Cardiovascular Flashcards
1
Q
Heart embryology
A
Embryonic structure—-> Gives rise to
- truncus arteriosus (TA)–> ascending aorta & pulmonary trunk
- bulbus cordis–> smooth parts (outflow tract) of left & right ventricles
- primitive ventricle–> trabeculated left & right ventricles
- primitive atria–> trabeculated left & right atria
- left horn of sinus venosus (SV)–> coronary sinus
- right horn of SV–> smooth part of right atrum
- right common cardinal vein & right anterior cardinal vein–> SVC
2
Q
Truncus arteriosus
A
- neural crest migration–> truncal & bulbar ridges that spiral & fuse to form the aorticopulmonary (AP) septum–>ascending aorta & pulmonary trunk
- Pathology: transposition of great vessels (failure to spiral), tetralogy of Fallot (skewed AP spetum development), perisistent TA (partial AP septum development)
3
Q
Interventricular septum development
A
- muscular ventricular septum forms. opening is called interventricular foramen
- AP septum rotates & fuses with muscular ventricular septum to form membranosus interventricular septum, closing interventricular foramen
- growth of endocardial cushions separates atria from ventricles and contributes to both atrial separation and membranous portion of the interventricular septum
Pathology: improper neural crest migration into the TA can result in transposition of the great arteries or a persistent TA.
-membranous septal defect causes an initial L-toR shunt shich later reverses to R-to-L shunt due to onset of pulmonary hypertension (Eisenmenger’s syndrome)
4
Q
Interarterial septum development
A
- foramen primum narrows as septum primum grows toward endocardial cushion
- perforations in septum primum form foramen secundum (foramen primum disappears)
- foramen secundum maintains R-to-L shunt as septum secundum begins to grow
- septum secundum contains a permanent opening (foramen ovale)
- foramen secundum enlarges and upper part of septum primum degenerates
- remaining portion of septum primum forms valve of foramen ovale
- Septum secundum and septum primum fuse to form the atrial septum
- foramen ovale usually closes soon after birth because of the increase LA pressure
Pathology: patent foramen ovale, caused by failure of the septum primum and septum secundum to fuse after birth
5
Q
fetal erythropoiesis
A
-fetal erythropoiesis occurs in: Yolk sac (3-10wks) Liver (6wks-birth) Spleen (15-30 wks) Bone marrow (22 wks to adult) ** Young Liver Synthesizes Blood Fetal hemoglobin= alpha2gamma2 Adult hemoglobin= alpha2beta2
6
Q
Fetal circulation
A
- Blood in umbilical vein has a PO2 of 30mmHg and is 80% saturated with O2
- umbilical arteries have low O2 saturation
- 3 important shunts
1. blood entering the fetus through the umbilical vein is conducted via the ductus venous into the IVC to bypass the hepatic circulation
2. most oxygenated blood reaching the heart via the IVC is diverted through the foramen ovale and pumped out the aorta to the head and body
3. deoxygenated blood entering the RA from the SVC enters the RV is expelled into the pulmonary artery, then passes through the ductus arterious into the descending aorta - at birth infant takes a breath; decrease resistance in pulmonary vasculature causes increase left atrial pressures vs. right atrial pressure; foramen ovale closes (now called fossa ovalis); increase O2 leads to decrease prostaglandins, causing closure of ducts arteriosus
- indomethacin helps close PDA
- prostaglandins E1 E2 keep PDA open
7
Q
Fetal-postnatal derivatives
- umbilical vein
- umbilical arteries
- ductus arterious
- ductus venous
- foramen ovale
- allantois
- notochord
A
- umbilical vein–>ligamentum teres hepatis; contained in falciform ligament
- umbilical arteries–> medial umbilical ligaments
- ductus arterious–>ligamentum arteriosum
- ductus venous–> ligamentum venosum
- foramen ovale–> fossa ovalis
- allantois–> urachus-median umbilical ligament; urachus is the part of the allantoic duct btw bladder & umbilicus. Urachal cyst or sinus is a remnant
- notochord–> nucleus pulposus of intervertebral disc
8
Q
Coronary artery anatomy
A
- SA & AV nodes are usually supplied by RCA
- Right dominant circulation= 85%=PD arises from RCA
- Left dominant circulation=8%=PD arises from LCX
- Codominant circulation=7%=PD arises from both LCX & RCA
- Coronary artery occlusion most commonly occurs in the LAD
- coronary arteries fill during diastole
- The most posterior part of the heart is the left atrium; enlargement can cause dysphagia (due to compression of the esophagus) or hoarseness (due to compression of the left recurrent laryngeal nerve, a branch of the vagus).
- Transesophageal echocardiography is useful for diagnosing left atrial enlargement, aortic dissection, thoracic aortic aneurysm.
9
Q
Cardiac output
A
-CO= stroke vol (SV) x HR
-Fickle principle:
CO= rate of O2 consumption/arterial O2 content- venous O2 content
-mean arterial pressure (MAP)= CO x total peripheral resistance
-MAP= 2/3 diastolic pressure + 1/3 systolic pressure
-pulse pressure= systolic pressure-diastolic pressure
-pulse pressure similar to stroke volumber (?)
-SV=CO/HR=EDV-ESV
-during the early stages of exercise, CO is maintained by increase HR and increase SV
-during the late stages of exercise, CO maintained by increase HR only (SV plateau)
-If HR is too high, diastolic filling is incomplete and CO decrease (ventricular tachy)
10
Q
cardiac output variables
A
- stroke vol affected by contractility, afterload, preload. Increase SV when increase preload, decrease afterload, increase contractility
- ***SV CAP
- contractility (and SV) increase with:
- catecholamines (increase activity of Ca2+ pump in sacroplasmic reticulum)
- increase intracellular Ca2+
- decrease extracellular NA+ (decrease activity of Na+/Ca2+ exchanger)
- digitalis (blocks NA+/K+ pump)–> increase intracellular Na+–> decrease Na+/Ca2+ exchanger activity–> increase intracellular Ca2+ - contractility (and SV) decrease with:
- beta 1 blockade (decrease cAMP)
- heart failure (systolic dysfunction)
- acidosis
- hypoxia/hypercapnea (decrease PO2/increase PCO2)
- non-dihydropyridine Ca2+ channel blockers
- SV increase in anxiety, exercise, pregnancy
- failing heart had decrease SV
- myocardial O2 demand is increase by:
1. increase (inc) afterload (arterial pressure)
2. inc contractility
3. inc HR
4. inc heart size (increase wall tension)
11
Q
preload & afterload
A
- preload=ventricular EDV
- afterload=mean arterial pressure (proportional to peripheral resistance)
- vEnodilators (nitroglycerin) decr preEload
- vAsodilators (hydrAlazine) decr Afterload (arterial)
- preload incr with:
1. exercise (slightly)
2. incr blood vol (overtransfusion)
3. excitement (incr sympathetic activity)
12
Q
Starling curve
A
- force of contraction is proportional to end diastolic length of cardiac muscle fiber (preload)
- increase contractility with sympathetic stimulation, catecholamines, digoxin
- decr contractility with loss of myocardium (MI), beta-blocker, calcium channel blockers
13
Q
Ejection fraction (EF)
A
EF= SV/EDV=EDV-ESV/EDV
- EF is an index of ventricular contractility
- EF is normally > or = 55%
- EF decr in systolic heart failure
14
Q
Resistance, pressure, flow
A
change of P= Q x R
- similar to Ohm’s law: change of V=IR
- resistance= driving pressure (delta P)/ flow (Q)= 8n (viscosity) x length/pi x r^4
- total resistance of vessel in series= R1 + R2 + etc
- 1/total resistance in parallel
- viscosity depends mostly on hematocrit
- viscosity increase in:
1. polycythemia
2. hyperproteinemic states (multiple myeloma)
3. hereditary spherocytosis - viscosity decrease in anemia
- pressure gradient drives flow from high pressure to low pressure
- resistance is directly proportional to viscosity and vessel length and inversly proportional to radius to 4th power
- arterioles account for most total peripheral resistance–> regulate capillary flow
15
Q
Cardiac cycle
A
Phases left ventricle:
- isovolumetric contraction-period btw mitral valve closure and aortic valve opening; period of highest O2 consumption
- systolic ejection-period btw aortic valve opening and closing
- isovolumetric relaxation-period btw aortic valve closing and mitral valve opening
- rapid filling- period just after mitral valve opening
- reduced filling-period just before mitral valve closure
Sounds:
- S1- mitral & tricuspid valve closure. Loudest at mitral area
- S2- aortic & pulmonary valve closure. Loudest at left sternal border
- S3- in early diastole during rapid ventricular filling phase. Associated with increase filling pressures (mitral regurgitation, CHF) and more common in dilated ventricles (but normal in children and pregnant women)
- S4- :atrial kick” in late diastole. HIgh atrial pressure. Associated with ventricular hypertrophy. L atrium must push against stiff LV wall.
16
Q
Splitting
- normal splitting
- wide splitting
- foxed splitting
- paradoxical splitting
A
- normal splitting
- inspiration–>drop in intrathoracic pressure–> increase venous return to the RV–> increased RV stroke vol–> increase RV ejection time–> delayed closure of pulmonic valve
- decrease pulmonary impedance (increase capacity of the pulmonary circulation) also occurs during inspiration, which contributes to delayed closure of pulmonic valve - wide splitting
- seen in condition that delay RV emptying (pulmonic stenosis, right bundle branch block)
- delay in RV empyting causes delayed pulmonic sound (regardless of breath)
- an exaggeration of normal splitting - foxed splitting
- seen in ASD–>L to R shunt–> incr RA & RV vol–> incr flow through pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed - paradoxical splitting
- seen in conditions that delay LV empyting (aortic stenosis, left bundle branch block)
- normal order of valve closure is reversed so that P2 sound occurs before delayed A2 sound
- on inspiration, P2 closes later and moves closer to A2, thereby paradoxically eliminating the split
17
Q
auscultation of the hear
“where to listen: APT M”
A
1.Aortic area: systolic murmur -aortic stenosis -flow murmur -aortic valve sclerosis 2. Left sternal border Diastolic murmur -aortic regurgitation -pulmonic regurgitation systolic murmur -hypertrophic cardiomyopathy 3. Pulmonic area: systolic ejection murmur -pulmonic stenosis -flow murmur (atrial septal defect, patent ductus arteriosus) 4. Tricuspid area Pansystolic murmur -tricuspid regurgitation -ventricular septal defect Diastolic murmur -tricuspid stenosis -atrial septal defect 5. Mitral area systolic murmur -mitral regurgitation Diastolic murmur -mitral stenosis
18
Q
Bedside maneuver—> effects
- inspiration
- expiration
- hand grip (increase systemic vascular resistance)
- valsalva (decr venous return)
- rapid squatting (incr venous return, incr preload, incr afterload with prolonged squatting)
A
- inspiration= incr intensity of R heart sounds
- expiration= incr intensity of L heart sounds
- hand grip (increase systemic vascular resistance)= incr intensity of MR, AR, VSD, MVP murmurs
- valsalva (decr venous return)= decr intensity of most murmurs
- rapid squatting (incr venous return, incr preload, incr afterload with prolonged squatting)= decr intensity of MVP, hypertrophic cardiomyopathy murmurs
- systolic heart sounds include aortic/pulmonic stenosis, mitral/tricuspid regurgitation, ventricular septal defect
- diastolic heart sounds include aortic/pulmonic regurgitation, mitral/tricuspid stenosis
19
Q
Heart murmurs: systolic
1. mitral/tricuspid regurgitation (MR/TR)
A
- mitral/tricuspid regurgitation (MR/TR)
- holosystolic, high-pitched blowing murmur
- mitral-loudest at apex and radiates toward axilla
- enhanced by maneuvers that incr TPR (squatting, hand grip) or LA return (expiration)
- MR often due to ishcemic heart disease, mitral valve prolapse, LV dilation
- tricupsid-loudest at tricuspid area and radiates to R sternal border
- enhanced by maneuvers that incr RA return (inspiration)
- TR can be caused by RV dilation
- Rheumatic fever and infective endocarditis can cause either MR or TR
20
Q
Heart murmurs: systolic
2. aortic stenosis (AS)
A
- aortic stenosis (AS)
- crescendo-decrescendo systolic ejection murmur following ejection click (EC; due to abrupt halting of valve leaflets)
- LV» aortic pressure during systole
- radiates to carotids/heart base
- pulsus parvus et tardus - pulses are weak with a delayed peak.
- can lead to syncope, angina, dyspnea on exertion (SAD)
- often due to age-related calcific aortic stenosis or bicuspid aortic valve
21
Q
Heart murmurs: systolic
3. VSD
A
- VSD
- holosystolic, harsh sounding murmur
- loudest at tricuspid area, accentuated with hand grip maneuver due to increased afterload
22
Q
Heart murmurs: systolic
4. mitral valve prolapse (MVP)
A
- mitral valve prolapse (MVP)
- late systolic crescendo murmur with midsystolic click (MC; due to sudden tensing of chordae tendinaea)
- most frequent valvular lesion
- best heard over apex
- loudest at S2
- usually benign
- can predispose to infective endocarditis
- can be caused by myxomatous degeneration, rhematic fever, chordae rupture
- enhanced by maneuvers that decr venous return (standing or Valsalva)
23
Q
Heart murmurs: diastolic
1. aortic regurgitation (AR)
A
- immediate high pitched “blowing” diastolic decrescendo murmur
- wide pulse pressure when chronic; can present with bounding pulses and head bobbing
- often due to aortic root dilation, bicuspid aortic valve, endocarditis, rheumatic fever
- incr murmur during hand grip
- vasodilators decr intensity of murmur
24
Q
Heart murmurs: diastolic
2. mitral stenosis (MS)
A
-follows opening snap (OS; due to abrupt halt in leaflet tips)
-delayed rumbling late diastolic murmur
LA» LV pressure during diastole
-often occurs secondary to rheumatic fever
-chronic MS can result in LA dilation
-enhanced by maneuvers that incr LA return (expiration)
25
Q
Heart murmurs: continuous
PDA
A
- continuous machine-like murmur
- loudest at S2
- often due to congenital rubella or prematurity
- best heard at left infraclavicular area
26
Q
ventricular action potential
-4 phases
A
-also occurs in bundle of His & Purkinjie fibers
Phase 0-= rapid upstroke-voltage gated Na+ channels open
Phase 1= initial repolarization-inactivation of voltage-gated Ca2+ channels balances K+ efflux
-Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction
Phase 3= rapid repolarization- massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels
Phase 4= resting potential- high K+ permeability through K+ channels
- in contrast to skeletal muscle:
1. cardiac muscle AP has a plateau, which is due to Ca2+ influx & K+ efflux, myocyte contraction occurs due to Ca2+ induced Ca2+ release from the sacroplasmic reticulum
2. cardiac nodal cells spontaneously depolarize during diastole resulting in automaticity due to I (f) channels (“funny current” channels responsible for a slow mixed Na+/K+ inward current)
3. Cardiac myocytes are electrically coupled to each other by gap junctions
27
Q
Pacemaker action potential
A
Occurs in SA & AV nodes. Key differences from the ventricular action potential include:
- Phase 0= upstroke-opening voltage-gated Ca2+ channels are permanently inactivated because of the less negative resting voltage of these cells. Results in a slow conduction velocity that is used by AV node to prolong transmission from the atria to ventricles
- Phase 2= plateau is absent
- Phase 3= inactivation of Ca2+ channels and incr activation of K+ channels–> incr K+ efflux
- Phase 4= slow diastolic depolarization- membrane potential spontaneously depolarizes as Na+ conductance incr (I f different from N Na in phase 0 of ventricualr AP)
- accounts for automaticity of SA and AV node
- the slope of phase 4 in SA node determines HR ACh/adenosine decr rate of diastolic depolarization and decr HR, while catecholamines incr depolarization and incr HR
- sympathetic stimulation incr chance that I f channels are open and thus incr HR
28
Q
torsades de pointes
A
- ventricular tachy, characherize by shifting sinusoidal waveforms on ECG, can progress to ventricular fibrillation
- anything that prolongs OT interval can predispose to torsades de pointes
- treatment includes magnesium sulfate
- congenital long QT syndromes are most often due to defects in cardiac sodium or potassium channels
- can present with severe congenital sensorineural deafness= Jervell & Lange-Nielson Syndrome
29
Q
Atrial fibrillation
A
chaotic & erratic basline (irregularly irregular) with no descrete P waves in btw irregularly spaced ORS complexes
- can result in atiral stasis and lead to stroke
- treatment includes rate control, anticoagulation, possible cardioversion
30
Q
atrial flutter
A
- rapid succession of identical, back-to-back depolarization waves
- identical appearance accounts for the “sawtooth appearance of flutter waves
- pharmacologic conversion to sinus rhythm: class IA, IC, III antiarrhythmics
- rate control: beta blocker or calcium channel blocker
31
Q
ventricular fibrillation
A
completely erratic rhythm with no identifibale waves
-fatal arrhythmia w/o immediate CPR & defibrillation
32
Q
AV block:
- 1 st degree
- 2nd degree (Mobitz type I or Wenckebach
- Mobitz II
- 3rd degree
A
1st degree
- PR interval is prolonged (>200 msec)
- asymptomatic
2nd degree
- progressive lengthening of PR interval until a beat is dropped (P wave not followed by a ORS complex)
- usually asymptomatic
Mobitz type II
- dropped beats that are not preceded by a change in the length of PR interval (as in type I)
- abrupt, nonconducted P waves result in a pathologic condition
- often found as 2:1 block, where there are 2 or more P waves to 1 QRS response
- may progress to 3rd degree block
- often treated with pacemaker
3rd degree
- atria & ventricles beat independently of each other
- both P waves & QRS complexes are present, although P waves bear no relation to QRS cmplexes
- atrial rate is faster than ventricular rate
- usually treated with pacemaker
- lyme disease can result in 3rd degree heart block
33
Q
atrial natriuretic peptide
A
- ANP is released from atrial myocytes in respponse to increase blood volume and atrial pressure
- causes generalized vascular relaxation and decrease Na+ reabsorption at the medullary collecting tubule
- constricts efferent renal arterioles and dilates afferent arterioles (cGMP mediated), promoting diuresis and contributing to the escape from aldosterone mechanism
34
Q
Baroreceptors & chemoreceptors
A
Receptors:
- aortic arch transmits via vagus nerve to solitary nucleus of medulla (responds only to inc BP)
- carotid sinus transmits via glossopharyngeal nerve to solitary nucleus of medulla (responds to decr & incr in BP)
Baroreceptors
- hypotension
- decr arterial pressure–> decr stretch–> decr afferent baroreceptor firing–> incr efferent sympathetic firing and decr efferent parasympathetic stimulation–> vasoconstriction, inc HR, incr contractility, incr BP
- important in the response to severe hemorrhage - carotid massage
- incr pressure on carotid artery–> incr stretch–> incr afferent baroreceptor firing–> decr HR - contributes to Cuhsing reaction (triad of hypertension, bradycardia, respiratory depression)
- incr intracranial pressure constricts arterioles –> cerebral ischemia & reflex sympathetic increase in perfusion pressure (hypertension)–> incr stretch–> reflex baroreceptor induced-bradycardia
Chemoreceptors
- peripheral
- carotid & aortic bodies are stimulated by decr PO2 (<60mmHg), incr PCO2, decr pH of blood - Central
- stimulated by changes in pH and PCO2 of brain interstitial fluid which in turn are influenced by arterial CO2
- do not directly respond to PO2
35
Q
circulation through organs
- lung
- liver
- kidney
- heart
A
- lung-organ with largest blood flow (100% of Cardiac output)
- liver- largest share of systemic cardiac output
- kidney- highest blood flow per gram of tissue
- heart- largest arteriovenous O2 difference because O2 extraction is 80%
- therefore incr O2 demand is met by incr coronary blood flow, not by incr extraction of O2
36
Q
normal pressure
A
PCWP
- pulmonary capillary wedge pressure (in mmHg) is good approximation of left atrial pressure
- in mitral stenosis, PCWP > LV diastolic pressure
- measured with pulmonary artery catheter (Swan-Ganz catheter)
37
Q
Autoregulation:
- heart
- brain
- kidneys
- lungs
- skeletal muscle
- skin
A
Autoregulation: how blood flow to an organ remains constant over a wide range of perfusion pressures
factors determing autoregulation
- heart- local metabolites (vasodilatory) CO2, adenosine, NO
- brain- local metabolites (vasodilatory) CO2 (pH)
- kidneys- myogenic and tubuloglomerular feedback
- lungs- hypoxnia causes vasocontriction
- skeletal muscle- local metabolites- lactate, adenosine, K+
- skin- sympathetic stimulation most important mechanism- temperature control
Note: the pulmonary vasculature is unique in that hypoxia causes vasoconstriction so that only causes vasodilationwell-ventilated areas are perfused. In other organs, hypoxia
38
Q
Capillary fluid exchange
A
Starling forces determine fluid movement through capillary membranes:
- Pc= capillary pressure- pushes fluid out of capillary
- Pi= interstitial fluid pressure- pushes fluid into capillary
- (symbol pi c)= plasma colloid osmotic pressure- pulls fluid into capillary, thus net filtration pressure= Pnet= [(Pc-Pi)]- (PIc-PIi)
Kf= filtration constant (capillary permeability) Jv= net fluid flow= (Kf)(Pnet)
Edema-excess fluid outflow into interstitium commonly caused by:
- incr capillary pressure (incr Pc; heart failure)
- decr plasma proteins (decr pi c; nephrotic syndrome, liver failure)
- incr capillary permeability (incr Kf; toxins, infections, burns)
- incr interstitial fluid colloid osmotic pressure (incr pi i; lympathatic blockage)
39
Q
Congenital heart disease:
Right-to-left shunts (early cyanosis)- “blue babies”
A
The 5 T’s:
- Tetralogy
- Transposition
- Truncus
- Tricuspid
- TAPVR
- Tetralogy of Fallot (most common cause of early cyanosis)
- Transposition of great vessels
- Persistent Truncus arteriosus- failure of truncus arteriosus to divide into pulmonary trunk & aorta; most pts have accompanying VSD
- Tricuspid atresia- characterized by absence of tricuspid valve and hypoplastic RV; requires both ASD & VSD for viability
- Total anomalous pulomary venous return (TAPVR)- pulomonary veins drain into right heart circulation (SVC, coronary sinus, etc); associated with ASD and sometimes PDA to allow for R-to-L shunting to maintain CO
40
Q
Congenital heart disease:
Left-to_right shunts (late cyanosis)- “blue kids”
A
- VSD (most common congenital cardiac anomaly)
- ASD (loud S1; wide, fixed split S2)
- PDA (close with indomethacin)
Frequency: VSD> ASD> PDA
41
Q
Eisenmenger’s syndrome
A
- uncorrected VSD, ASD, PDA causes compensatory pulmonary vascular hypertrophy, which results in progressive pulmonary hypertension
- as pulmonary resistance incr, shunt reverses from L-to-R to R-to-L, which causes late cyanosis, clubbing, polycythenia
42
Q
tetralogy of fallot
A
- tetralogy of fallot is caused by anterosuperior displacement of the infundibular septum
1. Pulmonary infundibular stenosis (most important determinant for prognosis)
2. RVH
3. Overriding aorta (overrides the VSD)
4. VSD
**PROVe
- early cyanosis (tet spells) caused by a R-to-L shunt across the VSD
- isolated VSDs usually flow L-to-R (acyanotic)
- in tetralogy, pulomary stenosis forces r-to-L (cyanotic) flow and causes RVH (on x-ray, boot-shaped heart)
Older patients historically learned to squat to relieve cyanotic symptoms. Squatting reduced blood flow to the legs, incr peripheral vascular resistance (PVR), and thus decr cyanotic R-to-L shunt across the VSD. Preferred treatment is early, primary surgical correction
43
Q
D-transposition of great vessels
A
- Aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior)–> separation of systemic & pulmonary circulations.
- not compatible with life unless a shunt is present to allow adequate mixing of blood (eg. VSD, PDA, patent foramen ovale)
- due to failure of the aorticopulmonary septum to spiral
- without surgical correction, most infants die within the first few months of life
44
Q
Coarctation of the aorta
- infantile type
- adult type
A
can result in aortic regurgitation
- infantile type
- aortic stenosis proximal to insertion of ductus arteriosus (preductal)
- associated with Turner syndrome
- infantile: in close to the heart
- check femoral pulses on physical exam - adult type
- stenosis is distal to ligamentum arteriosum (postductal)
- associated wtih notching of the ribs (due to collateral circulation), hypertension in upper extremities, weak pulses in lower extremities
- adult: distal to ductus
- most commonly associated with bicuspid aortic valve
45
Q
Patent ductus arteriosus
A
- in fetal period , shunt is R-to-L (normal)
- in neonatal period, lung resistance decr and shunt becomes L-to-R with subsequent RVH and/or LVH and failure (abnormal)
- associated with a continous, “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)
- endomethacin (indomethacin) ends patency of PDA; PGE kEEps it open (may be necessary to sustain life in conditions such as transposition of great vessels)
- PDA is normal in utero and normally closes only after birth
46
Q
Congenital cardiac defect associations
Disorder & Defect
A
- 22q11 syndrome- truncus arteriosus, tetralogy of Fallot
- Down syndrome- ASD, VSD, AV septal defect (endocardial cushion defect)
- congenital rubella- septal defects, PDA, pulomary artery stenosis
- turner syndrome- coarctation of aorta (preductal)
- Marfan’s syndrome- aortic insufficiency and dissection (late complication)
- infant of diabetic mother- transposition of great vessels
47
Q
Hypertension
A
- defined as BP> or equal 140/90 mmHg
- risk factors: incr age, obesity, diabetes, smoking, genetics, black>white>asian
- features: 90% of hypertension is primary (essential) and related to incr CO or incr TPR; remaining 10% mostly secondary to renal disease.
- Malignant hypertension is severe (>180/120mmHg) and rapidly progressing
- predisposes to- atherosclerosis, left ventricular hypertrophy, stroke, CHF, renal failure, retinopathy, aortic dissection
48
Q
Hyperlipidemia signs
A
- Atheromas-plagues in blood vessel walls
- xanthomas- plagues or nodules composed of lipid-laden histiocytes in the skin, especially the eyelids (xanthelasma)
- tendinous xanthoma- lipid deposit in tendon, especially Achilles
- corneal arcus- lipid deposit in cornea, nonspecific (arcus senilis)
49
Q
arteriosclerosis
- Monckeberg
- Arteriolosclerosis
- Atherosclerosis
A
- Monckeberg-
- Arteriolosclerosis
- Atherosclerosis
50
Q
Coarctation of the aorta
- infantile type
- adult type
A
can result in aortic regurgitation
- infantile type
- aortic stenosis proximal to insertion of ductus arteriosus (preductal)
- associated with Turner syndrome
- infantile: in close to the heart
- check femoral pulses on physical exam - adult type
- stenosis is distal to ligamentum arteriosum (postductal)
- associated wtih notching of the ribs (due to collateral circulation), hypertension in upper extremities, weak pulses in lower extremities
- adult: distal to ductus
- most commonly associated with bicuspid aortic valve
51
Q
Patent ductus arteriosus
A
- in fetal period , shunt is R-to-L (normal)
- in neonatal period, lung resistance decr and shunt becomes L-to-R with subsequent RVH and/or LVH and failure (abnormal)
- associated with a continous, “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)
- endomethacin (indomethacin) ends patency of PDA; PGE kEEps it open (may be necessary to sustain life in conditions such as transposition of great vessels)
- PDA is normal in utero and normally closes only after birth
51
Q
Patent ductus arteriosus
A
- in fetal period , shunt is R-to-L (normal)
- in neonatal period, lung resistance decr and shunt becomes L-to-R with subsequent RVH and/or LVH and failure (abnormal)
- associated with a continous, “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)
- endomethacin (indomethacin) ends patency of PDA; PGE kEEps it open (may be necessary to sustain life in conditions such as transposition of great vessels)
- PDA is normal in utero and normally closes only after birth
52
Q
Congenital cardiac defect associations
Disorder & Defect
A
- 22q11 syndrome- truncus arteriosus, tetralogy of Fallot
- Down syndrome- ASD, VSD, AV septal defect (endocardial cushion defect)
- congenital rubella- septal defects, PDA, pulomary artery stenosis
- turner syndrome- coarctation of aorta (preductal)
- Marfan’s syndrome- aortic insufficiency and dissection (late complication)
- infant of diabetic mother- transposition of great vessels
52
Q
Congenital cardiac defect associations
Disorder & Defect
A
- 22q11 syndrome- truncus arteriosus, tetralogy of Fallot
- Down syndrome- ASD, VSD, AV septal defect (endocardial cushion defect)
- congenital rubella- septal defects, PDA, pulomary artery stenosis
- turner syndrome- coarctation of aorta (preductal)
- Marfan’s syndrome- aortic insufficiency and dissection (late complication)
- infant of diabetic mother- transposition of great vessels
53
Q
Hypertension
A
- defined as BP> or equal 140/90 mmHg
- risk factors: incr age, obesity, diabetes, smoking, genetics, black>white>asian
- features: 90% of hypertension is primary (essential) and related to incr CO or incr TPR; remaining 10% mostly secondary to renal disease.
- Malignant hypertension is severe (>180/120mmHg) and rapidly progressing
- predisposes to- atherosclerosis, left ventricular hypertrophy, stroke, CHF, renal failure, retinopathy, aortic dissection
53
Q
Hypertension
A
- defined as BP> or equal 140/90 mmHg
- risk factors: incr age, obesity, diabetes, smoking, genetics, black>white>asian
- features: 90% of hypertension is primary (essential) and related to incr CO or incr TPR; remaining 10% mostly secondary to renal disease.
- Malignant hypertension is severe (>180/120mmHg) and rapidly progressing
- predisposes to- atherosclerosis, left ventricular hypertrophy, stroke, CHF, renal failure, retinopathy, aortic dissection
