CVS: Preload and Afterload Flashcards
(21 cards)
Define cardiac output
Vol blood ejected per min
Proportional to HR + SV ∴ CO = HR + SV
CO from right side (via pulmonary artery) and left side (via aorta) are same
CO determine blood pressure + blood flow
What is preload?
Stretching of heart during diastole, increases SV → Regulated by Starling’s law
What is contractility?
Strength of contraction at given diastolic loading, due to sympathetic nerves + circulating adrenaline increasing Ca2+
What is energy of contraction?
Work required to generate stroke volume, depends on Starling’s law + contractility
What are the 2 functions of stroke work?
- Increases chamber pressure> aortic pressure (isovolumetric contraction
- Ejection
Define Starling’s law
Energy of contraction of cardiac muscle is proportional to the muscle fibre length at rest
This means:
- Greater stretch of ventricle in diastole (resting muscle)
- Greater energy of contraction
- Greater SV achieved in systole (contracting muscle)
Intrinsic property of cardiac muscle (nerves, hormones etc. not involved)
Describe preload in terms of the molecular basis of Starling’s law
Un-stretched fibre:
- Overlapping actin/myosin - Less mechanical interference, less cross-bridge formation available for contraction
Stretched fibre:
- Less overlapping actin/myosin - More mechanical interference, potential for more cross-bridge formation, increased sensitivity to Ca2+ ions
What are the roles of Starling’s Law?
- Balances outputs of RV and LV → Prevents fluid congestion in heart
- Responsible for fall in CO following drop in blood volume (haemorrhage, sepsis), orthostasis (standing) leading to postural hypotension (dizziness, fainting)
- Contributes to increased CO during exercise
- Restores SV and CO in response to intravenous fluid transfusions
Breakdown of Starling’s law contributes to development of heart failure
What is afterload?
Force that opposes ejection, reduces SV → Regulated by Laplace’s law
Define Laplace’s law
Afterload opposes ejection of blood from the heart
Afterload is determined by Wall Stress → force through heart wall
More energy of contraction needed to overcome Wall Stress to produce ejection → Heart doesn’t function as efficiently with Wall Stress
Laplace’s law describes parameters that determine Afterload/Wall Stress (S):
- Pressure (P)
- Radius (r)
- Wall thickness (W)
Afterload (S) = P x r/2W
Afterload (S):
- Increased S- Produced by increasing Pressure and Radius
- Reduced S - Produced by increasing Wall Thickness
Therefore Laplace’s law states increased arterial blood pressure = Increased Afterload/Wall stress resulting in reduced ejection
How does afterload change when there’s smaller ventricular radius?
- Greater wall curvature
- More Wall Stress directed towards centre of chamber
- Less Wall stress directed through heart wall
- Better ejection - therefore less opposing force so decreased afterload
How does afterload change when there’s larger ventricular radius?
- Less wall curvature (Walls become thinner due to ventricular dilation)
- More wall stress directed through heart wall
- Greater afterload
- Less ejection
How does chronic high arterial blood pressure affect afterload?
- ⬆️Afterload/Wall Stress
- Increased energy expenditure
- Ultimately decreased SV/CO = Poor blood flow to end organs, poor perfusion of organs
How does Laplace’s law explain hypertrophy in heart failure?
- ⬆️r: Volume-overload heart failure
- E.g. MI causes poor stroke volume/ejection fraction
- Blood volume remains in heart
- ⬆️P: Pressure-overload heart failure
- E.g. Hypertension causes afterload which heart must work against
- S = P x r/ 2W therefore, increased r or P will increase afterload meaning less ejection
- To counteract this, the heart must compensate and it does this by:
- Increased Wall thickness (W) = hypertrophy (greater myocyte size)
- Same Wall stress but now over greater area (more sarcomeres)
- Less wall stress per sarcomere and less opposition to contraction of sarcomeres, greater SV/CO
- But requires more energy (as more sarcomeres used)
- This means greater O2 is needed, so ultimately contractility decreases, resulting in a circle of heart failure
What is the importance of Laplace’s law?
- Opposes Starling’s law at rest
- ⬆️Pre-load = ⬆️chamber radius
- Laplace’s law states that this will increase afterload, which will oppose ejection of blood from a ‘full’ chamber
- In a healthy heart, Starling’s law overcomes Laplace’s law to maintain good ejection
- Facilitates ejection during contraction
- Ventricular contraction = ⬇️chamber radius
- Laplace’s law states this will reduce afterload in ‘emptying’ chamber
- Aids ejection during reduced ventricular ejection phase of cardiac cycle
- Contributes to failing heart
- In failing heart, chamber often dilated, increasing chamber radius
- Reduction in ejection as Laplace’s law dictates that there is increased afterload opposing ejection
- Therefore, laplace’s law is good with small radii, but bad with large radii
How do changes in preload affect LV P-V loops?
Increased preload:
- Events that increase venous return such as venoconstriction during exercise or administration of intravenous fluids
- Increased end-diastolic volume = Increased Starling’s law = Increased SV
Decreased preload:
- Events causing loss of blood volume, e.g., haemorrhage, dehydration
- Decrease in EDV = decrease in Starling’s law = decreased SV
How do changes in afterload affect LV P-V loops?
Increased afterload:
- E.g. chronic hypertension
- Increased isovolumetric contraction to overcome greater aortic pressure and open aortic valves for ejection = Less energy left for ejection = reduced SV
Decreased afterload:
- E.g. Reduce blood pressure during dynamic exercise (running)
- Reduce isovolumetric contraction = easier to open aortic valve = more energy for ejection = increased SV
What is the primary determinant of preload in the context of cardiovascular physiology?
End diastolic volume - End-diastolic volume (EDV) is the volume of blood present in a ventricle of the heart at the end of diastole, just before systole begins. EDV is the primary determinant of preload, as it describes the degree of tension on the cardiac muscle fibres prior to contraction.
What is the primary determinant of after load in the context of cardiovascular physiology?
BP - BP, the force exerted by circulating blood upon the walls of blood vessels, is a primary determinant of afterload, not preload. Afterload is the pressure that the heart must overcome to eject blood during systole. This means that increased BP in the aorta causes an increase in afterload, as the left ventricular pressure needs to be higher than the aortic pressure to pump blood out of the heart
What term describes the difference between end-diastolic volume (EDV) and end-systolic volume (ESV)?
Stroke volume - it is the difference between the volume of blood in the left ventricle (LV) at the end of diastole (ventricular filling) and the volume of blood in the LV at the end of systole (ventricular contraction). This is a more accurate definition than the one that states it as the amount of volume ejected by the LV into the aorta per heartbeat, as this definition assumes that all the blood leaving the LV enters the outflow tract leading to the aorta, which will not be the case if there is aortic regurgitation or an interventricular septal defect leading to blood flow into the left atrium and right ventricle respectively.
On a 12-lead ECG, what leads represent the inferior region of the heart?
II, III, aVF
Leads II, III and aVF represent the inferior region of the heart. In 90% of people, this is supplied by the right coronary artery; in the remaining 10%, this is supplied by the left circumflex artery. By knowing what region of the heart and what arteries each ECG lead represents, you can identify where pathology in the heart is present. For example, ST elevation in leads II, III and aVF represents an inferior STEMI myocardial infarct, most likely caused by blockage to the right coronary artery. Having this information can then prepare the interventional radiology team for stent insertion or bypass surgery.
