cardiology Flashcards by sai bpudi

Truncus arteriosus GIVES RISE TO

Ascending aorta and pulmonary trunk

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Bulbus cordis GIVES RISE TO

Smooth parts (outflow tract) of left and right ventricles

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Endocardial cushion GIVES RISE TO

Atrial septum, membranous interventricular septum; AV and semilunar valves

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Primitive atrium GIVES RISE TO

Trabeculated part of left and right atria

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Primitive ventricle GIVES RISE TO

Trabeculated part of left and right ventricles

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Primitive pulmonary vein GIVES RISE TO

Smooth part of left atrium

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Left horn of sinus venosus GIVES RISE TO

Coronary sinus

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Right horn of sinus venosus GIVES RISE TO

Smooth part of right atrium (sinus venarum)

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Right common cardinal vein and right anterior cardinal vein GIVES RISE TO

Superior vena cava (SVC)

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First functional organ in vertebrate embryos

heart

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Primary heart tube loops to establish _____

left-right polarity

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Cardiac looping begins in week ____ of gestation.

week 4

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Defect in left-right dynein (involved in L/R asymmetry) can lead to ____

dextrocardia

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dextrocardia seen in____

Kartagener syndrome (primary ciliary dyskinesia)

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Septum secundum and septum primum fuse to form the___

atrial septum

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Patent foramen ovale is caused by ____

failure of septum primum and septum secundum

to fuse after birth

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Patent foramen ovale can lead to

paradoxical emboli

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abnormalities associated with failure of neural crest cells to migrate:

-Transposition of great vessels.
-Tetralogy of Fallot.
-Persistent truncus arteriosus.

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Aortic/pulmonary valve derived from ___

endocardial cushions of outflow tract

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Mitral/tricuspid valve derived from ___

fused endocardial cushions of the AV canal.

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3 important fetal circulation shunts:

1 Ductus venosus
2 Foramen ovale
3 Ductus arteriosus

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Blood entering fetus through the___

umbilical vein

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Blood entering fetus through the umbilical vein is conducted via the _____

ductus venosus

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Blood entering fetus through the umbilical vein is conducted via the ductus venosus into the ____

IVC

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Blood entering fetus through the umbilical vein is conducted via the ductus venosus into the IVC, bypassing ____

hepatic circulation

Most of the highly oxygenated blood reaching the heart via the ____

IVC

Most of the highly oxygenated blood reaching the heart via the IVC is directed through the __

foramen ovale

Most of the highly oxygenated blood reaching the heart via the IVC is directed through the foramen ovale and pumped into the ___

aorta

Most of the highly oxygenated blood reaching the heart via the IVC is directed through the foramen ovale and pumped into the aorta to supply the ____

head and body

Deoxygenated blood from the SVC passes through the RA -> 􏰀RV􏰀 ->____ -> ___ -> ___

main pulmonary artery patent ductus arteriosus descending aorta

At birth, infant takes a breath; ___ resistance | in pulmonary vasculature, causing ___ left atrial pressure vs right atrial pressure, causing ____ to close􏰀

↓ ↑ foramen ovale

At birth, infant takes a breath... __ O2 (from respiration) and ___ prostaglandins (from placental separation)􏰀 leads to closure of ____

ductus arteriosus

Indomethacin helps ___

close PDA

remnant of ductus arteriosus)

ligamentum arteriosum

Prostaglandins E1 and E2

kEEp PDA open

SA and AV nodes are usually supplied by ___

Right coronary artery (RCA)

RCA supplies ___

SA and AV nodes

Right-dominant circulation %

85%

Right-dominant circulation (85%) = PDA arises from __

RCA.

Left-dominant circulation ___

(8%)

Left-dominant circulation (8%) = PDA arises from ___

Left circumflex coronary artery (LCX)

Codominant circulation (7%) = PDA arises from both ____ and ___

LCX and RCA

Coronary artery occlusion most commonly occurs in the ___

Left anterior descending | artery (LAD)

Coronary blood flow peaks in __

early diastole

most posterior part of the heart

left | atrium

left atrium enlargement can cause ___ (due to compression of the ___) or ___ (due to compression of the____, a branch of the ___).

dysphagia esophagus hoarseness left recurrent laryngeal nerve vagus

Pericardium consists of 3 layers (from outer to inner):

``` 1) Fibrous pericardium 2) Parietal layer of serous pericardium 3) Visceral layer of serous pericardium ```

Pericardial cavity lies between __ and | __ layers.

parietal visceral

stroke volume (SV) × heart rate (HR)

Fick principle:

CO = rate of O2 consumption/ | arterial O2 content − venous O2 content

Mean arterial pressure (MAP) =

CO × total peripheral resistance (TPR)

2 ⁄3 diastolic pressure + 1⁄3 systolic pressure =

MAP

Pulse pressure =

systolic pressure – diastolic pressure

Pulse pressure is proportional to ___ and inversely proportional to ___

SV arterial compliance

proportional to SV, inversely proportional to arterial compliance.

Pulse pressure

SV =

= (EDV) − (ESV)

During the early stages of exercise, CO is maintained by ___

↑ HR and ↑ SV

During the late stages of exercise, CO is maintained by ___

↑ HR only (SV plateaus)

Diastole is preferentially shortened with ___ causing ___ filling time leading to ___ 􏰀􏰁(eg, ventricular tachycardia).

↑ 􏰂HR less ↓CO

Inc. in pulse pressure is seen in ___

hyperthyroidism aortic regurgitation

Dec. pulse pressure is seen in ___

aortic stenosis cardiogenic shock cardiac tamponade HF

↑ SV with: "SV CAP"

↑ Contractility (eg, anxiety, exercise) 􏰂 ↑ Preload (eg, early pregnancy) ↓ 􏰁Afterload

Contractility (and SV)􏰂 ↑ with:

Catecholamines increased 􏰂intracellular Ca2+ ↓ extracellular Na+

Catecholamines (inhibition of | ___ ) →__ Ca2+ entry into__→Ca2+ induced ___ release)

phospholamban increase sarcoplasmic reticulum􏰀 Ca2+

Contractility (and SV)􏰂 ↓ with:

- β1-blockade (􏰁 dec. cAMP) - HF with systolic dysfunction - Acidosis - Hypoxia/hypercapnia - Non-dihydropyridine Ca2+ channel blockers

↑ MyoCARDial O2 demand is􏰂 ↑ by: 􏰂 __ Contractility 􏰂 __ Afterload (proportional to ___) 􏰂heart Rate __ 􏰂Diameter of ventricle (􏰂__ wall tension)

↑ Contractility ↓ Afterload arterial pressure ↑ 􏰂Diameter of ventricle ↑ wall tension

Preload approximated by ___

ventricular EDV

VEnodilators (eg, ___) .... __ preload

nitroglycerin ↓ preload

Afterload approximated by ___

MAP

LV compensates for􏰂afterload by ___ in order to __ 􏰁wall tension

thickening (hypertrophy) ↓

VAsodilators (eg, ___) .... ___ 􏰁Afterload (Arterial).

hydrAlAzine ↓

ACE inhibitors and ARBs 􏰁both ____ preload and afterload.

↓

Chronic hypertension (􏰂__MAP) leads to ___.

increases 􏰀LV hypertrophy.

Left ventricular EF is an index of ____

ventricular contractility

normal EF is ___

≥ 55%

EF􏰁 ___ in systolic HF. | EF ___ in diastolic HF.

↓ normal

Force of contraction is proportional to ___

preload

increase 􏰂contractility with ___

- catecholamines | - positive inotropes (eg, digoxin)

decrease 􏰂contractility with ___

- loss of myocardium (eg, MI) - β-blockers (acutely) - non-dihydropyridine Ca2+ channel blockers - dilated cardiomyopathy

ΔP =

Q × R a change in pressure in a vessel is equal to flow times resistance this is similar to Ohm's law where a change in voltage is equal to current times resistance: ΔV = IR

Volumetric flow rate (Q) =

flow velocity (v) × cross-sectional area (A)

Resistance

(driving pressure ΔP) / (flow Q) = 8η (viscosity) x length / (πr4)

Total resistance of vessels in series:

RT = R1 + R2 + R3 . . .

Total resistance of vessels in parallel:

1/RT = 1/R1 + 1/R2 + 1/R3

Viscosity depends mostly on ____

hematocrit

Viscosity􏰂 increases in ____ states (eg, | _____ ) and _____

``` hyperproteinemic states (eg, multiple myeloma) ``` polycythemia

Viscosity decreases 􏰁in ____

anemia

Removal of organs in parallel arrangement (eg, ____)􏰀􏰁 = ___TPR and􏰂 ___CO.

nephrectomy ↓ TPR increase CO

Pressure gradient drives flow from __ pressure to ___ pressure.

high low

____ account for most of TPR.

Arterioles

___ provide most of blood storage capacity.

Veins

Inotropy curve Effects

Changes in contractility􏰀 → altered CO for a given RA pressure (preload) or EDV.

⊕ Intropy

Catecholamines digoxin

⊝ Intropy

Uncompensated HF narcotic overdose

Venous return curve Effects

Changes in circulating volume or venous tone → 􏰀altered RA pressure for a given CO. Mean systemic pressure (x-intercept) changes with volume/venous tone.

⊕ volume, venous tone

Fluid infusion, sympathetic activity

⊝ volume, venous tone

Acute hemorrhage spinal anesthesia

Total peripheral resistance curve Effects

At a given mean systemic pressure (x-intercept) and RA pressure, changes in TPR􏰀 → altered CO.

⊕ TPR

Vasopressors

⊝ TPR

Exercise AV shunt

exercise: __ 􏰂inotropy and ___ 􏰁TPR to maximize ___

↑ ↓ CO

HF: ___ 􏰁inotropy → 􏰀fluid retention to __ preload to maintain ___

↓ ↑ CO

fetal erythropoiesis WK 3-10

yolk sac

fetal erythropoiesis WK 6-birth

liver

fetal erythropoiesis WK 15-30

spleen

fetal erythropoiesis WK 22-adult

bone marrow

fetal hemoglobin

A2Y2

adult hemoglobin

A2B2

truncal and bulbar ridges spiral and fuse to form

aorticopulmonary septum

___ separates the ascending aorta and pulmonary trunk

aorticopulmonary septum

aorticopulmonary septum formed from ___

cardiac neural crest

notocord postanatal called ___

nucleus pulposus

foramen ovale postnatal called ____

fossa ovalis

period between mitral valve closing and aortic valve opening;

Isovolumetric contraction

period between aortic valve opening and closing

Systolic ejection

period between aortic valve closing and mitral valve opening

Isovolumetric relaxation

period just after mitral valve opening

Rapid filling

period just before mitral valve closing

Reduced filling

period of highest O2 consumption

Isovolumetric contraction

4 phases of cardiac cycle :

1. Isovolumetric contraction 2. Systolic ejection 3. Isovolumetric relaxation 4. Rapid filling 5. Reduced filling

mitral and tricuspid valve closure. heart sound?

S1 loudest at _____

mitral area

S2 Loudest at ____

left upper sternal border.

aortic and pulmonary valve closure. heart sound?

in early diastole during rapid ventricular | filling phase. heart sound?

heart sound associated with􏰂filling pressures (eg, mitral regurgitation, HF) and more common in dilated ventricles (but can be normal in children and young adults).

late diastole (“atrial kick”). heart sound?

heart sound best heard at apex with patient in left lateral decubitus position.

heart sound associated with ventricular noncompliance (eg, hypertrophy). Left atrium must push against stiff LV wall. Consider abnormal, regardless of patient age.

[JVP] a wave—

atrial contraction

Absent in atrial fibrillation (AF). [JVP]

a wave

c wave— [JVP]

``` RV contraction (closed tricuspid valve bulging into atrium). ```

x descent— [JVP]

atrial relaxation and downward | displacement of closed tricuspid valve during ventricular contraction.

Absent in tricuspid regurgitation. [JVP]

x descent

Prominent in tricuspid insufficiency and right HF. [JVP]

x descent

v wave— [JVP]

􏰂right atrial pressure due to filling (“villing”) against closed tricuspid valve.

y descent— [JVP]

RA emptying into RV

Prominent in constrictive pericarditis [JVP]

y descent

absent in cardiac tamponade. [JVP]

y descent

Continuous machine-like murmur. Loudest at S2. Often due to congenital rubella or prematurity.

Patent ductus arteriosus

Best heard at left infraclavicular area.

Patent ductus arteriosus

Holosystolic, harsh-sounding murmur. Loudest at tricuspid area.

Ventricular septal defect

continuous heart murmur

Patent ductus arteriosus

Diastolic heart murmurs:

Aortic regurgitation Mitral stenosis

Systolic Heart murmurs:

Aortic stenosis Mitral/tricuspid regurgitation Mitral valve prolapse Ventricular septal defect

Crescendo-decrescendo systolic ejection murmur

Aortic stenosis

murmur Loudest at heart base; radiates to carotids.

Aortic stenosis

murmur with “Pulsus parvus et tardus”—pulses are weak with a delayed peak.

Aortic stenosis

murmur Can lead to Syncope, Angina, and Dyspnea on exertion (SAD).

Aortic stenosis

Murmur most commonly due to age- related calcification in older patients (> 60 years old) or in younger patients with early-onset calcification of bicuspid aortic valve.

Aortic stenosis

Holosystolic, high-pitched “blowing murmur.”

Mitral/tricuspid regurgitation

murmur loudest at apex and radiates toward axilla.

Mitral regurgitation

murmur is often due to ischemic heart disease (post-MI), MVP, LV dilatation.

Mitral regurgitation

murmur loudest at tricuspid area and radiates to right sternal border

tricuspid regurgitation

murmur commonly caused by RV dilatation.

tricuspid regurgitation

Rheumatic fever and infective endocarditis can cause what murmurs?

Mitral regurgitation | tricuspid regurgitation

Late systolic crescendo murmur with midsystolic click (MC; due to sudden tensing of chordae tendineae).

Mitral valve prolapse

Murmur most frequent valvular lesion.

Mitral valve prolapse

Murmur loudest just before S2. Usually benign.

Mitral valve prolapse

Murmur best heard over apex.

Mitral valve prolapse

murmur can predispose to infective endocarditis.

Mitral valve prolapse

murmur can be caused by myxomatous degeneration (1° or 2° to connective tissue disease such as Marfan or Ehlers-Danlos syndrome), rheumatic fever, chordae rupture.

Mitral valve prolapse

High-pitched “blowing” early diastolic decrescendo murmur. Long diastolic murmur, hyperdynamic pulse, and head bobbing when severe and chronic. Wide pulse pressure.

Aortic regurgitation

murmur often due to aortic root dilation, bicuspid aortic valve, endocarditis, rheumatic fever. Progresses to left HF.

Aortic regurgitation

murmur follows opening snap (OS; due to abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips).

Mitral stenosis

murmur with delayed rumbling late diastolic murmur (􏰁interval between S2 and OS correlates with􏰂severity). LA >> LV pressure during diastole.

Mitral stenosis

murmur often occurs 2° to rheumatic fever. Chronic MS can result in LA dilatation.

Mitral stenosis

rapid upstroke and depolarization—voltage-gated Na+ channels open.

Myocardial action potential Phase 0

initial repolarization—inactivation of voltage-gated Na+ channels. Voltage-gated K+ channels begin to open.

Myocardial action potential Phase 1

plateau—Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux. Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction.

Myocardial action potential Phase 2

rapid repolarization—massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels.

Myocardial action potential Phase 3

resting potential—high K+ permeability through K+ channels.

Myocardial action potential Phase 4

In contrast to skeletal muscle ...Cardiac muscle: (3 differences)

1. Cardiac muscle action potential has a plateau, which is due to Ca2+ influx and K+ efflux. 2. Cardiac muscle contraction requires Ca2+ influx from ECF to induce Ca2+ release from sarcoplasmic reticulum (Ca2+-induced Ca2+ release). 3. Cardiac myocytes are electrically coupled to each other by gap junctions.

Occurs in the SA and AV nodes only

Pacemaker action potential

upstroke—opening of voltage-gated Ca2+ channels. Fast voltage-gated Na+ channels are permanently inactivated because of the less negative resting potential of these cells. Results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles.

Phase 0

what 2 phases are absent in Pacemaker action potential

Phases 1 and 2

inactivation of the Ca2+ channels and􏰂activation of K+ channels􏰀􏰂K+ efflux.

Phase 3

slow spontaneous diastolic depolarization due to If (“funny current”). If channels responsible for a slow, mixed Na+/K+ inward current; different from Ina in phase 0 of ventricular action potential. Accounts for automaticity of SA and AV nodes.

Phase 4

The slope of phase 4 in the SA node determines

ACh/adenosine ___ 􏰁the rate of diastolic depolarization and􏰁 ___HR

↓ ↓

catecholamines􏰂 ___ depolarization and ___ 􏰂HR

↑ ↑

Conduction pathway

SA node → 􏰀atria→ 􏰀AV node→􏰀bundle of His→􏰀right and left bundle branches→􏰀Purkinje fibers→􏰀ventricles

SA > AV > bundle of His/ Purkinje/ventricles.

Pacemaker rates

Purkinje > atria > ventricles > AV node.

Speed of conduction

Long QT interval predisposes to ____

torsades de pointes.

Polymorphic ventricular tachycardia, characterized by shifting sinusoidal waveforms on ECG; can progress to ventricular fibrillation (VF)

torsades de pointes.

Torsades de pointes caused by

drugs,􏰁 ↓ K+ ↓ 􏰁Mg2+ congenital abnormalities

Torsades de pointes tx

magnesium sulfate

Drug-induced long QT (ABCDE):

AntiArrhythmics (class IA, III) AntiBiotics (eg, macrolides) Anti“C”ychotics (eg, haloperidol) AntiDepressants (eg, TCAs) AntiEmetics (eg,ondansetron)

Inherited disorder of myocardial repolarization, typically due to ion channel defects

Congenital long QT syndrome

􏰂in Congenital long QT syndrome there is ↑ risk of ____ due to torsades de pointes.

sudden cardiac death (SCD)

Congenital long QT syndrome 2 types:

Romano-Ward syndrome Jervell and Lange-Nielsen syndrome

Congenital long QT syndrome type that is "autosomal dominant, pure cardiac phenotype (no deafness)."

Romano-Ward syndrome

Congenital long QT syndrome type that is "autosomal recessive, sensorineural deafness."

Jervell and Lange-Nielsen syndrome

Brugada syndrome genetically ___

Autosomal dominant disorder

Brugada syndrome most common in ___

Asian males

ECG pattern of pseudo-right bundle branch block and ST elevations in V1-V3.􏰂risk of ventricular tachyarrhythmias and SCD

Brugada syndrome

Prevent SCD with ____

implantable cardioverter-defibrillator (ICD).

Most common type of ventricular pre- excitation syndrome.

Wolff-Parkinson-White syndrome

Wolff-Parkinson-White syndrome ECG findings:

- characteristic delta wave - widened QRS complex - shortened PR interval

Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing AV node􏰀ventricles begin to partially depolarize earlier

Wolff-Parkinson-White syndrome

Wolff-Parkinson-White syndrome- May result in reentry circuit... leading to ___

supraventricular tachycardia.

cardiology Flashcards

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