Cardiology Flashcards
Bulbus cordis gives rise to…
Smooth/outflow parts of L and R ventricles
Endocardial cushion gives rise to…
Atrial septum
Membranous interventricular septum
AV and semilunar valves
Primitive pulmonary vein gives rise to…
Smooth part of L atrium
Right horn of sinus venosus gives rise to…
Smooth part of R atrium
Right cardinal veins give rise to…
SVC
Note - Target of central line
Embryologic mechanism of dextrocardia (e.g. Kartagener syndrome).
Defect in left-right dynein involved in L/R asymmetry during cardiac looping (4 weeks).
Age at which heart beats spontaneously
4 weeks
Steps of atrial separation (4)
Septum primum (top) grows towards endocardial cushion (bottom) narrowing foramen primum
Foramen secundum forms in septum primum as it continues to close foramen primum
Septum secundum (top) grows down to cover most of foramen secundum - residual is foramen ovale
Septum primum degenerates with remainder forming valve of foramen ovale - after birth fuse to form atrial septum due to increasing LA pressure
Note - Increasing RA pressure (straining) allows R to L shunt and may lead to cryptogenic stroke
Steps of ventricular separation (3)
Muscular interventricular septum (bottom) forms with opening called interventricular foramen
Aorticopulmonary septum (truncal/bulbar ridges) rotates and grows down to fuse with muscular septum - forms membranous interventricular septum and closes interventricular foramen
Endocardial cushions grow horizontally to separate atria from ventricles - also contributes to membranous interventricular septum
Mechanism of conotruncal abnormalities…
Persistent truncus arteriosus
Transposition of great vessels
Tetralogy of fallot
Failure of neural crest cells to migrate
Fetal circulation
Oxygenated blood from umbilical vein joins IVC via ductus venosus - mostly bypasses hepatic circulation
Enters RA and goes directly to LA via foramen ovale
Deoxygenated blood from SVC goes to RA, RV, and pulmonary artery, but is shunted to descending aorta (after left subclavian) via ductus arteriosus - due to high fetal pulmonary artery resistance (low O2 tension)
Deoxygenated blood returns via umbilical arteries off of internal iliacs
Mechanism of closure of fetal circulation
Decreased resistance in pulmonary vasculature leads to increased LA pressure - foramen ovale closes
Increased O2 and decreased prostaglandins (E1/E2) from placental separation lead to closure of ductus arteriosus - closed with Indomethacin
Postnatal derivative of... Allantois/urachus Ductus venosus Ductus arteriosus Notochord Umbilical arteries Umbilical vein
Median umbilical ligament Ligamentum venosum Ligamentum arteriosum Nucleus pulposus Medial umbilical ligaments Ligamentum teres
Right acute marginal artery supplies…
Right ventricle
Posterior interventricular/Posterior descending artery (PDA) supplies…
Note - 85% have PDA come off of RCA, while minority have PDA come off of LCX
Posterior ventricular walls
Posterior 1/3 of interventricular septum
Posteromedial papillary muscles
Left circumflex artery (LCX) supplies…
Lateral and posterior walls of LV
Anterolateral papillary muscles (via obtuse/marginal)
Anterior interventricular/Left anterior descending (LAD) supplies…
Anterior surface of LV
Anterior 2/3 of interventricular septum
Anterolateral papillary muscle
Blood supply to the SA and AV nodes…
Note - infarct may cause nodal dysfunction resulting in bradycardia and heart block
RCA
Fick’s principle
CO = rate O2 consumption/(arterial O2 - venous O2)
Maintenance of CO (SV x HR) during early and late exercise
Note - SV = EDV - ESV
Early both HR and SV
Late only HR - SV plateaus
Equation for MAP (afterload)
CO x TVR
OR
(2/3)Diastolic pressure + (1/3)Systolic pressure
Mechanism for decreased CO in VT
Diastole is preferentially shortened with increasing HR, decreasing filling time
Pulse pressure in... Hyperthyroidism Aortic regurgitation Aortic stiffening (isolated systolic HTN in elderly) OSA (sympathetic tone) Exercise
Increased
Pulse pressure in... Aortic stenosis Cardiogenic shock Cardiac tamponade Advanced HF
Decreased
Mechanism of catecholamine induced inotropy (and SV).
Phosphorylation of Phospholamban
Decreased inhibition of SERCA (Ca-ATPase)
Increased Ca entry into SR during relaxation
Upon next contraction…
Increased Ca-induced Ca release via RyR2 channels
Increased Ca-Troponin complex removal of Tropomyosin
Note - Na/Ca exchanger moves Ca out of cell instead of into SR during relaxation
Note - In smooth muscle Calmodulin instead of Troponin
Law explaining…
Increased O2 demand with increasing ventricular diameter
LV hypertrophy to compensate for increased afterload
LAPLACE’S LAW
Wall tension = (pressure x radius)/(2 x wall thickness)
Increased radius means increased wall tension/O2 demand
Increased wall thickness means decreased wall tension caused by increased afterload
Ejection fraction
Normal is > 55 - decreased in systolic HF but normal in diastolic HF
EF = SV/EDV = (EDV - ESV)/EDV
Action of the following on preload and afterload…
Venodilators (e.g. Nitrates)
Arteriolar vasodilators (e.g. Hydralazine)
Nitroprusside
Decreased preload (decreased O2 demand, reduced compression of coronary arteries during diastole)
Decreased afterload (activates RAAS)
Decreased preload and afterload (no effect on SV)
Note - ACEi/ARBs also affect both preload and afterload
Relationship between EDV and SV/CO (Frank-Starling curves)
Along a curve as EDV (preload) increases SV increases - force of contractility is proportional to end diastolic length of cardiac muscle fibers
As inherent contractility (inotropy) increases curve is shifted to the left - higher contractility at the same EDV
Volumetric flow rate equation
Q = flow velocity x cross sectional area (inverse of R)
Note - Capillaries have lowest velocity and highest cross sectional area
Relationship of RA pressure and venous return/CO (vascular function curves)
Increasing RA decreases venous return/CO via decreasing pressure gradient
When CO is at 0 (x-intercept) you get mean systemic pressure
When RA pressure is at 0 CO begins to plateau due to collapsing of vena cava
Location of pericardial cavity
Between fibrous pericardium/parietal pericardium and visceral pericardium.
Most posterior portion of the heart - responsible for dysphagia and hoarseness
Left atrium
Most anterior portion of the heart
Right ventricle
Note - Injury directly to LLSB will puncture lung pleura and right ventricle but not the lung
Relationship between Frank-Starling (cardiac) and vascular function curves.
Intercept of two curves is where the venous return and CO are equal = operating point of the heart
Note - cardiac function curves maintain an x/y intercept of 0
Cardiac/vascular function curve with increase in contractility
http://i.imgur.com/UFwPm59.png
Increased CO at lower RA pressure
Cardiac/vascular function curve with increase in volume/venous tone
http://i.imgur.com/Brgkvxj.png
Increased CO at higher RA pressure
Cardiac/vascular function curve with decrease in TPR (exercise, AV shunt)
http://i.imgur.com/QKvFuLN.jpg
Increased CO while maintaining same RA pressure
Note - alternatively, increase in TPR (vasopressors) will cause decreased CO while maintaining same RA pressure
Cardiac/vascular function curve in HF
http://i.imgur.com/VLyZQxu.png
Decrease in CO due to decreased inotropy (A to B) partially offset by increase in volume/venous tone (A to C)
Phases of left ventricular contraction (PV loop)…
Increased LVP at stable LVV (EDV)
Decreasing LVV (EDV to ESV) at increasing (rapid) then decreasing (reduced) LVP
Decreasing LVP at stable LVV (ESV)
Increasing LVV (ESV to EDV) at relatively stable LVP
Isovolumetric contraction - period between mitral valve closing and aortic valve opening (highest O2 consumption)
Systolic ejection - period between aortic valve opening and closing
Isovolumetric relaxation - period between aortic valve closing and mitral valve opening
Rapid/reduced filling - period between mitral valve opening and closing
Effect of increased afterload on PV loop
Increased ESV and maximum LVP - decreased SV (area in loop)
Effect of increased preload on PV loop
Increased EDV with stable ESV - increased SV (area in loop) without increase in EF
Effect of increased contractility on PV loop
Decreased ESV with stable EDV - increased SV (area in loop) and EF
Note - Line from origin of graph to top left point of loop is the Frank-Starling line
Valves/stage of cardiac cycle associated with S1 (loudest at mitral area/apex)
Closure of mitral and tricuspid valves at the beginning of isovolumetric contraction/systole
Valves/stage of cardiac cycle associated with S2 (loudest at LUSB)
Closure of aortic and pulmonary valves at the beginning of isovolumetric relaxation/diastole
Mechanism/stage of cardiac cycle associated with S3 (loudest at apex in LLD position at end expiration)
(“Kentuk-ey”)
Increased filling pressures (MR, HF) or dilated ventricle - occurs with rapid ventricular filling/early diastole
Note - may be normal in children and young adults
Mechanism/stage of cardiac cycle associated with S4 (loudest at apex in LLD position)
(“Ten-nessee”)
Increased atrial pressure and ventricular noncompliance (atrial kick against stiff LV) - occurs with atrial systole/late diastole
Stages of JVP…
a wave (absent in afib, prominent in tricuspid stenosis)
c wave
x descent (absent in tricuspid regurg)
v wave
y descent (absent in tricuspid stenosis and tamponade, prominent in constrictive pericarditis)
RA contraction
RV contraction resulting in tricuspid valve bulging into atrium
RA relaxation resulting in downward displacement of tricuspid valve during ventricular contraction
Increased RA pressure due to filling against closed tricuspid valve
RA emptying into RV prior to RA contraction
Mechanism of wide splitting as seen in pulmonary stenosis and RBBB
Delayed RV emptying delay pulmonic sound especially on inspiration
Exaggeration of normal splitting on inspiration due to increased venous return and decreased pulmonary impedance
Mechanism of fixed splitting as seen in ASD
Note - Also loud S1
L to R shunt increases RA/RV volumes so that there is increased flow through pulmonary valve regardless of inspiration
Mechanism of paradoxical splitting as seen in aortic stenosis and LBBB
Delayed aortic valve closure causes a “fixed split” during expiration - disappears during inspiration as pulmonary valve closure occurs later and “catches up” to aortic valve closure
Harsh crescendo-decrescendo systolic murmur
Loudest at mid systole - may eliminate S2
Loudest at RUSB (base)
Pulsus parvus et tardus
Radiates to carotids
Note - Concentric hypertrophy (pressure overload)
AORTIC STENOSIS
Calcification in older patients
Bicuspid aortic valve in younger patients
Holosystolic, high-pitched blowing murmur
Loudest at apex
Radiates to axilla
Note - Eccentric hypertrophy (volume overload)
MITRAL REGURGITATION
Treat with afterload reduction
Post-MI Infective endocarditis MVP LV dilation (functional/reversible) Acute rheumatic fever (initially)
Note - Acutely regurgitant syndromes present with increased pressure and decreased CO as heart has not had time to adapt
Holosystolic, high-pitched blowing murmur
Loudest at LLSB
Radiates to RSB
Note - Increases with inspiration (unlike MR)
TRICUSPID REGURGITATION
RV dilation
Infective endocarditis
Ebstein anomaly
Midsystolic click (chordae tendinae tensing) occurring earlier with inspiration
Late systolic crescendo murmur
Loudest right before S2
Loudest at apex
MITRAL VALVE PROLAPSE
Myxomatous degeneration
Chordae rupture
Predisposes to infective endocarditis
Holosystolic harsh murmur
Loudest at LLSB
VENTRICULAR SEPTAL DEFECT
Associated with fetal alcohol syndrome
High-pitched “blowing” diastolic decrescendo murmur
Loudest at early diastole - may eliminate S1
Loudest at LUSB and leaning forward
No inspiratory increase (unlike pulm regurg)
Hyperdynamic/bounding pulse (increased systolic, decreased diastolic) - may see head bobbing
Palpitations at night
Note - Eccentric hypertrophy (volume overload)
AORTIC REGURGITATION
Aortic root dilatation
Bicuspid aortic valve
Endocarditis
Note - Occasionally occurs from rheumatic fever (fusion of commissures) but will always occur with mitral valve stenosis
Early diastolic opening snap Rumbling mid diastolic murmur Decrescendo with presystolic accentuation Loudest at apex PCWP > LVEDP
Note - Patients also tend to have afib if severe, which might make accentuation disappear
MITRAL STENOSIS
Chronic rheumatic fever (late lesion) - commissural fusion
Note - More severe stenosis results in shorter A2-OS interval (earlier maximum diameter)
Continuous machine-like murmur
Loudest at left infraclavicular area
Lower extremity cyanosis
PATENT DUCTUS ARTERIOSUS
Congenital rubella
Prematurity
Note - Lower extremity cyanosis requires Eisenmenger’s syndrome
Diastolic and systolic murmurs loudest at LUSB
Systolic:
HOCM
Pulmonary stenosis
Flow murmur
Diastolic:
Aortic regurgitation
Pulmonary regurgitation
Diastolic and systolic murmurs loudest at LLSB
Systolic:
Tricuspid regurgitation
VSD
Diastolic:
Tricuspid stenosis
ASD
Effect of hand grip (increased afterload) on murmurs
Increased:
Mitral regurgitation
Aortic regurgitation
VSD
Decreased:
HOCM
Effect of valsalva/standing up (decreased preload) on murmurs…
Increased:
HOCM
MVP
Decreased: Most murmurs (including aortic stenosis)
Effect of rapid squatting/leg raise (increased preload, increased afterload) on murmurs
Increased: Most murmurs (including aortic stenosis)
Decreased:
HOCM
MVP
Phases (0-5) of cardiac action potential
Rapid depolarization due to voltage-gated Na channels
Initial repolarization due to inactivation of voltage-gated Na channels and opening of voltage-gated K channels
Plateau due to balance between voltage-gated K channels and voltage-gated Ca channels (Ca-induced Ca release)
Rapid repolarization due to massive efflux from voltage-gated slow K channels - Ca channels now closed
Resting potential maintained by high K permeability through K channels
Phases (0, 3, 4) of pacemaker action potential
Slow upstroke due to opening of voltage-gated L-Ca channels (allows for AV delay) - fast voltage-gated Na channels permanently inactivated due to high resting potential
Repolarization due to inactivation of L-Ca channels and increased activation of K channels
Slow spontaneous diastolic depolarization due to If/funny (Na) current - certain threshold opents T-type Ca channels
Mechanism of effect of Ach/adenosine, catecholamines, and sympathetic activation on HR
Ach/Adenosine decrease rate of diastolic depolarization decreasing SA activity, slow AV conduction, and prolong AV refractory period
Catecholamines increase rate of diastolic depolarization increasing SA activity, increasing AV conduction, and shortening AV refractory period
Note - SA node located near SVC opening
Relative speed of conduction of atria, AV node, Purkinje fibers, and ventricles
Purkinje (contraction) > atria > ventricles > AV node (delay)
Responsible for conduction to LA from SA node
Bachmann bundle
U-wave (after T wave) indicates…
Hypokalemia
Bradycardia
Mechanical action of heart during…
QRS (ventricular depolarization)
ST
T-wave (ventricular repolarization)
Mechanical function lags behind electrical activity
Isovolumetric contraction
Rapid ejection
Reduced ejection
Normal values for…
PR interval
QRS complex
QT interval
0.12 to 0.20
< 0.12
< 0.44 (men) or 0.46 (women)
Most common causes of acquired long-QT
“2 Hypos, 4 Antis”
Hypokalemia Hypomagnesemia Antiarrhythmics (class IA, III) Antibiotics (e.g. macrolides) Antipsychotics (e.g. haloperidol) Antidepressants (e.g. TCA) Antiemetics (e.g. ondansetron)
Inheritance pattern and presentation of…
Romano-Ward
Jervell/Lange-Nielsen
Congenital long QT - K channel defects causing defective myocardial repolarization
Romano-Ward - Autosomal dominant with no deafness
Jervell/Lange-Nielsen - Autosomal recessive with deafness
Asian male with…
ECG pattern of pseudo-RBBB
ST elevations in V1-V3
Increased risk of VT/sudden cardiac death
BRUGADA SYNDROME
Mutation in L-type Ca channels
Prevent with ICD
Delta wave
Wide QRS
Shortened PR
Increased risk of AV-reentrant tachycardia
WOLFF-PARKINSON WHITE
Abnormal fast accessory conduction pathway (bundle of Kent) from atria to ventricles bypasses rate-slowing AV node
Definitive treatment of atrial flutter
Catheter ablation of focus - isthmus between IVC and tricuspid annulus
Note - Focus for afib is AV node (interatrial septum near opening of coronary sinus/tricuspid orifice), or pulmonary veins in LA
Treatment of Vfib
Defibrillation
Regularly irregular rhythm
2nd degree Mobitz type I (Wenckebach) AV block
EKG presentation of 3rd degree heart block
Regular PR and RR intervals but no relationship between P wave and QRS
Note - associated with Lyme and 2nd degree type 2 block
Mechanisms (3) of ANP/BNP action in response to increased blood volume and atrial pressure
Note - Contributes to aldosterone escape
Increased cGMP
PKG induces smooth muscle relaxation
Decreased TPR
Decreased venous return/preload
Dilation of afferent renal arterioles
Constriction of efferent renal arterioles
Decreased Renin release
Increased GFR and Na filtration without compensatory Na resorption in distal nephron
Diuresis
Path of aortic arch/carotid body baro- and chemoreceptors to CNS
Aortic arch to Vagus to Solitary nucleus
Carotid body to Glossopharyngeal (IX) to Solitary nucleus
Mechanism of baroreceptor function
Decreased stretch leads to decreased afferent firing
Increased efferent sympathetic, with decreased efferent parasympathetic (vagus)
Results in increased PVR (sympathetic, RAAS), HR (sympathetic), contractility (sympathetic), and thus BP
Mechanism of Cushing reaction (HTN, bradycardia, respiratory depression)
Increased ICP Constriction of arterioles Cerebral ischemia Increased pCO2 and decreased pH Increased perfusion pressure (HTN) Increased stretch Baroreceptor induced bradycardia
Difference between central and peripheral (aortic arch, carotid body) chemoreceptors
Peripheral chemoreceptors response to decreasing PO2 as well, while central only response to increasing PCO2 and decreasing pH
Normal cardiac pressures for... RA RV PA LA/PCWP LV Aorta
~5 25/5 25/10 (rise in diastolic) ~10 (balloon inflation) 130/10 130/90
Note - PCWP approximates LA pressure, LV diastolic pressure,
Initial treatment of R to L shunts - “blue babies”
Maintenance of PDA with PGE1/2
Lack of aorticopulmonary septum formation
PERSISTENT TRUNCUS ARTERIOSUS
Most accompanied by VSD
Failure of aorticopulmonary septum to spiral
Associated with maternal diabetes
D-TRANSPOSITION OF GREAT VESSELS
Aorta anterior with pulmonary trunk posterior
Separation of systemic and pulmonary circuits require PDA (PGE1/2), VSD, or PFO to be compatible with life
Presents with ASD (required) and hypoplastic right heart
TRICUSPID ATRESIA
Caused by anterosuperior displacement of infundibular septum
TETRALOGY OF FALLOT
Pulmonary infundibular stenosis (prognosis)
RVH (boot-shaped heart on CXR)
Overriding aorta
VSD
Treat with…
Squatting (increased SVR reduces R to L shunt) during Tet spells
Pulmonary veins connected to SVC, coronary sinus, or portal/hepatic veins
TAPVR
Requires ASD or PDA
Mechanism for late cyanosis in L to R shunts - “blue kids” with cyanosis, clubbing, and polycythemia
VSD
ASD
PDA
EISENMENGER SYNDROME
Uncorrected L to R shunt increases pulmonary blood flow
PAH and RVH
Shunt reverses to R to L
Mechanism of lower extremity cyanosis in infantile form coarctation
Note - Associated with Turner syndrome (+bicuspid aortic valve) and Berry aneurysms
Coarctation occurs between subclavian and PDA (not present in adult form) - deoxygenated blood will enter aorta past the coarctation (now low pressure) and only reach the lower extremities
Most common causes of secondary hypertension
Fibromuscular dysplasia (string of beads) Primary hyperaldosteronism
Two histological types of arteriosclerosis of small arteries/arterioles
Hyaline thickening of vessel walls (essential HTN, diabetic microangiopathy) - results in glomerular scarring
Hyperplastic onion skinning and smooth muscle proliferation (malignant HTN) - results in fibrinoid necrosis
Arteriosclerosis of medium sized arteries presenting with pipestem appearance on XR
MONCKEBERG SCLEROSIS (MEDIAL CALCIFIC SCLEROSIS)
Medial band-like calcification of internal elastic lamina and media - does not involve intima/obstruct blood flow
Most common sites (5) of atherosclerosis (most common to least common) - common in elastic and muscular arteries
Abdominal aorta Coronary arteries Popliteal artery Carotid artery Circle of Willis
Mechanism of atherosclerosis
Endothelial cell dysfunction and fatty streaks Macrophage and LDL accumulation Foam cell formation/Platelet adhesion Smooth muscle migration (PDGF, FGF) Proliferation and ECM deposition Fibromuscular cap formation
Note - Risk of thrombotic occlusion depends on balance between macrophage Metalloproteinases and collagen deposition
Most common site of traumatic aortic rupture
AORTIC ISTHMUS
Distal to origin of L subclavian - most immobile due to ligamentum arteriosum
Risk factors for Aneurysm vs Dissection
Atherosclerosis
Cystic medial degeneration (HTN, bicuspid valve, connective tissue disease)
Classification of aortic dissections
AI
AII
B (III)
Ascending and descending aorta
Ascending aorta
Descending aorta
Note - Ascending tears begin at sinotubular junction, while descending tears begin at origin of L subclavian
Normal resting ECG
ST segment depression on exertion
STABLE ANGINA
Confirm with cath (>70% stenosis)
Reduce mortality with…
Aspirin
B-blockers (Atenolol or Metoprolol)
ST segment depression (endomyocardial)
T wave inversion
Normal biomarkers
UNSTABLE ANGINA
Due to incomplete occlusion - Reversible injury (swelling) just as in stable angina
LMWH (Enoxaparin) Supplemental O2 Symptom control with Nitrates/Morphine P2y12 blocker (Clopidogrel, Ticagrelor) ASA B-blockers ACEi
Chest pain at rest - usually at night
Transient ST segment elevation (transmural)
PRINZMETAL ANGINA (CORONARY ARTERY SPASM)
CCB
Nitrates
Smoking cessation
Avoid ASA/BBs
Mechanism of coronary steal.
Vessels maximally dilated at baseline distal to stenosis
Vasodilators (e.g. Dipyridamole) dilates normal vessels
Blood shunted towards well-perfused areas
Ischemia in post-stenotic region
ST segment depression
Elevated biomarkers
NSTEMI SUBENDOCARDIAL INFARCT
Complete occlusion of minor artery or partial occlusion of major artery - Irreversible damage after 30 minutes
LMWH (Enoxaparin)
Supplemental O2
Symptom control with Nitrates/Morphine
P2y12 blocker (Clopidogrel, Ticagrelor)
Reduce mortality with…
ASA
B-blockers
ACEi
Note - Within 60 seconds ATP is depleted but up to 30 minutes still only myocardial “stunning”
Age of MI showing…
Dark mottling
Pale with Tetrazolium stain
Coagulative necrosis (damaged/no nuclei)
Wavy fibers
Reperfusion injury
Contraction band necrosis
4 - 24 H
Notes:
Reperfusion injury is when increased blood flow leads to formation of ROS and further damage of myofibril membranes/mitochondria - troponins continue to rise after reperfusion
Also see contraction band necrosis (perpendicular to myocyte outlines) for same reason
Age of MI showing…
Yellow pallor (may see hyperemia initially)
Extensive coagulative necrosis
Extensive neutrophil invasion
Followed by macrophage invasion
Note - Macrophages laden with myoglobin and hemosiderin
1 - 7 D (FIRST WEEK)
Note - Risk for rupture especially if first MI
Age of MI showing…
Hyperemic border (granulation) Central yellow-brown softening
Granulation tissue (fibroblasts, collagen, blood vessels)
1 - 3 W (FIRST MONTH)
Age of MI showing…
Gray-white area of infarction
Contracted scar on histology
> 1 MONTH
Note - Eccentric hypertrophy (volume overload)
Timing of troponin…
Rise
Peak
Decline
4 hours (EKG before)
24 hours
7-10 days
Note - reinfarction can only be detected by CK-MB (decline at 3 d) prior to 7-10 days
ST elevations/Q waves in leads V1-V4
Reciprocal ST depression in III, aVF
LAD infarct
ST elevations/Q waves in leads I, aVL, V5-V6
LCX infarct (3rd most common)
ST elevations/Q waves in II, III, aVF
Reciprocal ST depression in I, aVL
RCA infarct (2nd most common)
Note - presents with bradycardia, hypotension, Kussmaul sign (increased JVP with inspiration)
ST depressions/tall R waves in V1-V3
PDA
MI complications within first 3 d
Arrhythmia (within 24 h)
Postinfarction fibrinous pericarditis (neutrophil damage if transmural)
MI complications (4) within first month
Papillary muscle rupture (esp. posteromedial - only PDA)
Interventricular septal rupture and shunt
Ventricular free wall rupture/tamponade
Ventricular pseudoaneurysm (cont. free wall rupture)
MI complications after first month
True ventricular aneurysm/mural thrombus
Dressler syndrome/autoimmune pericarditis
LVF and pulmonary edema
Heart failure S3 gallop Systolic dysfunction Mitral/Tricuspid regurgitation Dilation on echo Ballooning on CXR
DILATED CARDIOMYOPATHY
Eccentric hypertrophy (volume overload)
Treat with... Na restriction/Diuretics ACEi B-blockers Digoxin ICD/Heart transplant
Cardiomyopathy associated with…
Autosomal dominant inheritance Coxsackie myocarditis Alcohol Peripartum Chagas Doxorubicin Cocaine Hemochromatosis Beriberi (wet)
Dilated cardiomyopathy
Mechanism and treatment associated with…
Crescendo-decrescendo systolic murmur at LUSB and base
Murmur worse with decreased LV volume (decreased preload/SVR)
S4 gallop
Diastolic dysfunction
Mitral regurgitation (venturi forces)
HYPERTROPHIC CARDIOMYOPATHY
Autosomal dominant B-myosin heavy-chain (sarcomere) mutation leading to septal predominant myofibrillar disarray
Treat with…
Cessation of high-intensity athletics
B-blockers
Non-dihydropyridine CCB (eg. Verapamil)
Avoid... Nitrates Dihydropyridine CCBs ACEi Diuretics
Low voltage ECG
Diastolic dysfunction
Kussmaul sign
Increased atrial size with normal ventricular size
Thickened myocardium (endomyocardial fibrosis)
Eosinophilic infiltrate
LOFFLER SYNDROME
Restrictive cardiomyopathy
Note - in children differential includes endocardial fibroelastosis
HF treatments associated with reduced mortality
ACEi
B-blockers
Spironolactone
Hydralazine/Nitrates in African Americans
Hemosiderin-laden macrophages (HF cells) in lungs - golden cytoplasmic granules that turn blue with Prussian blue
Pulmonary edema
Decreased PCWP/preload
Decreased CO
Increased SVR
Cold/clammy skin
HYPOVOLEMIC SHOCK
Increased PCWP/preload
Decreased CO
Increased SVR
Cold/clammy skin
CARDIOGENIC/OBSTRUCTIVE SHOCK
Obstructive includes tamponade/PE
Decreased PCWP/preload
Increased CO
Decreased SVR
Warm/dry skin
SEPTIC/ANAPHYLACTIC SHOCK
Subtype of distributive shock
Decreased PCWP/preload
Decreased CO
Decreased SVR
Warm/dry skin
NEUROGENIC SHOCK
Subtype of distributive shock
Fever
New mitral regurgitation
Roth spots (white with surrounding hemorrhage) on retina
Painful Osler nodes on finger pads (vasculitis)
Painless Janeway erythema on palms/soles (microemboli)
Splinter hemorrhages (microemboli)
Glomerulonephritis
Arterial or pulmonary emboli
INFECTIVE ENDOCARDITIS
Treat with…
IV Vancomycin and Gentamicin
Endocarditis associated with…
IVDU/tricuspid regurgitation/pulmonary septic emboli Acute/normal valves Prosthetic valves Subacute/abnormal valves (RF, MVP) GU/GI manipulation Colon cancer Lupus/malignancy
S. aureus, Pseudomonas, Candida S. aureus S. epidermidis (coagulase- staph) Viridans strep (S. mutans, S. mitis) Enterococcus S. bovis Marantic/thrombosis
Disease associated with…
Aschoff bodies - Myocardial granuloma
Anitschkow cells - Histiocytes with wavy/rod-like nucleus
ACUTE RHEUMATIC FEVER MYOCARDITIS
Note - As opposed to viral myocarditis which shows predominant lymphocytic infiltration
Sharp pain on inspiration
Relief with sitting forward
Friction rub
Pulsus paradoxus
Widespread ST elevation with PR depression
Pericardial effusion
Associated with... Coxsackievirus Rheumatic fever STEMI/Dressler Radiation Neoplasia Autoimmune (SLE, rheumatoid arthritis) Uremia (no ST elevation)
ACUTE PERICARDITIS
Treat with…
NSAIDs
Glucocorticoids
Dialysis if uremic
CHF
Pericardial knock in early diastole
Kussmaul sign
Low QRS voltage with T-wave flattening
Increased pericardial thickness
Sharp halt in diastolic filling
Atrial enlargement
Associated with... Tuberculosis Surgery Radiation Neoplasia Uremia
CONSTRICTIVE PERICARDITIS
Treat with…
Diuretics
Pericardiectomy
Becks triad - Hypotension, JVD, distant heart sounds
Pulsus paradoxus
Low QRS voltage with electrical alternans
Equal pressures in all 4 chambers during diastole
Late diastolic collapse of RA
CARDIAC TAMPONADE
Diseases (5) associated with pulsus paradoxus - decreased of > 10 mmHg in systolic BP with inspiration
Mechanism - Equal diastolic pressures in RV/LV allows RV to bulge into LV with increased venous inflow on inspiration limiting LV outflow
Cardiac tamponade Pericarditis Asthma OSA Croup
Mechanism behind syphilitic heart disease
Tertiary syphilis disrupts vasa vasorum of aorta with subsequent atrophy of vessel wall
Note - also results in calcification of aortic root/ascending arch (tree bark aorta)
Constitutional symptoms
Multiple syncopal episodes
Mid-diastolic rumble at apex
Early diastolic plop sound
Scattered cells with mucopolysaccharide stroma
LEFT ATRIAL MYXOMA
Benign, pedunculated mesenchymal proliferation
Primary cardiac tumor in children associated with tuberous sclerosis
VENTRICULAR RHABDOMYOMA
Benign hamartoma
Mechanism behind Kussmaul sign
Negative intrathoracic pressure on inspiration not transmitted to heart - impaired filling of RV transmitted back to jugular veins
Often due to constrictive pericarditis, restrictive cardiomyopathy, and RA/RV tumors
Elderly female Constitutional signs Unilateral temporal headache Jaw claudication Ophthalmic artery occlusion/irreversible blindness
Elevated ESR
Affects carotid artery branches (elastic)
Medial granulomatous inflammation, Intimal thickening, Elastic lamina fragmentation
Associated with Polymyalgia Rheumatica
GIANT CELL (TEMPORAL) ARTERITIS
High-dose corticosteroids
Young asian female Constitutional signs Ocular disturbance Neurological disturbance Weak UE pulses
Elevated ESR
Affects aortic arch and proximal great vessels (elastic)
Medial granulomatous inflammation, Intimal thickening, Elastic lamina fragmentation
TAKAYASU ARTERITIS
Corticosteroids
Young adult Constitutional signs Hypertension Bowel angina with melena Neurologic dysfunction Livedo reticularis
Elevated ESR
Rosary sign mesenteric/renal aneurysms
Affects medium sized muscular vessels (spares lungs)
Transmural inflammation with fibrinoid necrosis
Immune-complex mediated
Associated with HBV
POLYARTERITIS NODOSA
Corticosteroids
Cyclophosphamide
Asian children Conjunctival injection Desquamating rash (including palms and soles) Hand-foot edema Cervical adenopathy Strawberry tongue Fever > 5 days
Early-onset coronary aneurysms/MI due to inflammation
KAWASAKI DISEASE (MUCOCUTANEOUS LYMPH NODE SYNDROME)
IVIG
ASA
Heavy middle-aged male smokers Intermittent claudication Gangrene and autoamputation of digits Superficial nodular phlebitis Raynaud's phenomenon
Necrotizing vasculitis of medium sized vessels
segmental vasculitis extending into contiguous veins and nerves
THROMBOANGIITIS OBLITERANS (BUERGER DISEASE)
Smoking cessation
Chronic sinusitis Nasopharyngeal ulceration Otitis media/Mastoiditis Cough Dyspnea Hemoptysis Hematuria due to RPGN
Large nodular densities on CXR
PR3-ANCA/c-ANCA positive
Affects small vessels…
Large necrotizing Granulomas
Adjacent necrotizing vasculitis
GRANULOMATOSIS WITH POLYANGIITIS (WEGENER)
Cyclophosphamide
Corticosteroids
Cough
Dyspnea
Hemoptysis
No nasopharyngeal involvement
Pauci-immune glomerulonephritis (minimal fluorescence)
MPO-ANCA/p-ANCA positive (cloverleaf fluorescence)
Affects small vessels…
Necrotizing vasculitis
No granulomas
MICROSCOPIC POLYANGIITIS
Cyclophosphamide
Corticosteroids
Asthma
Sinusitis
Skin nodules or purpura
Peripheral neuropathy
Peripheral eosinophilia
Pauci-immune glomerulonephritis
MPO-ANCA/p-ANCA positive
Affects small vessels…
Necrotizing Granulomas
Eosinophils
EOSINOPHILIC GRANULOMATOSIS WITH POLYANGIITIS (CHURG-STRAUSS)
URI in child followed by... Palpable purpura on buttocks/legs Arthralgia Abdominal pain Hematuria due to IgA nephropathy (Berger disease)
IgA immune complex deposition on small vessels
HENOCH-SCHONLEIN PURPURA (HSP)
Self-limited
Mechanism of Cor Pulmonale
Hypoxia due to chronic lung disease causes vasoconstriction of pulmonary vessels
Type of ASD associated with Trisomy 21
OSTIUM PRIMUM
Note - Aplasia of ostium secundum most common type
Most common metastases to heart
Note - Pericardial effusion
Breast
Lung
Melanoma
Lymphoma
Vertebral levels at which IVC…
Forms from iliacs
Crosses in front of R renal artery
Drains into RA
L4-L5
L1
T8
Derivatives of arch vascular derivatives (1-4, 6)
1 = Maxillary artery 2 = Hyoid/Stapedial 3 = Common/Internal carotid 4 = L (aortic arch) R (subclavian) 6 = Pulmonary arteries, PDA
Released by vascular endothelium to... Inhibit platelet aggregation Induce vasodilation Increase vascular permeability Stimulate leukocyte chemotaxis
Note - decreased in damaged endothelium (e.g. MI)
PROSTACYCLIN (PGI2)
From PGH2 via Prostacyclin Synthase
Note - opposes action of TXA2
Cause of supine hypotension (e.g pregnancy)
Aortocaval compression
Fixed-split S2
Midsystolic ejection murmur at LUSB due to increased flow across pulmonary valve
Mid-diastolic rumble murmur due to increased flow across tricuspid valve
ATRIAL SEPTAL DEFECT
Note - ASD, VSD, PFO associated with paradoxical embolisms especially on shunt reversal (straining, coughing)
Decreased LV length
Sigmoid septum with bulging
Atrophy of ventricle (increased connective tissue)
Lipofuscin pigment (brown perinuclear cytoplasmic inclusions)
NORMAL CARDIAC AGING
Subendocardial vacuolization and fibrosis
CHRONIC ISCHEMIC HEART DISEASE
Histological change in cardiac myocytes as a result of long-standing hypertension
Note - Diastolic dysfunction and LA enlargement
CONCENTRIC HYPERTROPHY
Note - Due to pressure overload and also seen in aortic stenosis
Benign congenital tumor composed of unencapsulated aggregates of thin-walled capillaries that grow before regressing by puberty
JUVENILE (STRAWBERRY) HEMANGIOMA
Border and contents of femoral triangle
Superiorly - Inguinal ligament
Medially - Adductor longus
Laterally - Sartorius
Contents (lateral to medial)... Nerve (not part of femoral sheath) Artery Vein Lymphatics
Note - Artery is midway between pubic symphysis and anterior superior iliac spine
Cardiomyocyte characteristic decreased with diastolic and systolic dysfunction, respectively.
Diastolic - Compliance (Normal EF, Normal LVEDV, increased LVEDP)
Systolic - Contractility (Reduced EF, Increased LVEDV, Increased LVEDP)
State causing... Increased CO/HR/RR Constant AO2 and ACO2 Decreased VO2 and increased VCO2 Modest increase in MAP Decreased PVR
EXERCISE
Increased tissue demand - more O2 removed and CO2 produced
Mechanism of acute pulmonary edema in a patient with aortic stenosis
Concentric hypertrophy means filling of LV becomes dependent on atrial kick which is lost in afib
Measurement of degree of AS
Difference between LVP and AOP during systole - point of maximum difference is point of maximum intensity of murmur
Note - In AR both increase dramatically together so no difference during systole
Review of CT imaging of thoracic anatomy
https://www.youtube.com/watch?v=b8qSXAH9WxQ
Pathologic findings associated with dicrotic pulse
High PVR and severe systolic dysfunction
Note - Accompanied by pulsus alternans
Pulsatile mass with thrill
Constant bruit
Increased preload
Decreased afterload
AV FISTULA
Note - Results in high-output cardiac failure
Modifiable risk factors for atherosclerosis
HTN
Hypercholesterolemia
Smoking
Diabetes
Mechanism of AAA in atherosclerosis
Fibrous cap prevents diffusion of O2 into vessel wall - below renal arteries no vasa vasorum for supply
Mechanism of enlarged coronary sinus in PAH
Note - Presents as loud S2
Increased RA pressure
Oral aphthous ulcers
Genital ulcers
Uveitis
BEHCET DISEASE
Mechanism of vasodilation via Ach, Shear stress, Bradykinin, and Substance P
Increase Ca (endothelium) Activation of eNOS Conversion of Arginine to NO NO diffuses into smooth muscle Increased cGMP
Note - NO is the single most important mediator of coronary vasodilation/autoregulation (Adenosine for coronary arterioles)
prominent intracytoplasmic granules that are tinged yellowish brown ina 78 yo male
lipofuscin accumulation due to lipid peroxidation
accumulating in aging cells
Advanced malignancy
sterile platelet rich thrombi on mitral valve leaflets
also associated with:
SLE
antiphospholipid syndrome
DIC
nonbacterial thrombotic endocarditis
endothelial injury due to circulating cytokines which trigger platelet deposition in presence of hypercoagulable state
Location of the left and right bundle branches
after leaving the AV node the AP enters the bundle of his and left and right bundle branches
along the interventricular septum
FASTEST (includes purkinje system) to ensure efficient contraction of the ventricles
contraction motion of ventricles
twisting motion fromt he apex toward the base (bottom-up)
Long term management for a patient who has a prosthetic valve
warfarin which competitively inhibits vitamin k epoxide reductase and depletes body of biologically active vitamin K
