Cardiology Flashcards
Truncus arteriosus gives rise to:
Ascending aorta and pulmonary trunk
Bulbous cordis gives rise to:
Smooth parts (outflow tract) of L and R Ventricles
Primitive atrium gives rise to:
Trabeculated part of L and R atria
Primitive ventricle gives rise to:
Trabeculated part of L and R ventricles
Primitive pulmonary vein gives rise to:
Smooth part of the L Atrium
Left horn of Sinus Venosus gives rise to:
Coronary Sinus
Right horn of Sinus Venosus gives rise to:
Smooth part of R A Atrium (Sinus Venarum)
Right common cardinal vein and Right anterior cardinal vein give rise to:
Superior Vena Cava (SVC)
When does the heart start beating?
Week 4 - first functional organ in vertebrate embryos
Kartagener Syndrome
Defect in L-R dynein (involved in L/R asymmetry) can lead to dextrocardia as seen in this disease.
Messes up embryological cardiac looping
Where does VSD commonly occur?
in the membranous septum
Patent Foramen Ovale
caused by failure of septum primum and septum secundum to fuse after birth
Most are left untreated
Can lead to paradoxical emboli (venous thromboemboli that enter systemic ARTERIAL circulation) - similar to those resulting from ASD
What are 3 common conotruncal abnormalities?
Transposition of the great vessels
Tetralogy of Fallot
Persistent truncus arteriosus
Sites of erythropoiesis
Yolk Sac (3-8 wks)
Liver (6 wks - birth)
Spleen (10-28 wks)
Bone marrow (18 wks to adult)
Only bone marrow is doing this ish after birth
What are 3 important shunts in fetal blood flow?
Ductus venosus
Foramen ovale
Ductus arteriosus
Allantois/urachus becomes…
Meidan umbilical ligament (urachus is part of allantoic duct btw bladder and umbilicus)
Ductus arteriosus becomes…
Ligamentum arteriosum
Ductus venosus becomes…
Ligamentum venosum
Foramen ovale becomes…
Fossa ovalis
Notochord becomes…
Nucleus pulposus
Umbilical arteries become…
Medial umbilical ligaments
Umbilical vein becomes…
Ligamentum teres hepatis (contained in falciform ligament)
What the most common coronary artery blockage?
LAD
Left coronary artery branches
LCX - supplies lateral and posterior walls of LV, anterolateral papillary muscle
Left Marginal (Obtuse) Artery
LAD - supplies anterior 2/3 of interventricular septum, anterolateral papillary muscle, and anterior surface of LV
PDA (rarely, but can happen) - If it does happen it would be a branch of LCX
Right coronary artery branches
Right marginal (Obtuse) Artery - supplies RV
PDA (usually) - supplies posterior 1/3 of interventricular septum, posterior walls of ventricles, and posteromedial papillary muscle.
RCA also supplies AV node most of the time
Cardiac output formula
CO = SV x HR
Fick’s principle
CO = [rate of O2 consumption]/[arterial O2 content - venous O2 content]
Mean arterial pressure (MAP) formula
MAP = 2/3(diastolic) + 1/3(systolic)
MAP = CO x TPR
Pulse pressure formula
PP = systolic - diastolic
Stroke volume formula
SV = EDV - ESV
SV = CO/HR
Wall Tension formula (Laplace’s Law)
Wall tension = (pressure x radius)/(2 x wall thickness)
Ejection Fraction formula
EF = SV/EDV = (EDV=ESV)/EDV
Resistance, Pressure, Flow formulas
Change in P = QR
R = P/Q = 8NL/Pi r^4
TR in series = R1 + R2..
TR in parallel: 1/TR = 1/R1 + 1/R2
Conditions that exhibit wide splitting of heart sounds
Pulmonic stenosis
R Bundle branch block
Conditions that delay RV emptying
Conditions that exhibit fixed splitting of heart sounds
ASD
Conditions that exhibit paradoxical splitting of heart sounds
Aortic stenosis
L Bundle branch block
Conditions that delay aortic valve closure
What is best heard over Aortic area?
Systolic murmur:
Aortic Stenosis
Flow murmur
Aortic valve sclerosis
What is best heard of left sternal border?
Diastolic murmur:
Aortic regurgitation
Pulmonic regurgitation
Systolic murmur:
Hypertrophic cardiomyopathy
What is best heard over left infraclavicular region?
Continuous murmur:
PDA
What is best heard over Pulmonic Area?
Systolic ejection murmur:
Pulmonic stenosis
Flow murmur (physiologic murmur)
What is best heard over Tricuspid Area?
Pansystolic murmur:
Tricuspid regurgitation
VSD
Diastolic murmur:
Tricuspid stenosis
ASD
What is best heard over Mitral Area?
Systolic murmur:
Mitral regurgitation
Diastolic murmur:
Mitral stenosis
What murmurs are systolic?
Aortic Stenosis Pulmonic Stenosis Mitral Regurgitation Tricuspid Regurgitation VSD MVP
What murmurs are diastolic?
Aortic Regurgitation
Pulmonic Regurgitation
Mitral Stenosis
Tricuspid Stenosis
Aortic stenosis findings
Crescendo-decrescendo systolic ejection murmur.
LV»_space; aortic pressure during systole
Loudest at heart base - radiates to carotids. “Pulsus parvus et tardus” - pulses are weak with a delayed peak.
Can lead to syncope, angina and dyspnea on exertion (SAD)
Often due to age-related calcification or early-onset calcification of bicuspid aortic valve.
Mitral/Tricuspid regurgitation findings
Holosystolic, high-pitched “blowing murmur”
Mitral - loudest at apex and radiates to axilla. MR is often due to ischemic heart disease (post MI), MVP, LV dilation
Tri - loudest at tricuspid area and radiates to right sternal border. TR commonly caused by RV dilation
Rheumatic fever and infective endocarditis can cause either MR or TR
MVP findings
Late systolic crescendo murmur with midsystolic click (MC; due to sudden tensing of chordae tendineae).
Most frequent valvular lesion.
Best heard over apex. Loudest just before S2.
Usually benign.
Can predispose to infective endocarditis. Can be caused by myxomatous degeneration ( primary or secondary to connective tissue disease such as Marfan or Ehlers-Danlos), rheumatic fever, chordae rupture.
VSD findings on auscultation
Holosystolic, harsh-sounding murmur. Loudest at tricuspid area.
Aortic regurgitation findings
High-pitched blowing early diastolic decrescendo murmur.
Long diastolic murmur and signs of hyperdynamic pulse when severe and chronic. Often due to aortic root dilation, bicuspid aortic valve, endocarditis, RF. Progresses to left HF.
Mitral stenosis findings
Follows opening snap (OS - due to abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips).
Delayed rumbling late diastolic murmur (smaller interval between S2 and OS correlates with increased severity).
LA»_space; LV pressure during diastole. Often occurs secondary to RF. Chronic MS can result in LA dilation
PDA findings on auscultation
Continuous machine-like murmur. Loudest at S2. Often due to congenital rubella or prematurity.
Best heard at left infraclavicular area
P wave
atrial depolarization
Atrial repolarization is masked by QRS
PR interval
time from start of atrial depolarization (start of P wave) to start of ventricular depolarization (start of QRS).
Normal = less than 200 ms
QRS complex
Ventricular depolarization
Normally less than 120 ms
QT interval
ventricular depolarization, mechanical contraction of the ventricles. ventricular repolarization. From start of QRS to end of T.
T wave
ventricular repolarization
T wave inversion may indicated recent MI
J point
junction between end of QRS complex and start of ST segment
ST segment
isoelectric, ventricles depolarized
U wave
caused by hypokalemia, bradycardia
Torsades de pointes
Polymorphic ventricular tachycardia, characterized by shifting sinusoidal waveforms on ECG; can progress to VFib.
Long QT interval predisposes to torsade de pointes. Caused by drugs, decreased K, decreased Mg, other abnormalities.
Tx = magnesium sulfate
Congenital long QT syndrome
Inherited disorder of myocardial repolarization, typically due to ion channel defects.
Higher risk of sudden cardiac death (SCD) due to torsades de pointes. Includes:
1) Romano-Ward Syndrome: autosomal dominant, pure cardiac phenotype (no deafness)
2) Jervell and Lange-Nielson Syndrome: autosomal recessive, sensorineural deafness
Drug-induced long QT caused by:
ABCDE
anti Arrhythmics (class 1A, III) anti Biotics (macrolides) anti "C" ychotics (haloperidol) anti Depressants (TCAs) anti Emetics (ondansetron)
Brugada Syndrome
Autosomal dominant disorder most common in Asian males
ECG pattern of pseudo-right bundle branch block and ST elevations in V1-V3.
Higher risk of ventricular tachyarrhtymias and SCD. Prevent SCD with implantable cardioverter-defribrillator (ICD)
Wolff-Parkinson-White Syndrome
Most common type of ventricular pre-excitation syndrome.
Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing AV node
This leads to ventricles beginning to partially depolarize earlier leading to characteristic delta wave with widened QRS complex and shortened PR interval on ECG.
May result in reentry circuit leading to supraventricular tachycardia
AFib on ECG
Chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes.
Associated with: (7) HTN CAD Rheumatic heart disease Binge drinking (holiday heart) HF Valvular disease Hyperthyroidism
Can result in atrial stasis and lead to cardioembolic events.
Tx includes antithrombotic therapy (warfarin), rate control (B blockers, non-dihydropyridine Ca channel blockers, digoxin), rhythm control (class 1C or 3 antiarrhtymics) and or/ cardioversion (pharm or electrical)
Atrial flutter on ECG
A rapid succession of identical, back-to-back atrial depolarization waves. The identical appearance accounts for the “sawtooth” appearance of the flutter waves.
Management similar to Afib (rate control, anticoagulation, caridoversion). Definitive treatment is catheter ablation
VFib on ECG
A completely erratic rhythm with no identifiable waves. Fatal arrhythmia without immediate CPR and defibrillation
1st degree AV block on ECG
The PR interval is prolonged (greater than 200 ms). Benign and asymptomatic. No Tx required
2nd degree AV block - Mobitz type 1 (Wenckebach) on ECG
Progressive lengthening of PR interval until a beat is “dropped” ( a P wave not followed by a QRS complex).
Usually asymptomatic.
Variable RR interval with a pattern (regularly irregular)
Mobitz type II on ECG
Dropped beats that are not preceded by a change in the length of PR interval (as in type 1). May progress to 3rd degree block.
Often treated with pacemaker
3rd degree (complete) AV block on ECG
The atria and ventricles beat independently of each other. Both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes. Atrial rate faster than ventricular rate.
Usually treated with pacemaker.
Lyme Disease can result in 3rd degree block
Atrial natriuretic peptide
Released from atrial myocytes in response to increased blood volume and atrial pressure.
Acts via cGMP.
Causes vasodilation and lower Na reabsorption at the renal collucting tubule. Dilates afferent renal arterioles and constricts efferent arterioles, promoting diuresis and contributing to “aldosterone escape” mechanism
B-type (Brain) naturietic peptide
Released from ventricular myocytes in response to increased tension. Similar physiologic action to ANP, with longer half-life. BNP blood test used for diagnosing HF (very good negative predictive value)
Available in recombinant form (nesiritide) for treatment of HF
Cushing reaction triad
Hypertension
Bradycardia
Respiratory depression
Right to Left Shunts
Congenital heart defects
Early cyanosis - “blue babies.” Often diagnosed prenatally or become evident immediately after birth. Usually require urgent surgical correction and/or maintenance of a PDA.
5 T’s
1) Truncus arteriosus (1 vessel)
2) Transposition (2 vessels)
3) Tricuspid atresia (3 = tri)
4) Tetralogy of Fallot (4 = tetra)
5) TAPVR (5 letters)
Persistent Truncus arteriosus
Congenital heart defect
Truncus arteriosus fails to divide into pulmonary trunk and aorta due to lack of aorticopulmonary septum formation. Most patients have accompanying VSD.
D-Transposition of great vessels
Congenital heart defect
Aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior). This leads to separation of systemic and pulmonary circulations. Not compatible with life unless a shunt is present to allow mixing of blood (e.g. VSD, PDA, or patent foramen ovale)
Due to failure of the aorticopulmonary septum to spiral
Without surgical intervention, most infants die within the first few months of life.
Tricuspid atresia
Congenital heart defect
Absence of tricuspid valve and hypoplastic RV - requires both an ASD and VSD for viability
Tetralogy of Fallot
Congenital heart defect
Caused by anterosuperior displacement of the infundibular septum. Most common cause of early childhood cyanosis.
1) Pulmonary infundibular stenosis (most important determinant for prognosis)
2) Right ventricular hypertrophy - boot shaped hear on CXR
3) Overriding aorta
4) VSD
Pulmonary stenosis forces R-L flow across VSD leading to early cyanotic “tet spells,” RVH.
Squatting: Increases SVR, lowers R-L shunt and improves cyanosis
Tx = early surgical correction
Total anomalous pulmonary venous return (TAPVR)
congenital heart defect
Pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc): associated with ASD and sometimes PDA to allow for R-L shunting to maintain CO.
Left-Right shunts
LATE cyanosis - blue kids
VSD
ASD
PDA
Frequency: VSD > ASD > PDA
Ventricular septal defect
Most common congenital cardiac defect. Asymptomatic at birth, may manifest weeks later or remain asymptomatic throughout life. Most self resolve; larger lesions may lead to LV overload and HF
Atrial septal defect
Defect in interatrial septum; loud S1; wide, fixed split S2.
ostium secundum defects are most common and usually occur as isolated findings.
Ostium primum defects are rarer yet usually occur with other cardiac anomalies.
Symptoms range from none to HF. Distinct from patent foramen ovale in that septa are missing tissue rather than unfused.
Patent ductus arteriosus
In fetal period, shunt is R-L (normal). In neonatal period, lower lung resistance leads to shunt becoming L-R leading to progressive RVH and/or LVH and HF
Associate with a continuous, “machine-like” murmur. Patency is maintained by PGE synthesis and low O2 tension. Uncorrected PDA can eventually result in late cyanosis in the lower extremities (differential cyanosis)
Indomethacin ends patency of PDA; PGE keeps it open (may be necessary to sustain life in conditions such as transposition of the great vessels).
PDA is normal in utero and normally closes only after birth
Eisenmenger syndrome
Uncorrected L-R shunt (VSD, ASD, PDA) lead to increased pulmonary blood flow leading to pathologic remodeling of vasculature leading to pulmonary arterial HTN. RVH occurs to compensate leading to shunt becoming R-L.
Causes late cyanosis, clubbing, and polycythemia. Age of onset varies.
Coarctation of the aorta
Aortic narrowing near insertion of ductus arteriosus (juxtaductal). Associated with bicuspid aortic valve, other heart defects, and Turner Syndrome.
HTN in upper extremities and weak, delayed pulse in lower extremities (brachial-femoral delay). With age, collateral arteries erode ribs (notched appearance on CXR)
Alcohol exposure in utero (fetal alcohol syndrome) leads to what congenital heart defects?
VSD
PDA
ASD
Tetralogy of Fallot
Congenital rubella leads to what congenital heart defects?
Septal defects
PDA
Pulmonary artery stenosis
Down Syndrome leads to what congenital heart defects?
AV Septal defect (endocardial cushion defect)
VSD
ASD
Infant of diabetic mother leads to what congenital heart defects?
Transposition of great vessels
Marfan Syndrome leads to what congenital heart defects?
MVP
Thoracic aortic aneurysm and dissection
Aortic regurgitation
Prenatal lithium exposure leads to what congenital heart defects?
Ebstein anomaly
Turner Syndrome leads to what congenital heart defects?
Bicuspid aortic valve
Coarctation of aorta
Williams Syndrome leads to what congenital heart defects?
Supravalvular aortic stenosis
22q11 syndromes lead to what congenital heart defects?
Truncus arteriosus
Tetralogy of Fallot
Anteroseptal infarct (LAD) on ECG
V1-V2
Anteroapical (distal LAD) infarct on ECG
V3-V4
Anterolateral (LAD or LCX) infarct on ECG
V5-V6
Lateral (LCX) infarct on ECG
I, aVL
Inferior (RCA) infarct on EKG
II, III, aVF
Dressler Syndrome
Autoimmune phenomenon resulting in fibrinous pericarditis several weeks post-MI)
Acute bacterial endocarditis - organisms
S. aureus (high virulence)
Large vegetations on previously normal valves. Rapid onset.
Subacute bacterial endocarditis - organisms
strep viridans (low virulence). Smaller vegetations on congenitally abnormal or diseased valves. Sequela of dental procedures. Gradual onset.
Bacterial endocarditis - organism present in colon cancer
S. bovis
Bacterial endocarditis - organism present on prosthetic valves
S. epidermidis
bacterial endocarditis - culture is negative
Coxiella burnetii
Bartonella
HACEK
Haemophilus Actinobacillus Cardiobacterium Eikenella Kingella
Bacterial endocarditis signs
FROM JANE
Fever
Roth spots
Osler nodes
Murmur
Janeway lesions
Anemia
Nail-bed hemorrhage
Emboli
Beck triad for cardiac tamponade
Hypotension
Distended neck veins
Distant heart sounds
Angiosarcoma
a vascular tumor
Rare blood vessel malignancy typically occurring in the head, neck, and breast areas. Usually in elderly, on sun-exposed areas. Associated with radiation therapy and chronic postmastectomy lymphedema.
Hepatic angiosarcoma associated with vinyl chloride and arsenic exposure. Very aggressive and difficult to resect due to delay in diagnosis.
Bacillary angiomatosis
vascular tumor
benign capillary skin papules found in AIDS patients. Caused by bartonella henselae infections. Frequently mistaken for Kaposi sarcoma, but has a neutrophilic infiltrate
Cherry hemangioma
Vascular tumor
Benign capillary hemangioma of the elderly.
Does not regress. Frequency higher with age
Cystic hygroma
Vascular tumor
Cavernous lymphangioma of the neck
Associated with Turner Syndrome
Glomus tumor
Vascular tumor
Benign, painful, red-blue tumor under fingernails.
Arises from modified smooth muscle cells of the thermoregulatory glomus body
Kaposi Sarcoma
Vascular tumor
Endothelial malignancy most commonly of the skin, but also mouth, GI tract, and respiratory tract.
Associated with HHV-8 and HIV.
Frequently mistaken for bacillary angiomatosis, but has lymphocytic infiltrate
Pyogenic granuloma
Vascular tumor
Polypoid capillary hemangioma that can ulcerate and bleed
Associated with trauma and pregnancy
Strawberry hemangioma
Vascular tumor
Benign capillary hemangioma of infancy
Appears in first few weeks of life (1/200 births): grows rapidly and regresses spontaneously by 5-8 years old
