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From Flashcardlet big > Cardiac physiology > Flashcards

Cardiac physiology Flashcards

1
Q

Describe the principles of mixed venous saturation measurement

A

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

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2
Q

Describe central venous pressure waveform

A

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

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3
Q

Describe how inotropes increase cardiac contractility

A

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

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4
Q

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

A

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.

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5
Q

Draw the oxygen dissociation curve

A

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

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6
Q

Describe the stages of hemostasis

A

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

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7
Q

What is thrombo-elastogram (TEG)

A

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.

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8
Q

What is Laplace Law

A

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

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9
Q

What are the components of the myocardial oxygen supply demand relationship

A

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.

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10
Q

What regulates blood flow

A

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

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11
Q

Describe endothelial function and give examples of endothelial effectors

A

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,

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12
Q

Describe and draw the arterial waveform

A

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

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13
Q

What are the arterial waveforms in severe major conditions

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

A

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.

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14
Q

What is the fick method for calculating Cardiac output

A

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

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15
Q

How do you calculate shunt fraction

A

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

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16
Q

The mechanisms of injury during reperfusion include

A

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

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17
Q

What is mechanism of Heparin Induced thrombocytopenia and thrombosis

A

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.

18
Q

What are two test for HIT

A

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.

19
Q

What is management of HIT

A

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

20
Q

What does in IABP do

A 
LV systolic pressure -------decrease
LV diastolic pressure------decrease/likely stay the same 
Aortic diastolic pressure 
	early 			increases
	late 				decrease
Aortic systolic pressure	decrease
21
Q

List two peptides that can distinguish CHF from COPD in ER

A

Brain Natriuretic peptide

Atrial Natriuretic peptide

22
Q

What are physiological effects of BNP

A

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

23
Q

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

A

Diuretics
ACE
Beta Bloclers
Aldosterone antagnoist

24
Q

What are the key aspects of cerebral blood flow

A

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

25
Q

What are the cerebral consequenes of rewarming

A

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

26
Q

How are coronary collateral vessels generated

A
  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%
27
Q

What is Bohr effect

A

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

28
Q

List mechanism of ischemia-reperfusion injury

A 
Oxygen-free radical formation: interstitial edema/endothelial injury
calcium influx
leucocyte production 
lactate accumulation 
high-energy phosphate depletion
29
Q

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

A

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

30
Q

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

A

The pressure volume loop goes to the right

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

31
Q

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

A

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.

32
Q

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

A

Poiseuilles’ Law

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

33
Q

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

A

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

34
Q

When does collateral flow occur

A

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

35
Q

What happens during repefusion injury

A

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,

36
Q

What is physiology of myocardial ischemia

A

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.

37
Q

What is physiology of stunned myocardium

A

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.

38
Q

What is physiological response of hibernating myocardium

A

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.

39
Q

What is involved in ventricular remodeling in heart failure

A

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.

40
Q

What is BNP

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

also stimulated by fibrosis, arrhytmias, ischemia, cardiac hypertrophy

41
Q

What is the binding protein in catechoalmines for calcium contraction effects

A

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

42
Q

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

A

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

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