CV Anatomy modules 10-18 Flashcards
When is the mitral valve open and aortic valve closed
During:
Rapid ventricular filling
Diastasis
Atrial systole
What valve is open when LA pressure is greater than LV pressure
Mitral valve
What valve is open when LV pressure is greater than aortic pressure
Aortic valve
What happens to the aortic valve when aortic pressure exceeds LV pressure
It closes (producing the second heart sound), then causes retrograde flow from aorta toward aortic valve (Dicrotic notch)
What happens to the mitral valve when LV pressure exceeds LA pressure
It closes producing the 1st heart sound
Identify the status of the mitral valve during each phase of the cardiac cycle: Atrial systole Ventricular ejection Isovolumetric ventricular relaxation Isovolumetric ventricular contraction Rapid ventricular filling
Atrial systole-MV open
Ventricular ejection-MV closed
Isovolumetric ventricular relaxation-MV closed
Isovolumetric ventricular contraction-MV closed
Rapid ventricular filling-MV open
Identify the status of the aortic valve during each phase of the cardiac cycle Atrial systole Ventricular ejection Isovolumetric ventricular relaxation Isovolumetric ventricular contraction Rapid ventricular filling
Atrial systole-AV closed
Ventricular ejection-AV open
Isovolumetric ventricular relaxation-AV closed
Isovolumetric ventricular contraction-AV closed
Rapid ventricular filling-AV closed
What does each element represent in the cardiac PV loop Height Width Corners Area of PV loop
Height = ventricular pressure
Width = ventricular volume
Corners = where valves open and close
Area of PV loop = myocardial workload
What happens to myocardial external workload if the volume axis widens or the pressure axis increases heaight
Each will increase workload
Determine the severity of cardiac dysfunction based on EF >50% 41-49% 26-40% <25%
>50% = normal 41-49% = mild dysfunction 26-40% = moderate dysfunction <25% = severe dysfunction
What alterations affect the morphology of the cardiac PV loop
Preload
Contractility
Afterload
How does preload change the cardiac PV loop
Increased = wider PV loop Decreased = narrower loop
How does a change in contractility affect the cardiac PV loop
Increased = PV loop is wider, taller, and shifts LEFT Decreased = PV loop is narrower, shorter, and shifts RIGHT
How do changes to afterload affect the PV loop
Increased = PV loop is narrower, taller, and shifts ESV to right Decreased = PV loop is wider, shorter, and shifts ESV left
What arteries arise from the LCA
Left anterior descending
circumflex arteries
What does the left anterior descending artery perfuse
Anterolateral and apical wall of LV
Anterior 2/3 of interventricular septum
Perfusion changes caused by the left anterior descending will be seen in which lead
EKG V1-V4
What does the circumflex artery supply?
Left atrium
Lateral and posterior walls of ventricle
Perfusion changes caused by the circumflex artery will be seen in which leads
Leads I, aVL, V5 - 6
What does the right coronary artery perfuse
Right atrium
Right ventricle
Interatrial septum
Posterior third of interventricular septum
Perfusion changes caused by the right coronary artery are seen in which leads
Leads II, III, aVF
What does the posterior descending artery perfuse
Inferior wall
Where is the coronary sinus
The heart’s posterior surface
Where does the coronary sinus return blood
To the right atrium
How is the coronary sinus used during bypass
It can be cannulated to administer retrograde cardioplegia solution
Describe the unique properties of the Thebesian circulation
It returns deoxygenated blood to the left side of the heart
Contributes to small amount of anatomic shunt
When using TEE/TTE, what is the best view for diagnosing myocardial ischemia
Midpapillary muscle level in short-axis
Where do the left and right coronary arteries originate
The aortic root
How is PDA coronary dominance defined
Defined by origin:
right dominance = RCA gives rise to PDA
Left dominance = circumflex
Codominance = RCA and circumflex
What coronary supplies the SA node
RCA
The RCA supplies which cardiac node
SA node
AV node in 80% pts
What coronary artery supplies the AV node
RCA in ~80% of patients
What coronary supplies the Bundle of His
LCA in 75% of pts
What nodes does the LCA supply
Bundle of His
Left and right bundle branches
What coronary supplies the left and right bundle branches
LCA
What are the 3 main coronary veins
Great cardiac vein
Middle cardiac vein
Anterior cardiac vein
What blood drains into the coronary sinus
Most of the blood returning from the LV
Which veins carry most of the blood returning from the right ventricle
Anterior cardiac vein
What type of coronary vessels are the RCA, LAD, and CxA
Epicardial vessels
Describe the function of collateral vasculature in the heart
They provide redundancy of blood flow to poorly perfused areas
They develop from different branches of the same coronary artery or between 2 different coronary arteries
Single fed vessels are at risk if occlusion develops proximal to collateral branch
Lateral leads
I, aVL, V5, V6
Inferior leads
II, III, aVF
Septal leads
V1 - V4
What is coronary blood flow at rest? What percent of CO?
225-250 mL/min
4-7% of CO
What are the variables in the equation for coronary blood flow?
Coronary BF = (Coronary perfusion pressure)/(Coronary vascular resistance)
What range is coronary BF MAP autoregulated?
MAP between 60-140 mmHg
What is the most important determinant of coronary vessel diameter
Local metabolism
How does cardiac metabolism impact coronary vessels
It affects the coronary vessel diameter
What percent of O2 is consumed by myocardium in coronary blood flow
70%
Definition = To ensure constant amount of blood flow over a wide range of perfusion pressures
Autoregulation
What is coronary BF autoregulation?
The constant amount of blood flow over a wide range of perfusion pressures
MAP 60-140 mmHg
Allows for constant coronary BF over a wide range of BPs
How is coronary BF affected when out of autoregulation range
BF is dependent on CPP
What is coronary reserve
The difference between coronary BF at rest and maximal dilation
Coronary reserve = resting coronary BF - Maximal dilation BF
What is the difference between resting coronary BF and coronary BF at maximal dilation
Coronary reserve
What does coronary reserve allow for during stress
Allows CBF to increase in times of hemodynamic stress or exercise
Describe coronary reserve in the patient with atherosclerosis
When O2 demand increases, atherosclerotic vessels are maximally dilated at rest and can’t dilate further
Patient has DECREASED coronary reserve
What is autoregulation of coronary BF affected by
Local metabolism
Myogenic response
Autonomic nervous system
What metabolic byproducts cause coronary vasodilation
Adenosine, a byproduct of ATP metabolism
What are some mediators of coronary vasodilation
Nitric oxide PGs Hydrogen (decreased pH, increased CO2) Potassium CO2
What are the effects of vasodilation on coronary blood flow (3)
- Decreases vascular resistance
- Increases coronary perfusion
- Flushes out products of metabolism
How does hypocarbia affect coronary blood flow
It causes vasoconstriction, decreasing CBF
What muscarinic mediators cause coronary artery vasodilation
Nitric oxide
Which receptors lead to coronary artery vasodilation
Beta-2
Histamine-2
Muscarinic
What receptors lead to coronary artery vasoconstriction
Alpha
Histamine-1
What 2 pressures determine coronary perfusion pressure
CPP = Aortic DBP - LVEDP
What 3 responses are responsible for autoregulation of coronary BF
- Local metabolism
- Myogenic response
- Autonomic nervous system
Why does LCA endocardial vessel flow decrease dramatically during systole
LV contraction compresses the endocardial vessels during systole due to the large mass of the LV
Describe the coronary flow via the RCA during the cardiac cycle
Flow remains relatively constant throughout the cardiac cycle
Why is the RV coronary flow more constant versus the LV coronary flow
RV has a thinner wall that doesn’t generate high enough pressures to occlude blood supply during systole
How does P50 affect myocardial O2 consumption
Left shift means less O2 is released to myocardium
Decreases supply
How does end-diastolic volume affect myocardial O2 consumption
Decreased EDV reduces wall stress
Decreased demand
How does heart rate affect myocardial O2 consumption
Reduces supply and increases demand
Increased heart rate decreases DIASTOLIC filling time
How does aortic diastolic BP affect myocardial O2 consumption
Decreased DBP means decreased supply and reduced CPP
What 2 components maintain myocardial O2 balance
Supply and demand
What are 3 determinants of O2 delivery (supply)
Coronary BF
CaO2
O2 extraction
What are 4 determinants of O2 demand
Preload
Afterload
Contractility
Wall stress
How is tachycardia detrimental to the ischemic heart?
It decreases O2 SUPPLY and increases O2 DEMAND
How does afterload affect coronary perfusion pressure
it INCREASES CPP
When do most perioperative myocardial infarctions occur
within 24-48 hours of surgery
What is normal coronary sinus O2 saturation?
~30%
What does the amount of myocardial O2 extraction mean for myocardial O2 delivery/demand
The heart cannot meaningfully increase O2 extraction ratio when O2 demand increases
What 2 factors must increase to meet myocardial O2 demand
Coronary BF or CaO2
List factors that increase myocardial O2 demand (7)
Tachycardia HTN SNS stimulation INC wall tension INC LV EDV INC afterload INC contractility
List factors that decrease myocardial O2 delivery
Decreased coronary flow
- Tachycardia
- DEC aortic pressure
- DEC vessel diameter (hypocapnia, spasm)
- INC LV EDV
Decreased CaO2
- Hypoxemia
- Anemia
Decreased O2 extraction
- DEC P50 (left shift)
- DEC capillary density
How does tachycardia affect myocardial O2
It can decrease supply by
-decreasing diastolic filling time
Increase demand
-increasing cardiac contraction and cycles requires more energy/ATP and O2 utilization
How does increased aortic diastolic pressure affect myocardial O2
Increased supply
- It increases coronary artery perfusion
- INC aortic DBP - LVEDP = INC CPP
Increased demand
- Increased wall tension to overcome afterload
- Myocardium requires higher pressures to overcome AV
How does increased preload affect myocardial O2
Decreased supply
-Increased EDV decreases CPP
Increased demand
-higher preload increases wall stress (pressure)
Describe the relationship between nitric oxide and hgb
NO is inactivated by hgb, which is why it has a short half-life (5 seconds)
It is inactivated before entering systemic circulation
What 4 responses regulate vascular smooth muscle tone
Autonomic nervous system
Renin-angiotensin-aldosterone system
Local metabolism
Myogenic response
How does Ca++ affect vessel diameter
INCREASED CA++ = vasoconstriction
DECREASED Ca++ = vasodilation
List the second messenger systems that modulate vascular tone by altering Ca++ concentrations
G-protein cAMP -Increased cAMP = vasodilation Nitric oxide cGMP -Increased cGMP = vasodilation Phospholipase C -Increased IP3 and DAG = vasoconstriction
Describe the process of the G-protein cAMP pathway to vasodilation
Norepi => beta-2 receptor => G-protein => adenyl cyclase => cAMP increase => PKA => decreased Ca++ => vasodilation
How does PKA affect excitation-contraction coupling
Leads to vasodilation via
- Inhibition of voltage-gated Ca++ channels in sarcolemma
- Inhibition of SR release of Ca++ release
- Myofilament reduced Ca++ sensitivity
- Ca++ reuptake into SR via SERCA2 pumps facilitated
DECREASES available Ca++ in sarcolemma, from SR, sequesters Ca in SR and decreases myofilament Ca sensitivity
What mediators increase nitric oxide production (8)
ACh Substance P Bradykinin Serotonin Vasoactive intestinal peptide Thrombin Shear stress
What is the role of NOS in the nitric oxide pathway
NOS is an enzyme that catalyzes conversion of L-arginine to NO
How does NO travel into smooth muscle
diffusion
What activates guanylate cyclase?
Role of activated guanylate cyclase?
nitric oxide
converts guanosine triphosphate to cyclic guanosine monophosphate (cGMP)
How does phosphodiesterase (PDE) contribute to vessel diameter
It deactivates cGMP to guanosine monophosphate (Ca++ availability increases?)
What mediators activated the PLC pathway? The result?
Mediators = phenylephrine, norepinephrine, angiotensin 2, endothelin-1
Result = vasoconstriction
Describe the PLC pathway to vasoconstriction
Angiotensin 2 etc => ATII receptor => Gq G-protein => PLC => IP3, DAG => Increased Ca++ => vasoconstriction
What 2 second messengers are activated by PLC
IP3
DAG