Cardiac physiology

Question 0

Describe the principles of mixed venous saturation measurement

Answer 0

MVO2 represent the difference in oxygen delivered and oxygen consumed by the tissues and is used as an indirect measure of cardiac output.

assessed from blood contained from the pulmonary artery to ensure adequate mixing of blood from the coronary sinus (maximal oxygen extraction) and the superior and inferior vena cava
Normal is 60 to 80%
Low = low cardiac output; anemia; reduced arterial saturation/hyperthermia/pain/shivering
High = decreased oxygen consumpption or extraction, secondary to hypothermia, sepsis or shunting

Question 1

Draw and describe the changing pressure wavefroms during flotation of a Swan-Ganz Catheter

Answer 1

1) Central venous pressure
2) Right ventricular pressure with systolic pressure increasing as the catheter passes across the tricuspid valve
3) Pulmonary arterial pressure–with increased diastolic pressure as the catheter passes across the pulmonary valve
4) pulmonary artery wedge pressure

Question 2

Describe central venous pressure waveform

Answer 2

a wave atrial systole
c wave isovolumetric contraction of the right ventricle with bulging of the closed tricuspid valve– rise in right atrial pressure
x descent atrial diastole. Relaxation of the atrial muscle results in reduced in right atrial pressure
V wave venous return again a closed tricuspid valve
y descent opening of the tricuspid valve resulting in emptying of the right atrium

Question 3

Describe how inotropes increase cardiac contractility

Answer 3

Most inotropes work by increasing the intracellular cyclic adenosine monophosphate (cAMP) levels which occurs by

a) stimulation of adenylate cyclase, which catalyses the conversion of ATP to cAMP (dopamine, adrenaline, noradrenaline)
b) inhibition of phosphodiesterase enzyme which normally converts cAMP to inactive 5 AMP (milrinone

cAMP augments calcium influx into myocardial cells thereby increasing contractility

Question 4

How does the cardiac action potential differ in the purkinje cells and pacemaker cells

Answer 4

Purkinje cells have a more negative resting potential and the upstroke of phase is more rapid

action potential of the pacemaker cells of the SA node and AV node differ from normal cardiomyocytes:

a) automaticity—depolarize spontaneously in a rhythmic manner without requiring initiation of the action potential by adjacent cell
b) phase 0 is less rapid than normal cardiomyocytes
c) phase 4 progressively increases due to gradual spontaneous depolarization rather then being almost flat with normal cardiomyocytes.

Question 5

Draw the oxygen dissociation curve

Answer 5

the relationship between arterial oxygen saturation (SaO2) and arterial partial pressure (PaO2) is non-linear

Above a PaO2 of 60 mmHg rises and falls in the PaO2 make very little difference to the SaO2

Below a PaO2 of 60 mmHg however, a small drop in the PaO2 procedures a large fall in the SaO2

Question 6

Describe the stages of hemostasis

Answer 6

1) vascular phase
2) platelet phase
3) clotting phase

Question 7

What is thrombo-elastogram (TEG)

Answer 7

TEG allows the measurement of the kinetics and tensile strength (viso-elastic properties of clot formation and fibrinolysis

assesses several different variables in the coagulation process

a) R time (normal range 4 to 8 minutes) that measure the time to initial formation
b) K time (normal range 1 to 4 minutes) and alpha angle (normal range 54- 67 degrees) which measure fibrinogen-platelet interaction
c) maximal amplitude (MA) normal range 59-68 mm) measures platlete aggregation
d) amplitude 60 minutes after the maximum, which represents the degree of fibrinolysis.

Question 8

What is Laplace Law

Answer 8

T = tension; P = Pressure; r = radius; h = wall thickness

T = P x r/2h

The 3 rules of LaPlace:
The higher the pressure the higher the tension
The thicker the wall the less the tension
The larger the radius the higher the tension

Question 9

What are the components of the myocardial oxygen supply demand relationship

Answer 9

The supply of coronary blood flow depends on:
oxygen carrying case capacity which depends on Fi02, Hg, and Fe
Coronary blood flow, which depends on
blood pressure: diastolic
Resistance, which is R1 epicardial resistance (trivial when normal),R2 prearteriolar (25-30%) and arteriorlate (40-50%) resistance, and R3 microvascular or precapillary sphincter (20-45%).
R1 is affected by proximal CAD, R2 by neurohormonal factors (an inotropes) and R3 is affected by LVH, DM, and microvascular CAD.

Coronary demand depends on; HR, Contractility, and LV wall tension
The normal coronary blood flow range is 8- 15 ml/100gm/min in a beating heart and 1.5 ml/100gm/min in an arrested heart.

Question 10

What regulates blood flow

Answer 10

Coronary autoregulation: the ability to match supply to demand given a mean BP of 40 to 130. Severe hypotension sets an ischemic spiral.
Metabolic regulation
NO: released as a response to hypoxia that leads to coronary dilation
Adenosine: ATP degradation leads to Adenosince release which is coronary dilator
Neural control
Parasympathetic stimulation increases flow. Sympathetic stimulation varies
Myogenic control
intracavitary pressure and intramural conaries

Question 11

Describe endothelial function and give examples of endothelial effectors

Answer 11

Monolayer between the blood and the elastic laminia covering the covering the vascular wall. It is capable of controlling both the vascular wall and the blood.
Endothelial effectors include: NO or EDRF, prostacyclin, endothelium derived factor (EDHF) and bradykinin
Endothelial vasoconstrictors: eddothelin-1 (ET), Angiotensis II, and thromboxane A2
Antiproliferative: NO, Prostacyclin, TGF beta, heparin
Proliferative: ET1, Angiotensin II, PDF
Antiothrombotic: NO
Inlammatory: ICAM, VCA,

Question 12

Describe and draw the arterial waveform

Answer 12

a wave: atrial contraction (follows the ECGs p wave)
x descent: atrial diastole
c wave: ventricular systole leading to AV closure
v wave: atrial filling against closed AV valve, ventricular systole
y decent: ventricular diastole of AV valve

Question 13

What are the arterial waveforms in severe major conditions

a) cardiac tamponade
b) TR
c) constrictive pericarditis
d) pacemaker syndrome

Answer 13

Cardiac tamponade: the waveform shows attenuated y descent (reduced atrial filling)

tricuspid regurgitation: large v waves

constrictive pericarditis: the waveform shows an exaggerated y descent. also the ventricular wave form shows the dip and plateua pattern

In pacemaker syndrome the wavefom shows cannon a waves, due to atrial contraction against a closed triscuspid valve.

Question 14

What is the fick method for calculating Cardiac output

Answer 14

The total uptake or release of a substance from an organ is a product of the blood flow through the organ and the arterial-venous difference in that substance content

The Fick Euation

CO = CI x BSA

CI = O2 (ml/min) uptake/A02 content- VO2 content

Question 15

How do you calculate shunt fraction

Answer 15

Let Qp = pulmonary blood flow and Qs = systemic blood flow. PV = pulmonary venous and PA = pulmonary arterial and SA= systemic arterial and MV = mixed venous oxygen saturation
then

Qp/Qs = SA02 - MVO2/ PVO2 - PAO2

Question 16

The mechanisms of injury during reperfusion include

Answer 16

Increased MAC present in the injured area results in incoming neutrophil adhesion and activation
C3a leads to neutrophil chemotaxis
Accelerated release of oxygen free radicals due to abundance of oxygen during reperfusion
Reduced capacity to secrete NO
Increased intracellular calcium
Edema

Question 17

What is mechanism of Heparin Induced thrombocytopenia and thrombosis

Answer 17

Heparin binds to platelets and releases s small amount of platelet factor 4. PF4 avidly binds to heparin to form a heparin-PLF4 complex, which is antogenic in some people

IgG antibodies to the H-PL4 complex are produced within 45 to 15 days after exposure and continue to circulate 3 to 6 months.

Question 18

What are two test for HIT

Answer 18

Serotonin release test—detects the release of radioactive serotonin from normal platelets washed by the patients serum

Enzyme immunoassay measures IgG anti-H-PL4 antibodies directly.

Question 19

What is management of HIT

Answer 19

Stop all heparin
Examine patient for DVT
Management should be focused on prevention of further events
Full anticoagulation with 1) argatroban, bivaliruden, Lepirudin (also called hirudin)

Hirudin- cleared via kidney, the therapeutic level should be between 3.5 yo 4.5 ug/ml during CPB

Question 20

What does in IABP do

Answer 20

LV systolic pressure -------decrease
LV diastolic pressure------decrease/likely stay the same 
Aortic diastolic pressure 
	early 			increases
	late 				decrease
Aortic systolic pressure	decrease

Question 21

List two peptides that can distinguish CHF from COPD in ER

Answer 21

Brain Natriuretic peptide

Atrial Natriuretic peptide

Question 22

What are physiological effects of BNP

Answer 22

Promote execretion of sodium and water
relax vascular smooth muscle cells to improve myocyte relaxation during diastole
decrease myocardial fibrosis/remodelling

Question 23

List 4 medications that every patient with HF (EF < 20%) should be taking

Answer 23

Diuretics
ACE
Beta Bloclers
Aldosterone antagnoist

Question 24

What are the key aspects of cerebral blood flow

Answer 24

Cerebral perfusion is the most important. It’s MAP - ICP
Cerebral blood flow has two determinants , the CPP (repressure) and the resistance. The resistance depends on autoregulation, hormonal and neuro effects

Question 25

What are the cerebral consequenes of rewarming

Answer 25

Secondary injuries may be occur due to reperfusion
Brain hyperactivity can occur which causes the release of glutamate–big time neurotoxin
Hyperglycemia also leads to cellular acidosis
Cerebral vascular and resistance and energy metabolism are impaired in proportion to ischemia
Increase rate of oxygen extraction

Question 26

How are coronary collateral vessels generated

Answer 26

1. Stage 1 (within 24 hours)
   a. passive widening of preexisting channels
   b. Activation of endothelias cells
2. Stage 2. (1-4 days)
   a. infmallation and cellular proliferation
   b. angiogenesis
3. Stage 3. (2-6 months)
   a. cellular maturation and matrix deposition
   * new collaterals form when stenosis is 70%

Question 27

What is Bohr effect

Answer 27

Factors that cause a right shift in the oxygen dissociation curve, thereby encouraging oxygen release to the tissues.

Question 28

List mechanism of ischemia-reperfusion injury

Answer 28

Oxygen-free radical formation: interstitial edema/endothelial injury
calcium influx
leucocyte production 
lactate accumulation 
high-energy phosphate depletion

Question 29

Describe what happens with an acutely ischemic heart on the pressure volume loop

Answer 29

Decreases the diastolic compliance (increases EDPVR) and contractility
The pressure volume loop goes to the right and upward to maintain stroke volume

Question 30

Describe what happens toto a dilated heart of chronic congestive heart failure

Answer 30

The pressure volume loop goes to the right

The EDPVR does not actually move. the compliance does not change

Question 31

What happens to the pressure volume loop with a positive inotropic agent

Answer 31

Shifts the ESPVR line to the left and the degree of dilation would be reduced and both the stroke volume and ejection fraction be increased.

Question 32

What law describes the resistance of viscous fluid to laminar flow (

Answer 32

Poiseuilles’ Law

Resistance is inversely proportional to the 4th power of the radius and directly to the length of the narrowing

Question 33

List facts of percentage of stenosis reduction and it’s effect on resistance

Answer 33

80% has a 16 times greater resistance then 60%
90% has a 256 times greater resistance then 60%

also stenotic lesions change laminar to turbulent flow and this effects resistance

also athersclerosis also effects endothelium and therefore greater vasoconstriction can occur

Question 34

When does collateral flow occur

Answer 34

will occur immediately but only modest collateral flow

gradually begins 8 to 24 hours

doubling by the 3rd day after total occlusion

appears nearly complete after 1 month

Question 35

What happens during repefusion injury

Answer 35

impairs NO generation and therefore vasoconstriction may predominate mediated by relative overexpression of endothelin-1
When NO is impaired leukocytes and platelets adhere to endothelium and this causes damage
Then you have a trigger of cytokine reactions IL-1; IL-6; IL-8, complement C3a C5a, oxygen radicals,

Question 36

What is physiology of myocardial ischemia

Answer 36

progressive loss of adenine nucleotides and elevation of intracellular and intramitochandrial calcium may lead to cellular death and necrosis

a period of days is necessary for recovery of ATP levels of adenine nucleotides must be resynthesized. During this time contractile processes are impaired.

Question 37

What is physiology of stunned myocardium

Answer 37

reversible damage to the contractile proteins such that their responsiveness to cytosolic levels of calcium is diminished. The magnitude of the cytosolic pulse of calcium which each heartbeat appears to be nearly normal but the magnitude of the contraction is reduced.

this will improve over time.

Question 38

What is physiological response of hibernating myocardium

Answer 38

chronic hypoperfusion, oxygen delivery is reduced but above the level required for cell viability.

decrease in the magnitude of the pulse of calcium involved in the excitation-contraction process such that the calcium levels developed within the cytosol during each heart beat are inadequate fro effective contraction to occur.

with reperfusion, hibernating myocardium can quickly resume effective contraction.

Question 39

What is involved in ventricular remodeling in heart failure

Answer 39

Angiotensin and aldosterone stimulate collagen formulation and proliferation of fibroblasts in the heart, leading to an increase in the ratio of interstitial tissue to myocardial tissue in the noninfarcted regions of the heart.

Question 40

What is BNP

Answer 40

increased in heart failure
ventricular myocyte stretch
effects are 
a. natriuesis
b. vasodilation
c. neurohumoral changes

also stimulated by fibrosis, arrhytmias, ischemia, cardiac hypertrophy

Question 41

What is the binding protein in catechoalmines for calcium contraction effects

Answer 41

Beta agonists—bind to adenylate cyclase via the transmembrane GTP binding protein. This leads to increase cAMP synthesis (this acts as second messenger) for a series of intraceullar reaction resulting in higher levels of cytosolic calcium