Pathophysiology Flashcards
Venous Thromboembolism
(VTE)
DVT and PE
DVT
Epidemiology
- 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
UE DVT
Risk Factors
- Central venous line
- Pacemakers
- Trauma
- Extrinsic compression @ thoracic inlet
DVT
Presentation
- 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
SVC Syndrome
Can be caused by UE DVT
- Facial swelling
- Blurred vision
- Dyspnea
DVT
Diagnosis
- D-Dimer
- Fibrin degradation product
- Nonspecific
- Duplex US
- Sensitivity⇒ proximal DVT (90-100%), distal DVT (40-90%)
- Contrast venography ⇒ gold standard
DVT
Treatment
- Anticoagulation
- IVC filter
- Should be avoided unless can’t anticoag
- Dec. risk of PE short term
- Inc. risk of recurrent DVT
Thromboplebitis
Superficial inflammation and pain involving a vein.
- Risk ⇒ Virchow’s triad
- Presentation ⇒ firm, tender palpable cord
- Treatment ⇒ local heat and NSAIDS
PR Interval
0.12 - 0.2 secs
or
< 1 large box
QRS Complex
< 0.1 secs
QT interval
< 0.45 secs
Axis Determination
Use lead II or aVF
Inferior Wall
Leads
II, III, aVF
Anterior Wall
Leads
I, aVL, V1-V3
Anterolateral Wall
Leads
V5, V6
Lateral Wall
Leads
I, aVL, -aVR
EKG Leads
Summary
Left Anterior Descending
(LAD)
Anterior wall of both ventricles
Anterior 2/3 of septum
Anterior papillary muscles
Diagonal branches of LAD
Anterior surface of LV
Left Circumflex
Left atrium
Posterior and lateral left ventricle
Right coronary artery (RCA)
Right atrium and right ventricle
SA and AV nodes
Posterior septum
Right marginal artery
RV
Posterior descending artery
Inferior and posterior walls of right ventricle
Posterior 1/3 of septum including posterior papillary muscles
Coronary Circulation
Summary
CAD
Risk Factors
CAD
Biomarkers
Typical CAD History
Levine’s sign ⇒ pt comes in clutching hand to chest
Chest Pain
Patterns
Physical Exam
During Ischemia
Xanthomas ⇒ cholesterol deposits around joints
Xanthelasmas ⇒ cholesterol deposits around eyes
EKG Lead
Patterns
Stable Angina
Treatment
- 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
-
Modify risk factors
- Interventional therapy
- PCI / stent
Cardiac Cath
Indications
Prinzmetal Angina
S3 gallop
Due to volume overload with poor LV function
S4 heart sound
Due to noncompliant left ventricle
ACS
Treatment
STEMI
Treatment
NSTEMI and Unstable Angina
Treatment
Dressler Syndrome
Acute Bacterial Endocarditis
- Normal valve
- Virulent organism
- Onset days - few weeks
- Mortality rate higher
Subacute Bacterial Endocarditis
- Abnormal valve ⇒ congenital or degenerative
- Less virulent organism
- Viridans strep
- S. epidermidis
- Enterococcus
- Onset weeks to many months
Endocarditis
Risk Factors
- 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)
Endocarditis
Pathogenesis
- 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
Endocarditis
Lesion Locations
Valve surface facing lower pressure chamber
- Ventricular surface of semilunar valves
- Atrial surface of AV valves
Acute Bacterial Endocarditis
Agents
S. aureus most common
Subacute Bacterial Endocarditis
Agents
Viridans strep most common
IE Overall
Agents
S. viridans most common cause overall
Native Valve Endocarditis
Both Staph and Strep ⇒ 70-80% of cases
- Abnormal valves
- Strep including viridans
- S. sanguis, S. salivarius, S mutans
- S. bovis (group D strep)
- Strep including viridans
- Normal valves
- S. aureus
- Enterococci
- S. pneumoniae
- S. pyogenes
Prosthetic Valve Endocarditis
-
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
IV Drug Users
Endocarditis
- Agents
- S. aureus most likely
- Enterococci, Pseudomonas, Candida, beta-hemolytic strep
- Can be polymicrobial
- Location
- Tricuspid valve most often
Healthcare Associated NVE
S. aureus
Coag-neg strep
Enterococci
Dental-Associated
Endocarditis
Viridans strep
GI/GU Associated
Endocarditis
Strep. bovis
Enterococci
Fungal
Endocarditis
- Seen with immunocompromised hosts
- Vegetations larger and bulkier
- Valvular/chordal perforation possible
- Micro ⇒ PMNs, fibrin, platelets, fungi
Culture-Negative
Endocarditis
- 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
Non-infective Endocarditis
- Non-bacterial thrombotic endocarditis
- Libman Sacks Endocarditis
Non-bacterial Thrombotic Endocarditis
(NBTE)
- 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
Libman Sacks Endocarditis
-
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
Acute Bacterial Endocarditis
Symptoms
- Generally more fulminant picture
- High fevers
- Heart murmur
Subacute Bacterial Endocarditis
Symptoms
- Low grade fever
- May not be present if pt used abx
- May not have murmur
Endocarditis
Other Symptoms
- Nonspecific sx common
- Fatigue, night sweats, anorexia, chills, weight loss
- CNS symptoms
- HA, AMS
- Myalgias or arthralgias
- Other sx related to complications
Endocarditis
Physical Exam
- 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
Endocarditis
Complications
- 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
- Left-sided lesions
- 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
Endocarditis
Diagnosis
- 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
- Major
Endocarditis
Treatment
- Prolonged abx therapy with bactericidal drugs
- Empiric therapy in suspected IE
Endocarditis
Prophylaxis
Acute Rheumatic Fever
Acute, immune mediated multisystem inflammatory disease that follows GAS pharyngitis by 10 days to 6 weeks.
Mostly in children.
ARF
Clinical Presentation
- 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
ARF
Diagnosis
- 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
ARF
Pathology
Anistschkow cells ⇒ Mφ with abnormal chromatin
Aschoff body ⇒ multinucleated Anistschkow cells
ARF
Pericarditis
Chronic Rheumatic Heart Disease
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
Rheumatic Mitral Valve Disease
- 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
Cardiac Valve
Histology
Mixed Lesion
Stenosis and insufficiency within the same valve
Pure disease
Only stenosis or insufficiency within a valve
Isolated disease
Involvemen of a single valve
Combined disease
Involvement of more thatn one valve
Valvular Lesions
Consequences
- 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
Congenital vs Acquired
Valvular Lesions
- Acquired stenosis of aortic and mitral ⇒ 2/3 of all valve diseases
- Congenital malformations may inc. severity of acquired disease
Mitral and Aortic Valvular Disease
Etiologies
Aortic Stenosis
- 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
Calcific Aortic Stenosis
- Due to senile degeneration
- Otherwise normal valve
- Bulky calcific deposits in Sinus of Valsalva
- ± osseous metaplasia
Bicuspid Aortic Valve
- Most common congenital valve anomaly
- See early calcific stenosis
- 60-70 y/o
- Two patterns
- Anterior/posterior
- Right/left
- Raphe ⇒ false commissure
Unicommissureal Aortic Valve
Acommissural Aortic Valve
Aortic Stenosis
Presentation
- Asymptomatic for years until stenosis severe
- Onset of sx ⇒ inc. mortality
- Angina ⇒ syncope ⇒ heart failure
Aortic Stenosis
Diagnosis
- 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
-
Systolic ejection murmur, crescendo-decrescendo, best heard in the right 2nd intercostal space
- 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
Aortic Insufficiency
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
Acute Severe AR
- 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
Chronic Severe Aortic Regurgitation
Clinical Presentation
- Exertional dyspnea
- Orthopnea
- Fatigue
- Occational chest pain
Chronic Severe Aortic Regurgitation
Diagnosis
-
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
-
Diastolic decrescendo mumur best heard at left or right sternal border with pt leaning forward at end-expiration
- TTE to confirm dx
- CXR ⇒ progressive cardiomegaly
Chronic Severe Aortic Regurgitation
Treatment
- Pt may be asymptomatic for years
- Indications for aortic valve replacement
- Severe symptomatic AR
- Severe asympatomatic AR w/ structural LV changes
Mitral Valve Insufficiency
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
-
Abnormalities of leaflets and commissures
Acute Severe MR
- 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
Chronic MR
- 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
-
Mitral valve replacement
Mitral Valve Prolapse
“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%
MVP
Microscopic Appearance
- Myxomatous degeneration of valve
- ↑ mucopolysaccharides
- ↓ collagen
- Expansion of spongiosa w/ disruption of fibrosa
- Type III collagen lost ⇒ ↓ structual integrity
MV Prolapse
Murmur
Mid systolic click
MVP
Complications
Seen in 3% of patients.
Higher risk in men, older patients.
- Infective endocarditis
- Mitral insufficiency requiring surgery
- Stroke / systemic infarct
- Arrhythmias
Mitral Annular Calcification
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
Mitral Stenosis
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
Mitral Stenosis
Presentation
- Progressive dyspnea or fatigue with exertion
- Exacerbated by tachycardia
- A. fib with RVR poorly tolerated
Mitral Stenosis
Diagnosis
- 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
-
“Opening snap” followed by a low-pitched diastolic rumble
-
With increasing severity
- Loss of opening snap
- S1 softens and eventually disappears
-
Early on when leaflets still pliable
- EKG ⇒ LA enlargement and ultimately RA enlargement with RBBB
- CXR ⇒ LA enlargement, pulmonary artery dilatation, RV enlargement in advanced cases
- TTE ⇒ gold standard
Mitral Stenosis
Treatment
- 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
Peripheral Arterial Disease
(PAD)
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
Claudication
- Calf ⇒ femoral-popliteal disease
- Thigh, hip, or butt ⇒ aortoiliac disease
- Pseudo-claudication ⇒ spinal stenosis or MSK
- Not relieved with rest
