4. Cardiac System

Question 1

What is the breakdown of an electrocardiogram (ECG)?

Answer 1

P wave- depolarization of atria
QRS complex- depolarization of ventricles
T wave- repolarization of ventricles
U wave- unknown, possible repolarization if papillary muscles

Slides 4-6 sept 19

Question 2

What are the 2 main events of the cardiac cycle?

Answer 2

1. Ventricular systole (contraction)
   Isovolumic ventricular contraction
   Ventricular ejection (rapid ejection phase and reduced ejection phase)
2. Ventricular diastole (relaxation)
   Isovolumic ventricular relaxation
   Ventricular filling (rapid filling phase and reduced filling phase)

Question 3

How does ventricular systole work?

Answer 3

Blood volume during this period is known as end-diastolic volume (EDV) or preload
Starts with closure of AV (mitral) valve (this generates first low pitched heart sound)
Ejection starts by opening semilunar valve (AV valves now closed) and sharp increase in ventricular and aortic pressure (rapid then reduced ejection phase

Slides 8-9 sept 19

Question 4

How does ventricular diastole work?

Answer 4

Blood volume in ventricles during this period is known as end-diastolic volume (ESV)
Begins with closure of semilunar (aortic) valve which generates 2nd higher pitched heart sound
The ventricle filling begins with opening of AV (mitral) valve (semilunar valves are now closed)
Majority of ventricular passive filling occurs (rapid filling 70%) reduced filling with atrial contraction follows

Slides 10-11 sept 19

Question 5

What is stroke volume (SV)?

Answer 5

The amount of blood pumped out of the ventricle per beat (normal value of 70mL for resting man)

End-diastolic volume - end systolic volume

SV=EDV-ESV

Slide 23 sept 19

Question 6

What is the ventricular pressure-volume loop?

Answer 6

It identifies the sequential dynamic changes in the left ventricle for one complete cardiac cycle
Generated by plotting the left ventricular pressure against left ventricular volume (provides info on left ventricular function)

Slide 14 sept 19

Question 7

What is cardiac output and it’s determinants?

Answer 7

Output of heart per unit time
Normal value is 5-6 L/min

Cardiac output= heart rate x stroke volume
CO=HR x SV

Determined by cardiac factors heart rate and myocardial contractility and by coupling factors preload and afterload

Question 8

What is the cardiac index (CI)?

Answer 8

This value is used to minimize the influence of body size in cardiac output
It is the cardiac output per body surface area (BSA) in meters squared (m^2)
BSA= square root of height (cm) times weight (kg) divided by 3600

Ranges between 2.6-4.2 L/min/m^2

Question 9

What is the heart rates effect cardiac output (CO) and stroke volume (SV)?

Answer 9

Increasing HR alone will have an inverse effect on SV because the ventricular filling time is decreased as the diastolic period decreases

Increasing HR will increase CO, but up to a limit because of the drastic decrease on ventricular filling time during tachycardia attack

Question 10

Why, while exercising, the percentage of CO increase is generally more than that if the HR? (3 reasons)

Answer 10

1. Reduction in peripheral vascular resistance
2. Positive ionotropic effect to the contractile myocytes primarily caused by the increase of sympathetic activity
3. Compressing action of the contracting skeletal muscles together with the venous valves to enhance the venous return

Question 11

What are the 3 parameters that can influence stroke volume (SV)?

Answer 11

1. Preload (affecting EDV)
2. Afterload
3. Contractility (inotropy)

Afterload and contractility have direct effect on ESV

Question 12

What is preload (EDV)?

What is it determined by?

Answer 12

EDV=ESV + venous return
Increase in preload will increase SV
Preload is affected by the degree of stretching of the cardiac myocytes prior to contraction and therefore related to the sarcomere length at the end of diastole
Also directly related to the end diastolic ventricular blood volume and the intra-myocardial wall stress of the ventricle at the end of diastole

Determined by: ventricular compliance, venous return, length-tension relationship, heart rate (lesser extent)

Question 13

What is ventricular compliance?

Answer 13

The change in volume divided by the change in pressure
ΔV/ΔP = compliance (C)
VP/ΔV = stiffness

High compliance means heart can be easily stretched during diastole (enhance venous return)
Low compliance means the heart will resist expansion during diastole (stiff)
Initially ventricle has a high compliance, compliance decreases when the myocytes reach their elastic limit

Slides 27-31 sept 19

Question 14

How does ventricular dilation affect end-diastolic volume (preload)?

Answer 14

Use ventricular compliance/filling curve slide 5 sept 24

With ventricular dilation, there is an increase in ventricular compliance (ΔV/ΔP) or the slope of LVEDPVR is lower
Ventricle can have a greater EDV without causing a large increase in EDP (enhancing venous return->increase preload)

Question 15

How does ventricular hypertrophy affect end-diastolic volume (preload)?

Answer 15

Use ventricular compliance/filling curve slide 6 sept 24
For ventricular hypertrophy (up in thickness) there is a decrease in ventricular compliance
Decrease compliance increases EDP at a given EDV (deterring venous return)

Question 16

What is the effect of venous return in preload?

Answer 16

An increase in venous return will increase ventricular filling and therefore increase preload (end-diastolic volume)
Increase in EDV also causes an increase in end diastolic pressure for a given heart

Increase preload, stretch myocardial contractile myocytes, increase force of contraction, increase stroke volume, increase cardiac output

Question 17

What is frank starling mechanism or starlings law?

Answer 17

The observed increase in force of contraction by the heart in response to an increase in preload is contributed by frank starling mechanism or starlings law

Ensures the outputs if both the ventricles are matched over time and to prevent shifting of blood between pulmonary and systemic circulations

Question 18

What does an increase in LVEDV do? (Left ventricle end diastolic volume)

Answer 18

Increases in LVEDV always leads to increase in LVEDP which increases stroke volume
Slide 11 sept 24

Question 19

What happens when you increase preload (EDV) by increasing venous return but leave all cardiac and coupling factors constant?

Answer 19

Instantaneous increase in stroke volume which results in increase in cardiac output without any change to end systolic volume

The increase of SV by increasing EDV alone does not alter the contractility if a given heart (frank starling mechanism)

Slides 12-13 sept 24

Question 20

What is the length tension relationship of the ventricle?

Answer 20

Illustrates relationship between changes of the initial length of a myocyte (preload) to the contractile force (tension) developed by the heart muscle
Increase in preload, increase in active tension (^ EDV= ^ stretching)
Increase in active tension is accompanied by an increase in the velocity of tension development (velocity of muscle shortening)

Explains why an increase in EDV will result in an increase in SV with no change in ESV

Slides 15-17 sept 24

Question 21

What is afterload?

Answer 21

Defined as the ventricular wall tension (stress) developed during ventricular ejection (systole)

Magnitude of wall tension is directly related to resistance, impedance or pressure that ventricle must be able to overcome before blood can be ejected

Also defined as the lid against which the heart must counteract before blood can be ejected out (aortic pressure major component of afterload for left ventricle)

Question 22

What is Laplace’s law?

Answer 22

Ventricular wall stress (σ) can be estimated by the laplaces law for a sphere
Wall stress is proportional to the product of the intra-ventricular pressure (p)and ventricular radius (r), divided by the wall thickness (h)

σ α (p•r) / 2h

Slide 20-21 sept 24

Question 23

What is afterloads effect on stroke volume?

Answer 23

Using frank starling curve (relationship between LVEDV/LVEDP (preload to SV)

Increase in afterload shift the frank sterling curve down and right
Due to increase in afterload, the heart have to generate a much higher pressure in order to eject the same volume of blood (open aortic valve) (decrease velocity of fiber shortening which results in decrease SV)
Increases ESV also with normal venous return results in increase EDV

Slides 23-24 sept 24
Slides 29-30 sept 24

Question 24

What is the Vmax on a force-velocity relationship curve?

Slide 25 sept 24

Answer 24

The y intercept represents an extrapolated value for the maximum velocity (Vmax) that can be achieved by the muscle fiber in the absence of any load (it is extrapolated because one cannot measure the velocity of shortening of a muscle fiber in the absence of any load)

Vmax is an indicator for the inotropic condition of a contractile muscle in a given physiological condition

Question 25

What is the x intercept on the force velocity relationship curve?

Answer 25

X intercept represents the maximum force that the heart can generate at a given preload condition
For a given heart at a given inotropic condition, any elevation in preload will result an increase in afterload, but no effect on Vmax

Slide 26 sept 24