4. Cardiac System Flashcards
What is the breakdown of an electrocardiogram (ECG)?
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
What are the 2 main events of the cardiac cycle?
- Ventricular systole (contraction)
Isovolumic ventricular contraction
Ventricular ejection (rapid ejection phase and reduced ejection phase) - Ventricular diastole (relaxation)
Isovolumic ventricular relaxation
Ventricular filling (rapid filling phase and reduced filling phase)
How does ventricular systole work?
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
How does ventricular diastole work?
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
What is stroke volume (SV)?
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
What is the ventricular pressure-volume loop?
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
What is cardiac output and it’s determinants?
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
What is the cardiac index (CI)?
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
What is the heart rates effect cardiac output (CO) and stroke volume (SV)?
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
Why, while exercising, the percentage of CO increase is generally more than that if the HR? (3 reasons)
- Reduction in peripheral vascular resistance
- Positive ionotropic effect to the contractile myocytes primarily caused by the increase of sympathetic activity
- Compressing action of the contracting skeletal muscles together with the venous valves to enhance the venous return
What are the 3 parameters that can influence stroke volume (SV)?
- Preload (affecting EDV)
- Afterload
- Contractility (inotropy)
Afterload and contractility have direct effect on ESV
What is preload (EDV)?
What is it determined by?
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)
What is ventricular compliance?
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
How does ventricular dilation affect end-diastolic volume (preload)?
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)
How does ventricular hypertrophy affect end-diastolic volume (preload)?
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)
What is the effect of venous return in preload?
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
What is frank starling mechanism or starlings law?
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
What does an increase in LVEDV do? (Left ventricle end diastolic volume)
Increases in LVEDV always leads to increase in LVEDP which increases stroke volume
Slide 11 sept 24
What happens when you increase preload (EDV) by increasing venous return but leave all cardiac and coupling factors constant?
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
What is the length tension relationship of the ventricle?
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
What is afterload?
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)
What is Laplace’s law?
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
What is afterloads effect on stroke volume?
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
What is the Vmax on a force-velocity relationship curve?
Slide 25 sept 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
What is the x intercept on the force velocity relationship curve?
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
