The Heart-Starlings Law and the Control of Cardiac Output PDF

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Summary

Understand the factors that regulate cardiac output
Understand the principle of the Frank-Starling law of the heart
Understand how the heart adjusts cardiac output and venous pressure
Understand the consequences of heart failure
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Description

The Heart: Starling’s Law and the Control of Cardiac Output Starling observed using an isolated heart-lung preparation that the larger the diastolic volume of the heart the greater the energy of the contraction. The energy of contraction is proportional to the resting muscle fibre length. Direct relationship between end diastolic volume and end systolic pressure. Main role of the Law is to balance the output from both sides so automatically the 2 sides of the heart stay in balance. He mimicked the resistance of the arterioles with a Starling resister and he measured the cardiac output by collecting the blood pumped around the circuit. By varying the height of the venous reservoir he showed that the greater the pressure and hence the stretch the grater the cardiac output. Below a Starling resister acts as a TPR. Pressure was measured with mercury manometers and the blood collected to measure the cardiac output. The degree of stretch of the cardiac muscle can be varied by altering the height of the venous reservoir. In vivo the cardiac nerves vary the rate of the heart do he cut all the neural connections to have a pure myogenic preparation. The extent of preload will affect the force of contraction and stroke volume during systole. Systolic pressure rises until diastolic volume reaches 30ml.

Cardiac Output Cardiac output (CO) is controlled by two factors: 1. SV (stroke volume) 2. HR (heart rate) CO = SV  HR   

CO varies from 4 to 7 L per min depending on body size and fitness. When sleeping it falls to its lowest value and is raised in pregnancy. Athletes can increase their CO by up to six fold by increasing both the HR and to a limited extent the SV.

Ventricular Function Curves (Starling Curve)  Plateau phase doesn’t occur in humans as there are mechanisms to prevent this from happening.

The ascending part of the curve the heart compensates from the increase in venous pressure.  Once the curve reaches a plateau decompensation occurs and the heart is less efficient at following Frank – Starling Law. Length – Tension Relationship The energy of contraction is proportional to the resting fibre length which reflects the degree of overlap between the myosin and actin fibres. 

Balancing Venous and Arterial Pressure  Preload of the ventricles is provided by central venous pressure (CVP) Afterload of the ventricles is provided by arterial blood pressure (BP).  Exercise will increased cardiac output and the heart can adapt to this.  If the output of the left side of the heart was increased by 1 % compared to the right side. More blood would go into the systemic circulation and the pulmonary circulation would be completely emptied.  Input into the right and output from the left side of the heart must stay exactly in balance or blood would be transferred into the pulmonary circuit which has a limited capacity. Family Curves  In Starling’s heart-lung preparation, the nervous control of heart contraction is not present.  In the intact system there are a family of Starling curves under the influence of sympathetic nerve activity. This means that for any given length the cardiac output depends on which curve the heart is operating on.  The cardiac output can be adjusted depending on need (e.g. exercise).  The body can adapt the heart to fall on different Starling curves depending on the neural activity. Neural Control The heart rate is a balance between: 1. The influence of the sympathetic and parasympathetic nervous system on the heart rate. 2. The natural rate of depolarisation of the SA node.  ACh decreases the rate at which the SA node depolarises, slowing the generation of the SA action potential. Parasympathetic system is dominant.  Sympathetic nervous system is part of the peripheral nervous system. The neurotransmitter is noradrenaline. Noradrenaline increases heart contraction by activating β 1-adrenoceptos in the heart.  Adrenaline is released form the adrenal medulla and reached the heart via the blood stream and also increases heart rate. Sympathetic Innervation and the Starling Curve  In exercise a greater CO is produced for a given fibre length as the sympathetic drive moves the heart onto a more efficient Starling curve.  Increased sympathetic activity will increase heart rate/muscle contraction (shift curve up and left)

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Decreased sympathetic activity will decrease heart rate/muscle contraction (shift curve down and right)

Heart Failure Congestive Heart Failure - The heart is over filled with blood (left ventricle) and is unable to compensate for the change in volume. Initially changes in volume can be compensated by increasing heart contraction (rate) and shifting the curve upward and to the left. However if the heart is failing, the curve is depressed and moves into the decompensated or plateau phase. If the right ventricle of the heart begins to fail it cannot maintain the balance and the Starling curve becomes less steep. Initially by moving up the Starling curve the right side of the heart keeps the situation in balance over the short term. Once the right side of the heart cannot keep up with the left side fluid floods into the lungs and the patients goes into pulmonary oedema. The first symptom is difficulty with breathing as the lung engorged with blood becomes stiff. In heart failure a higher venous pressure produces a smaller CO also a higher end diastolic volume is required for a given energy of stroke work. •

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As the left ventricle becomes impaired insufficient blood is pumped from the systemic circulation and this leads to peripheral oedema. The capillary filtration pressure exceeds 25 mmHg, the COP so fluid moves into the tissues. This gives oedema of the lower limbs, swollen ankles, ascites in the gut (fluid filled sack) and pulmonary vascular congestion (dyspnoea). Symptoms  Weaker pumping action of the heart  Pulmonary oedema  Coughing, Tiredness, Shortness of breath  Swelling in veins above the heart (jugular vein in neck) and excess fluid in the extremities (ankles and legs) Causes  High blood pressure (chronic overload)  Artery disease and a restriction in coronary blood supply  Myocardial infarction (heart attack) and the loss of functional heart tissue  Diseased valves (leaky or stiff) Treatments The main approaches for treating heart failure: 1. Reduce work of the heart by reducing arterial resistance with vasodilators 2. Reduce cardiac dilatation by reducing the plasma volume with diuretic drugs (frusemide)

3. Improve myocardial contractility by cardiac glycosides (digoxin) or b1adrenoceptor agonists (dobutamine) 4. Digoxin prolongs the plateau phase of the cardiac AP by blocking Na/K pump and increasing Na build up in the cell, and increasing the build up of Ca within the cell->increase contractility Angiotensin Converting Enzyme reduces water retention and vasoconstriction. ACE inhibitors reduce blood pressure by reducing water and sodium retention. They prevent the production of angiotensin II and aldosterone. Angiotensin II increases blood pressure and generates more work for the heart to pump blood. Aldosterone retains Na and water, this increases blood volume. Beta blockers inhibit Beta adrenoceptors that are responsible for increasing heart rate (and thus contraction) and vasoconstriction. Pacemaker Cells and Neaural Activity Parasympathetic Hyperpolarises pacemaker activity. Increases time period to next AP.

Sympathetic Increases pacemaker activity. Reduces time period to next AP....