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Cardiology - Physiology / Anatomy (Normal Heart Chamber Pressures…
Cardiology - Physiology / Anatomy
*Pressure Volume Loops
MAAM COCO
--> start at right bottom corner
M = mitral valve
A = Aortic Valve
C = close
O = open
Clinical Cases
Pressure Volume loop example
Notes
:
note when there is just an increase in width of PV loop, then nothing else changed
--> NO left upper corner slope change = no contractility change
Just a volume increase
--> normal saline infusion
Example
:
Clinical Case
Notes
:
note that
Clinical Case
Pressure Volume Loops with CHF
CHF has lower contractility of the heart
ESPVR = end-systolic pressure volume relationship
--> slope measures the contractility of the LV
Notes
:
the PV loop width = SV
SV = volume during each stroke of ventricle
Top line of P/V loop for LV = afterload
:
note the top of the pressure-volume loop for the ventricle is the highest pressures reach in the ventricle
increasing the afterload will raise the pressure in the LV
thus the top line = afterload
Drug Effects on P/V Loop
Nitroprusside = equal vein and artery vasodilator
Nitroprusside
= equal vein and artery vasodilator
Cardiac Surgeries
Cathederization
either femoral or radial
femoral Vein Cathederization - Left Atrial Pressure
- direct vs indirect left atrial pressure measurement
note for catheterization to get to the left atrium or left ventricle
go through femoral vein to right atrium
punch small hole in the atrial septum where the fossa ovalis is
--> thin fibrous layer
heals spontaneously
Direct Left Atrial Pressure
puncture through Fossa ovalis
Femoral vein catheder to left atrium case
Notes
:
note that
Clinical Case
INdirect Left Atrial Pressure
measure indirectly by go to the pulmonary venules
measure the PCWP = pulmonary capillary Wedge Pressure
estimates the left atrium pressure
Left Atrium Ventricular and Aorta pressure Diagram
LV / aorta pressure case
DONT forget the isovolumetric contraction and relaxtion are where the valves are closed and the pressures are equallized fro a moment
BOTH valves are closed at this time
Clinical Case
Notes
:
note that
LV / aorta pressure case 2
Clinical Case
Notes
:
note solution = B
Notes:
note that the dichrotic notch is where the aorta closes and there is a quick increase in the aorta pressure
--> think of the aortic valve closing and giving a quick push of pressure into the aorta
*JVP = Jugular Venous Pulse and Atrium Waves
Notes:
JVP = jugular Venous Pulse waves
= atrial pressures
Waves A / C / X / V / Y
A
= atrial contraction
C
= RV contraction
X
= Exiting of ventricle blood --> makes x ddescent in right atrium
V
= VILLING of the atrium
Y
= Emptying of the aorta passively into the ventricle
--> VILLING and Empting...
Cardiac *Action Potentials
Pacemaker Cells
just phases 4, 0 ,3
NO phase 1 and 2
Notes
:
phase 4 = Funny Leak channels ALWAYS stay open
--> they are funny for 2 reasons
--> they ALWAYS stay open and they allow both Na+ and K+ into the cell
phase 0 = voltage gate Ca++ channels
--> remember the cardiac cells are ALL about the calcium
--> Ca++ causes upstroke phase 0 in pacemakers and plateau in myocytes
phase 3 = same for all cells
--> K+ reflux out of the cell
--> return to negative baseline
SLOPE
of phase 4 = funny leak channels and T type calcium channels = transition type calcium channels
--> determines the HR
PAcemaker Cells automatocity from funny leak channels and T type calcium channels
note there is a transition in phase 4 from funny leak channels to transition type = t type calcium channels
then in phase 0 of pacemaker = L type = long type calcium channels that stay open for long time
= stopped eventually by the outgoing K+ efflux in phase 3
Myocyte Cells potentials
phases 0-4
Notes
:
pLateau in myocytes = L for L type calcium channels
*Arrhythmias
bradyarrythmias and tachy AR
Brady AR
HR < 60 bpm
Tachy AR
HR > 100 bpm
3 causes generally
3 causes of tachy ARs
1 = higher slope of funny channels phase o
--> higher automaticity = higher HR
2 = triggered activity from outside the heart
3 = reentry on conduction
--> ex = Wlf-Parkinson White syndrome where conduction from ventricles reenters the atrium
*CO = Cardiac Output Physiology
Tetralogy case
Clinical Case
Notes
:
note that
*Exercise Physiology
Short Term Changes to Heart and CVS from Exercise
CO changes and TPR = Resistance in Exercise
decreased TPR in exercise case
Notes
:
note that in exercise although the SNS is activated releaasing epi and NE, this causes vasoconstriction
but the key thing in exercise is the release of local metabolites
these cause local vasodilation in all the muscles that are working and need more blood
--> these local metabolites are actually able to overcome the EPI in terms of vasoconstriction and TPR
thus overall TPR in exercise is lowered
Clinical Case
Arterial Blood gases stay normal in exercise
compensated b hyperventialtion, CO, and improved V/Q matching
note it is the venous blood gases that would have higher CO2 and lower O2 than normal due to tissues using more OXygen
Clinical Case
Clinical Case
Notes
:
note that
Long Term Changes to Heart and CVS from Exercise
Heart adaptations for long distance runners and weight lifters
long distance = dilated athletes heart
weight lifters = hypertrophies athletes heart
Long Distance athlete dilated heart
note that comes with increased diastolic function
key is that it is not a pathology since they also develop a better coronary network to perfuse the heart, get a slower resting heart rate and more efficient heart overall
*RAAAS System
Renin triple AAA system
angiotensin aldosterone ADH System
RAAS summary map
ANP and BNP
ANP / BNP Reverse effect on RAAS
ANP = atrial natriuretic peptide
= NATURAL diuretic peptide
--> from the atrium
BNP = brain natriuretic peptide
--> from the ventricles
the natriuretic peptides are the ways for the 2 chambers of the heart = atrium and ventricles to communicate with the kideny to tell it to diuretic = lose water
ANP case
Notes
:
note that
Clinical Case
Notes:
ANP is a peptide that is release form the right atrium of the heart
when it sense wall stress from high volume of blood return
ANP works in 3 ways all at the KIDNEY to counteract the RAAS system and lower the BP
kidney --> ANP increases the GFR to remove water from the vascular system
kidney --> ANP stops aldosterone from reabsorbing at the PCT
kidney --> ANP stops juxtaglomerular cells from secreting renin for the RAAS
--> shuts down RAAS at the source
ANP and BNP MOA
Guanylate Cyclase activators
increase cGMP --> protein Kinase G
ANP... easy as cGMP... BNP easy as cGMP... Viagra... easy as cGMP ... and PDE
ANP and BNP relation to Viagra = sildenafil MOA
Guanylate Cyclase activators
increase cGMP --> protein Kinase G
ANP... easy as cGMP... BNP easy as cGMP... Viagra... easy as cGMP ... and PDE
sildenafil inhibits PDE5, which breaks down cGMP
--> thus same pathway as ANP and BNP to cause vasodilation
Clinical Case
Notes
:
note that
Clinical Case
RAAAS and antiHTN antiRAAAS Drugs
ACEIs and ARBs
implantable *pacemaker or cardioverter-defibrillator
can be dual chamber
--> meaning both right atrium and right ventricle = through the mitral valve
note that you can get secondary mitral regurge from dual pacemakers
Clinical Cases
Dual pacemaker implant with sequelae mitral regurgitation case
Notes
:
note that
Clinical Case
Dual Chamber Right sided only Pacemaker
Biventricular Pacemaker
both left and right ventricles
Cases
Clinical Case
Clinical Case
Notes
:
note that
Notes
recall that the coronary sinus and great coronary vein path drain the left ventricle
this both run along the atrioventricular groove in the posterior portion of the heart
*Coronary Arteries and Veins
Interventricualr Septum Blood supply
note that the interventricular septum gets its blood supply from the two major Coronary arteries from the front and back
anterior 2/3 from the LAD = left anterior descending artery
posterior 1/3 of the interventricular septum from the RPD = right posterior descending artery
--> note the exception is when people may not be right dominant heart
*Coronary Blood Flow
in myocardium lowest during systole for the LV
--> highest during diastole whent he heart muscles relax
note in the RV the pressures aren't that high
--> thus flow is relatively constant throughout
Coronary autoregulation of blood flow by local metabolites
--> adenosine and NO both cause local vasodilation and increase flow
--> autoregulation ONLY within 60-140
--> reason why HTN stage 1 = 140 systolic and hypotension below 60 is dangerous
--> lose autoregulation
CASES
Myocardium blood flow case
Notes
:
solution = Left myocardium
Clinical Case
Coronary Blood Flow Depends on Relaxation of the Ventricles
Length of Diastole is actually the most important factor
more important since relaxes the ventricles longer
note the blood flow is linear and not dependent on the intraventricular pressure
Coronary Blood Flow Autoregulation (local metabolites)
Adenosine
NO
CASES
Clinical Case
Clinical Case
Notes
:
note that
AV Coronary Artery ? Discrepancy from UWORLD and USMLE
comes from the dominant side of the heart
most = 90% of people are right heart dominant
--> meaning the PDA comes from the RCA
10% of people are left dominant heart
--> PDA comes from the
Right vs Left Dominance
95% are right dominant
remaining 5% are left dominant
Normal Heart Chamber Pressures
Notes:
430 rule for cathedar and right atrium and pulmonary wedge blood pressures
--> right atrium mean is about = 4 (1-6)
--> right ventricle goes from 430 = (4-30)
--> the pulmonary artery is similar and the PCWP = 6-12
note that the left ventricle diastolic pressure has to come down as low as 5-10 to meet the same as the left atrium to allow in blood
same with the right ventricle, its diastolic has to go as low as 1-6
clinical case
Clinical Case
Notes
:
note that
*Heart conduction System
SA node
AV ndoe
*Right Atrium structures and SA and AV Nodes Anatomy
AV Node location in the right atrium
right next to the coronary sinus
think of the coronary sinus as a mini-Vena Cava that opens right next to it into right atrium
AV Node location in the right atrium
Clinical Case
Notes
:
note that
Speed of Conduction
"Park AT Venture AVenue"
fastest to slowest
*Anatomy of the Heart
Heart structures on XRAY
Notes
:
note the right atrium is at the same level as the middle lobe of the right lung
Cardiac Blood *Flow Physiology
FLOW of blood is the SAME throughout the whole system
--> because it is a closed system the blood flow is the same everywhere in the system
~ 5 L/min.
Blood Flow = Q = V x
Clinical Cases
AP to Muscle *Contraction
Dihydro rec / RyR calcium induced calcium release
troponin blocker of tropomyosin removed by Ca++
*Sarcomeres
see musculoskeletal notes
*Calcium in Muscle Contractions
calcium induced calcium release
--> Dihydros to RyR
--> only in cardiac muscle cells and SM
--> NOT in skeletal muscle
*DIRTY USMLE
CARDIAC physiology
CO = HR x SV
*frank starling
CONTRACTILITY
= the slop of the curve
recall that the 3 things that effect SV are
preload
afterload
contracitly
--> so when the slope changes
--> the ESV will always move left to give higher SV
*Pressure volume loops
