Cardio Flashcards
Truncus arteriosus–>
Ascending aorta and pulmonary trunk
Bulbus cordis–>
smooth parts (outflow tract) of left/right ventricles
Endocardial cushion–>
Atrial septum, membranous IV septum, AV and semilunar valves
Primitive atrium–>
Trabeculated part of rt/lt atria
Primitive ventricle–>
Trabeculated part of rt/lt ventricle
Primitive pulmonary vein–>
Smooth part of lt atrium
Left horn of sinus venosus–>
coronary sinus
Right horn of sinus venosus–>
Smooth part of rt atrium (sinus venarum)
Right common cardinal vein and rt anterior cardinal vein
SVC
What part of IV septum most often malformed in VSD?
Membranous
Ductus venosus
Allows bypass of hepatic circulation
Foramen ovale
Allows bypass of pulmonary circulation
Ductus arteriosus
Allows blood to leave pulmonary circulation
Closed foramen ovale
Fossa ovalis
What causes ductus arteriosus closure?
Low prostaglandins – can use indomethacin
Allantois–>
Urachus–>mediaN umbilical ligament
Ductus arteriosus–>
Ligamentum arteriosum
Ductus venosus–>
Ligamentum venosum
Notochord–>
nucleus pulposus
Umbilical aa’s–>
MediaL umbilical ligaments
Umbilical vvs–>
Ligamentum teres hepatis (round ligament) in the falciform ligament
SA and AV nodal blood supply
RCA
LCX goes to
Lateral/post walls of left ventricle, antlat papillary muscle
LAD goes to
Anterior 2/3 of IV septum, anterlat papillary muscle, anterior surface of lft ventricle
PDA goes to
AV node, posterior 1/3 IV septum, post 2/3 walls of ventricles, posteromed papilary muslce
Right marginal a goes to
Right ventricle
Innervation of pericardium
Phrenic n (referred shoulder pain)
CO=
SV*HR
Fick principle
CO=rate O2 consumed/(art O2-venousO2)
MAP=
CO*TPR
or
2/3 diastolic P+1/3systolic P
Pulse pressure
Systolic-diastolic
Proportional to SV, inverse proportional to arterial compliance
SV
EDV-ESV
Increase pulse pressure states
Hyperthyroidism, aortic regurg, aortic stiffening, OSA, exercise
Lower pulse pressure states
Aortis stenosis, cardiogenic show, cardiac tamponade, advanced HF
SV increases with…
Higher contractility
Higher preload
Lower afterload
Contractility increases with…
B1 activation (calcium channels opened, phospholamban phosphorylation) Catecholamines More IC Ca Lower EC Na Dig (blocks Na/K pump)
Contractility decreases with…
B1 block (less cAMP) Loss of myocardium Dilated cardiomyopathy HF w/ systolic dysfxn Acidosis Hypoxia/hypercapnia Non DHP Ca channel blockers
Oxygen demand for heart increased with…
Increased Contractility
Increased Afterload (proportional to art. P)
Increased hR
Increased Diameter of ventricle
CARD
Wall tension =
Walls stress =
Tension= P*r
Stress=(Pr)/(2wall thickness)
Approximation, contributors, pharm affecting preload
Ventricular EDV
Depends on venous tone and circulating blood volume
Lowered w/ nitroglycerin (venous vasodil.)
Afterload approximation, pharm affecting
MAP
Lowered with arterial vasodilators like hydralazine, ACE inhibs/ARBs (lower preload and afterload)
Response to high afterload
LV hypertrophy (increase wall thickness) to decrease wall tension
EF=
SV/EDV
or
(EDV-ESV)/EDV
Index of ventricular contractility (lower in systolic HF)
Starling princiciple
Force of contraction is proportional to end diastolic length of cardiac muscle fiber (preload) up to a point where the increased tension impedes hearts ability to pump
ChangeP=
Q*R
Where Q=volumetric flow rate
Q=
Flow velocity(v)*Cross sectional area(A)
R=
changeP/Q
or
8n(viscosity)length/(pir^4)
SO RADIUS IS THE BIG VARIABLE
Total resistance in series
R=R1+R2+R3…
Total resistance in parallel
1/R=1/R1+1/R2+1/R3…
What accounts for most of TPR?
Arterioles
What provides storage capacity?
Venous circ
a wave
Atrial contraction (absent in A fib)
c wave
RV contraction (closed tricuspid bulges into atrium)
x descent
Downward displacement of close tricuspid valve during rapid vent. ejection phase
Reduced/absent in tricuspid regurg, right HF because lower pressure gradient
v wave
Increased RAP due to filling against closed tricuspid valve
Y descent
RA emptying into RV
Prominent in constrictive pericarditis
Absent in cardiac tamponade
Wide splitting
In conditions that delay RV emptying (e.g. pulmonic stenosis, right branch bundle block)–exaggeration of normal splitting
Fixed splitting
Heard in ASD, i.e. lft–>rt shunt–>delayed closure of pulmonic valve
Paradoxical splitting
Delay aortic valve closure (aortic stenosis, lft bundle branch block), A2 after P2; On inspiration P2 moves closer to A2 (I.e. split best heard in exhalation)
Inspiration’s effect on heart sounds
Increases venous return to rt atrium –> increased intensity of rt heart sounds
Hand grip’s effect on heart sound
Increases afterload –> increased intensity of MR, AR, VSD murmurs
- -> lowered intensity of hypertrophic cardiomyopathy, AS murmurs
- -> later click in MVP
Valsalva/standing effect on heart sound
Decreases preload –> decreased intensity of most murmurs
Increased intensity of hypertrophic cardiomyopathy
Earlier click in MVP
Rapid squatting effect on heart sound
Increases venous return, increases preload, increases afterload
Decreased intensity of hypertrophic cardiomyopathy murmur
Increased intensity of AS, MR, VSD
Later click in MVP
Aortic stenosis
Crescendo-decrescendo systolic (w/ or w/o ejection click)
Heard loudest at heart base, radiates to carotids
Can lead to syncope, angina, dyspnea on exertion
Usually due to age related calcification or in younger patients with congenital bicuspid aortic valve (e.g. Turners)
Mitral/tricuspid regurg
Holosystolic, high pitched, blowing
Mitral – loudest at apex and radiates towards axilla; often due to iscehmic heart disease after MI, MVP, LV dilatation
Tricuspid – loudest at tricuspid area; usually caused by RV dilatation
Can be caused by rheumatic fever/infective endocarditis
MVP
Late systolic crescendo w/ mid systolic click (sudden tensing of chordae tendinae) – loudest just before S2
Most frequent lesion, usually benign
Best heard over apex
Causes: myxomatous degeneration (e.g.in Margans), rheumatic HD, chordae rupture
VSD
Holosystolic harsh sounding murmur heard best at tricuspid area
aortic regurg
High pitched “blowing” early diastolic decrescendo murmur
Long diastolic murmur, hyperdynamic pulse, head bobbing when severe/chronic, wide pulse pressure
Usually due to aortic root dilatation, bicuspid aortic valve, endocarditis, rheumatic fever
Progresses to lft HF
Mitral Stenosis
Follows opening snap (abrupt half in leaflet motion in diastole – after rapid opening due to fusion at leaflet tips)
Delayed rumbling mid/late diastolic murmur
(Prognosis worse if closer to S2)
Highly specific for late rheumatic fever and can lead to LA dilatation
PDA
Continuous machine-like murmur loudest at S2 – congenital rubella or prematurity; best heard at left infraclavicular area
Phase 0 (myocardium)
Rapid upstroke/depol due to opening of voltage gated Na channels
Phase 1 (myocardium)
Initital repol due to inactivation of Na channels – voltage gated K channels begin to open
Phase 2 (myocardium)
Plateau due to Ca influx through voltage gate Ca channels (balances K efflux) –> triggers Ca release from SR and myocyte contraction
Phase 3 (myocardium)
Rapid repolarization due to K efflux – opening of slow K channels and Ca channels close
Phase 4 (myocardium)
Resting potential characterized by high K permeability
Phase 0 (nodal)
Upstroke due to opening of voltage gated Ca channels, fast voltage gated Na chennels permanently inactivated because resting potential is less negative –> slow conduction velocity to prolong transmission from atria to ventricles
Phase 3 (nodal)
Inactivation of Ca channels and increased activation of K channels –> K efflux
Phase 4 (nodal)
Slow spontaneous diastolic depol due to If funny current –> slow Na/K inward current; gives automaticity and slope determines HR
Ach/Adenosine decrease rate of diastolic depol/HR
Catecholamines increase rate of diastolic depol/HR (sympathetic stim opens If)
SA node location
Near entry of SVC
AV node location
Posterinferior part of interatrial septum near opening of coronary sinus
Pacemaker rates
SA>AV>bundle of His/Purkinje/Ventricles
Speed of conduction
Purkinje>atria>vent>AV node
P wave
Atrial depol
QRS
Ventricular depol (<120s)
QT interval
Vent depol, contraction, repol
T wave
Vent repol
J point
Jxn between end of QRS and start of ST
ST segment
Isoelectric – vents are depol
U wave
Prominent in hypokalemia and bradycardia
Causes of Torsades
Low K Low Mg Congenital abnormalities (long QT syndrome -- ion channel defects --> risk of SCD and torsades) Drugs AntiArrhythmics (IA, III) AntiBiotics (macrolides) AntiCychotics (Haloperidol) AntiDepressants (TCAs) AntiEmetics (Odansetron) ABCDE
Romano Ward
AD pure cardiac congenital long QT syndrome; K channel
Jervell Lange Nielsen
AR, congenital long QT syndrome w/ sensorineural deafness; K channels
Brugada syndrome
AD in Asian males; pseudo right branch bundle block w/ ST elevations in V1-V3; increased risk of vent tachyarrhymthias and SCD – give implantable cardioverter-defibrilator
Wolff Parkinson White
Most common ventricular preexcitation syndrome
Abnormal fast accessory pathway from atria to ventricle (bundle of Kent) that bypasses rate slowing AV node resulting in partial ventricular depol earlier –> delta wave with widened QRS and shorter PR
Can cause reentry circuit –> SVT
Risk factors for A fib
HTN, CAD
1st degree heart block
PR >200ms
2nd degree type I/Wenckebach HB
Progressive lengthening of PR interval until beat dropped
2nd degree type II HB
Dropped beats not preceeded by change in length of PR interval
3rd degree HB
Atria and ventricles independent (Arate>Vrate)
Can be caused by lyme disease
ANP release from
Atrial myocytes in response to increased blood volume/atrial P
ANP actions
via cGMP –> vasodilation and less Na reabsorption at renal collecting tubule, dilates afferent renal arterioles and contricts efferent –> diuresis and contributes to aldosterone escape
BMP release from
Ventricular myocytes in response to increased tension
Aortic arch receptor
Transmits via vagus to solitary nuc of medulla in response to BP change
Carotid sinus receptor
Transmits via glossopharyngeal (9) to solitary nucleus of medulla in response to BP change
Peripheral vs central chemoreceptors
Peripheral respond to O2, CO2 and pH while central only CO2 and pH
How do you measure LAP?
PCWP
Heart autoregulation of blood flow
Local vasodilatory metabolites: adenosine, NO, CO2, low O2
Brain autoregulation of blood flow
Local vasodilatory metabolites: Co2 (pH)
Kidneys autoregulation of blood flow
Mygenic and tubuloglomerular feedback
Lungs autoregulation of blood flow
Hypoxia –> vasoconstriction (this is weird but maintains ventilation/perfusion match)
Skeletal muscle autoregulation of blood flow
Local metabolites during exercise: lactate, adenosine, K, H, CO2
Skin autoregulation of blood flow
Symp stim helps in temp control
Net fluid flow equation
Jv=Kf[(Pc-Pi)-C(pic-pii))]
Kf = capillary permeatbility to fluid
Right to left shunts
Truncus arteriosus (1 vessel) Transposition (2 switched vessels) Tricuspid atresia Tetralogy of fallot TAPVR (5Ts)
Persistent truncus arteriosus
Doesn’t divide into aorta/pulmonary trunk due to lack of aorticopulmonary septum formation (usually accompanied by VSD)
D-transposition of great vessels
Septation did not spiral – must have shunt present for mixing w/ blood
Tricuspid atresia
Absence of tricuspid valve and hypoplastic RV (requires ASD and VSD)
Tetralogy of fallot
Anterior superior displacement of infundibular septum – most common cause of early childhood cyanosis
-Pulmonary infundibular stenosis/RVOTO (PROGNOSIS!)
-Right ventricular hypertrophy (boot shaped heart)
-Overriding aorta
-VSD
Squatting –> increases SVR –> less right/left shunt (higher left sided pressure) –> improves cyanosis
TAPVR
Total anomalous pulmonary venous return
Pulonary veins drain into right heart – assoc w/ ASD/PDA to allow right–>left shunting to maintain CO
Ebstein anomaly
Displacement of tricuspid vavle leaflets down into RV, “atrializing” the ventricle –> tricuspid regurg and right HF
Assoc w/ utero Li exposure
Left to right shunts
VSD>ASD>PDA
ASD
Loud S1, wide fixed split S2
Ostium secundum defects are common
Eisenmenger syndrome
Uncorrected left–>rt shunt –> increased pulmonary blood flow –> pathologic remodeling of vascularture –> pulmonary arterial HTN–>RVH to compensate–>rt to lft shunt (reversed) –> late cyanosis, clubbing, polycythemia
Coarc of aorta
Aortic narrowing near insertion of ductus arteriosus
Assoc w/ bicuspid aortic valve, Turner syndrome
HTN in upper extremities and weak lower extremity pulses
W/ time intercostal aas enlarge to create collateral circ –> erode into ribs –> notched appearance on CXR
Complications: HF, increased risk of cerebral hemorrhage (berry aneurysm), aortic rupture, endocarditis
Alcohol exposure in utero–>
VSD, PDA, ASD, tet oF
Congenital rubella–>
PDA, pulm a. stenosis, septal defects
Diabetes in mother –>
Transposition of great vessels
DS–>
AVSD (endocard cushion defect), VSD, ASD
Marfan –>
MVP, thoracic aortic aneurysm and dissection, aortic regurg
Li exposure in utero–>
Ebstein anomaly
Turner syndrome–>
Bicuspid aortic vavle, coarc
Williams syndrome
Supravalvular aortic stenosis
22q11 syndromes–>
Truncus arteriosus, Tet oF
Hypertensive urgency
> 180/>120 w/ no end organ damage
Hypertensive emergency
evidence of acute end organ damage – encephalopathy, stroke, retinal hemorrhages/exudates, papilledema, MI, HF, aortic dissection, kidney injury, microangiopathic hemolytic anemia, eclampsia
HTN predisposes to
CAD, LVH, HF, a fib, aortic dissection, aortic aneurysm, stroke, CKD (hypertensive nephropathy), retinopathy
Hyaline arteriolosclerosis
Thickening of vessel walls as in essential HTN or diabetes
Hyperplastic arteriolosclerosis
Onionskinning in in severe HTN w/ proliferation of smooth muscle cells
Monckeberg sclerosis
Aka medial calcific sclerosis – medium sized arteries
Calcifications of internal elastic lamina and media –> vascular stiffening without obstruction
Pipstem appearance on x ray, does not obstruct blood flow and intima NOT involved
Atherosclerosis
Large/medium sized muscular arteries – arteriolosclerosis caused by cholesterol plaques
Location of atherosclerosis
Abdominal aorta>coronary artery>popliteal artery>carotid artery
GF involved in smooth muscle cell migration in atherosclerosis
FGF, PDGF
Abdominal aortic aneurysm risk factors and sxs
Atherosclerosis, tobacco use, age, male, family hx
Present: palpable pulsatile abdominal mass
Thoracic aortic aneurysm risk factors
Assc w/ cystic medial degeneration, risk factors: HTN, bicuspid aortic valve, Marfans, 3o syphillis (obliterative endarteritis of the vasa vasorum) –> aortic root dilatation –> aortic regurg
Traumatic aortic rupture
Trauma/deceleration injury –> at aortic isthmus most often (just distal to origin of lft subclav a.)
Associations w/ aortic dissection
HTN, bicuspid aortic vavle, connective tissue disorders
Aortic dissection presents
Tearing sudden pain radiating to back, can have unequal BP in arms, CXR shows mediastinal widening
Types of aortic dissection
Stanford A: proximal –> ascending aorta, may extend to aortic arch or descending, may cause acute aortic regurge or tamponade (REQ SURG)
Stanford B: distal –> only descending aorta (Tx w/ B blockers and then vasodilators)
Risk factors for prinzmetal angina
Smoking (not HTN or hypercholestrol)
Coronary steal
Give a vasodilator and causes dilation in normal coronary vessels rather than stenosed; pharm stress tests
STEMI
Transmural w/ ST elevation
NSTEMI
Subendocardial infarct w/ ST depression
First 24 hours post MI
Wavy fibers –> neutrophils appear; complications: Vent arrhythmia, HF, cardiogenic shock
1-3 days post MI
Extensive coag necrossis w/ neutrophils; complication postinfarction fibrinous pericarditis
3-14 days post MI
Macrophages and then granulation tissue; complications: free wall rupture –> tamponade, papillary m rupture –> mitral regurge, IV septal rupture (macrophage mediated structural degradation), LV pseudoaneurysm
2 weeks-months post MI
Contracted scar; complications: Dressler syndrome, HF, arrhthmias, true vent aneurysm (mural thrombus)
Troponin rises in x hours and peaks at x hours then remains elevated for x days
4, 24, 7-10
CK-MB rises in X hours, peaks at X hours, returns to normal in X hours
6-12, 16-24, 48 – making it good to follow
Anteroseptal MI
LAD – V1-V2
Anteroapical MI
distal LAD – V3-V4
Anterolateral MI
LAD or LCX – V5-V6
Lateral MI
LCX – I, aVL
Inferior MI
RCA–II, III, aVF
Posterior MI
PDA V7-V9; depression in V1-3 w/ tall R waves
Tx for NSTEMI/unstable angina
Anticoag, antiplt, ADP receptor inhib (clopedogrel), B blocker, ACE inhib, statins, symptoms controlled w/ nitroglyerin and morphin
Tx for STEMI
NSTEMI + Reperfusion therapy
Dilated cardiomyopathy causes
Alcohol, wet Beriberi, Coxsacki B viral myocarditis, chornic Cocaine use, Chagas, Doxorubicin, hemochromatosis, sarcoidosis, peripartum cariomyopathy
ABCCCD
Findings in dilated cardiomyopathy
HF, S3, regurg murmur, dilated heart on echo, balloon appearance on CXR; leads to systolic dysfuction, eccentric hypertrophy
Tx for dilated cardiomyopathy
Na restriction, ACE inhib, B blockers, diuretics, dig, ICD, heart transplant
Takotsubo cardiomyopathy
Ventricular apical balooning due to increased sypathetic stim (stress)
Hypertrophic cardiomyopathy causes
Mostly familial – mutations in sarcomeric proteins like myosin binding prot C and beta myosin heavy chain, assc w/ Freidrich ataxia
Hypertrophic cardiomyopathy sx
Syncope during exercise, can lead to sudden death, S4, systolic murmur, mitral regurge due to impaired mitral valve closure; leads to diastolic dysfxn; has marked concentric hypertrophy and myofibrillar disarray/fibrosis
Hypertrophic obstructive cardiomyopathy
Hypertrophic CM w/ asymmetric septal hypertrophy/systolic anterior motion of mitral valve–>outflow obstruction–>dyspnea, syncope
Tx of hypertrophic CM
Cessation of high-intensity athletics, Bblockers or nonDHP CCBs, ICD if high risk
Restrictive/infiltrative CM causes
Postradiation fibrosis, Loffler syndrome, Endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), amyloidosis, sarcoidosis, hemochromatosis (though more often dilated)
Puppy LEASH
Restrictive/infiltrative CM results in
Diastolic dysfxn – low voltage ECG despite thick myocardium (esp w amyloid)
Loffler endocarditis
Assc. w/ hypereosinophilic syndrome; histology shows eosinophilic infiltrate in myocardium
HF syndrome
Cardiac pump dysfxn –> congestion, low perfusion; sx: dyspnea, orthopnea, fatigue, S3, rale, JVD, pitting edema
Systolic dysfxn
Reduced EF, higher EDV, lower contractility (2o to ischemia/MI or dilated CM)
Diastolic dysfxn
Preserved EF, normal EDV, lower compliance (2o to myocardial hypertrophy)
Drugs that decrease mortality in HF
ACE Inhibs or ARBs, B blockers (EXCEPT acute decomp), spirinolactone
Hypovolemic shock causes
Hemorrhage, dehydration, burns
Hypovolemic shock skin, PCWP, CO, SVR
Cold clammy skin
Much lower PCWP (preload)
Lower CO
Increased SVR
Tx of hypovolemic shock
IV fluids
Cardiogenic shock causes
Acute MI, HF, valvular dysfxn, arrhythmia
Obstructive shock causes
Cardiac tamponade, PE, tension pneumothorax
Cardiogenic/obstructive skin, PCWP, CO, SVR
Cold, clammy skin
PCWP can go either way
CO much lower
SVR goes up
Tx of cardiogenic shock
Inotropes, diuresis
Tx of obstructive shock
Relieve obstruction
Distributive shock cause
Sepsis, anaphylaxis, CNS injury
Sepsis/anaphylaxis shock skin, PCWP, CO, SVR
Skin warm
Lower PCWP
Higher CO
Much lower SVR
CNS injury shock skin, PCWP, CO, SVR
Skin dry
Lower PCWP
Lower CO
Much lower SVR
Tx of distributive shock
IV fluids, presors
Roth spot
White spot on retina surrounded by hemorrhage, found in bacterial endocarditis
Osler nodes
Painful notes on fingers. toe pads due to immune complex deposition, found in bact ECitis
Janeway lesions
Small, painless erythematous lesions in palm or sole, found in bact ECitis
Most common bact. endocarditis buts
Acute: s.auerus (large veg on perviously normal valve, rapid onset)
Subacute: viridians strep – smaller veg on damaged/abnormal valve after dental procedure, gradual onset
S bovis in colon cancer
S. epi on prosthetic valves
Causes of NBTE
Malignancy, hypercoagulable state, lupus
Most frequently involved valve in Bact EC itis
Mitral
Tricuspid valve ECitis associations
IVDU, S. aureus, Pseudomonas, candida
Culture negative ECItis bugs
Coxiella burnietti, Bartonella, HACEK (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella)
Early and late lesion in rheumatic fever
Early – mitral regurg
Late – mitral stenosis
Histology of rheumatic fever
Aschoff bodies (granduloma) and Anitschkow cells (large macs w/ ovoid/wavy rod-like nucleus)
Type of hypersensitivity of RF
Type II (abs to M protein cross react – molecular mimicry)
Tx/prophylaxis of RF
Penicillin
JONES criteria
Joint (migratory polyarthritis) Oheart (carditis) Nodules in skin (subcutaneous) Erythema marginatum Sydenham chorea
Presentation of acute pericarditis
Sharp pain aggravated by inspiration and relieved by sitting up/leaning forward, friction rub, widespread ST segment elevation or PR depression; can have effusion
Acute pericarditis causes
Idiopathic (most, probably viral), confirmed infxn (e.g. coxsackie), neoplasia, autoimmune (e.g. SLE, RA), uremia, cardiovascular (acute STEMI, Dressler), radiation
Cardiac tamponade findings
Beck triad (hypotension, distended neck veins, distant heart sounds), increased HR, pulsus paradoxus (large lowered BP on inspiration), low voltage QRS and electrical alternans
Where is pulsus paradoxus seen?
Cardiac tamponade, asthma, OSA, pericarditis, croup
3o syphillis effect on heart
Disrupts vasa vasorum–>dilatation of aorta and valve ring–>atrophy of vessel wall (looks like tree bark)
May see calcification of aortic roots, ascentidng archm thoracic aorta, aneurysm of ascending aorta, arch or aortic insufficiency
Most common heart tumor
Metastatis
Most common primary cardiac tumor in adults
Myxoma – ball vavle ovstruction in lft atrium assc w/ syncopal episodes, may auscultate plop
Myxoma histology
Myxioid gelatinous material, myxoma cells in GAGs
Most frequent cardiac tumor in kiddos
Rhabdomyoma (assc w/ tuberous sclerosis) – basically a hamartoma
Kussmaul sign
Increased JVP on inspiration (normal is decreased)
Seen w/ constrictive pericarditis, restrictive cardiomyopathies, right atrial/ventricular tumors
