colon cancer/IBD
83
Q

bacterial endocarditis: typical pathogens

A

80% Gram Positive Cocci (GPC)
∗ 32% S. Aureus
∗ 18% S. Viridans
∗ 11% Enterococcus

IV drug users: 60% Staph Aureus, 20% Strep Viridans

Prothetic valves: 30-35% S. Epidermidis (usually non-pathologic skin flora)

84
Q

bacterial endocarditis: signs and sxs

A

fever, rigors (chills), night sweats, arthralgia / bone pain / septic joint, malaise/weakness, weightless, SOB, abd pain, rashes/skin changes

Hx of predisposing structural cardiac abnormalities / bacteremia risk

85
Q

bacterial endocarditis: PE findings

A

fever, skin conditions, CV (new murmur, CHF signs), GI (splenomegaly, abd tender to palpation), MSK (bone TTP), neuro (neuologic signs, Roth spots on fundoscopic exam)

Note: sxs all over body

86
Q

bacterial endocarditis: skin conditions associated

A

Petechiae: soft palate or extremities

Janeway Lesions: non-tender erythematous/hemorrhagic macular/nodular lesions on palms/soles

Osler’s Nodes: painful, immune-complex related inflammatory nodules on finger pads
- more common in SBE

Splinter Hemorrhages: linear, red hemorrhages in nails
- more common in SBE

87
Q

bacterial endocarditis: lab findings and tests

A

Blood cultures x 3 sets (minimum) prior to giving antibiotics

CBC: leukocytosis (ABE), normocytic anemia

ESR: elevated, often > 100 (specific to only a couple conditions – one is endocarditis)

Creatinine: assure renal fx preserved

Urinalysis: microscopic hematuria (common), glomerulonephritis (proteinuria, RBC casts = GN = not common = big hint)

EKG: heart blocks

88
Q

bacterial endocarditis: imaging

A

Trans-esophageal echocardiogram is best: 81.4% positive for vegetation on valve

89
Q

bacterial endocarditis: Modified Duke Criteria

A

Major Criteria:

  • Sustained bacteremia (3/4 sets 1 hr apart OR 2 sets 12 hr apart)
  • Endocardial involvement: vegetation (oscillating intracardiac mass), valve abscess/ perforation, prosthetic dehiscence (come undone) OR New Valvular regurgitation

Minor Criteria:

  • Predisposing medical condition (abnormal valve or bacteremia-prone)
  • Fever (>38°C)
  • Vascular phenomena (septic emboli, mycotic aneurysm, Janeway lesion)
  • Immune phenomena (glomerulonephritis, Osler’s nodes, Roth spots, RF+)
  • Blood cx + or evidence of infection
90
Q

bacterial endocarditis: diagnosis

A

Definite pathologic: micro-organism demonstrated in vegetation or cardiac abscess OR pathology of vegetation shows active endocarditis
- rare, need heart surgery

Definite clinical: 2 major OR 1 major/3 minor OR 5 minor criteria

Possible: 1 major/1 minor OR 3 minor

91
Q

bacterial endocarditis: treatment

A

6 weeks of IV ABX:

Native valve ABE: empiric therapy while waiting for cx results
- Nafcillin/Gentamicin (tx staph - most common) OR Vancomycin/Gent (if suspect MRSA)

Native valve SBE: likely wait for return of cx results (Ampicillin/Gentamicin)

Prosthetic valve: Vanco/Gent/Rifampin

92
Q

bacterial endocarditis: surgical indications:

A

Incompetent valve causing CHF despite maximal medical therapy (must fix valve)

Heart block worsening (due to conduction system involvement)

Cardiac abscess (must go in and drain)

Recurrent emboli on medical therapy

Fungal infection: indication to remove valve, esp. if prosthetic

93
Q

bacterial endocarditis: meds to avoid

A

Anticoagulation (heparin/Coumadin) contra-indicated: potential for hemorrhage from emboli

However, anti-coag is generally accepted (despite ↑ risk) in following conditions:
o Prosthetic heart valve
o Acute coronary syndrome

94
Q

bacterial endocarditis: prophylaxis

A

Amoxicillin (clindamycin if pcn-allergic) prior to dental procedures for at-risk patients:

  • congenital Cyanotic Heart Disease: unrepaired or repaired with residual defects
  • prosthetic valve
  • prior endocarditis hx
  • heart transplant recipients who develop “valvulopathy”
95
Q

pericarditis: definition and causes

A

infection of pericardium

1/3: infectious (viral, TB, fungal)
2/3: neoplastic, immune-mediated (post-cardiac surgery – called “Dressler’s Syndrome, etc.), uremic (end-stage renal disease), idiopathic, drug-induced, traumatic (MVI / chest trauma), immediate post-MI (larger infarcts)

96
Q

pericarditis: clinical presentation

A

Positional pleuritic chest pain: better leaning forward, worse supine

Fever (esp. if infectious cause)

Pericardial friction rub (classic finding; brown paper bag crumpling)

If pericardial effusion is present: distant heart sounds, fainter friction rub

97
Q

pericarditis: EKG findings

A

diffuse ST elevation (acute pericarditis)

pericardial effusion: low voltage throughout all leads

98
Q

pericarditis: diagnosis:

A

2 or more of the following 4:• Chest pain
Pericardial friction rub
Appropriate EKG changes
Pericardial effusion

99
Q

pericarditis: expanded lab and test work-up

A

EKG (as seen already)

Labs: thyroid testing (TSH): thyroid dz can cause, renal function (creatinine), ANA, rheumatoid factor (b/c SLE or RA can cause)

Consider TB/fungal evaluation in appropriate pt (immunosuppressed, TB exposures)

Consider evaluation for recent MI (e.g., wall motion abnormalities by ECHO, troponin less helpful because often ↑ in pericarditis)

HIV testing: if at risk

Cancer W/U:

100
Q

pericarditis: treatment

A

Non-steroidal anti-inflammatory medications (NSAIDs) – consistent w/ viral infection
- treatment is for sxs / tolerance to sxs (not to fix issue)

Colchicine or Steroids (Prednisone) (if NSAIDs ineffective)

101
Q

pericarditis: medication to avoid

A

anticoagulants: may cause hemorrhage and cardiac tamponade (same as for endocarditis, but for different reason – potential for hemorrhage from emboli in endocarditis)
• Caveat: if immediate post-MI period continue aspirin/heparin unless pericardial effusion > 1 cm or tamponade sx develop

102
Q

cardiac tamponade: sxs and tx

A

complication of pericarditis (10-15% of acute pericarditis)

Sxs: “Becks triad” – distant heart sounds, hypotension, JVD; pulsus paradoxus; pericardial friction rub

tx: pericardiocentesis

103
Q

constrictive pericarditis: sxs and tx

A

chronic pericardial inflammation causes fibrosis and scar

sxs: HF, normal BP, elevated JVP - similar to cardiac tamponade but slower in progression

Dx: CXR and Echo give hints; dx via heart catheterization

Tx: surgical resection of pericardium

Adult Clinical Medicine (5 decks)

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