Cardiovascular Flashcards
Truncus arteriosus
Ascending aorta and pulmonary trunk
Bulbus cordis
Smooth parts (outflow tract) of left and right ventricles
Endocardial cushion
- Atrial septum, membranous interventricular septum
- AV and semilunar valves
Primitive atrium
Trabeculated part of left and right atria
Primitive ventricle
Trabeculated part of left and right ventricles
Primitive pulmonary vein
Smooth part of left atrium
Left horn of sinus venosus
Coronary sinus
Right horn of sinus venosus
Smooth part of right atrium (sinus venarum)
Right common cardinal vein and right anterior cardinal vein
Superior vena cava
Heart begins to beat spontaneously at
Week 4 of development
Cardiac looping
- Primary heart tube loops to establish left-right polarity
- Begins in week 4 of gestation
- Defect in left-right dynein (involved in L/R asymmetry) can lead to dextrocardia, as seen in Kartagener syndrome (primary ciliary dyskinesia)
Conotruncal abnormalities associated with failure of neural crest cells to migrate
- Transposition of great vessels
- Tetralogy of Fallot
- Persistent truncus arteriosus
What causes a patent foramen ovale
- Caused by a failure of septum primum and septum secundum to fuse after birth
- Most are left untreated
- Can lead to paradoxical emboli, similar to those resulting from ASD
Where do ventricular septal defects usually occur
- Usually occurs in membranous septum
- Most common congenital cardiac anomaly
Allantois → urachus
- Median umbilical ligament
- Urachus is part of allantoic duct between the bladder and umbilicus
Ductus arteriosus
Ligamentum arteriosum
Ductus venosus
Ligamentum venosum
Foramen ovale
Fossa ovalis
Notochord
Nucleus pulposus
Umbilical arteries
Medial umbilical ligaments
Umbilical vein
- Ligamentum teres hepatis
- Contained in falciform ligament
3 layers of pericardium
- Fibrous pericardium
- Parietal layer of serous pericardium
- Visceral layer of serous pericardium
- Pericardial cavity lies between parietal and visceral layers
CO during exercise
- EARLY: CO is maintained by ↑ HR and ↑ SV
- LATE: CO is maintained by ↑ HR only (SV plateaus)
With ↑ HR, what becomes preferentially shortened
- Diastole is preferentially shortened with ↑ HR
- Less filling time → ↓ CO (eg ventricular tachycardia)
Conditions that ↑ pulse pressure
- Hyperthyroidism
- Aortic regurgitation
- Aortic stiffening (isolated systolic hypertension in elderly)
- Obstructive sleep apnea (↑ sympathetic tone)
- Exercise (transient)
Conditions that ↓ pulse pressure
- Aortic stenosis
- Cardiogenic shock
- Cardiac tamponade
- Advanced heart failure
Ejection fraction in diastolic vs systolic heart failure
- ↓ in systolic HF
- Normal in diastolic HF
How does the left ventricle compensate for ↑ afterload
LV compensates for ↑ afterload by thickening (hypertrophy) in order to ↓ wall tension
Force of contraction is proportional to
End diastolic length of cardiac muscle fiber (preload)
What do AV shunts do to total peripheral resistance and cardiac output
AV shunts ↑ CO and ↓ TPR
Which phase of the cardiac cycle consumes the most O2
Isovolumetric contraction is the period of highest O2 consumption
S1
- Mitral and tricuspid valve closure
- Loudest at mitral area
S2
- Aortic and pulmonary valve closure
- Loudest at left upper sternal border
S3
- Early diastole during rapid ventricular filling phase
- Associated with ↑ filling pressures (eg mitral regurgitation, HF)
- More common in dilated ventricles (can be normal in children and young adults)
S4
- Late diastole (“atrial kick”)
- Best heart at apex with patient in left lateral decubitus position
- High atrial pressure
- Associated with ventricular noncompliance (eg hypertrophy)
- Left atrium must push against stiff LV wall
- Considered abnormal, regardless of patient age
Order of jugular venous pulse
a wave → c wave → x descent → v wave → y descent
a wave
- Atrial contraction
- Absent in atrial fibrillation
c wave
RV contraction (closed tricuspid valve bulging into atrium)
x descent
- Atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction
- Absent in tricuspid regurgitation
- Prominent in tricuspid insufficiency and right HF
v wave
↑ right atrial pressure due to filling against closed tricuspid valve
y descent
- RA emptying into RV
- Prominent in constrictive pericarditis
- Absent in cardiac tamponade
Normal splitting
- Inspiration → drop in intrathoracic pressure → ↑ venous return → ↑ RV filling → ↑ RV stroke volume → ↑ RV ejection time → delayed closure of pulmonic valve
- ↓ pulmonary impedance (↑ capacity of the pulmonary circulation) also occurs during inspiration, which contributes to delayed closure of pulmonic valve
Wide splitting
- Seen in conditions that delay RV emptying (eg pulmonic stenosis, right bundle branch block)
- Causes delayed pulmonic sound (especially on inspiration)
- An exaggeration of normal splitting
Fixed splitting
- Heard in ASD
- ASD → left to right shunt → ↑ RA and RV volumes → ↑ flow through pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed
Paradoxical splitting
- Heard in conditions that delay aortic valve closure (eg aortic stenosis, left bundle branch block)
- Normal order of valve closure is reversed so that P2 sound occurs before delayed A2 sound
- Therefore, on inspiration, P2 closes later and moves closer to A2, therby “paradoxically” eliminating the split (usually heard on expiration)
Effect of inspiration
↑ intensity of right heart sounds
Effect of hand grip
- ↑ afterload
- ↑ intensity of MR, AR, VSD murmurs
- ↓ hypertrophy cardiomyopathy murmurs
- MVP: later onset of click/murmur
Effects of valsalva (phase II), standing up
- ↓ preload
- ↓ intensity of most murmurs (including AS)
- ↑ intensity of hypertrophic cardiomyopathy murmur
- MVP: earlier onset of click/murmur
Effect of rapid squatting
- ↑ venous return, ↑ preload, ↑ afterload
- ↓ intensity of hypertrophic cardiomyopathy murmur
- ↑ intensity of AS murmur
- MVP: later onset of click/murmur
How is cardiac muscle different from skeletal muscle
- Cardiac action potential has a plateau, which is due to Ca2+ influx and K+ efflux
- Cardiac muscle contraction requires Ca2+ influx from ECF to induce Ca2+ release from SR (Ca2+ induced Ca2+ release)
- Cardiac myocytes are electrically coupled to each other by gap junctions
Why are voltage gated Na+ channels permanently inactivated in pacemaker action potential
Due to less negative resting potential of these cells
Which phases are absent in pacemaker action potential
1 & 2
What determines heart rate
Slope of phase 4 in SA node
Rank speed of conduction
Purkinje > atria > ventricles > AV node
Treatment of torsades de pointes
Magnesium sulfate
Congenital long QT syndromes
Inherited disorder of myocardial repolarization typically due to ion channel defects
Romano-Ward syndrome
- Congenital long QT syndrome
- AD
- Pure cardiac phenotype (no deafness)
Jervell and Lange-Nielsen syndrome
- Congenital long QT syndrome
- AR
- Sensorineural deafness
Brugada syndrome
- AD
- Asian males
- ECG pattern of pseudo-right bundle branch block and ST elevations in V1-V3
- ↑ risk of ventricular tachyarrhythmias
Wolf-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 → ventricles begin to partially depolarize earlier → characteristic delta wave with widened QRS complex and shortened PR interval on ECG
- May result in reentry circuit → supraventricular tachycardia
Action of atrial natriuretic peptide
- Acts via cGMP
- Causes vasodilation and ↓ Na+ reabsorption at the renal collecting tubule
- Dilates afferent renal arterioles and constricts efferent arterioles, promoting diuresis and contributing to “aldosterone escape” mechanism
- B-type natriuretic peptide has a longer half-life, is used for diagnosing HF, and is available in recombinant form (nesiritide)
Normal pressure of right atrium
Normal pressure of right ventricle
25/5
Normal pressure of pulmonary artery
25/10
Normal pressure of left atrium
Normal pressure of left ventricle
130/10
Normal pressure of aorta
130/90
Autoregulation of heart
Local metabolites (vasodilatory): adenosine, NO, CO2, ↓ O2
Autoregulation of brain
Local metabolites (vasodilatory): CO2 (pH)
Autoregulation of kidneys
Myogenic and tubuloglomerular feedback
Autoregulation of lungs
Hypoxia causes vasoconstriction
Autoregulation of skeletal muscle
Local metabolites during exercise: lactate, adenosine, K+, H+, CO2 →→ “CHALK”
At rest: sympathetic tone
Autoregulation of skin
Sympathetic stimulation most important mechanism: temperature control
What causes ↑ interstitial fluid colloid osmotic pressure
Lymphatic blockage
Right-to-left shunts
- Truncus arteriosus (1 vessel)
- Transposition (2 switched vessels)
- Tricuspid atresia (3 = tri)
- Tetralogy of Fallot (4 = tetra)
- TAPVR (5 letters in name)
Cause of persistent truncus arteriosus
- Truncus arteriosus fails to divide into pulmonary trunk and aorta due to lack of aorticopulmonary septum formation
- Most patients have accompanying VSD
Cause of D-transposition of great vessels
- Due to failure of the aorticopulmonary septum to spiral
- Not compatible with life unless a shunt is present to allow mixing of blood (eg VSD, PDA, or patent foramen ovale)
Cause of tetralogy of Fallot
- Anterosuperior displacement of the infundibular septum
- Most common cause of childhood cyanosis
Cause of Ebstein anomaly
- Displacement of tricuspid valve leaflets downward into RV, artificially atrializing the ventricle
- Associated with tricuspid regurgitation and right HF
- Lithium exposure in utero
VSD vs ASD O2 saturation
- VSD: O2 saturation ↑ in RV and pulmonary artery
- ASD: O2 saturation ↑ in RA, RV and pulmonary artery
How do ASD and patent foramen ovale differ
With ASD, septa are missing tissue rather than unfused (patent foramen ovale)
Uncorrected PDA results in
Late cyanosis in the lower extremeties (differential cyanosis)
Eisenmenger syndrome
- Uncorrected left-to-right shunt (VSD, ASD, PDA) → ↑ pulmonary blood flow → pathologic remodeling of vasculature → pulmonary arterial hypertension
- RVH occurs to compensate → shunt becomes right to left
- 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
- Hypertension in upper extremities and weak, delayed pulse in lower extremities (brachial-femoral delay)
- With age, intercostal arteries enlarge due to collateral circulation → arteries erode ribs → notched appearance on CXR
- Complications: HF, ↑ risk of cerebral hemorrhage (berry aneurysms), aortic rupture, and possible endocarditis
Is endocarditis a possible complication of coarctation of the aorta
Yes, along with HF, ↑ cerebral hemorrhage (berry aneurysms), aortic rupture and possible endocarditis
Alcohol exposure in utero (fetal alcohol syndrome)
- VSD
- ASD
- PDA
- Tetralogy of Fallot
Congenital rubella
- PDA
- Pulmonary artery stenosis
- Septal defects
Down syndrome
- AV septal defect (endocardial cushion defect)
- VSD
- ASD
Infant of diabetic mother
Transposition of great vessels
Marfan syndrome
- MVP
- Thoracic aortic aneurysm and dissection
- Aortic regurgitation
Prenatal lithium exposure
Ebstein anomaly
Williams syndrome
Supravalvular aortic stenosis
22q11 syndromes
- Truncus arteriosus
- Tetralogy of Fallot
Hypertensive urgency vs emergency
Hypertensive urgency → severe (>180/>120 mmHg) hypertension WITHOUT acute end-organ damage
Hypertensive emergency → severe hypertension with evidence of acute end-organ damage (eg encephalopathy, stroke, retinal hemorrhages and exudates, papilledema, MI, HF, aortic dissection, kidney injury, microangiopathic hemolytic anemia, eclampsia)
Xanthoma
Plaques or nodules composed of lipid-laden histocytes in skin, especially the eyelids (xanthelasma)
Tendinous xanthoma
Lipid deposit in tendon, especially Achilles
Corneal arcus
Lipid deposit in cornea. Common in elderly (arcus senilis) but appears earlier in life in hypercholesterolemia.
Location of atherosclerosis
Abdominal aorta > coronary artery > popliteal artery > carotid artery
Progression of atherosclerosis
Endothelial cell dysfunction → macrophage and LDL accumulation → foam cell formation → fatty streaks → smooth muscle cell migration (involves PDGF and FGF), proliferation and extracellular matrix deposition → fibrous plaque → complex atheromas
Difference in association of thoracic vs abdominal aortic aneurysms
Abdominal aortic aneurysm → atherosclerosis
Thoracic aortic aneurysm → cystic medial degeneration, hypertension, bicuspid aortic valve, connective tissue disease, tertiary syphilis
0-24 hours after MI
- Early coagulative necrosis, release of necrotic cell contents into blood
- Edema, hemorrhage, wavy fibers
- Neutrophils appear
- Reperfusion injury, associated with generation of free radicals, leads to hypercontraction of myofibrils through ↑ free calcium influx
- COMPLICATIONS: ventricular arrhythmia, HF, cardiogenic shock
1-3 days after MI
- Extensive coagulative necrosis
- Tissue surrounding infarct shows acute inflammation with neutrophils
- COMPLICATIONS: postinfarction fibrinous pericarditis
3-14 days after MI
- Macrophages
- Granulation tissue at margins
- COMPLICATIONS: free wall rupture → tamponade; papillary muscle rupture → mitral regurgitation; interventricular septum rupture due to macrophage-mediated structural degradation; LV pseudoaneurysm (risk of rupture)
2 weeks to several months after MI
- Contracted scar complete
- COMPICATIONS: Dressler syndrome, HF, arrhythmias, true ventricular aneurysm (risk of mural thrombus)
ST elevation or Q wave in V1-V2
Anteroseptal (LAD)
ST elevation or Q wave in V3-V4
Anteroapical (distal LAD)
ST elevation or Q wave in V5-V6
Anterolateral (LAD or LCX)
ST elevation or Q wave in I, aVL
Lateral (LCX)
ST elevation or Q wave in II, III, aVF
Inferior (RCA)
ST elevation or Q wave in V7-V9, ST depression in V1-V3 with tall R waves
Posterior (PDA)
Cardiac arrhythmia
Occurs within first few days after MI. Important cause of death before reaching the hospital and within the first 24 hours post-MI.
Postinfarction fibrinous pericarditis
Occurs 1-3 days after MI. Friction rub.
Papillary muscle rupture
Occurs 2-7 days after MI. Posteromedial papillary rupture ↑ risk due to single blood supply from posterior descending artery. Can result in severe mitral regurgitation.
Interventricular septal rupture
Occurs 3-5 days after MI. Macrophage mediated degradation → VSD.
Ventricular pseudoaneurysm formation
Occurs 3-14 days after MI. Contained free wall rupture. ↓ CO, risk of arrhythmia, embolus from mural thrombus.
Ventricular free wall rupture
Occurs 5-14 days after MI. Free wall rupture → cardiac tamponade.
True ventricular aneurysm
Occurs 2 weeks to several months after MI. Outward bulge with contraction (“dyskinesia”), associated with fibrosis.
Dressler syndrome
Occurs several weeks after MI. Autoimmune phenomenon resulting in fibrinous pericarditis.
LV failure and pulmonary edema
Can occur secondary to LV infarction, VSD, free wall rupture, papillary muscle rupture with mitral regurgitation.
Dilated cardiomyopathy - systolic or diastolic dysfunction
Systolic dysfunction
Hypertrophic cardiomyopathy - systolic or diastolic dysfunction
Diastolic dysfunction
Restrictive/ infiltrative cardiomyopathy
Diastolic dysfunction
Etiologies of dilated cardiomyopathy
Often idiopathic or familial. Other etiologies include chronic Alcohol abuse, wet Beriberi, Coxsackie B viral myocarditis, chronic Cocaine use, Chagas disease, Doxorubicin toxicity, hemochromatosis, sarcoidosis, peripartum cardiomyopathy.
“ABCCCD”
What type of cardiomyopathy is associated with Friederich ataxia
Hypertrophic cardiomyopathy
Etiologies of restrictive/ infiltrative cardiomyopathy
Sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), Loffler syndrome (endomyocardial fibrosis with a prominent eosinophilic infiltrate) and hemochromatosis (although dilated cardiomyopathy is more common)
What is special about the ECG of restrictive/ infiltrative cardiomyopathy
Low voltage ECG despite thick myocardium (especially amyloid)
Findings of dilated cardiomyopathy
- HF
- S3
- Systolic regurgitant murmur
- Dilated heart on echocardiogram
- Balloon appearance of heart on CXR
Treatment of dilated cardiomyopathy
- Na+ restriction
- ACE inhibitors
- β blockers
- Diuretics
- Digoxin
- ICD
- Heart transplant
Findings of hypertrophic cardiomyopathy
- S4
- Systolic murmur
- May see mitral regurgitation due to impaired mitral valve closure
Treatment of hypertrophic cardiomyopathy
- Cessation of high-intensity athletics
- Use of β blockers or non-dihydropyridine Ca2+ channel blocker
- ICD for high risk patients
Obstructive hypertrophic cardiomyopathy
- Subset of hypertrophic cardiomyopathy
- Asymmetric septal hypertrophy and systolic anterior motion of mitral valve → outflow obstruction → dyspnea, possible syncope
HF with systolic dysfunction
- Reduced EF
- ↑ EDV
- ↓ contractility often secondary to ischemia/MI or dilated cardiomyopathy
HF with diastolic dysfunction
- Preserved EF
- Normal EDV
- ↓ compliances often secondary to myocardial hypertrophy
When should β blockers not be used in patients with HF
Acute decompensated HF
Hypovolemic shock
- Caused by hemorrhage, dehydration and burns
- Skin is cold and clammy
- ↓↓ PCWP/preload
- ↓ CO
- ↑ SVR/ afterload
- Treat with IV fluids
Cardiogenic shock
- Caused by acute MI, HF, valvular dysfunction, arrhythmia
- Skin is cold and clammy
- ↑ PCWP/ preload
- ↓↓ CO
- ↑ SVR/ afterload
- Treat with inotropes and diuresis
Obstructive shock
- Caused by cardiac tamponade, pulmonary embolism
- Skin is cold and clammy
- ↑ PCWP/ preload
- ↓↓ CO
- ↑ SVR/ afterload
- Treat by relieving obstruction
Distributive shock caused by sepsis and anaphylaxis
- Skin is warm
- ↓ PCWP/ preload
- ↑ CO
- ↓↓ SVR/ afterload
- Treat with IV fluids and pressors
Distributive shock caused by CNS injury
- Skin is dry
- ↓ PCWP/ preload
- ↓ CO
- ↓↓ SVR/ afterload
- Treat with IV fluids and pressors
Nonbacterial endocarditis
- Marantic/ thrombotic
- Secondary to malignancy, hypercoaguable state, or lupus
In what condition do you see equilibration of diastolic pressures in all 4 chambers
Cardiac tamponade
Beck triad
- Associated with cardiac tamponade
- Hypotension
- Distended neck veins
- Distant heart sounds
Pulsus paradoxus is associates with
↓ amplitude of systolic BP by > 10 mm Hg during inspiration
- Cardiac tamponade
- Asthma
- Obstructive sleep apnea
- Pericarditis
- Croup
Kussmaul sign
- ↑ JVP on inspiration instead of normal ↓
- Inspiration → negative intrathoracic pressure not transmitted to heart → impaired filling of right ventricle → blood backs up into vena cavae → JVD
- Constructive pericarditis
- Restrictive cardiomyopathies
- Right atrial or ventricular tumors
