Afterload AND Preload - CVS PDF

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HEART: PRELOAD AND AFTERLOAD Cardiac Output (CO) – volume of blood ejected from the heart per minute. Determines blood pressure and blood flow. CO = heart rate (beats per minute) x stroke volume (blood ejected per beat) Cardiac output from the right side (pulmonary artery) and left side (aorta) is the same. It changes according to demand – 70bpm x 70ml = 5 litres/min during rest and increases to 22 litres/min (180bpm x 120ml) Blood pressure = cardiac output x total peripheral resistance Blood flow (CO) = BP/TPR - If cardiac output is low, blood pressure is also low. - Good cardiac output shows that there is good blood flow to brain and heart. What controls stroke volume? Preload – stretching of the heart at rest, filling pressure, increases SV (Starling’s Law) Afterload – opposes ejection is the blood pressure in the systemic circulation and reduces SV (Laplace’s law). Energy of contraction – amount of work required to generate stroke volume i.e. how much energy and oxygen is required to produce a contraction in the presence of afterload and preload. Heart rate – modulated by sympathetic and parasympathetic nerves Contractility – strength of contraction at a given resting loading, due to sympathetic nerves and circulating adrenaline increases [Ca2+] Stroke work increases chamber pressure greater than aortic pressure (isovolumetric contraction) and ejects blood. - Preload increases energy of contraction and enhances SV. - Afterload requires greater energy of contraction and opposes SV.

Preload - Starling’s Law of the Heart Energy of contraction of the cardiac muscle is proportional to the muscle fibre length at rest. - Greater stretch of ventricle in diastole (resting muscle), greater energy of contraction, greater SV achieved in systole (contracting muscle). - Intrinsic property of cardiac muscle (e.g. nerves and hormones are not involved) Increase in venous return increases end-diastolic volume, it stretches the muscle more. This increases the strength of cardiac contraction and increases stroke volume (more blood ejected)

Difference between end systolic volume (lower – some blood is still left in the heart) and end diastolic volume (higher) is stroke volume. Aortic blood pressure fluctuates between when you are contracting and relaxing the heart. Central venous pressure – pressure of blood in the great veins. Increasing blood volume – increases central venous pressure, increase in end-diastolic volume, increase in stroke volume. Decrease in volume leads to less preload, less stroke volume, end-diastolic volume falls and central venous pressure falls. Ascending limb – as CVP goes up, stroke volume goes up as you are stretching the heart muscle more at rest. It plateaus as there is a limit to its stretching ability. If it is not stretched, actin and myosin can interact but they still cannot shorten that much. There is interaction between the myosin and actin filaments. When you stretch it, the interactions between actin and myosin are removed. They interact better to produce contraction. Increased sensitivity to calcium means that a low calcium level can still cause good contraction.

Preload - Molecular Basis of Starling’s Law Actin

Un-stretched fibre

Roles of Starling’s Law Overlapping actin/myosin - Mechanical inference Myosin  Balances outputs of RV and LV Less cross-bridge formation available for contraction What enters on the right leaves on the Z band How Does Stretching left. movement Increase Energy of There is no congestion in the pathway Contraction? – this goes wrong in heart failure.  Responsible for fall in cardiac output after drop in blood volume e.g. haemorrhage and sepsis. Less blood Stretched fibre back to the heart leads to less stretch. Less overlapping actin/myosin  Responsible for fall in cardiac output - Less mechanical inference Potential for more cross-bridge formation during orthostasis (standing) leading to Increased sensitivity to Ca ions postural hypotension (dizziness and fainting). Blood pools in the veins in the feet and there is less return to the heart.  Restores cardiac output in response to intravenous fluid transfusions to increase CVP.  Increased cardiac output during exercise e.g. during exercise the increased CVP, increases end-diastolic and then increased stroke volume to lungs and then increased end-diastolic volume in LV increases stroke volume to the body. 2+

Afterload – Laplace’s Law Afterload opposes ejection of blood from the heart. Determined by wall stress directed through the heart wall – more energy of contraction is needed to overcome this wall stress to produce ejections and the heart doesn’t function as efficiently. P = 2T/r

Wall tension (T), Pressure (P) and Radius (r) in a chamber e.g. ventricle.

2x wall tension because a chamber has two dimensions of curvature. Tension (T) is made up of wall stress (S) and wall thickness (w) P = 2Sw/r or S = P x r/2w Afterload (S) is increased by increasing pressure and radius and decreasing wall thickness. More afterload means more opposition to contraction. Afterload – Radius and Wall Stress S =P x r / 2w S

S

S

Small ventricle radius Greater wall curvature

Larger ventricle radius

More Wall Stress directed towards centre of chamber

Less wall curvature

Less Afterload

More Wall Stress directed through heart wall

Better ejection

More Afterload Less Ejection

Normally, Starling’s Law wins to maintain proper stroke volume and ejection. During contraction, as the chamber gets smaller, it gets better at contracting and ejecting blood out of it. - Maintains ejection even when pressure is reducing in the chamber. When a heart is failing because it is congested and dilated, there is a large radius so increased afterload. Starling’s law is not working efficiently.

High arterial blood pressure – more energy is needed to open valves in isovolumetric contraction. There is also increased afterload to get over. - Baroreflex should reduce blood pressure. Heart Failure Volume-overload – heart doesn’t contract very much and it just fills up with blood (radius increases) To compensate we have to increase wall thickness (w) and so there is hypertrophy (same number of cells but they are thicker – more sarcomeres). Effect of Preload on Ventricular Pressure-Volume Loop Effect of

Afterload on Ventricular Pressure-Volume Loop More energy used during isovolumetric contraction – pressure has to be raised over the pressure in aorta because of the high blood pressure. There is less energy for ejection as so much is used opening the valve....