USMLE - Cardiology Part 1

Ascending Aorta and Pulmonary Trunk

Transposition of the Great Vessels (failure to spiral), Tetralogy of Fallot (skewed AP septum), Persistent TA (partial AP septum development)

Smooth part (outflow tract) of L and R Ventricles

Trabeculated Ventricles

Trabeculated Atria

Coronary Sinus

Smooth part of RA

SVC

Neural Crest Cells. Truncal and bulbar ridges spiral and fuse to form AP septum giving rise to the Ascending Aorta and the Pulmonary Trunk

Muscular ventricular septum forms with interventricular foramen

AP septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing interventricular formane

Growth of endocardial cushions separate atria from ventricles and contributes to both atrial separation and membranous portion of interventricular septum

L-R shunt which later reverses to R-L shunt due to onset of PHTN (Eisenmengers syndrome)

Foramen primum narrows as septum primum grows towards endocardial cushions

Perforations in septum primum form foramen secundum and FP disappears

FS maintins R-L as suptum secundum begins to grow

Septum Secundum contains FO (permanent opening)

Foramen secundum enlarges and upper part of septum primum degenerates

Remaining portion of septum primum forms valve of FO

Septum secundum and septum primum fuse to form atrial septum

FO closes soon after birth because of increased LA pressure

Failure of Septum Primum and Septum Secundum to fuse after birth

"Young Livers Synthesize Blood"

Yolk Sac: weeks 3-10

Liver: week 6 - birth

Spleen: 15-30 weeks

Bone Marrow: 22 weeks to adulthood

PO2 = 30mmHg

O2 Sat = 80%

Low

Umbilical vein –> ductus venosus –> IVC to bypass liver

RA –> FO –> LA

Pulmonary Artery –> Ductus Arteriosus –> Aorta

Decreased resistance in pulmonary vasculature –> increased P in LA –> FO closes

Increased O2 –> decreased prostaglandins –> ductus arteriosus closes

Indomethacin closes the PDA

PGE keeps in open

Ligamentum teres hepatis contained in the falciform ligament

Medial umbilical ligaments

Ligamentum arteriosum

Ligamentum venosum

Fossa Ovalis

Urachus - median umbilical ligament. The Urachus is part of the allantoic duct between bladder and the umbilicus

Urachal cyst or sinus is a remnant

Nucleus pulposus of IV disc

RCA

PDA arises from RCA in 85% of individuals

From LCX in 8%

Both in 7%

LAD > RCA > CFX

Diastole

Acute Marginal, PDA (80%)

CFX, LAD

Dysphagia (compression of esophagus) + Hoarseness (compression recurrent laryngeal nerve)

Transesophageal Echocardiography

LA Enlargement, Aortic Dissection, Thoracic Aortic Aneurysm

Ant 2/3 of IV septum, anterior papillary muscles, anterior surface of LV

Lateral and Posterior walls of LV

Posterior 1/3 of IV septum and posterior walls of ventricles

CO = SV x HR

Fick Principle

CO = (Rate of O2 consumption)/(arterial O2 - venous O2)

MAP = CO x TPR

MAP = 2/3 Diastole + 1/3 Systole

PP = Systolic - Diastolic

| PP α SV

EDV - ESV

Early: Increases in HR and SV

Late: HR only, SV plateaus

Diastolic filling is incomplete and CO decreases resulting in ventricular tachycardia

SV CAP

| Contractility, Afterload, Preload

BACH

β Blockers (decreased cAMP), Acidosis, Ca Channel Blockers (non-dihydropyridine), Hypoxia/Hypercapnea, Systolic Heart Failure

Catecholamines (increase activity of Ca pump in SR). Digitalis (Increased intracellular Na --> increased intracellular Ca)

Pregnancy, Exercise, Anxiety

CARS

| Increased Contractility, Afterload, Rate, Size (wall tension)

EDV

MAP

| Proportional to peripheral resistance

Venodilators like Nitroglycerin

Vasodilators like Hydralazine

Exercise, Volume, Excitement

Preload

EF = SV/EDV

Index for ventricular contractility

Normally ≥ 55%

Decreases in Systolic HF

P = Q x R

R = P/Q = (8 x viscosity x length)/π(r^4)

Hct

| Increases with Polycythemia, Hyperproteinemic state (multiple myeloma), Hereditary spherocytosis

Anemia

Arterioles

Mitral and Tricuspid valves close

| Loudest in Mitral area

Aortic and Pulmonary valves close

| Loudest at L sternal border

In early diastole

Associated with increased filling pressures

MR, CHF

Sign of dilated ventricles

Normal in Pregnants and Children

Atrial Kick in late diastole

Caused by high atrial pressure

Associated with ventricular hypertrophy

a: atrial contraction

c: RV contraction (tricuspid valve bulges into atrium)

x: atrial relaxation

v: RA filling

y: blood flow from RA to RV

S1 - A2-P2

Inspiration --> drop in intrathoracic pressure --> increased venous return to RV --> increased RV SV --> increased RV ejection time --> delayed closure of pulmonic valve

Inspiration also leads to increased capacity of pulmonary circulation which also delays P closing

Due to delayed RV emptying

| Pulmonic stenosis, R bundle branch block

ASD. L-R shunt --> ⇑ RA and RV volumes --> ⇑ flow through pulmonic valves such that regardless of breath, valve closure greatly delayed

Seen in conditions that delay LV emptying (Aortic Stenosis, Left Bundle Branch Block).

Reversal of A2 and P2

Systolic murmors: AS, Flow Murmur, Aortic Valve Sclerosis.

Diastolic murmurs: AR, PR

| Systolic murmurs: HOCM

Systolic ejection murmur: Pulmonic stenosis, Flow murmur from ASD or PDA.

Pansystolic murmurs: Tricuspid Regurg, VSD

| Diastolic murmurs: Tricuspid stenosis, ASD

Systolic: MR

Diastolic: MS

"Drs press forward"

Diastolic rumble and pulmonary flow murmur

Blood flow across ASD does not cause the murmur because there is no pressure gradient

The murmur later progresses to a louder diastolic murmur of pulmonic regurgitation from dilation of pulmonary artery

Left infraclavicular region. Continuous machine like murmur. Loudest at S2

Often due to congenital rubella or prematurity

Increased intensity of R heart sounds

Increased intensity of L heart sounds

⇑systemic vascualr resistance.

⇑ intensity of MR, AR, VSD, MVP

⇓ intensity of AS, HOCM

⇓ venous return

Bedside Maneuver: Valsala

⇑ MVP and HOCM

⇑ venous return, ⇑ preload, ⇑ afterload (if prolonged)

| ⇓ MVP and HOCM

Holosystolic high pitched blowing murmur.

Loudest at apex and radiates towards axilla

Enhanced by maneuvers that ↑ TPR (squatting, hand grip) and ↑ LA return (expiration)

Most often due to Ischemic heart disease, MVP, LV dilation, RF, infective endocarditis

Holosystolic high pitched blowing murmur.

Loudest at tricuspid area and radiates to R sternal border

Enhanced by maneuvers ↑ RA return (inspiration)

Most often due to RV dilation, RF, infective endocarditis

Crescendo-decrescendo systolic ejection murmur following ejection click (due to abrupt halting of valve leaflets) that radiates towards carotids and loudest at heart base

P in LV > P in Aorta

"SAD" --> Syncope, Angina, Dyspnea

Pulsus Parvus et Tardus

Age related calcification or bicuspid valve

Holosystolic, harsh sounding murmur loudest at tricuspid area and ↑ by handgrip (increased afterload)

Late systolic crescendo murmur with midsystolic click (from sudden tensing of chordae tendineae)

Best heard over apex during S2

Predisposes to infective endocarditis

Caused by myxomatous degeneration, RF, chordae rupture.

Enhanced by maneuvers that ↓ venous return (standing, valsala)

MVP

Immediate high pitched blowing diastolic decrescendo murmur.

Wide pulse pressure, bounding pulse, head bobbing.

Due to aortic root dilation, bicuspid endocarditis, RF.

↓ by vasodilators

↑ by hand grip

Delayed rumble in late diastole with opening snap (abrupt halting of leaflets due to fusion)

P in LA (measured by PCWP) > P in LV

Due to RF and can lead to LA dilation

Enhanced by maneuvers that ↑ LA return (expiration)

Bundles of His and Purkinje fibers

0: INa

1: Na channels inactivated, K channels open

2: Plateau. Ca channels open

3: Repolarization. K channels open. Ca channels close

4: Resting Potential. High K permeability

Ca induced Ca release

0: Ca mediated upstroke

2: no plateau

3: Inactivation of Ca channels, Opening of K

4: Slow diastolic depolarization because of Na funny channels

ACh and Adenosine --> ↓ Slope --> ↓ HR

| Catecholamines --> ↑ Slope --> ↑ HR

Atrial depolarization

Purkinje > atra > ventricles > AV node

SA > AV > Bundle of His/Purkinje/Ventricles

Conduction delay through AV node

| Normally < 200 msec

Ventricular depolarization

| Normally < 120 msec

Mechanical contraction of the ventricles

Ventricular repolarization

| T wave inversion may indicate recent MI