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Emergency Med rotation > Cardio part 1 > Flashcards

Cardio part 1 Flashcards

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1
Q

Pathophys of infective endocarditis

A

Bacteremia that delivers the organisms to the surface of the valve
Adherence of the organisms
Eventual invasion of the vavular leaflets

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2
Q

Etiology of endocarditis

A 
Native valve:
Rheumatic valvular disease- primarily involving the mitral valve
Congenital heart disease
Mitral valve prolapse
Degenerative heart disease
Prosthetic valve endocarditis:
Local abscess and fistula formation, valvular dehiscence
IVDA
New therapeutic modalities
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3
Q

S/sx of infective endocarditis

A 
Fever
Chills
Anorexia
Wt loss
Malaise
HA
Myalgias
Night sweats
SOB
Cough
Joint pains
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4
Q

What is the difference between acute and subacute endocarditis?

A

Subacute is characterized by a hx of an indolent process
Subacute process is caused by S. viridans
Interval between onset and dx averages about 6 wks
Acute is much more aggressive

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5
Q

PE of infective endocarditis

A 
Fever
Heart murmur
Petechiae
Subungual hemorrhages
Osler nodes
Janeway nodes
Roth spots
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6
Q

Workup of infective endocarditis

A 
CBC
CMP
Glucose
Coag panel
UA
Three sets of blood cultures
Echo- transthoracic
U/s
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7
Q

Tx of infective endocarditis

A

Treat any congestive heart failure
Native valve- pen G and gentamicin
IVDU- vanc and gentamicin
Prosthetic valve- Vanc and gentamicin and rifampin
Consider linezolid sub for vanc with unstable renal function

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8
Q

Indications for surgery in infective endocarditis

A

CHF refractory to standard medical therapy
Fungal infective endocarditis (except H. capsulatum)
Persistent sepsis after 72 hrs of appropriate antibiotic tx
Recurrent septic emboli
Rupture of an aneurysm of the sinus of Valsalva
Conduction disturbances caused by a septal abscess
Kissing infection of the anterior mitral leaflet in pts with IE of the aortic valve

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9
Q

Pathophysiology of angina pectoris

A

Myocardial ischemia develops when coronary blood flow becomes inadequate to meet myocardial oxygen demand
Angina pectoris is the MC clinical manifestation of myocardial ischemia
Caused by chemical and mechanical stimulation of sensory afferent nerve endings in the coronary vessels and myocardium

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10
Q

Precipitating factors of angina pectoris

A 
Severe anemia
Fever
Tachyarrhythmias
Catecholamines
Emotional stress
Hyperthyroidism
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11
Q

S/sx of angina pectoris

A 
Retrosternal chest discomfort:
-Pressure
-Heaviness
-Squeezing
-Burning
-Choking sensation
Locations:
-Epigastrium
-Back 
-Neck
-Jaw
-Shoulders
Radiation:
-Arms
-Shoulders
-Neck
Precipitated by exertion, eating, exposure to cold, or emotional stress
Stable: Lasts 1-5 mins and relieved by rest of nitroglycerin
Intensity does not change with respiration, cough, or change in position
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12
Q

PE of angina pectoris

A

Positive Levine sign

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13
Q

Workup of angina pectoris

A

CXR
Exercise stress test
Stress echo
Nuclear imaging for those with baseline EKG abnormalities
EKG
Procedures for those with inconclusive noninvasive study results or unstable angina despite maximal medical tx

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14
Q

Tx of angina pectoris

A 
Treat RFs
-Statins
Daily aspirin
Nitro
Beta blockers
Lifestyle modifications
Consider revascularization with left main artery stenosis >50%, 2- or 3-vessel dz and LV dysfunction, poor prognostic signs during noninvasive studies, or severe sx despite maximum medical therapy
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15
Q

Pathophys of cardiac tamponade

A

Phase I- The accumulation of pericardial fluid impairs relaxation and filling of the ventricles, requiring a higher filling pressure
Phase II- With further fluid accumulation, the pericardial pressure increases above the ventricular filling pressure, resulting in reduced cardiac output
Phase III- A further decrease in cardiac output occurs, which is due to the equilibration of pericardial and left ventricular filling pressures
Marked reduction in diastolic filling
Systemic venous return is altered

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16
Q

What is the MCC of cardiac tamponade?

A

Malignant diseases

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17
Q

S/sx of cardiac tamponade

A 
Dyspnea
Tachycardia
Tachypnea
Decreased urine output
Confusion
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18
Q

PE of cardiac tamponade

A 
Elevated JVP
Hepatomegaly
Diminished heart sounds
Pericardial friction rub
Some may present with dizziness, drowsiness, or palpitations
Cold, clammy skin
Weak pulse
Pulsus paradoxus
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19
Q

What is Beck’s triad?

A 
Indicates cardiac tamponade
Increased JVP
Hypotension
Diminished heart sounds
Y descent in jugular venous or right atrial waveform
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20
Q

Workup for cardiac tamponade

A 
CXR
CK and isoenzymes
Renal profile and CBC with diff
Coag panel
Antinuclear antibody assay
ESR
RF
HIV testing
PPD
EKG- electrical alternans
21
Q

Tx of cardiac tamponade

A

Pericardiocentesis or pericardiotomy

Pericardial window in hemodynamically unstable pts

22
Q

Pathophys of atrial fibrillation

A

Electrical remodeling
Contractile remodeling
Structural remodeling

23
Q

RFs of AFib

A 
Hemodynamic stress
Atrial ischemia
Inflammation
Noncardiovascular respiratory causes
EtOH and drug use
Endocrine d/os
Neurologic d/os
Genetic factors
Advancing age
24
Q

S/sx of AFib

A 
Wide variety
Palpitations
Dyspnea
Fatigue
Dizziness
Angina
Decompensated heart failure
Poor exercise tolerance
Presyncope or syncope
Generalized weakness
25
Q

PE of AFib

A

Irregularly irregular pulse
Tachycardia
May have exophthalmos, thyromegaly, elevated JVP, or cyanosis
May have heart failure, wheezes, or diminished breath sounds
May have displaced PMI or S3
Prominent P2 with pulmonary HTN
May have ascites, hepatomegaly, or hepatic capsular tenderness
Cyanosis, clubbing, or edema of lower extremities

26
Q

Workup for AFib

A 
EKG
CBC
Serum electrolytes and BUN/creatinine
CK and/or troponin
BNP
D-dimer
Thyroid function studies
Digoxin level
Toxicology testing or ethanol level
Echo
CTA if D-dimer pos
CT or MRI if ablation is planned
27
Q

RFs of stroke in pts with AFib

A 
Advancing age
Female
HTN
DM
Heart failure
Hx of stroke/TIA/thromboembolism
CAD
PAD
Valvular heart disease
28
Q

Management of new-onset AFib

A

BBs and CCBs are 1st line for rate control
Amiodarone for those intolerant or unresponsive to other agents
Anticoagulation
Cardioversion may be necessary

29
Q

When should cardioversion be done on an AFib pt?

A 
Hemodynamically unstable
Severe dyspnea or CP
Preexcited AFib
Rate-control is not working
Echo does not reveal any valvular or functional abnormality of the heart
30
Q

Pathophys of atrial flutter

A

Single reentrant circuit with circus activation in the right atrium around the tricuspid valve annulus, with an area of slow conduction between tricuspid valve annulus and the coronary sinus ostium

31
Q

Etiology of atrial flutter

A 
Coronary artery disease
Hypertensive heart disease
Rheumatic heart disease
Congenital heart disease
Pericarditis
Cardiomyopathy
Hypoxia
COPD
PE
Hyperthryoidism
Pheochromocytoma
DM
Electrolyte imbalance
EtOH consumption
Obesity
Digitalis toxicity
Myotonic dystrophy in childhood
32
Q

Typical sx of atrial flutter

A

Palpitations
Fatigue or poor exercise tolerance
Mild dyspnea
Presyncope

33
Q

Less common sx of atrial flutter

A

Angina
Profound dyspnea
Syncope

34
Q

Workup for atrial flutter

A 
EKG
Vagal maneuvers if flutter waves are not seen
Adenosine
Exercise testing
TTE
35
Q

Tx of atrial flutter

A

CCBs or BBs for rate control
May need cardioversion
Anticoagulation
Consider radiofrequency ablation

36
Q

Etiology of SVT

A 
Triggered by a reentry mechanism
Premature atrial or ventricular ectopic beats
Other triggers:
-Hyperthyroidism
-Stimulants
-Alcohol
37
Q

Hs and Ts of arrhythmias

A 
Toxins
Thromboses
Temperature
Tension pneumo
Tamponade
Trauma
Hypoxia
Hypovolemia
Hypokalemia/hyperkalemia
Hydrogen
38
Q

Common sx of SVT

A 
Palpitations
Dizziness
SOB
Syncope
CP
Fatigue
Diaphoresis
Nausea
39
Q

Workup of SVT

A 
Cardiac enzymes
Electrolyte levels
CBC
Thyroid studies
Digoxin level
Electrophysiologic studies
EKG
CXR
TTE
40
Q

Tx of SVT

A

Hypotensive or unstable: immediate cardioversion

Stable: try vagal maneuvers, then if unsuccessful, adenosine

41
Q

Pathophys of VTach

A

Caused by electrical reentry or abnormal automaticity

42
Q

Etiology of VTach

A 
Ischemic heart dz
Structural heart dz with disruption of nl conduction patterns
Congenital structural cardiac d/os
Acquired channelopathies
Inherited channelopathies
Electrolyte imbalances
Sympathomimetic agents
Digitalis toxicity
Systemic diseases causing infiltrative cardiomyopathy or scar
43
Q

S/sx of VTach

A 
Palpitation
Lightheadedness
Syncope
CP
Can also be asymptomatic
44
Q

PE of VTach

A 
Hypotension
Tachypnea
Diminished LOC
Pallor
Diaphoresis
High JVP
Mental status changes:
Anxiety
Agitation
Lethargy
Coma
45
Q

Workup of VTach: labs

A

Electrolytes
Serum levels of therapeutic drugs
Toxicology
Serum cardiac markers

46
Q

Workup of VTach: imaging, other

A

Echo
EKG
Holter monitoring with recurrent syncope or palpitations

47
Q

Tx of VTach: stabilization

A

VT associated with loss of consciousness or hypotension needs immediate cardioversion with 100-200J biphasic
Address reversible RFs
Lidocaine if pts have ongoing myocardial ischemia
Pulseless VT- high-dose unsynchronized energy

48
Q

Tx of VTach: postabilization management

A

Referral to a cardiologist
Admission to a monitored bed
Further studies, such as electrophysiologic study
Consideration for radiofrequency ablation
Consideration for ICD placement

49
Q

Tx of VTach: long-term tx

A

Depends on cause:
Amiodarone in combo with BBs for pts with left ventricular dysunction d/t previous MI
Heart failure: BB, ACE, aldosterone antagonists
Stains for coronary heart disease

Emergency Med rotation (12 decks)

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