Cardio part 1 Flashcards

(49 cards)

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
PE of AFib
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
Workup for AFib
``` 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
RFs of stroke in pts with AFib
``` Advancing age Female HTN DM Heart failure Hx of stroke/TIA/thromboembolism CAD PAD Valvular heart disease ```
28
Management of new-onset AFib
BBs and CCBs are 1st line for rate control Amiodarone for those intolerant or unresponsive to other agents Anticoagulation Cardioversion may be necessary
29
When should cardioversion be done on an AFib pt?
``` 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
Pathophys of atrial flutter
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
Etiology of atrial flutter
``` 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
Typical sx of atrial flutter
Palpitations Fatigue or poor exercise tolerance Mild dyspnea Presyncope
33
Less common sx of atrial flutter
Angina Profound dyspnea Syncope
34
Workup for atrial flutter
``` EKG Vagal maneuvers if flutter waves are not seen Adenosine Exercise testing TTE ```
35
Tx of atrial flutter
CCBs or BBs for rate control May need cardioversion Anticoagulation Consider radiofrequency ablation
36
Etiology of SVT
``` Triggered by a reentry mechanism Premature atrial or ventricular ectopic beats Other triggers: -Hyperthyroidism -Stimulants -Alcohol ```
37
Hs and Ts of arrhythmias
``` Toxins Thromboses Temperature Tension pneumo Tamponade Trauma Hypoxia Hypovolemia Hypokalemia/hyperkalemia Hydrogen ```
38
Common sx of SVT
``` Palpitations Dizziness SOB Syncope CP Fatigue Diaphoresis Nausea ```
39
Workup of SVT
``` Cardiac enzymes Electrolyte levels CBC Thyroid studies Digoxin level Electrophysiologic studies EKG CXR TTE ```
40
Tx of SVT
Hypotensive or unstable: immediate cardioversion | Stable: try vagal maneuvers, then if unsuccessful, adenosine
41
Pathophys of VTach
Caused by electrical reentry or abnormal automaticity
42
Etiology of VTach
``` 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
S/sx of VTach
``` Palpitation Lightheadedness Syncope CP Can also be asymptomatic ```
44
PE of VTach
``` Hypotension Tachypnea Diminished LOC Pallor Diaphoresis High JVP Mental status changes: Anxiety Agitation Lethargy Coma ```
45
Workup of VTach: labs
Electrolytes Serum levels of therapeutic drugs Toxicology Serum cardiac markers
46
Workup of VTach: imaging, other
Echo EKG Holter monitoring with recurrent syncope or palpitations
47
Tx of VTach: stabilization
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
Tx of VTach: postabilization management
Referral to a cardiologist Admission to a monitored bed Further studies, such as electrophysiologic study Consideration for radiofrequency ablation Consideration for ICD placement
49
Tx of VTach: long-term tx
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