Cardio Flashcards
Where are the auscultation points for normal valve sounds
1) Aortic –> over aorta (R 2nd intercostal space at the right sternal border)
2) Pulmonic –> over pulmonary trunk (L 2nd intercostal space at the left sternal border)
3) Tricuspid –> over right ventricle (L 5th intercostal space at the left sternal border)
4) Mitral –> over left ventricle (L 5th intercostal space at midclavicular line (3 inches to left of the sternum) ie the apex of the heart)
Where are the auscultation points for valvular murmurs
Aortic stenosis (systolic) --> aorta (R 2nd intercostal space at sternal border) Aortic regurgitation (diastolic) --> left ventricle (L 5th intercostal space at apex of heart) Pulmonic stenosis (systolic) --> pulmonary trunk (L 2nd intercostal space at sternal border) Pulmonic regurgitation (diastolic) --> right ventricle (L 5th intercostal space at sternal border) Tricuspid stenosis (diastolic) --> right ventricle (L 5th intercostal space) Tricuspid regurgitation (systolic) --> right atrium (R 5th intercostal space at sternal border, to the right of the auscultation point for tricuspid) Mitral stenosis (diastolic) --> left ventricle (L 5th intercostal space) Mitral regurgitation (systolic) --> left atrium (L upper border of axilla, since left atrium is mostly posterior heart)
What is the blood supply of the heart?
What is right vs left dominance?
What are the anastamoses?
1) Blood supply: Ascending aorta –> R and L coronary artery (holes in walls of R and L aortic sinuses)
Right coronary artery - supplies R atrium, R ventricle, AV node, SA node, interatrial septum
-posterior interventricular artery - supplies R and L ventricles
-marginal artery - supplies R ventricle
Left coronary artery - v short
-left anterior interventricular artery - supplies R and L ventricles and interventricular septum
-circumflex - supplies L atrium and L ventricle
2) Right dominance - posterior interventricular artery branches from right coronary artery (80%)
Left dominance - PDA branches from circumflex branch of Left coronary artery (20%)
3) Right coronary artery and circumflex branch of left coronary artery – pathway of collateral flow for tissues
What is the venous drainage of the heart?
Great + middle + small cardiac veins –> great cardiac vein becomes coronary sinus –> Drains into Right atrium
anterior cardiac veins –> directly into right atrium
least cardiac veins –> directly into underlying chamber –> explains why blood in left ventricle is not 100% saturated
What is the structure of the pericardium and its relation to cardiac tamponade
1) Visceral pericardium - covers external surface of heart and roots of the vessels
Parietal pericardium - continuous with visceral at roots of the vessels –> Creates sinuses
transverse sinus - open at both ends, anteriorly bounded by pulmonary trunk and ascending aorta, posteriorly bounded by SVC
oblique sinus - blind recess, bounded by IVC and 4 pulmonary veins
fibrous pericardium - fused with parietal pericardium, inelastic tough layer
2) Cardiac tamponade: accumulation of fluid in pericardial space –> cavity cannot expand outwards bc of fibrous pericardium so it expands inwards –> compresses the heart –> restricts filling during diastole –> reduces cardiac output (need to do pericardiocentesis to remove fluid)
Explain the cardiac conduction system
Composed of Purkinje fibers, NOT nerve cells/nervous tissue
SA node: located in wall of right atrium near where SVC comes in; pacemaker of the heart
fibrous skeleton: layer of dense collagenous connective tissue running across heart at atrioventricular boundary – layer of insulation between atrial muscles and ventricular muscles
AV bundle: defect in fibrous skeleton – only electrical connection between atria and ventricles
AV node: located in wall on right side of interatrial septum; retards the wave of depolarization
0.15 second gap between atrial and ventricular depolarization
Describe innervation to the heart
Heart can function without innervation but it has nerve supply that modulates cardiac cycle
1) Parasympathetic: slow down SA node, lengthen interval of AV node
- preganglionic - vagus nerve
- postgang- cardiac plexus in wall of the heart
2) Parasympathetic sensory: afferent limb of cardiac reflexes (not conscious levels)
- enter CNS at medulla
- cell bodies in inferior vagus ganglion
3) Sympathetic: speed up SA node, reduce interval of AV node
- preganglionic - upper thoracic spinal cord
- postgang - cervical and upper thoracic ganglia
4) Sympathetic sensory: reach conscious levels eg ischemia
- enter CNS at upper thoracic spinal cord levels
- cell bodies in dorsal root ganglia
- brain perceives pain/angina from upper thoracic dermatomes (T1-T4) –> upper chest and medial arm
Describe the SNS system of neurotransmission
Input at spinal cord (T1-L2)
Preganglionic SNS fiber: cholinergic = acetylcholine neurotransmitter
short preganglionic neurons synapse at ganglia in paravertebral column
Postganglionic SNS fiber: synapse at cholinergic-nicotinic receptor (N2-R); noradrenergic = norepi neurotransmitter (synthesized in axon termini of postgang fibers)
Adrenergics diffuse across synapse and bind to adrenoreceptors on post synaptic membrane of effector(/target) tissue: synapse at type alpha and beta adrenergic receptors
Describe how specificity of effector response is achieved within the SNS and PSNS.
Identify the isoforms of adrenoceptors, and major tissues that express these isoforms.
1) specific receptor isoforms expressed on target effector tissue determines specificity of response to adrenergic stimulation (can have different effects from a single compound)
2) Alpha: alpha1 (vascular smooth muscle), alpha2
Beta: beta1 (SA node, ventricular myocytes, renal JG cells)
beta2 (myocardium heart muscle, bronchial smooth muscle, vascular smooth muscle of skeletal muscles meaning smooth muscle of blood vessels that supply skeletal muscle)
beta3
Describe the function of COMT, MAO, and cholinesterase.
COMT and MAO- degrade adrenergics (eg norepi at synapse of SNS effector postsynaptic membrane); alternatively norepi can diffuse back across presynaptic membrane for recycling
Cholinesterase- degrades ACh at synapse of PSNS effector postsynaptic membrane; alternatively choline form of ACh can be reuptaken by presynaptic membrane
Describe the basic histology and function of the adrenal gland in the context of ANS physiology
Adrenal gland sits on top of kidneys, supports upfront, quick SNS response when SNS is activated
outer cortex
inner medulla: pregang SNS fibers (ACh) synapse with chromaffin postganglionic fibers at cholinergic-nicotinic receptors–> secretes catecholamines–> epi (and a little norepi) into circulation
epi supports norepi secreted from local postganglionic SNS fibers
Which of the following responses are DECREASED during elevated SNS activity?
1) arterial BP due to increased cardiac output, vasoconstriction
2) blood flow to contracting skeletal muscle
3) glycolysis in liver and skeletal muscle
4) gluconeogenesis in liver, plasma glucose level
5) insulin secretion
6) muscle contractility
7) mental activity, awareness
8) rate of blood coagulation, release of RBCs from spleen
9) GI motility
10) lipolysis in adipocytes
5) insulin secretion decreases
9) GI motility and secretion decreases
Describe the PSNS system of neurotransmission
Input at brainstem, sacral spinal cord
preganglionic PSNS fiber: cholinergic = ACh
Postganglionic PSNS fiber: synapse at N2-R, cholinergic = ACh neurotransmitter
Effector(/target) tissue: synapse at cholinergic-muscarinic (CM) receptors - 5 isoforms, including one in SA node (CM2-R)
Describe the autonomic control over cardiac function (blood pressure)
Receptor: high pressure baroreceptors in carotid sinus, aortic arch; low pressure baroreceptors in right atrium and pumonary arteries
signal carried on afferent fibers (CN IX and X) to medulla (cardioinhibitory, cardioaccelatory, and vasomotor centers)
interneurons release neurotransmitters - activation of SNS is accompanied with inhibition of PSNS and vice versa
Preganglionic efferents synapse with postganglionic efferents
Sympathetic efferents - increase heart rate (beta1), vasoconstriction (alpha1) –> increase blood pressure
Parasympathetic efferents - (CM2-R in SA node)–> decrease heart rate
Describe the formation of the embryonic heart tube
When: 3rd week of devlpt
Where: splanchnic mesoderm, induced by endoderm
What: angiogenic clusters
medial –> dorsal aortae
lateral –> R and L endocardial tubes –> heart tube (4th week)
aortic arch = communication between heart tube and dorsal aorta
What are the regions of the heart tube and what are their adult derivatives?
Blood flows caudally to cranially
caudal end: sinus venosus - receives venous return from placenta, yolk sac, embryo –> becomes sinus venarum (smooth-walled part of right atrium where veins enter)
primitive atrium –> becomes trabeculated parts of right and left atria (ie pectinate muscle)
primitive ventricle –> becomes trabeculated part of left ventricle (trabeculae carnae)
bulbus cordis:
- proximal third –> becomes trabeculated part of right ventricle (trabeculae carnae)
- conus cordis –> becomes smooth parts of the right and left ventricles
- truncus arteriosus –> roots of ascending aorta and pulmonary trunk
Describe the development of the smooth portion of the left atrium
primitive atrium = rough-walled section of LA (pectinate muscle)
pulmonary veins = smooth-walled section of LA
the pulmonary vein grows out of the atrium towards the lungs
then starts getting resorbed back into the wall of the left atrium
end result: 4 pulmonary veins branching from left atrium and v large smooth wall portion
Describe the effects of heart tube folding
heart tube folds on itself:
atrium becomes cranial to the ventricle
veins enter on posterior wall of heart (back wall of right atrium)
arteries leave from anterior wall of heart (front wall of left ventricle)
What are the 2 major functional requirements for heart tube septation?
1) need communication between R and L sides of the heart in the fetus
oxygenated blood is coming from placenta –> IVC –> R atrium, so it needs to go to left side to distribute to body
2) Communication needs to be closed when baby is born
since oxygenated blood is now coming from L side (lungs)
Describe the formation of the atrial septum (end of 4th week – beg of 6th week)
1) Septum primum grows from wall of atrium towards the 4 atrioventricular endocardial cushions (comprised of neural crest cells)
2) Foramen primum - narrowing gap between septum primum and endocardial cushions
3) Foramen secundum - perforation in septum primum formed due to apoptosis, before closure of foramen primum
4) Septum secundum forms on right side of septum primum covering foramen secundum –> is thicker and more rigid
(-part of septum primum not covered by septum secundum –> becomes fossa ovalis
-free edge of septum secundum –> becomes limbus of fossa ovalis)
5) R–>L pressure gradient in the fetus –> blood flows through tunnel called foramen ovale
6) When fetus is born, pressure gradient becomes L–>R (lungs start working) –> closure of foramen ovale
Describe the two types of atrial septal defects and whether they are cyanotic
1) Primum type: failure of septum primum to fuse with the endocardial cushions (neural crest migration defect, association with valvular defects) –> persistent opening in foramen primum
results in L to R shunt –> acyanotic
2) Secundum type: septum secundum doesnt completely cover foramen secundum –> incomplete closure of foramen ovale
results in L to R shunt –> acyanotic
What is Eisenmenger’s syndrome?
when an acyanotic L to R shunt caused by a congenital heart defect overloads pulmonary circuit over time –> causes pulmonary hypertension –> shunt reverses to R to L shunt –> becomes cyanotic
Describe the formation of the ventricular septum (end of 5th week – beg of 7th week)
1) embryonic ventricular septum- formed from cardiac muscle –> becomes muscular septum in adults
2) aorticopulmonary/spiral septum - ingrowth of neural crest cells that divides the truncus arteriosus in half (R side pulmonary trunk and L side aorta) –> becomes membranous septum in adult
Describe the following types of ventricular septal defects and whether they are cyanotic:
1) Tetralogy of Fallot
2) Persistent truncus arteriosus
3) Transposition of the great arteries
4) Patent ductus arteriosus
1) Tetralogy of Fallot - aorticopulmonary septum displaced to the right (pulmonary side)
-pulmonary stenosis
-overriding aorta
-ventricular septal defect - failure of fusion of aorticopulmonary septum with embryonic ventricular septum
-right ventricular hypertrophy
results in R to L shunt –> cyanotic (most common)
2) Persistent truncus arteriosus - aorticopulmonary septum doesnt form at all
-also membranous ventricular septal defect
-bc deoxy blood and oxy blood is mixed when blood enters systemic and pulmonary circuits –> cyanotic
3) Transposition of the great arteries - spiral septum is not spiral –> aorta and pulmonary trunk positions are reversed
-cyanotic
right ventricle (deoxy) –> aorta
left ventricle (oxy) –> pulmonary trunk
babies must have other septal defects to survive
4) Patent ductus arteriosus - connects pulmonary artery to descending aorta in fetus
reversal of pressure gradient at birth results in L to R shunt: 02 blood shunted from aorta to pulmonary artery–> acyanotic (putting more oxy blood back into the lungs unnecessarily)
more common in preemies (prostaglandin decreases at 9 mos devlpt, needed to close ductus arteriosus)
Describe the differences in prenatal and postnatal circulation
1) Prenatal circulation:
-oxygenated blood from umbilical vein –> ductus venosus (shunt to bypass liver) –> IVC (mixes with deoxy blood)–> right atrium –> foramen ovale shunt –> left atrium –> ascending aorta –> (supplies brain) –> Descending aorta –> umbilical arteries
-deoxy blood from SVC –> right atrium –> tricuspid valve –> right ventricle –> pulmonary trunk –> pulmonary artery –> ductus arteriosus shunt –> descending aorta –> umbilical arteries
2) postnatal circulation:
umbilical vein closes –> becomes ligamentum teres
umbilical arteries close –> become medial umbilical ligaments
ductus venosus closes –> becomes ligamentum venosum
reversed L to R gradient closes foramen ovale
increased 02, decreased prostaglandin (around 9 mos devlpt)–> ductus arteriosus closes –> becomes ligamentum arteriosum
What is the clinical significance of cardiac-specific troponin and creatine kinase?
elevated plasma levels of cardiac specific troponin (cTnI, cTnT) and to a lesser extent creatine kinase (CK-MB) are reliable markers of myocardial injury eg MI
What are the properties of cardiomyocytes that allow for greater contractile force compared to skeletal muscle?
1) slight stretch from resting position L0 signals cardiomyocyte to release intracellular Ca2+ from SR and mitochondria –> increased contractile force
2) cardiomyocytes develop more tension from stretch than other types of muscle –> increased filling = more forceful contraction
(myocardial biomechanics) Explain what happens during diastole and systole in left ventricle. What is the clinical impact of hypertension?
1) Diastole: myocardium is relaxed, low intraventricular pressure and low arterial BP
Early diastole: aortic valve closed, mitral valve ready to open; fibers have no load
mitral valve opens due to increased left atrium filling (/pressure)
filling –> stretch from L0 –> preload –> increased wall tension (since T = p x r)
mitral valve closes when ventricular pressure > atrial pressure
2) Systole: myocardium contracts, high intraventricular pressure and high arterial BP
LV muscle fibers stretched to optimal length –> increased intracellular Ca2+
Early systole = isovolumetric contraction; mitral and aortic valves closed, increase in LV blood pressure
afterload=opposing aortic blood pressure (ie systemic BP)
preload (contractile force) > afterload (aortic pressure) –> aortic valve opens –> LV ejects blood into aorta –> systolic contraction ends
3) Hypertension = increased aortic/systemic blood pressure
heart esp LV has to work much harder to pump blood
What is the function and mechanism of Digitalis (digoxin)?
Function: positive inotrope - use for impaired cardiac function eg decreased ejection fraction
increases contractile force (inotropy)
increases end diastolic volume
increases contraction velocity
increases cardiac output
also slows SA and AV nodal conduction (used in heart failure)
sensitizes baroreceptors - reduces SNS afferent activity (downregulates SNS tone)
Mechanism:
- Normally, the NA+/K+ ATPase pumps Na+ out and K+ in
- NCX takes advantage of the gradient to pump Na+ in and pump Ca2+ out –> decrease in sarcoplasmic Ca2+ –> relaxation
- Digoxin inhibits Na+/K+ ATPase –> increased sarcoplasmic Na+ –> NCX inhibited –> increased sarcoplasmic Ca2+ –> increased contractility –> increased cardiac output
Describe the effect of SNS and PSNS tone on SA pacemaker activity and the mechanism behind this effect
Mechanism: increase in positive charge in an electrogenic cell (eg Na+ influx) increases resting membrane potential (from its resting -85 mV) –> decreases time to reach threshold, and vice versa
SNS: increased Na+ permeability at AV and SA node –> decreased time to reach depolarization threshold –> increased rate of rise of depolarization –> increased heart rate (decreased interval between peaks) compared to basal HR
PSNS: increased K+ permeability at AV and SA node –> decreased rate of rise of depolarization (time to reach threshold) –> increased interval between peaks compared to basal rate –> decreased heart rate
Describe arrhythmias associated with the SA node:
- what are the characteristics of sinus rhythm? Normal sinus rhythm?
1) Sinus tachycardia
2) Sinus bradycardia
*Sinus rhythm: rhythm set by the SA node (P waves)
Normal sinus rhythm: P before QRS, regular P-P intervals and QRS-QRS intervals (regular rhythm), HR 60-100 bpm
1) Sinus tachycardia: HR >100 bpm
decreased P-P interval
2) Sinus bradycardia: HR
Describe arrhythmias associated with the AV node:
1) primary heart block
2) second degree heart block
3) tertiary/complete heart block
1) primary heart block - delayed conduction through AV node/bundle of His
- prolonged PR interval
- still 1 P before QRS
2) second degree heart block - increased refractory period for AV node
- not every P wave is followed by QRS interval
3) tertiary/complete heart block - no atrial impulses reach the ventricles
- P and QRS are at regular intervals separately but not coordinated with each other
- escape rhythm: junctional escape (if block is at AV node, around 50 bpm) or ventricular escape (if block is distal to AV node, around 30 bpm by His-Purkinje pacemaker)
Describe circus rhythms caused by the phenomenon of reentry.
What is the clinical abnormality that results?
How does afib manifest on EKG? What are the types of afib? What is one serious risk associated with afib?
1) Normal: unidirectional spread of action potential (depolarization) through the myocardium; retrograde conduction prevented by effective refractory period
Reentry: results in formation of ectopic pacemaker (outside of SA node) because damaged cells allow retrograde conduction
if time for retrograde conduction is longer than effective refractory period – AP hits myocytes when they are active again –> creates circus rhythm circuit –> self-sustaining ectopic pacemaker
-abnormal circus rhythm can spread to myocytes in relative refraction period and doesnt self-terminate
2) fibrillation - twitches of myofibrils but no coordinated contractions of the entire muscle
atrial fibrillation - no recognizable P wave (bc no uniform atrial depolarization), irregularly irregular interval
ventricle doesnt beat at 200+ beats/minute bc of AV nodal delay
generally localized to left atrium
Types: Recurrent (resolves itself), paroxysmal (in and out of sinus and afib)
Risk: atrial thrombus –> PE or stroke
