Transcript AOA Cardiology Review

AOA Cardiology Review
Deepa Patadia
Luke Poth
March 22, 2011
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Anatomy
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Know normal
pressures:
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RA: < 5
RV: < 25/5
RV=PA: < 25/5
PCWP=LA: < 12
LV: < 130/10
Aorta: < 130/90
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Conduction System
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Fast Action Potential
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Variations in conductance of voltage gated ion
channels
Spatially arranged so to create a domino effect
Resting membrane potential negative due to
intracellular proteins
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AP Propagation
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AP propagates down
the sarcolema (Plasma
membrane)
Down T-Tubules
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Cardiac Muscle Excitation Contraction
Coupling
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AP propagates down TTubules to Sarcoplamic
Reticulum (Ca2+
stores)
Get Ca2+ induced
Ca2+ release
Digoxin binds to
Na+/K+ atpase
exchanger (not shown)
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Its all about Cardiac Output
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CO = Stroke volume x Heart rate (liters/min)
Stroke volume
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Preload volume of blood at the end of diastole
Afterload  LV wall stress needed to pump blood
into the aorta
Contractility  function of biochemistry of cardiac
muscle
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Preload
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Cardiac Output as function of preload is commonly
referred to as Frank Starling Curve
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Afterload
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Law of Laplace
Afterload = (Aortic Pressure x Radius)/wall
thickness
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Increased pressure, increased ventricular
diameter, or decreased wall thickness increases
afterload
In order to maintain constant afterload, an
increase in BP overtime leads to increased wall
thickness
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Contractility
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Based on changes in biochemistry within the
muscle fiber
Primarily mediated via the sympathetic and
parasympathetic nervous system
Most drugs modulate Cardiac Output by
affecting contractility
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LV Diastolic Pressure Volume Curve
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Pressure Volume Loop for LV
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Increased Preload
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Increased Afterload
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Increased Contractility
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CO/Venous Return Curve
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Fast Regulation of Arterial Pressure
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Slow Regulation of BP
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Rhythms
healthguide.howstuffworks.com
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Rhythms
http://www.aafp.org/afp/2003/0801/p483.html
cardionetics.com
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Rhythms
medictube.com
easypediatrics.com
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Rhythms
ncbi.nlm.nih.gov
medictube.com
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Rhythms
ambulancetechnicianstudy.co.uk
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Rhythms
cardionetics.com
http://library.med.utah.edu/kw/ecg/ecg_outline/Lesson6/index.html
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Rhythms
http://en.wikipedia.org/wiki/File:CHB.jpg
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Murmurs General Rules
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Expiration increases intensity of right sided
murmurs
Inspiration increases intensity of left sided
murmurs
Can identify etiology of murmur by finding
location on chest wall where murmur is heard
the loudest
S1…..S2 (A2 P2)
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Common Murmurs
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Mitral/Tricuspid Regurgitation
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Holosystolic blowing murmur
Location where murmur is heard loudest
indicates whether mitral or tricuspid
Any process which remodels LV can cause
mitral regurg
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Aortic Stenosis
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Ejection click followed cresendo-decrescendo
murmur
Radiates to carotids, paroxical splitting
Etiology: Dystophic calcification or bicuspid
valve
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VSD
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Holosytolic and harsh
Larger the defect the softer the murmur
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Mitral Valve Prolapse
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Late systolic click then murmur which peaks
in intensity at S2
Decreased preload causes murmur to move
towards S1
Increased preload moves to S2
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Aortic Regurgitation
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Immediate blowing diastolic murmur
Wide pulse pressure
Etiology: (1) aortic valve root dilation most
common (2) Infective endocarditis
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Mitral Stenosis
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OS delayed rumbling late diastolic murmur
Severity measured by time interval between
S2 and OS
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Shorter time interval more severe
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HOCM Murmur
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Increases in intensity with reduced preload
(standing up, expiration)
Decreases in intensity with increased preload
(B-blocker, lying flat)
Sounds like aortic stenosis but loudest at left
parasternal border 4th intercostal space
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Pathology
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Congenital Heart Disease
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Early cyanosis (right to left shunt)
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Tetralogy of Fallot
Transposition of the great vessels
Truncus arteriosus
Tricuspid atresia
Total anomalous pulmonary venous return
Late Cyanosis (left to right shunt)
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VSD
ASD
PDA
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Hypertension
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BP>140/90
Primary vs. secondary
Predisposes to: atherosclerosis, LVH, stroke, CHF,
renal failure, retinopathy, aortic dissection
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Atherosclerosis
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Risk factors: smoking, htn, DM, hyperlipidemia,
family history
Pathogenesis: endothelial cell dysfunction  LDL
and macrophage accumulation  foam cell
formation  fatty streaks  smooth muscle
migration  fibrous plaques
Complications: aneurysms, ischemia, infarcts,
peripheral vascular disease, thrombus, emboli
Symptoms: angina, claudication, or asymptomatic
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Ischemic Heart Disease
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Angina
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Stable
Unstable
MI
Chronic ischemic heart disease
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Myocardial Infarction
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Day 1: risk for arrhythmia
Day 2-4: risk for arrhythmia
Day 5-10: risk for free wall rupture, papillary
muscle rupture, interventricular septal rupture
Week 7: risk for ventricular aneurysm
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MI Diagnosis
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EKG (ST elevation, ST depression, Q waves)
Cardiac troponin (rises after 4 hours; remains elevated for 710 days)
CK-MB
AST
ecglibrary.com
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Cardiomyopathies
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Dilated
 Systolic dysfunction
 Eccentric hypertrophy
 Etiologies: alcohol, wet beriberi, coxsackie B myocarditis,
chronic cocaine use, Chagas’ disease, doxorubicin toxicity,
hemochromatosis, peripartum cardiomyopathy
Hypertrophic
 Diastolic dysfunction
 Concentric hypertrophy, outflow tract obstruction
 Autosomal dominant
Restrictive
 Diastolic dysfunction
http://eurheartj.oxfordjournals.org/content/29/7.cover-expansion
 Etiologies: sarcoidosis, amyloidosis, postradiation fibrosis,
endocardial fibroelastosis, Loffler’s syndrome, hemochromatosis
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CHF
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Clinical syndrome that occurs due to
diminished cardiac pumping function
Right heart failure most often due to left heart
failure; isolated right heart failure can occur
due to cor pulmonale
Signs/Symptoms: dyspnea on exertion,
cardiac dilation, pulmonary edema,
paroxysmal nocturnal dyspnea, orthopnea,
hepatomegaly, dependent edema, JVD
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Endocarditis
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Strep viradans most
common
Staph aureus most common
in drug users
Strep bovis most common
in UC or colon cancer
Tricuspid valve endocarditis
think drug users
Mitral valve most common
valve
Osler nodes
Janeway lesions
Roth spots
Splinter Hemorrhages
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Roth Spots
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Not unique tpo
endocarditis
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Pericarditis
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Etiology: rheumatic (SLE, rheumatoid
arthritis), viral infection (coxsackie most
common), uremia, post MI (Dressler’s
Syndrome)
EKG: diffuse ST elevations, PR depressions
Symptoms: Pleuritic chest pain and chest
pain lessened by leaning forward
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Effusion/CardiacTamponade
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Fluid surrounding the heart
Equivalent pressure in all four chambers
EKG: Electrical Alternans
Pulsus Paradoxus: Non palapable radial
pulse on inspiration
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Vascular Disorders
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Raynaud’s disease
Wegener’s
Granulomatosis
Churg-Strauss
syndrome
Sturge-Weber disease
Henoch-Schonlein
purpura
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Buerger’s disease
Kawasaki disease
Polyarteritis nodosa
Takayasu’s arteritis
Temporal arteritis
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Thank you!
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