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1. HDS Cardiology > Pathophysiology > Flashcards

Pathophysiology Flashcards

1
Q

Venous Thromboembolism

(VTE)

A

DVT and PE

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2
Q

DVT

Epidemiology

A
  • Risk higher in men
  • Most common in LE
    • Esp. calf veins
    • 15-30% propagate to proximal calf veins without treatment
  • Risk of PE much higher in proximal DVT
    • 40-50% vs 5-10% distal
  • UE DVT much less common
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3
Q

UE DVT

Risk Factors

A
  • Central venous line
  • Pacemakers
  • Trauma
  • Extrinsic compression @ thoracic inlet
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4
Q

DVT

Presentation

A
  • Pain and swelling of the area
  • Many asympatomatic w/ normal exam
  • Exam
    • TTP, erythema, warmth, swelling distal to DVT
    • Palpable tender “cord” in area of DVT
    • Dilated superficial veins
    • Low grade fever
    • Homan’s sign ⇒ calf pain with dorsiflexion
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5
Q

SVC Syndrome

A

Can be caused by UE DVT

  • Facial swelling
  • Blurred vision
  • Dyspnea
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6
Q

DVT

Diagnosis

A
  • D-Dimer
    • Fibrin degradation product
    • Nonspecific
  • Duplex US
    • Sensitivity⇒ proximal DVT (90-100%), distal DVT (40-90%)
  • Contrast venography ⇒ gold standard
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7
Q

DVT

Treatment

A
  • Anticoagulation
  • IVC filter
    • Should be avoided unless can’t anticoag
    • Dec. risk of PE short term
    • Inc. risk of recurrent DVT
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8
Q

Thromboplebitis

A

Superficial inflammation and pain involving a vein.

  • Risk ⇒ Virchow’s triad
  • Presentation ⇒ firm, tender palpable cord
  • Treatment ⇒ local heat and NSAIDS
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9
Q

PR Interval

A

0.12 - 0.2 secs

or

< 1 large box

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10
Q

QRS Complex

A

< 0.1 secs

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11
Q

QT interval

A

< 0.45 secs

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12
Q

Axis Determination

A

Use lead II or aVF

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13
Q

Inferior Wall

Leads

A

II, III, aVF

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14
Q

Anterior Wall

Leads

A

I, aVL, V1-V3

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15
Q

Anterolateral Wall

Leads

A

V5, V6

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16
Q

Lateral Wall

Leads

A

I, aVL, -aVR

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17
Q

EKG Leads

Summary

A
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18
Q

Left Anterior Descending

(LAD)

A

Anterior wall of both ventricles

Anterior 2/3 of septum

Anterior papillary muscles

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19
Q

Diagonal branches of LAD

A

Anterior surface of LV

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20
Q

Left Circumflex

A

Left atrium

Posterior and lateral left ventricle

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21
Q

Right coronary artery (RCA)

A

Right atrium and right ventricle

SA and AV nodes

Posterior septum

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22
Q

Right marginal artery

A

RV

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23
Q

Posterior descending artery

A

Inferior and posterior walls of right ventricle

Posterior 1/3 of septum including posterior papillary muscles

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24
Q

Coronary Circulation

Summary

A
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25
Q

CAD

Risk Factors

A
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26
Q

CAD

Biomarkers

A
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27
Q

Typical CAD History

A

Levine’s sign ⇒ pt comes in clutching hand to chest

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28
Q

Chest Pain

Patterns

A
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29
Q

Physical Exam

During Ischemia

A

Xanthomas ⇒ cholesterol deposits around joints

Xanthelasmas ⇒ cholesterol deposits around eyes

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30
Q

EKG Lead

Patterns

A
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31
Q

Stable Angina

Treatment

A
  • Medical therapy
    • Modify risk factors
      • Lipid lowering drug
      • Control BP
    • Drugs to prevent/relieve angina
      • Nitrates
      • β-blockers
      • CCB
      • Late sodium current blockers
        • Ranolazine - if fail all others
    • Antiplatelet agents
  • Interventional therapy
    • PCI / stent
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32
Q

Cardiac Cath

Indications

A
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33
Q

Prinzmetal Angina

A
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34
Q

S3 gallop

A

Due to volume overload with poor LV function

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35
Q

S4 heart sound

A

Due to noncompliant left ventricle

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36
Q

ACS

Treatment

A
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37
Q

STEMI

Treatment

A
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38
Q

NSTEMI and Unstable Angina

Treatment

A
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39
Q

Dressler Syndrome

A
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40
Q

Acute Bacterial Endocarditis

A
  • Normal valve
  • Virulent organism
  • Onset days - few weeks
  • Mortality rate higher
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41
Q

Subacute Bacterial Endocarditis

A
  • Abnormal valve ⇒ congenital or degenerative
  • Less virulent organism
    • Viridans strep
    • S. epidermidis
    • Enterococcus
  • Onset weeks to many months
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42
Q

Endocarditis

Risk Factors

A
  • Significant MR ⇒ most common
  • MVP ⇒ 20% of NVE cases
  • RHD
  • Congenital heart disease ⇒ 15% with NVE
    • TOF ⇒ highest IE risk
    • VSD, bicuspid valve, aortic coarctation
  • Degenerative valves ⇒ SBE in elderly pts
    • Mitral valve most common
  • Hypertrophic cardiomyopathy or asymmetrical septal hypertophy ⇒ aortic valve IE (rare)
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43
Q

Endocarditis

Pathogenesis

A
  • Portal of entry for organism into bloodstream
  • Turbulent flow ⇒ endothelial damage ⇒ deposition of fibrin/platelets
    • Deposition gives rise to non-bacterial thrombotic endocarditis (NBTE)
  • Bacteria adhere to NBTE and multiply
    • More platelet/fibrin deposition ⇒ creates vegetation where bacteria replicate
  • There can be direct invasion of virulent organism in ABE without underlying endothelial damage
44
Q

Endocarditis

Lesion Locations

A

Valve surface facing lower pressure chamber

  • Ventricular surface of semilunar valves
  • Atrial surface of AV valves
45
Q

Acute Bacterial Endocarditis

Agents

A

S. aureus most common

46
Q

Subacute Bacterial Endocarditis

Agents

A

Viridans strep most common

47
Q

IE Overall

Agents

A

S. viridans most common cause overall

48
Q

Native Valve Endocarditis

A

Both Staph and Strep ⇒ 70-80% of cases

  • Abnormal valves
    • Strep including viridans
      • S. sanguis, S. salivarius, S mutans
    • S. bovis (group D strep)
  • Normal valves
    • S. aureus
    • Enterococci
    • S. pneumoniae
    • S. pyogenes
49
Q

Prosthetic Valve Endocarditis

A
  • Early
    • Within 2 months after surgery
    • Usually due to contamination from surgery
    • More virulent pathogens
      • S. epidermitis most common
      • S. aureus, GNR like Pseudomonas, Enterococci, Candida, Corynebacterium
  • Late
    • > 60 days after surgery
    • Valve is endothelialized
    • Pathogens less virulent
      • S. epidermitis ⇒ most common months 2-12
      • Strep including viridans ⇒ most common > 12 months
      • Also S. aureus, Entoerocci, Candida
50
Q

IV Drug Users

Endocarditis

A
  • Agents
    • S. aureus most likely
    • Enterococci, Pseudomonas, Candida, beta-hemolytic strep
    • Can be polymicrobial
  • Location
    • Tricuspid valve most often
51
Q

Healthcare Associated NVE

A

S. aureus

Coag-neg strep

Enterococci

52
Q

Dental-Associated

Endocarditis

A

Viridans strep

53
Q

GI/GU Associated

Endocarditis

A

Strep. bovis

Enterococci

54
Q

Fungal

Endocarditis

A
  • Seen with immunocompromised hosts
  • Vegetations larger and bulkier
  • Valvular/chordal perforation possible
  • Micro ⇒ PMNs, fibrin, platelets, fungi
55
Q

Culture-Negative

Endocarditis

A
  • May have vegetations, murmur, symptoms of IE with negative cultures
  • Causes
    • Prior abx therapy
    • Fastidious organisms
      • HACEK group
      • Legionella, Brucella, Coxiella
    • Non-infective endocarditis
    • Atrial myxoma
56
Q

Non-infective Endocarditis

A
  • Non-bacterial thrombotic endocarditis
  • Libman Sacks Endocarditis
57
Q

Non-bacterial Thrombotic Endocarditis

(NBTE)

A
  • Small vegetations of fibrin on leaflets
  • No microorganisms
  • Can produce emboli
  • See in debilitated patients
    • Esp. lymphoma, lung CA, pancreatic CA
  • Frequently occurs along with DVT/PE
58
Q

Libman Sacks Endocarditis

A
  • Mitral and tricuspid valvulitis with small, sterile vegetations
    • May be located on undersurfaces of AV valves, valvular endocardium cords, mural
  • Associated with SLE ⇒ commonly occurs with antiphospholipid syndrome
  • Micro ⇒ finely granular, fibrinous eosinophilic material
59
Q

Acute Bacterial Endocarditis

Symptoms

A
  • Generally more fulminant picture
  • High fevers
  • Heart murmur
60
Q

Subacute Bacterial Endocarditis

Symptoms

A
  • Low grade fever
    • May not be present if pt used abx
  • May not have murmur
61
Q

Endocarditis

Other Symptoms

A
  • Nonspecific sx common
    • Fatigue, night sweats, anorexia, chills, weight loss
  • CNS symptoms
    • HA, AMS
  • Myalgias or arthralgias
  • Other sx related to complications
62
Q

Endocarditis

Physical Exam

A
  • Fever and murmur
  • Arterial emboli ⇒ 20-50%
  • Splenomegaly ⇒ 15-50%
  • Clubbing ⇒ 10-20%
  • Petechiae ⇒ 10-40%
  • Janeway lesions ⇒ hemorrhagic, non-painful macules of palms/soles
  • Osler nodes ⇒ painful, subcutaenous nodules on distal pads of fingers or toes
  • Splinter hemorrhages
  • Roth spots ⇒ retinal hemorrhages with small central clearing
63
Q

Endocarditis

Complications

A
  • Cardiac
    • Valvular destruction
    • CHF
    • Myocardial abscess or valve ring abscess
    • Suppurative pericarditis
    • Emboli
  • Embolic complications
    • Left-sided lesions
      • CVA or brain abscess
      • Roth spots
      • MI
      • Splenic abscess or infarct
      • Renal abscess or infarct
    • Right-sided
      • Pulmonary septic emboli, infarct, PNA
  • Mycotic (infected) aneurysms
    • Cerebral vessels most common
    • Also AA, splenic, coronary, plumonary, mesenteric
  • CNS
    • Cerebral emboli ⇒ MCA most common
    • CVA, arteritis, abscess, cerebritis, meningitis
  • Renal
    • Embolic infarct
    • Multiple abscesses
    • Interstitial nephritis
    • Glomerulonephritis
64
Q

Endocarditis

Diagnosis

A
  • Tests
    • Blood cultures
    • ECHO
  • Duke Criteria
    • Major
      • Microbiologic
      • Evidence of endocardial involvement
    • Minor
      • Predisposing heart condition or IVDU
      • Fevere
      • Vascular phenomena
      • Immunologic phenomena
      • Microbiologic findings that aren’t major
65
Q

Endocarditis

Treatment

A
  • Prolonged abx therapy with bactericidal drugs
  • Empiric therapy in suspected IE
66
Q

Endocarditis

Prophylaxis

67
Q

Acute Rheumatic Fever

A

Acute, immune mediated multisystem inflammatory disease that follows GAS pharyngitis by 10 days to 6 weeks.

Mostly in children.

68
Q

ARF

Clinical Presentation

A
  • Migratory polyarthritis with fever
  • Carditis
    • Pericardial friction rubs
    • Tachycardia and arrhythmias
    • Cardiac dilatation from myocarditis
      • Resultant mitral insufficiency or CHF
  • 1% die from fulminant RF
69
Q

ARF

Diagnosis

A
  • Major criteria
    • Carditis
    • Polyarthritis
    • Chorea
    • Erythema Marginatum
    • Subcutaneous nodules
  • Minor criteria
    • Arthralgia
    • Fever
    • Elevated ESR and CRP
    • Prolonged PR interval
  • Jones Criteria
    • ASO titer + 2 major or 1 major and 2 minor criteria
70
Q

ARF

Pathology

A

Anistschkow cells ⇒ Mφ with abnormal chromatin

Aschoff body ⇒ multinucleated Anistschkow cells

71
Q

ARF

Pericarditis

72
Q

Chronic Rheumatic Heart Disease

A

Acute rheumatic carditis of ARF can progress to chronic RHD.

  • Valve distribution of chronic RHD
    • Mitral ⇒ 65-70%
    • Mitral and aortic ⇒ 25%
    • Tricuspid and pulmonic ⇒ rare
73
Q

Rheumatic Mitral Valve Disease

A
  • Commissural fusion
  • “Fish mouth” mitral valve
  • Thickening, shortening, and fusion of chordae tendinae
  • Diffuse fibrous thickening of valve cusp
  • Fibrosis of leaflets
    • Primarily at margin of closure
  • Post-inflammatory neovascularization
  • Chronic inflammation
  • Mineralization
74
Q

Cardiac Valve

Histology

75
Q

Mixed Lesion

A

Stenosis and insufficiency within the same valve

76
Q

Pure disease

A

Only stenosis or insufficiency within a valve

77
Q

Isolated disease

A

Involvemen of a single valve

78
Q

Combined disease

A

Involvement of more thatn one valve

79
Q

Valvular Lesions

Consequences

A
  • Effect varies from mild to fatal
  • Degree of stenosis/insufficiency related to rate of development
  • Secondary changes in other organs
    • Lungs and liver most
    • Pulmonary HTN
80
Q

Congenital vs Acquired

Valvular Lesions

A
  • Acquired stenosis of aortic and mitral ⇒ 2/3 of all valve diseases
  • Congenital malformations may inc. severity of acquired disease
81
Q

Mitral and Aortic Valvular Disease

Etiologies

82
Q

Aortic Stenosis

A
  • Critical AS ⇒ 2/3 reduction in area or >50 mmHg gradient
  • Untreated ⇒ usu. die of CHF, 10-20% die suddenly d/t lethal arrhythmia
  • Major causes
    • Degenerative calcific aortic stenosis ⇒ most common
    • Bicuspid Aortic Valve ⇒ most common congenital valve anomaly
    • Senile degeneration
    • Chronic RHD
    • Diffuse post-inflammatory scarring with commissural fusion
    • Congenital aortic stenosis
83
Q

Calcific Aortic Stenosis

A
  • Due to senile degeneration
  • Otherwise normal valve
  • Bulky calcific deposits in Sinus of Valsalva
  • ± osseous metaplasia
84
Q

Bicuspid Aortic Valve

A
  • Most common congenital valve anomaly
  • See early calcific stenosis
    • 60-70 y/o
  • Two patterns
    • Anterior/posterior
    • Right/left
  • Raphe ⇒ false commissure
85
Q

Unicommissureal Aortic Valve

86
Q

Acommissural Aortic Valve

87
Q

Aortic Stenosis

Presentation

A
  • Asymptomatic for years until stenosis severe
  • Onset of sx ⇒ inc. mortality
  • Angina ⇒ syncope ⇒ heart failure
88
Q

Aortic Stenosis

Diagnosis

A
  • Physical exam
    • Systolic ejection murmur, crescendo-decrescendo, best heard in the right 2nd intercostal space
      • Murmur radiates to carotid arteries
      • May radiate to apical region ⇒ Gallivardin’s phenomenon
      • Mild AS ⇒ early peaking murmur
      • Severe AS ⇒ late peaking murmur
        • Paradoxically split S2 (A2 after P2)
      • Critical AS ⇒ A2 component inaudible/absent
    • Low amp. carotid pulse ⇒ pulsus parvus
    • Delay in carotid upstroke ⇒ pulsus et tardus
    • Sustained apical impulse
  • Possible EKG findings
    • LVH
    • LBBB
    • Heart block
  • Possible CXR findings
    • LV prominence
    • AV calcification
    • Post-stenotic aortic dilatation
  • TTE ⇒ gold standard
  • TEE ⇒ cath or stress test if still unsure
89
Q

Aortic Insufficiency

A

A portion of the total SV regurgitates back into the LV.

  • Due to failure of leaflet coaptation in diastole
  • AR ⇒ ventricular dilatation ⇒ inc. EDV ⇒ volume overload
  • Majr etiologies
    • Aortic root dilatation
    • Chronic RHD
    • Infective endocarditis
    • Diet drug (Phen-Fen) valvulopathy
90
Q

Acute Severe AR

A
  • Presentation
    • Acute heart failure
    • Cardiogenic shock
    • Fulminant pulmonary edema
  • Diagnosis
    • Tachycardia, hypotension, tachypnea
    • Diastolic Decrescendo murmur
      • May be soft and short w/ early termination
    • CXR ⇒ nl LV size w/ pulmonary edema
    • TTE/TEE to confirm
  • Treatment
    • Diuretics to improve pulmonary edema
    • Hemodynamic stabilization
    • Urgent surgery
91
Q

Chronic Severe Aortic Regurgitation

Clinical Presentation

A
  • Exertional dyspnea
  • Orthopnea
  • Fatigue
  • Occational chest pain
92
Q

Chronic Severe Aortic Regurgitation

Diagnosis

A
  • Physical exam
    • Diastolic decrescendo mumur best heard at left or right sternal border with pt leaning forward at end-expiration
      • Diastolic flow murmur @ left sternal border without MS ⇒ Austin-Flint murmur
    • Soft systolic murmur possible
    • Laterally displaced and diffuse PMI
    • Large pulse pressure
    • Soft S1
    • S3 possible in absence of CHF
    • Quincke’s pulse ⇒ systolic plethora and diastolic nail bed blanching with pressure
    • Musset’s sign ⇒ head bobbing
    • Corrigan’s pulse ⇒ bounding full carotid pulse with rapid downstroke
  • TTE to confirm dx
  • CXR ⇒ progressive cardiomegaly
93
Q

Chronic Severe Aortic Regurgitation

Treatment

A
  • Pt may be asymptomatic for years
  • Indications for aortic valve replacement
    • Severe symptomatic AR
    • Severe asympatomatic AR w/ structural LV changes
94
Q

Mitral Valve Insufficiency

A

Failure of MV to close completely allows reverse flow from LV to LA during systole.

  • Major causes
    • Abnormalities of leaflets and commissures
      • MVP
      • RHD
      • IE
    • Abnormalities of tensor apparatus
      • Papillary muscle/chordae rupture or dysfunction
    • Left ventricular abnormalities
      • LV dilatation
    • Abnormalities of mitral annulus
      • Mitral annular calcification
95
Q

Acute Severe MR

A
  • Presentation
    • Pts acutely ill
    • Hypotension and shock
    • Acute pulmonary edema and acute HF
  • Diagnosis
    • Classic holosystolic murmur may be absent
    • Acute onset of pulmonary edema/HF
    • TTE to confirm
    • TEE or cath if unclear
  • Treatment
    • Requires urgent surgery
    • Intra-aortic balloon pump ⇒ dec. afterload
    • Diuretics ⇒ reduce pulmonary edema, hypotension may be prohibitive
    • Nitroprusside and hydralazine ⇒ reduce afterload
96
Q

Chronic MR

A
  • Presentation
    • Remains asympatomatic for prolonged period
    • Progressive exertional dyspnea and fatigue
    • CHF sx during late stages
  • Physical exam
    • Classic holosystolic murmur best heard at LV apex with radiation to axilla
    • S3 gallop
    • Soft S1
  • TTE for confirmation and evaluation
  • Treatment
    • Mitral valve replacement
      • Severe MR with LV dysfunction or new A. Fib or symptomatic
    • Prophylactic MV repair
      • Preserves subchordal apparatus and IV geometry
      • Consider mortality risk, surgeon, and pt anatomy
97
Q

Mitral Valve Prolapse

A

“Floppy mitral valve”

Excess valve tissue results in billowing of tissue between chordal attachments.

  • Affected leaflets enlarged, redundant, thick, rubbery, and nearly translucent
  • Chordae stretched and abnormal
    • Can thin and rupture ⇒ “flail leaflet” and MR
  • One of the most common valvular disorders
  • Etiology usu. unknown
  • Commonly seen with CT disorders
  • Tricuspid valve also affected in 20-40%
98
Q

MVP

Microscopic Appearance

A
  • Myxomatous degeneration of valve
  • ↑ mucopolysaccharides
  • ↓ collagen
  • Expansion of spongiosa w/ disruption of fibrosa
  • Type III collagen lost ⇒ ↓ structual integrity
99
Q

MV Prolapse

Murmur

A

Mid systolic click

100
Q

MVP

Complications

A

Seen in 3% of patients.

Higher risk in men, older patients.

  • Infective endocarditis
  • Mitral insufficiency requiring surgery
  • Stroke / systemic infarct
  • Arrhythmias
101
Q

Mitral Annular Calcification

A

Stony hard calcific nodules occuring behind MV leaflets.

  • May not affect function
  • Can cause regurgitation or stenosis
  • Site for thrombi formation
  • Site for infective endocarditis
  • Most common
    • Women over 60 y/o
    • Myxomatous mitral valve
    • Elevated LV pressure
102
Q

Mitral Stenosis

A

Obstruction to flow from LA to LV leads to pressure gradient across the MV during diastole.

  • Etiology
    • RHD
    • Infective endocarditis
    • Tumor
    • Metabolic
    • Mitral annular calcification
  • Gradual ↑ LA pressure ⇒ pulmonary congestion ⇒ pulmonary edema ⇒ right HF
  • Long standing MS ⇒ marked LA enlargement ⇒ risk of developing A. Fib
103
Q

Mitral Stenosis

Presentation

A
  • Progressive dyspnea or fatigue with exertion
  • Exacerbated by tachycardia
  • A. fib with RVR poorly tolerated
104
Q

Mitral Stenosis

Diagnosis

A
  • Physical exam
    • Early on when leaflets still pliable
      • “Opening snap” followed by a low-pitched diastolic rumble
        • Best heard with the bell with patient in the left lateral decubitus position
      • Prominent S1
    • With increasing severity
      • Loss of opening snap
      • S1 softens and eventually disappears
  • EKG ⇒ LA enlargement and ultimately RA enlargement with RBBB
  • CXR ⇒ LA enlargement, pulmonary artery dilatation, RV enlargement in advanced cases
  • TTE ⇒ gold standard
105
Q

Mitral Stenosis

Treatment

A
  • Mechanical intervention ⇒ Percutaneous balloon mitral valvuloplasty (PBMV)
    • Symptomatic severe MS
    • Asymptomatic severe MS w/ significant pulmonary HTN
    • Asymptomatic severe MS w/ new A. Fib
    • Symptomatic women during pregnancy
  • If poor candidate for PBMV ⇒ surgical commissurotomy or valve replacement
  • Anticoagulate if A. Fib present or hx of prior embolic event
  • Diuretics
  • Rate control
106
Q

Peripheral Arterial Disease

(PAD)

A

Atherosclerotic vascular disease primarily in BLE.

  • Epidemiology
    • 20-30% of ppl > 70
    • Men > women
    • Same risk factors as CAD
  • Common @ branch points and turbulent areas
  • 50-70% of cases asymptomatic
  • Usually present with claudication
107
Q

Claudication

A
  • Calf ⇒ femoral-popliteal disease
  • Thigh, hip, or butt ⇒ aortoiliac disease
  • Pseudo-claudication ⇒ spinal stenosis or MSK
    • Not relieved with rest

1. HDS Cardiology (7 decks)

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