Cardiology Flashcards
Truncus arteriosus gives rise to
Ascending aorta and pulmonary trunk
Bulbus cordis gives rise to
smooth parts )Outflow tract of LV and RV)
Primitive ventricle/atrium gives rise to
trabeculated part of L & R ventricles and atrIa
L horn of sinus venosus gives rise to
Coronary sinus
R horn of sinus venosus gives rise to
smooth part of R atrium ( sinus venarum)
Endocardial cushion gives rise to
Atrial septum, membranous IV septum, AV and semilunar valves
R common cardinal & R anterior cardinal vein gives rise to
SVC
Posterior cardinal, subcardinal and supracardinal veins
IVC
Primitive pulmonary vein
Smooth part of LA
The heart is the first functional organ in vertebrae embryos. beats spontaneously by ______ week of development
4
In atrial septation, what is the name of the first septum to form?
Septum primum
What is the name of the opening created when the septum primum grows towards endocardial cushions?
Ostium primum
Why does septum primum closes against septum secundum, sealing the foraman ovale soon after birth?
Increased LA pressure and decreased RA pressure
What two septums fuse during infancy/early childhood forming the atrial septum
Septum secundum & septum primum
Patent foramen ovale etiology
Failure of septum primum and septum secundum to fuse after birth
- Most left untreated
What is the most common congenital cardiac anomaly?
Ventricular septal defect
Explain outflow tract formation
Neural crest cell migration–>truncal and bulbar ridges that spiral and fuse to form aorticopulmonary septum –>ascending aorta & pulm trunk
1st aortic arch derivatives develop into arterial system
part of maxillary artery (branch of external carotid)
2nd aortic arch derivatives develop into arterial system
Stepedial artery and hyoid artery
3rd aortic arch derivatives develop into arterial system
Common carotid artery and proximal part of internal carotid artery
4th aortic arch derivatives develop into arterial system
Aortic arch & proximal part of right subclavian artery
4th aortic branch corresponding nerve
Right recurrent laryngeal nerve (loops around R subclavian artery)
6th aortic arch derivatives develop into___ arterial system
proximal part of pulm arteries & ductus arteriosus (left only)
6th aortic branch corresponding nerve
Left recurrent laryngeal nerve (loops around ductus arteriosus)
Ductus arteriosus gives rise to
ligamentum arteriosum
Ductus venosus
ligamentum venosum
Foramen ovale
fossa ovalis
Umbilical arteries
medial umbilical ligamentes
Umbilical veins
Ligamentum teres (hepatis)
Umbilical vein carries
oxygenated blood
Umbilical arteries carry
Deoxygenated blood
What are the 3 layers of the heart wall
- Endocardium: innermost layer, lines the interior of the heart chambers, covers valves
- Myocardium: middle layer- composed of cardiac muscle
- Epicardium: outermost layer aka visceral layer of serous pericardium - forms valve rings, helps anchor muscle fibers
What are the 3 layers of pericardium (outer to inner)?
- Fibrous pericardium - external
- parietal pericardium- internal
- Visceral pericardium aka Epicardium
Pericardial space lies b/n
Parietal layer of serous pericardium and visceral layer of serous pericardium (epicardium)
What is myocardium composed of?
Cardiac muscle, responsible for the contractile function of the heart
What is epicardium composed of?
Covered by the visceral layer of pericardium, contains coronary blood vessels and nerves
Pericardium is innervated by ____nerve
Phrenic nerve
What are the three tunics of an artery wall?
- Tunica intima: innermost layer
- Tunica media: middle layer
- Tunica adventitia: outermost layer
What is the composition of tunica intima?
- Endothelial cell layer, CT, & internal elastic membrane
What is the composition of tunica media?
smooth muscle fibers, elastic and collagenous tissues
What is tunica adventitia composed of?
Loose collagenous CT, blood and lymph vessels, nerves and fibroelastic CT, vasa vasorum
Contractility and (SV) increases with
- Catecholamine stimulation via B1 receptors
- inc intracellular Ca2+
- dec extracellular Na+ (dec activity of Na/Ca exchanger)
Apex (anterior left) formed mainly by
LV
Base of the heart (posterior aspect) formed mainly by
LA
Diaphragmatic (inferior surface)
L&R ventricles
Anterior (sternocostal surface) formed mainly by
RV
Pulmonary (left surface located in the cardiac impression of L lung) formed mainly by
LV
What is the most posterior part of the heart
LA
Explain etiology and sx of Ortner syndrome
LA enlargement can be cause by Mitral stenosis. Enlargement of the LA chamber will cause compression of the esophagus causing- dysphasia and compression of L laryngeal nerve causes hoarseness
What is the most anterior part of the heart
RV (commonly injured in trauma)
Boundaries of the heart (inner to outer)
Endocardium > Myocardium > Epicardium (visceral layer of serous pericardium) > Parietal layer of serous pericardium > Fibrous pericardium
Draw major vessels of the heart
List AV and semilunar valves
AV: Tricuspid and Mitral (bicuspid) valves
SV: Pulmonary and aortic valves
Mitral valve: location, function, auscultation
Location: Between the left atrium and left ventricle
Function: prevents backflow from the LV to LA during ventricular systole
Auscultation: 5th ICS MCL ( Apex)
S1:Mitral and tricuspid Close, loudest at mitral area (systole)
Blood flow through the heart
deoxygenated blood IVC and SVC –> R atrium –> TRICUSPID V–>Right ventricle –>PULMONIC V–>pulmonary arteries (R,L)–> lungs–>oxygenated blood enters through pulmonary veins –>L atrium–>MITRAL V–>L ventricle–> AORTIC V–> Aorta –> to the rest of the body
S1 sound is heard during ————–at the beginning of —————–
closure of AV vlaves- isometric contraction
Systole
S2 sound is heard during —————at the beginning of —————-
closure of semilunar valves- isometric relaxation
Diastole
S3 sound
benign in kids and trained athletes. if heard later in life = indication of HF
Stenosis occurs during ———-
late diastole
Regurgitation occurs during —————
early diastole
Vascular dysfunction during diastole
(ARMS & PaRTS)
Aortic regurgitation
Mitral stenosis
Pulmonic regurgitation
Tricuspid stenosis
Vascular dysfunction during systole
(Opposite of ARMS & PaRTS)
Aortic stenosis
Mitral regurgitation
Pulmonic stenosis
Tricuspid regurgitation
Mitral regurgitation murmur
holosystolic murmur
Mitral stenosis murmur
diastolic murmur
Mitral valve prolapse
Systolic murmur (midsystolic click)
Tricuspid valve: location, function, auscultation
location: b/n RA and RV
function: prevents back flow from RV to RA during ventricular systole
Auscultation: 5th L ICS - during S1 (systole)
Tricuspid regurgitation murmur
Holosystolic murmur
Tricuspid stenosis murmur
diastolic murmur
Ventricular septal defect
holosystolic murmur
Pulmonic valve: location, function, auscultation
location: b/n RV and pulmonary artery
function: prevents backflow from the pulmonary artery to RV during ventricular diastole
Auscultation: 2nd L ICS
Pulmonic stenosis, atrial septal defect, and flow murmurs are all ______murmurs
Systolic ejection murmurs
Aortic valve: location, function, auscultation
location: between the LV and aorta
function: prevents backflow from aorta to LV during ventricular diastole
What murmurs can be appreciated at Erb’s point? 3rd L ICS
- Aortic regurgitation- Diastolic murmur
- Pulmonic regurgitation- diastolic murmur
- Hypertrophic cardiomyopathy - systolic murmur
S3 sound is heard during
Early diastole eg. can be normal, mitral regurgitation, HF
S4 sound is heard during
Late diastole. Always abnormal, hypertrophy
Cardiac muscle intercalated discs
cell membranes that separate individual cardiac muscles from one another
Gap junctions function
found at each intercalated disc. allows transfer of ions and small molecules including
what is syncytium of cardiac muscle
Atrial wall contraction followed by ventricular walls contraction due to the rapid spread of AP from one cardiac cell to the next through intercalated discs
5 phases of cardiac muscle AP
0- rapid depolarization
1- initial repolarization
2- Plateau (unique to cardiac AP)
3- Rapid repolarization
4- Resting membrane potential
Ion flow during AP phase 0
- SA node stimulates the conduction system
- Voltage gated fast Na channels open
- rapid flow of Na +1 depolarizes the cell membrane
- Membrane potential becomes more positive
- Volgage gated slow Ca 2+ channels open and influx 2+ making cell more positive
Ion flow during AP phase 1
- voltage gated fast Na
channels close - voltage gated fast K +1 channels open and leave the cell = (repolarization at the peak)
- Ca is still entering in the background
ion flow during AP phase 2
- Voltage gated (fast) K channels close
- Voltage gated slow Ca channels still open triggers more Ca release from sarcoplasmic reticulum —> myocyte contraction
ion flow during AP phase 3
- Voltage gated slow Ca channels close
- Voltage gated (slow) K channels open Efflux +1 leaving cell
ion flow during AP phase 4
- high K permeability - brings it to resting AP.
k high intracellularly
Na high extracellularly
how does the cell reset after AP/Excitation contraction coupling
- Ca gets pumped back to sarcoplasmatic reticulum using calcium ATPase pump
- some calcium leaves the cells through Ca2+/Na+ exchanger
- Na+ leaves cell and K+ enters cell via Na+/K+ channels ATPase pump
Cardiac muscle vs skeletal muscle
Cardiac muscle:
- Myocytes coupled by gap junctions and intercalated discs
- AP plateau
- Ca influx from ECF induces Ca release from sarcoplasmic reticulum
Skeletal muscle:
- myocytes not coupled via intarcalated discs
- AP no plateau
- No Ca releaase from sarcoplasmic reticulum
P wave on EKG
Atrial depolarization (K+ leaves the cell)
PR intervnal on EKG
Time from start of atrial to ventricular depolarization
QRS on EKG
Ventricular depolarization
QT interval on EKG
Ventricular depolarization/ventricular contraction/ventricular repolarization
Long QTI can is associated with or predispos individuals to ______condition
Torsades de pointes
What are the risks associated with Torsades de pointes?
- Congenital abnormalities
- hypomagnesemia, hypokalemia, and hypocalcemia
- Drugs: antiarrhythmics, antibiotics, antipsychotics
T wave on EKG
Ventricular repolarization
Inversion of the T wave is associated with
ischemia, recent MI
U wave on EKG is associated with
Papillary muscle relaxation - final muscle to relax to prevent regurgitation of blood
hypokalemia
What kind of heart block presensents with elongation of PR interval
Primary heart block
What kind of heart block presents with elongation of the PR interval until TWO atrial depolarization occur
Mobitz I
What kind of heart block presents with non-conducting P waves with no elongation of the PR interval, likely progresses to complete heart block
Mobitz II
What kind of heart block presents with no QRS wave
Complete heart block (Bundle branch block)
Where does Pacemaker AP occur?
Primarily in the SA node (to maintain regular rhythm and rate of the heart)
Pacemaker action potential phase 4, 0, 3
Phase 4 = spontaneous depolarization driven by funny currents, t-type Ca2+ channels, and reduced K+ efflux
Phase 0 = rapid depolarization primarily due to L-type Ca2+ channels
Phase 3 = Repolarization facilitated by K+ efflux and closure of Ca2+ channels
Regulatory mechanisms of the cardiac cycle: what are the receptors
- Aortic arch: transmits via vagus nerve > solitary nucleus in medulla in response to BP changes
- Carotid sinus: transmits via glossopharyngeal nerve > solitary nucleus in medulla in response to BP changes
Regulatory mechanisms: Chemoreceptors
- Peripheral: carotid and aortic bodies are stimulated by inc PCo2, dec blood pH, and dec in PO2
- Central: stimulated by changes in pH and PCo2 of CSF (influenced by arterial CO2)
T/F central chemorectptors become less responsive with chronically inc PCO2 (eg (COPD)
True. depends on peripheral chemoreceptors to detect dec O2 to drive respiration
Regulatory mechanisms: Baroreceptors
- Hypotension: ↓ Arterial pressure > ↓ Stretch > ↓ Afferent baroreceptor firing > ↑ Efferent sympathetic firing > ↓ Efferent PS stimulation = Vasoconstriction ↑HR ↑Contractility ↑BP
- Carotid massage: ↑ Pressure on carotid sinus > ↑ Stretch > ↑ Afferent BR > ↑ AV Node refractory period = ↓ HR
- Cushing reflex: (Triad of HTN, bradycardia, respiratory depression) ↑ Intracranial pressure > Constricts arterioles > Cerebral ischemia > ↑ pCO2 > ↓ pH > Central reflex sympathetic ↑ in perfusion pressure/HTN > ↑ Stretch > Bradycardia
What 2 branches of coronary arteries comes from the aortic root
RCA and LCA
RCA branches into
- Acute (R marginal artery)
- Posterior descending artery (PDA)
LCA branches into
- Left anterior descending artery (LAD)
- Left circumflex artery (LCx
LAD supplies ______
2/3 of interventricular septum, anterolateral papillary muscle and anterior surface of LV
Which coronary artery is most commonly occluded?
LAD
PDA supplies ______
1/3 of interventricular septum, posterior 2/3 walls of ventricles, and posteromedial papillary muscle
RCA supplies _______
AV node and SA node
Right (acute marginal) artery supplies_______
RV
What does coronary dominance refers to?
Which artery supplies the posterior descending artery (PDA)
Right dominant
PDA from RCA (60-80% people)
Left dominant
PDA from LCx (10-20%)
Co-dominant
PDA from both RCA and LCx (20%)
Draw Aorta branches
inferior phrenic, celiac trunk (foregut), middle suprarenal arteries, renal arteris, SMA (midgut), testicular arteries, IMA (hindgut), lumbar arteries, common iliac arteries
Frank-starling law
Stroke volume increases proportionally to an increase in the volume of blood filling the heart
Cardiac output
The amount/volume of blood the heart pumps/1min
CO = HR X SV
what affects CO
Increased stretch
ANS stimulation
Stroke volume (SV)
The amount of blood pumped from the ventricles/beat
SV = End diastolic volume (EDV) - End systolic volume (ESV)
what is the average stroke volume
70-90 mL
How does the PNS affects the heart rate (HR)
- PNS: Right vagus nerve - decreases intrinsic rate of the SA node. Left vagus nerve - slows conduction of AV node —> dec force of contraction of atria (not ventricles)
How does the SNS affects the heart rate (HR)
increases rate in times of stress (frequency, conduction, force of contraction of atria and ventricles)
How does thyroid hormones affect the heart rate (HR)
End diastolic volume
The amount of blood filled in the ventricles approx 100 mL
Ejection fraction
The amount of blood ejected from the ventricles (notable that all of the blood in the ventricles are not ejected) approx 60% is ejected, 40% remains
EF = ejected /filled = SV/EDV= 60/100 = 60%
End systolic volume
The amount of blood that remains in the ventricle after contraction = ESV = 40 mL
What 3 factors is Stroke volume dependent on?
- Contractility = force of the heart muscle contraction
- Preload = degree of stretch of cardiac myocytes at the end of ventricular filling = EDV
- Afterload = resistance the ventricle overcomes to eject blood
What factors affect the afterload
Pressure in the LV must be > systemic pressure for the aortic valve to open (same for pulmonic side)
Example:
HTN > higher vascular pressure > dec in afterload > reduce ejected blood
Stenosis > dec in afterload> reduce ejected blood
SV increases with
- Inc in contractility
- Inc preload
- Dec afterload
Contractility and (SV) decreases with
- B blockade (dec cAMP)
- HF with systolic dysfunction
- Acidosis
- Hypoxia/hypercapnia (dec Po2/inc pCO2)
Force of contraction changes in the presence of
- increased end diastolic volume/increased cardiac stretch
- Sympathetic stimulation
PP is increased in the following situations
Hyperthyroidism, aortic regurgitation, aortic stiffening = isolated systolic HTN), OSA, anemia, exercise
Pulse pressure (PP)
SBP-DBP
PP is decreased in the following situations
Aortic stenosis, cardiogenic shock, cardiac tamponade, advanced HF
Mean arterial pressure
average arterial pressure throughout one cardiac cycle, (systole and diastole)
MAP = CO X total peripheral resistance (TPR)
= 2/3 DBP + 1/3 SBP = DBP + 1/3 pp
Pressure- Volume loops
Watch Dr. Pershows video
Cardiac cycle
1) Isovolumetric relaxation (ventricular diastole early)
2) Ventricular filling (ventricular diastole late)
3) Atrial systole (atrial contraction- happens during diastole, in which 20% of filling to ventricles)
4) Isovolumetric contraction
5) Ventricular contraction (ventricular systole first phase)
6) Ventricular ejection (ventricular systole second phase)
Pathway of electrical conduction of the heart
SA node > Atria > AV node > IV septum/bundle of his > L&R Bundle branches > Purkinje fibers > ventricles
What is the intrinsic firing rate of the SA node?
60-100 depolarizations/minute
Early systole
- Pressure within the ventricles increases —-> AV valves close
- semilunar valves remain closed and ventricular pressure continues to rise
Late systole
- Semilunar valves are forced to open —-> blood enters the aorta and pulmonary trunk
- Remaining ventricular blood = End systolic volume
Early diastole
- Brief repolarization phase
- Ventricles relax and pressure drops rapidly
- Semilunar valves close, AV valves remain closed
- Atrial pressure > ventricular pressure ——> Causes AV valves to open
Mid-Late Diastole
- Ventricle fill passively
- AV valves are open
- Semilunar valves are closed
- Pressure increases in both atria
- SA node fires at the end of diastole causing atrial depolarization and contraction
What are the 2 phases and subphases of cardiac cycle. Explain what happens during each phase
Phase 1- Systole
- AV valves close
- Acute ejection of blood from vent –> circulation
3 subphases:
1) isovolumic contraction (W/out emptying)
2) Ejection
3) Isovolumic relaxation (Ventricles relax)
Phase 2- Diastole
- AV valves open
- Filling of the ventricles
3 subphases
1) Rapid inflow
2) Diastole
3) Atrial systole (contraction of atria happens during diastole, in which 20% of filling to ventricles)
Both opening and closing of the AV and semilunar valves occur passively when pressure gradient pushes blood backward or forward? T/F
True
