Cardio- Embryology and Physiology Flashcards
Truncus Arteriosus
Gives rise to ascending aorta and pulmonary trunk
Issues with this can cause transposition of great vessels
Right common cardinal vein and right anterior cardinal vein
Gives rise to SVC
Cardiac looping
Begins at 4 wks of development
Dynein defects (Kartagener- ciliary dyskinesia)- can lead to dextrocardia
Septation of chambers- Atria
- Septum primum
- Foramen secundum
- Septum secundum
- Foramen ovale
- Septum secundum and primum fuse (forming atrial septum)- failure of fusion: patent foramen ovale
- Foramen ovale closes due to increased LA pressure
Separation of chambers- Ventricles
Endocardial cushions separates atria form ventricles and contributes to atrial and membranous portion of interventricular septum
VSD: most common congenital cardiac anomaly
Usually occurs in membranous septum
Conotruncal abnormalities
Associated with failure of neural crest cell to migrate
Valves
Derived from endocardial cushions
Outflow tract- A&P
AV canal- M&T
Fetal circulation
Two main circuits to the aorta:
Mom –> Umbilical vein (oxy blood from mom) –> ductus venosus –> IVC –> foramen ovale –> LA –> LV –> aorta –>
brain + body –> back through IVC & SVC –> RA –> RV –> Pulmonary artery –> Ductus arterioles –> Aorta –>
Aorta –> Umbilical arteries –> Mom
Ductus Arteriosus- steroids vs. prostaglandins
Indomethacin (NSAID)- closes PDA
Prostaglandins (E1 and E2)- kEEp PDA open
Umbilical arteries and veins
2 umbilical arteries, one umbilical vein (think smiley face)
AllaNtois
Carries gas and waste
Become mediaN umbilical ligament
UmbiLilcal arteries
Become mediaL umbilical ligaments
RCA (Right coronary artery)
Supplies SA and AV node (can cause heart block if damaged)
More common for PDA (posterior descending artery) to come from RCA- called” right-dominant circulation”, but can come from LCA or both (co-dominant)
LAD (Left anterior descending)
More common site of coronary artery occlusion
Supplies anterior LV
Most posterior part of heart
LA; enlargement can cause dysphagia (compression of esophagus) and hoarseness (compression of the left recurrent laryngeal nerve)
Pericardium
3 layers: parietal, visceral, and fibrous
Oxygen extraction
Highest in myocardium (coronary arteries)
3 main features of heart circulation
- Muscle perfused in diastole
- High O2 extraction
- O2 demand and coronary blood flow are tightly coupled
Cardiac output
= SV * HR = rate of O2 consumption (aka VO2)/ (a. - v. O2 content)
Early exercise: CO maintained by increased HR and SV
Late exercise: CO maintained by increased HR only (SV plateaus)
Increased HR
Diastole preferentially shortened (less filling time –> decreased CO)
MAP
= CO * TPR = 2/3 diastolic pressure + 1/3 systolic pressure
Pulse pressure
Systolic - diastolic pressure
Proportional to SV, inversely prop to compliance
SV
EDV - ESV
Increased pulse pressure
Hyperthyrodism, aortic regurg, aortic stiffening, obstructive sleep apnea
Decreased pulse pressure
Aortic stenosis, cardiogenic shock, tamponade, HF
SV
Increased with increased:
Contractility and preload
Increased with decreased:
Afterload
Contractility
Increased with:
Catecholamines (increase Ca2+ release)
Decreased Na+ extracellularly
Digitalis (increases Na+ and Ca2+ intracellularly)
Decreased with B1 blockers HF with systolic dysfunction Acidosis Hypoxia/ hypercapnea Non-DHP Ca2+ blockers (verapamil and diltiazem- mainly target heart)
Myocardial oxygen demand- CARD
Increased by:
Increased CARD: Contractility, After load, heart Rate, Diameter of ventricle
Tension
= PR(Radius) / (2t(wall thickness))
Preload
Approximated by ventricular EDV (increased preload, increased EDV)
vEnodilators decrease prEload
Afterload
Approximated by MAP (increased after load, increased MAP, increased wall tension)
vAsodilators decrease Afterload
Ejection fraction
= SV/ EDV = EDV - ESV/ EDV
Svedv
EF decreased in systolic failure
EF normal in diastolic failure (harder to tx)
Starling curve
Increase in end-diastolic length of muscle fiber increases the force of contraction
Viscosity of blood
Depends mostly on hematocrit (higher hematocrit, higher viscosity)
Arterioles
Account from most of TPR
Inotropy
Contractility
Increased by digoxin, catecholamines
Decreased in uncompensated HF and narcotics overdose
Venous return
Increased by fluid infusion, sympathetic activity
Decreased in acute hemorrhage or spinal anesthesia
Total Peripheral Resistance
Increased with vasopressors
Decreased with exercise (to perfuse organs) and AV shunt
See page 269 of FA for more details on effect on graph
Pressure volume curves
Increased preload: shifts right part of curve further right (same ESV, but higher EDV)
Increased after load: elongates curve (upward) with same EDV, but higher ESV
Increased contractility: shifts left part of curve further left (lower ESV, but same EDV)
S1
mItral and trIcuspid valves close (remember- sounds are heard mainly when the door CLOSES not opens)
S2
aortic and pulmonic valves close
S3
Can be normal in children or adults
Pathologic: dilated ventricles
S4 (PHour)
Pathologic always: hypertroPHIC ventricle
JVP
a wave- atrial contraction
c wave- tricuspid closure/ RV contraction
x descent- atrial relaXation (absent in tricuspid regard)
v wave- atrial filling (“Villing”)
y descent- RA emptYing into RV (passive)
Normal Splitting of S2
During inspiration (I) distance between A2 and P2 closure increase due to increased venous return (caused by decreased intrathoracic pressure)
Wide Splitting of S2
Not much difference seen between A2 and P2 closure during I and E; delayed P2 closure
Caused by pulmonic stenosis and RBBB
Fixed Splitting of S2
No difference between A2 and P2 closure during I or E; delayed P2 closure
Heard in ASD (because larger L–> R shunt causes larger volume in LA and therefore takes longer for LA to empty and P2 to close)
Paradoxical splitting
Delayed A2 closure; P2 sound occurs before A2 (and paradoxically split is less during inspiration –> as opposed to normally when it is more clear during inspiration)
Caused by aortic stenosis and LBBB
Inspiration (increases venous return to RA)
Increased intensity of rIght heart sounds
Handgrip (increased after load)
Increases MR, AR, VSD (backflow probs)
Decreases hypertrophic cardiomyopathy murmurs
Delays MVP click
Valsalva and standing up (decreases preload)
Decreases intensity of most murmurs EXCEPT hypertrophic cardiomyopathy
Early MVP click
Rapid squatting (increases preload and after load)
Shunts blood from L –> R; used in pts with Tet to force more blood to go through pulmonary circulation by increasing SVR
Decreases intensity of hypertrophic cardiomyopathy murmur
Increases intensity of AS
Delays MVP click (similar to handgrip)
Systolic heart sounds
A & P stenosis M & T regurg VSD (heard at T) MVP Hypertrophic cardiomyopathy
Diastolic heart sounds
A & P regurg
M & T stenosis
ASD (heard at T)
Aortic stenosis
Crescendo-decrescendo
Radiates to carotids
Pulsus parvus et tardus (pulses are weak with delayed peak)
SAD: leads to Syncope, Angina, and Dyspnea
Mitral regurgitation
Holosystolic, high pitched blowing murmur
Loudest at apex and radiates to axilla
Left sided S3 indicates more severe MR (higher regurgitant volume)
Commonly caused by rheumatic fever
Tricuspid regurgitation
Holosystolic, high pitched blowing murmer (like MR)
Radiates to right sternal border
Caused by RV dilation
Increases in intensity with inspiration
Mitral valve prolapse
Late systolic crescendo murmur beginning with mid systolic click (delayed by increased after load, earlier with decreased preload)
VSD
Harsh, holosystolic murmur
Loudest at T
Accentuated by increased after load (more back flow through hole)
Hypertrophic cardiomyopathy
Systolic crescendo-decrescendo murmur
Caused by left ventricular outflow obstruction
Increased with valsalva
Aortic regurgitation
High-pitched blowing diastolic decrescendo murmur
Hyperdynamic pulse/ head bobbing when severe/chronic
Wide pulse pressure
Loudest when sitting up and leaning forward
Mitral stenosis
Follows opening snap- OS (mitral valve snapping open)
Rumbling, late diastolic murmur
Increased severity as S2 and OS interval decreases
LA»_space; LV pressure during diastole (blood is retained in LA and not filling in LV as atria are contracting, due to stenosis of the mitral valve)
PDA
Continuous (machine-like) murmur
Loudest at S2
Due to congenital rubella or prematurity
Best heard in left infraclavicular area
Myocardial action potential- Phase 0
Sky rocket: Na+ (into cell) channels open
Myocardial AP- Phase 1
Dip: K+ (out of cell) channel open
Myocardial AP- Phase 2
Plateau: Ca2+ (into cell) open while K+ (out) channels remain open
Myocardial AP- Phase 3
Descent: K+ (out) dominates and Ca2+ channels close
Myocardial AP- Phase 4
Low plateau: K+ stay open- membrane reaches resting potential
Memory tool for myocardial AP: Na-K-Ca-K-K-K
Knack-Cak-K-K
- Na (into cell)
- K (out of cell)
- Ca (into cell) + K (out of cell)
- K (out of cell)
- K (out of cell)
Difference from skeletal muscle
- Plateau: Cardiac has plateau phase due to Ca2+ influx (during K+ efflux)
- Ca2+ induced Ca2+ release: Require Ca2+ influx into cell to release Ca2+ from SR (sarcoplasmic reticulum)
- Gap junctions: Cardiac myocytes are electrically coupled
Pacemaker AP (occurs in SA and AV nodes)- Phase 0
- Upstroke: Ca2+ (into cell) open
Pacemaker AP- Phase 1 and 2 DO NOT EXIST
DO NOT EXIST
Pacemaker AP- Phase 3
- Descent: K+ (out of cell) open, Ca2+ close
Pacemaker AP- Phase 4 (Four- Funny)
- Funny: K+ (INTO cell) and Na+ (into cell) via “funny current”
Rate at which ions enter cells determines the HR (via adjusting the number of open funny current channels)
Adenosine/ ACh- decreases HR
Catecholamines- increases HR
Conduction Pathway
SA node –> atria -> AV node –> Bundle of His –> Right and left bundle branches –> Purkinje fibers –> ventricles
Pacemaker rates (comparison)
SA > AV > Bundle/Purkinje
Speed of conduction
Purkinje > atria > ventricles > AV node
P wave
Atrial depol
PR
Time from atrial to ventricular depol
QRS
Ventricular Depol (+ atrial repol)
QT
Time between ventricular deploy and repol
T
Ventricular repol
ST
Isoelectric, ventricles depolarized
U (after T wave)
Seen with hypokalemia and bradycardia
Torsades de pointes
Polymorphic ventricular tachycardia
Caused by drugs, decreased K+, decreased Mg2+
Long QT predisposes to this
Drugs that induce long QT (ABCDE)
Anti-Arrythmics (Class IA, III) Anti-Biotics (macrolides) Anti-Cychotics (haloperidol) Anti-Depressants (TCADs) Anti-Emetics (ondansetron)
Torsades de Pointes- tx
magnesium sulfate
Congenital Long QT Syndrome
Due to ion channel defects- specifically with K+ channel proteins
Increased risk of ventricular tachy, sudden death
Two types:
Romano-Ward Syndrome: AD- no deafness
Jervell and Lange-Nielsen: AR with deafness
Brugada Syndrome- ABCD
Autosomal dominant, seen in Asian males
Characterized by pseudo RBBB (presence of R’- QRS split into two humps) and ST elevations in V1-V3
Causes increased risk of ventricular tachyarrythmias
Asian male
Brugada
Cardioverter-defib tx
Dominant
Wolff-Parkinson-White
Most common ventricular pre-excitation syndrome
Causes by reentrant loop (bundle of Kent) that bypasses the AV node
Characterized by delta wave (shortened PR and widened QRS)
Can result in SVT
Atrial fibrillation
No discrete P waves, varying RR intervals, narrow QRS complexes
Irregularly irregular pattern; AV node generally determines rate of ventricular contraction
RF: HTN, CAD
Afib-tx
anti-coag, rate control, rhythm control, cardioversion
Atrial flutter
Sawtooth pattern
Caused by back-to-back atrial depolarization
Can be due to reentrant loop around tricuspid valve
Tx: catheter ablation
Vfib
Erratic rhythm with no identifiable waves
Fatal in not tx
Tx: CPR and defibrillation
AV block- 1st degree
PR interval is prolonged (>200ms)
PR is PRo1onged
AV block- 2nd degree (Mobitz Type I)
Progressively elongating PR interval, that causes a missed QRS
“Regularly irregular”
AV block- 2nd degree (Mobitz Type II)
Occasional missed beat (P that is not followed by QRS)
Tx: pacemaker (to prevent progression to 3rd degree heart block)
AV block- 3rd degree
P and QRS are independent of one another
Can be caused by Lyme disease
Tx: pacemaker
How to calculate HR
Look at number of boxes between two QRS peaks
300 –> 150 –> 100 –> 75 –> 60 –> 50
Atrial Natriuretic Peptide
Released from atrial myocytes in response to INCREASED volume to promote natriuresis
Acts via cGMP (like NO)
Dilates afferent arterioles and constricts efferent arterioles to promote filtration and diuresis
Brain Natriuretic Peptide
Released from ventricular myocytes in response to increased tension
Longer half life than ANP
BNP blood test- to diagnose HF
Nesiritide (recombinant BNP) available for HF treatment
Net effects of ANP and BNP (3)
Increase GFR
Inhibits renin secretion- Increases natriuresis and diuresis
Prevent reabsorption of Na+ at PCT
Baroreceptors
General path: baroreceptors detect stretch
Carotid massage
If stretch is detected –> baroreceptors fire –> decreases sympathetic stim and increases parasymp stim –> increases AV node refractory period –> Decreases HR
Opposite for hypotension
Cushing reaction
Triad of hypertension, bradycardia and respiratory depression
(Mnemonic: CHBE- cushing: HTN, Bradycardia, and decreased Exhalation)
Caused by increased intracranial pressure –> stimulates vasoconstriction of a. to brain –> cerebral ischemia –> increases pCO2 and decreases pH (note: brain does not respond to PO2 changes!!) –> sympathetic reflex increases –> causes HTN –> periphery detects increased stretch –> causes bradycardia
Afferent vs. Efferent baroreceptor signals
Afferent/ Sensory:
IX: Glossopharyngeal- via carotid baroreceptors (e.g. during carotid massage)
X: Vagus- via aortic baroreceptors
Efferent:
Parasympathetic: via vagus nerve (affects heart- SA and AV nodes)
Sympathetic: via sympathetic chain (affects blood vessel and heart)
Processing occurs in the medulla
Chemoreceptors- Peripheral
Peripheral: Located in similar regions to baroreceptors (aortic arch, carotid)- stimulated by decreased pO2 and increased pCO2 (decreased pH)
Chemoreceptors- Central
Central: Stimulated by changes in pH and pCO2 of brain interstitial fluid (affected by arterial CO2)
Does NOT directly respond to pO2
Normal cardiac pressure
RA: 5
RV: 10
LA (PCWP): 25
LV: 100
PCWP (wedge pressure)
Estimates LA pressure
Gathered by inflating a balloon in pulmonary artery and measuring downstream pressure
Autoregulation
Blood flow (flow rate) stays the same despite variation in perfusion pressures
Pulmonary vs. systemic vasculature
Pulmonary: hypoxia causes vasoCONSTRICTION
Systemic vasculature: hypoxia causes vasoDILATION
Chemicals that help with auto regulation- CHALK
CHALK CO2 H+ Adenosine Lactate K+
Normal changes in an aging heart (5)
Decrease in LV chamber size (apex to base)
Sigmoid shaped ventricular septum
Myocardial atrophy (increases collagen deposition)
Accumulation of cytoplasmic lipofuschin w/in myocytes (product of lipid peroxidation)
Dilated aortic root
Capillary fluid exchange
Jf (net fluid flow) = Permeability to fluid * (Capillary pressure - Interstitial pressure) - Permeability to protein * (Plasma oncotic (colloid osmotic) pressure - Intestitial oncotic pressure)
