Cardiology - Physiology / Anatomy
*Pressure Volume Loops
- MAAM COCO
--> start at right bottom corner - M = mitral valve
- A = Aortic Valve
- C = close
- O = open
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
Cardiac *Action Potentials
Pacemaker Cells
- just phases 4, 0 ,3
- NO phase 1 and 2
Myocyte Cells potentials
- phases 0-4
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
*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
click to edit
Tetralogy case
Clinical Case
Notes:
- note that
*Exercise Physiology
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
*RAAAS System
- Renin triple AAA system
- angiotensin aldosterone ADH System
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
Dual Chamber Right sided only Pacemaker
*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
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
RAAS summary map
*Heart conduction System
- SA node
- AV ndoe
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
RAAAS and antiHTN antiRAAAS Drugs
- ACEIs and ARBs
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
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
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
*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
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
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
*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
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
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
Notes:
- pLateau in myocytes = L for L type calcium channels
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
Clinical Case
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 Blood Flow Autoregulation (local metabolites)
- Adenosine
- NO
Clinical Case
CASES
Clinical Case
Clinical Case
Notes:
- note that
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
*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
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
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...
*DIRTY USMLE
CARDIAC physiology
CO = HR x SV
click to edit
*frank starling
*Pressure volume loops
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
