Cardiovascular- Anatomy and Physiology Flashcards
What artery supplies the right ventricle?
right (acute) marginal artery
What artery supplies the SA and AV node?
the right coronary a. (note that RCA infarct can cause complete heart block)
What are the main branches of the left main coronary a.?
- left circumflex coronary a. (LCX)
- left anterior descending a. (LAD)
What does the LCX supply?
the lateral and posterior walls of the left ventricle and the anterolateral papillary muscles
What does the LAD supply?
the anterior 2/3rds of the interventricular septum, anterolateral papillary muscle, and the anterior surface of the left ventricle
The majority (85%) of people are ‘right-heart dominant’. What does this mean?
the PDA (posterior descending a.) arises from the RCA
What does left-heart dominant mean?
the PDA arises from the LCX (co-dominant= arises from the LCX and the RCA)
Coronary artery occlusion most commonly occurs where?
LAD
When does coronary artery blood flow peak?
early diastole
Enlargement of what part of the heart is associated with dysphagia due to compression of the esophagus or hoarseness due to compression of the left recurrent laryngeal nerve?
the most posterior part, the left atrium
What is the eqn for CO?
HR X SV or via the Fick principle:
CO= rate of O2 consumption/ (arterial O2 content- venous O2 content)
What is the eqn for mean arterial pressure?
CO x TPR, or
MAP= 2/3 diastolic pressure + 1/3 systolic pressure
What is pulse pressure?
What is the eqn for SV?
end diastolic volume - end systolic volume
How does SV and HR change during exercise?
during the early stages of exercise, both HR and SV increase, and eventually SV plateaus
What are some things associated with increased pulse pressure?
- hyperthyroidism
- aortic regurg
- aortic stiffening
- obstructive sleep apnea
- exercise (transient)
Isolated increased systolic pressure in the elderly suggests what?
aortic stiffening
What are some things associated with decreased pulse pressure?
- aortic stenosis
- cardiogenic shock
- cardiac tamponade
- heart failure
What are the three variables that affect stroke volume?
- contractility
- preload and afterload
What things increase contractility?
- catecholamines (increase the activity of SR Ca2+ pumps)
- increased intracellular Ca2+
- decreased extracellular Na+ (via decreased activity of the Na/Ca2+ pump)
- Digitalis
How does digitalis increase contractility?
by blocking Na/K pumps leading to increased intracellular Na+, decreasing Na/Ca exchanger activity, and thus leading to elevated levels of Ca2+
What are some things that decrease contractility?
- B1-blockade (decreased cAMP)
- acidosis
- acidosis
- hypoxia/hypercapnia
- non-dihydropyridine CCBs
What are some things that increase myocardial oxygen demand?
What is the eqn for cardiac wall tension (aka thickness)?
WT= (pressure*radius)/(2*wall thickness)
Venodilators such as nitroglycerin ______ preload
decrease
How does the left ventricle compensate to increased afterload?
by thickening to decrease wall tension
Vasodilators such as hydralazine ______ afterload
decrease
How do ACEIs and ARBs affect pre- and afterload?
they decrease both
What is the eqn for equation fraction?
SV/EDV= (EDV- ESV)/EDV
Normal EF = 55+%
How is EF affected by systolic HF? diastolic HF?
systolic HF: decreased
diastolic HF: normal
What is inotropy?
An inotrope is an agent that alters the force or energy (aka contractility) of muscular contractions. Negatively inotropic agents weaken the force of muscular contractions. Positively inotropic agents (e.g. digoxin) increase the strength of muscular contraction.
Contractility is proportional to what?
the end-diastolic length of cardiac muscle fibers (aka preload)
How does organ removal affect TPR and CO?
it increases TPR and decreases CO
_______ account for most of TPR
Arterioles
What is the period of heart contraction with the highest O2 consumption?
isovolumetric contraction
What is S1?
mitral and tricuspid valve closure. Loudest at the mitral area
When does S1 occur?
at the start of isovolumetric contraction
What is S2?
closure of the aortic and pulmonary valves
When does S2 occur?
at the end of systolic ejection when the aortic pressure generated becomes higher than that of the left ventricle
Where is S2 best heard?
left upper sternal border
When is S3 heard (pathologic)?
in early diastole during the rapid ventricular filling phase
What things cause an S3?
associated with increased filling pressure (e.g. mitral regurg, HF) and more common in dilated ventricles (but normal in children and pregnant women)
When is S4 heard (pathologic)?
in late diastole (aka atrial kick)
Where is S4 best heard?
at the apex with the pt. left lateral decubitus
What things cause an S4?
high ventricular pressure/hypertrophy
What causes the ‘a’ wave of jugular venous pulse?
atrial contraction (absent in a fib)
What causes the ‘c’ wave of jugular venous pulse?
RV contraction (closed tricuspid valve bulging into the atrium)
What causes the ‘x’ descent of jugular venous pulse?
atrial relaxation and downward displacement of the closed tricuspid valve during ventricular contraction (absent in tricuspid regurg)
What causes the ‘v’ wave of jugular venous pulse?
increased right atrial pressure due to filling against a closed tricuspid valve
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Describe the murmur of aortic stenosis
It is a crescendo-descrendo systolic ejection murmur (between S1 and S2) caused by LV pressure being higher than aortic pressure during systole
Where is aortic stenosis best heard?
at the heart base; radiates to the carotids
A common finding with aortic stenosis is ________
pulsus parvus el tardus (pulses are weak and delayed)
What is the most common cause of aortic stenosis?
age-related calcification or early-onset calcification of bicuspid aortic valves
Describe the murmur of mitral/tricuspid regurg
It is a holosystolic, high-pitched ‘blowing’ murmur
Where is a mitral regurg murmur best heard?
at the apex and radiates toward the axilla
What commonly causes mitral valve regurg?
ischemic heart disease (post-MI) or LV dilation
Where is a tricuspid mumur best heard?
the tricuspid area- 5th right intercostal space at the sternal border
_________ and ________ can cause either MR or TR
Rheumatic fever and infective endocarditis
Describe the murmur of mitral valve prolapse
it is a late systolic crescendo (building) murmur with a midsystolic click (this is the most common valvular lesion)
What causes the midsystolic click in mitral valve prolapse?
sudden tensing of chordae tendineae
Where is MVP best heard?
over the apex
What are some common causes of MVP?
-myxomatous degeneration (primary or secondary to CT disease such as Marfan or Ehlers-Danlos syndrome)
rheumatic fever
chordae rupture
Describe the murmur of a VSD
It is a holosystolic, harsh-sounding murmur
Where is a VSD murmur best heard?
the tricuspid area
Describe aortic regurg murmurs
it is a high-pitched, ‘blowing’ early diastolic (right after S2) descrescendo murmur
What is the other murmur heard in diastole (after S2) besides aortic regurg?
mitral stenosis
Describe a mitral stenosis murmur
It follows opening snap after S2 with a delayed rumbling late diastolic murmur
T or F. Decreased interval between S2 and OS in mitral stenosis correlates with increasing severity
T.
Describe the murmur of a PDA
It is a continuous (systolic and diastolic- only one) machine-like murmur loudest at S2
Where is a PDA murmur best heard?
the left infraclavicular area
A PDA murmur commonly arises after what?
congenital rubella or prematurity
What is the resting potential of a myocardial cell?
-85 mV
Describe Phase 0 of the myocardial action potential
rapid upstroke and depolarization as voltage-gated Na+ channels open and Na+ influx into the cell
Describe Phase 1 of the myocardial action potential
Initial reploarization caused by inactivation of voltage-gated Na+ channels and opening of some K+ channels
Describe Phase 2 of the myocardial action potential
plateua phase, in which Ca2+ influx balances K+ efflux / Ca2+ influx riggers additional Ca2+ release from the SR and myocyte contraction
Describe Phase 3 of the myocardial action potential
Padily repolarization due to massive K+ efflux
Describe Phase 0 of SA/AV node action potentials
initial depolarization/upstroke once the nodes reach a potential of -40mV due to opening of voltage-gated Ca2+ channels
Why are fast volatge-gated Na+ channels inactive in the SA/AV nodes?
because of the less negative resting voltage of these cells. This results in a slow conduction velocity that is used by the nodes to prolong transmission from the atria to the ventricles
Phases 1 and 2 are absent in the SA/AV nodes. Describe Phase 3
inactivation of Ica2+ channels and activation of K+ channes causes K+ efflux and repolarization back to a potential around -65mV
Describe Phase 4 of the AV/SA action potential
this is a slow spontaneous diastolic depolarization as Na+ conductance increases due to If channels (aka ‘funny current channels’)- this accounts for the autmaticity of the nodes
What determines HR?
the slope of phase 4 in the SA node
What is occurring during the P wave of the EKG curve?
atrial depolarization
Why is atrial REpolarization not seen on an EKG curve?
it is masked by the QRS complex
What does the PR interval represent?
the time from the start of atrial depolarization to the start of ventricular depolarization, normally less than 200 ms
What does the QRS complex represent and what is the normal length?
ventricular depolarization; 120msec
What does the QT interval represent?
the time for:
ventricular depolarization, contraction, and repolarization
What does the T wave represent and what would an inverted T wave suggest?
ventricular repolarization; recent MI
What would an additional ‘U’ wave after the T wave suggest?
caused by hypokalemia or bradycardia
What is the conduction pathway of the heart?
SA node -> atria -> AV node -> common bundle -> bundle branches -> fascicles/Purkinje fibers -> ventricles
What parts of the conduction pathway move the fastest?
Purkinje > atria > ventricles > AV node
What is the blood supply to the AV node?
RCA
What is this?
Torsades de pointes- venticular tachycardia (can progress to v. fib)
What predisposes to TDP?
long QT interval
What drugs can cause an elongated QT interval?
ABCDE
AntiArrhythmics (clas IA, III)
AntiBiotics (e.g. macrolides)
Anti”C“ychotics (e.g. haloperidol)
AntiDepressants (e.g. TCAs)
AntiEmetics (e.g. ondansetron)
What is Congenital long QT syndrome?
inherited disorder of myocardial reploarization, typically due to ion channel defects. Includes:
Romano-Ward Syndrome and Jervell and Lange-Neilson Syndrome
What is the difference between Romano-Ward Syndrome and Jervell and Lange-Neilson Syndrome?
Romano-Ward Syndrome is AD with no deafness
Jervell and Lange-Neilson Syndrome is AR with sensorineural deafness
What is Brugada Syndrome?
an AD disorder that presents with an ECG pattern of pseduo-right bundle branch block and ST elevation in V1-V3
Brugada syndrome is particularly common in _______
Asian males
What is this?
Wolff-Parkinson-White Syndrome
What causes Wolff-Parkinson-White Syndrome?
Abnormally fast accessory conduction pathway from the atria to venticles through the bundle of Kent, which bypasses the slow V node, causing the venticles to begin partially depolarizing earlier giving rise to the characteristic DELTA WAVE
The worst potential sequelae of WPW is _______
may result in a reentry circuit causing supraventicular tachycardia
Changes in BP are sensed by a series of chemo, baro, and mechanoreceptors in the periphery. How do the aortic arch receptors work?
they transmit via the vagus nerve to the solitary nucleus of the medulla in response to changes in BP
How does the carotid sinus transmit to the solitary nucleus of the medulla in response to changes in BP?
via the glossopharyngeal n.
How do baroreceptors (like those found on the aortic arch and the carotid sinus) work?
they sense hypotension which decreased baroreceptor firing while increasing sympathetic firing to cause vasoconstriction, increased HR and contractility.
What occurs during a ‘carotid massage’?
pressure on the carotid sinus increased afferant baroreceptor firing, which increased the AV node refractory period, decreasing HR
What is the classic triad of a Cushing rxn?
HTN, bradycardia, and respiratory depression
What causes a Cushing rxn?
increased intracranial pressure constricts arterioles leading to cerebral ischemia and increased pCO2 (leading to acidosis). This causes the central CNS to increase sympathetics causing HTN which then causes a peripheral-reflex baroreceptor-induced bradycardia
