Control of Cardiac Output Flashcards
Definition of preload
Filling pressure of right ventricle, related to the CVP
Degree of stretch immediately before contracting
Definition of after load
Resistance to outflow from left ventricle, related to the MABP
Force against which the LV pumps to eject blood => aorta
Definition of end diastolic volume
Related to the filling pressure fo the heart
CVP=EDP
Definition of heart failure
Inability of heart to maintain a CO sufficient to adequately supply the tissues and organs of the body with blood
Can occur acutely and chronically
Definition of ANREP response
Autoregulation method where myocardial contractility increases with afterload
Definition of central venous pressure
Amount of blood and also capacitance of the veins
Describe the central venous system
What is the venous return equal to?
When is this not the case?
CVS is a closed system
CO=venous return
Except in transient events. In orthostasis, CO>VR as some pools in lower extremities. Due to the fact that there is more blood in the venous system than arteriole system
What influences cardiac output
Preload and afterload
Contractility
HR
What is the preload
Degree of stretch of the heart immediately before it contracts
What is the afterload
What is it due to?
What is it influenced by
Force against which the LV pumps to eject blood into the aorta
Mainly due to aortic P
Influenced by TPR and aortic stiffness (particularly with age)
What is the end diastolic volume
Related to the filling pressure of the heart
CVP=EDP
Describe the results of the Frank experiment
As filling pressure increases, ventricular P increases
The energy released during contraction depends on initial fibre length
- Filling P increases
- Fibre length increases
- Force increases
Hyperbolic relationship
What is the relationship between EDP and EDV
EDP is easier to measure but relationship to EDV can change if V stiffens
Why does force increase with increased tension
Cross bridge theory
Maximum stretch present when there is max overlap between actin and myosin and the longest sarcomere possible forms
If there is too much overlap between actin filaments and no more cross bridges forming = shorter sarcomere length, results in a smaller % of max tension.
Gives a similar hyperbolic shape (sarcomere length vs % of max tension)
Describe the differences in cardiac and skeletal length tension curves
Steeper in cardiac than skeletal
So relatively small changes in preload/stretch => large change in force
How does Ca sensitivity and length dependence affect the amount of stretch and tension
As [Ca] increases, tension increases
Probably involves troponin C
What are the consequences of Starling’s Law
SV of LV = SV of RV
CVP determines CO (assuming constant SNS input)
CO maintained even if afterload increases/contractility decreases
How is the RV and LV output made equal
Increase in RV output Increase in BV in pulmonary veins Increase in LA P and V Increased filling of LV and LVEDP Increased stretch Increased force of contraction Increased SV and LV output LV output = RV output
How is the RV and LV output made equal, shown on a ventricular function curve
Initially, SV of both LV and RV are the same
However as RV has thinner walls, P and V is higher here
When RV increases, out of sync with LV
LV will match SV of RV by increasing the EDP
What is the compliance of a chamber
Change in V with a given change in P
What is heart failure
When is it acute?
When is it chronic
What is it characterized by?
Inability of the heart to maintain a CO sufficient to adequately supply tissues and organs with blood
Can be acute (MI, muscle not working)
Can be chronic (chronic heart failure, microstructure deteriorates)
Characterized by a lower amplitude CO curve
Describe the 3 compensatory mechanisms in heart failure
Decreased BP => decreased Na and water excretion
This increases BV and CVP => increases SV
Decreased BP and renal F activates SNS and RAAS
This increases water retention, +ve ionotrope and chronotrope, vasoconstriction => increased SV and EDP
Increased venous BV and VC
This increases CVP and EDP
Describe the long term effects of the compensatory mechanisms in heart failure
Muscles continually weaken so EDP increases to maintain a SV sufficient for survival which continues to fall
What is the effects of afterload on cardiac output
Increased AL => decreased SV because ejection cannot start until VP> AP
If AP increases, ejection is delayed so there is less time and energy for ejection
Describe the mechanism to overcome increased afterload
What happens as a result
Ejection fraction falls, more blood remains in the heart at the end of systole so EDV/EDP increases. Restored SV due to Starling mechanism
ANREP effect, release of substances that increase [Ca] in myocytes, increased ionotropy
Depression of CO by baroreceptors, SNS inhibited
CO and SV overall does not change as a result
How is the preload regulated, CVP dependent
When does regulation occur?
CVP, function of amount of blood in veins and capacitance
Increased SNS => Increased VC => Increased P => Increased CVP
-Occurs in exercise so RV output = Increased LV output for working muscle
Changes in BV can alter CVP
-Occurs in hemorrhage, blood loss decreases CVP => decreased CO
Compensation
- Increased VC to restore CO
- Increased renal fluid retention
- Shift of fluid from interstitium => plasma => increased BV
Describe cardiac contractility and what is it regulated by?
Amount and rate of cardiac tension developed and ability to eject a SV
Regulated by [Ca] in myocytes via SNS/pH and pO2
NA increases contractility by stimulating B1 and B2
How does exercise affect cardiac contractility
Increases contractility and venoconstriction => increase EDP and CO
How does transfusion and exercise affect cardiac contractility?
Increased CVP and CO due to increased BV
Describe the SAN and the pacemaker potentials
Primary pacemaker with diastolic depolarization (funny current haha)
Has non selective channels for Na, Ca
Effects of the ANS agonists on the SNS
NA/A
Increased If
Increased rate of diastolic depolarisation (+ lusitrope)
Increased HR (+ chronotrope)
Effects of the ANS agonists on the PNS
Ach
Decreased If
Opens KAch
Decreased rate of diastolic depolarisation (- lusitrope)
Decreased HR (-ve chronotrope)
