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CVS Physiology part 4

Dr Swapnil Pawar January 31, 2020 267 5


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APPLIED CARDIOVASCULAR PHYSIOLOGY

Outline the important features of a left ventricular pressure-volume loop

The left ventricular pressure volume loops plot the left ventricular volume in millilitres is plotted on the x axis against the left ventricular pressure in mmHg on the y axis over the cardiac cycle. The LV pressure-volume loop can be divided into four basic stages; ventricular filling, isovolumetric contraction, ventricular ejection and isovolumetric relaxation. If we start at the beginning of ventricular filling when the mitral valve opens and the end systolic volume of the LV is about 50mls, we can call this point A. The ventricles fill and the LV pressure slowly rises to a point where the LV pressure rises above atrial pressure and the mitral valve closes, this can be termed point B which represents the end diastolic pressure and end-diastolic volume which is usually around 130mls. The line from point A to B is phase 1 and represents ventricular filling, this horizontal distance is stroke volume. Phase 2 then begins which is isovolumetric contraction where the volume in the ventricle remains the same as all valves are closed but the pressure rises rapidly. This continues until the intraventricular pressure exceeds the aortic diastolic pressure, often at about 80mmHg, and the aortic valve opens, or point C. Phase 3 then begins which is the period of ventricular ejection. During phase 3 the systolic pressure rises to about 120mmHg and ventricular volume decreases as blood is ejected. There is a fall of pressure to about 100mmHg at the end of systole to a point and when the LV pressure drops below that of the aorta and the aortic valve closes or point D. This point marks end systolic volume. Phase 4 is isovolumetric relaxation where both the aortic and mitral valve closes so there is no change in volume but the ventricular pressure returns back to its diastolic level. When the intraventricular pressure falls below the atrial pressure the mitral valve opens or point A and the whole cycle begins again.

The LV pressure-volume loop can provide some important information about the heart. This includes:

  • LV end diastolic volume or point B on the loop is an indicator of pre-load. Increased pre-load will shift the curve the right but end diastolic volume will increase more than end systolic volume so that stroke volume is increased
  • Afterload is illustrated by the slope of the line connecting end diastolic volume or point B with end systolic volume or point D. Increased afterload will increase the slope of the afterload line as end diastolic volume/pressure or point B will not change but end systolic pressure and volume will increase. Therefore, there will also be a reduction in stroke volume.
  • Contractility can be represented by the slope of the end systolic pressure volume line, that is the angle of the line between the end systolic point or point D and the x axis. With increased contractility the end systolic pressure/volume point is moved to the left and slightly upwards thus increasing the gradient of the end systolic pressure volume line.
  • The slope of the line from point A or when the mitral valve opens and point B or end diastolic volume gives the elastance of the ventricle and this line is known as the end diastolic pressure volume relationship. Increased elastance such as in diastolic dysfunction will increase the slope of this line, that is, ventricular pressure will be higher for any given ventricular volume.
  • The area within the pressure volume loop represents stroke work

What is shock and how can it be classified?

Shock is a broad term for a clinical condition characterised by the failure to deliver and/or utilise adequate amounts of oxygen to supply the needs of the body. Shock can be classified according to the major component of the circulation that is affected;

  • Hypovolemic shock: inadequate preload
  • Cardiogenic shock: pump failure
  • Obstructive shock: obstruction to the pump outflow
  • Distributive shock: altered vascular capacitance

Shock can also be classified physiologically into:

  • Hypoxic: inadequate oxygenation in the lungs
  • Anaemic: adequate oxygenation but inadequate oxygen carriage in the blood
  • Stagnant: adequate oxygenation but inadequate blood flow in the body
  • Histotoxic: adequate oxygenation but tissues unable to utilise the supplied oxygen

Both classification systems can be overly simplistic and shock may be caused by multiple categories within these groups. 

Describe the cardiovascular changes that occur following the acute loss of 1L of blood in an adult

1L of blood loss is a significant amount, being about 20% of total blood volume in an average 70kg person. This will result in a decrease in venous return and thus a decrease in cardiac output via the Frank Starling mechanism. The body’s cardiovascular changes occur with an aim to reduce further blood loss and ensure adequate blood flow to vital organs. The following cardiovascular changes occur:

  • Decreased systolic blood pressure but a smaller decrease or even an increase in diastolic blood pressure, resulting in a narrow pulse pressure. The mean arterial blood pressure is usually decreased. The body is able to maintain a normal arterial pressure for longer than it is able to maintain a normal cardiac output.
  • Initially there will be no change in haemoglobin or haematocrit as whole blood is lost
  • Activation of the baroreflex: the decrease in arterial pressure reduces the firing rate of the baroreceptors. This causes a decrease in vagal tone and an increase in sympathetic tone resulting in increased heart rate and contractility. Within the vasculature, increased sympathetic stimulation causes arteriolar constriction which increases systemic vascular resistance, and venoconstriction which helps to increase venous return. This baroreceptor response can compensate for a 10 -15% loss of total blood volume without significantly affecting cardiac output.
  • Blood flow is redistributed from less important organs to the brain and the heart in order to preserve sufficient oxygen supply to these vital organs. Both the cerebral and coronary circulations have good local blood flow autoregulation, thus helping them to maintain adequate perfusion. The decreased perfusion to other organs can lead to acidosis which activates the chemoreceptors thus causing increased sympathetic activity
  • The Barcroft-Edholm or ‘depressor’ reflex: blood loss causes decreased right atrial pressure. At a certain right atrial pressure the ‘depressor’ reflex is activated by mechanoreceptors within the atrium which then overrides the baroreceptor reflex. This reflex results in increased vagal tone which reduces heart rate and decreases cardiac output, thus hopefully promoting haemostasis by slowing circulation which hopefully reduces bleeding and promotes clot formation. The Barcroft-Edholm reflex is activated after about 15-20% blood loss. However, this reflex is often suppressed in acute blood loss due to increased sympathetic activity from the injury itself, pain and fear.
  • Increased sympathetic activation also stimulates the release of catecholamines from the adrenal gland which further increases sympathetic activity. It also increases the release of cortisol.
  • Renin release is stimulated by increased sympathetic activity, decreased afferent arteriolar pressure and reduced flow of sodium and chloride to the distal tubules. This results in increased levels of angiotensin 2 and aldosterone which results in vasoconstriction, renal afferent and arteriolar vasoconstriction, antidiuretic hormone release and increased renal reabsorption of sodium and water.
  • Cardiopulmonary baroreceptors are activated which also causes the secretion of anti-diuretic hormone from the posterior pituitary. This results in vasoconstriction via the V1 receptors and retention of water in the kidneys via V2 receptors.
  • There is a decrease in capillary hydrostatic pressure due to increased sympathetic activation causing arteriolar vasoconstriction whereas oncotic pressure remains the same. This new imbalance causes a transcellular shift of fluid from the interstitial to the intravascular space which works to restore volume within the intravascular space. This, combined with the renal retention of sodium and water, results in haemodilution and a drop in haemoglobin and haematocrit.
  • There is increased release of erythropoietin within 24 hours of haemorrhage

What are the cardiovascular consequences of PEEP?

Positive end expiratory pressure is the application of positive pressure to expiration so that airway pressure is artificially kept above atmospheric pressure.

Cardiovascular consequences of PEEP differ depending on the cardiac function and fluid status of the patient.

  • Effect on preload
    • Increased PEEP results in increased intrathoracic pressure. Venous return is determined by the gradient between mean systemic venous pressure and right atrial pressure. The right atrial pressure is increased with PEEP which results in a decrease in venous return and thus a decrease in preload. However, this effect is minimised by a compensatory increase in sympathetic tone and an increase in intra-abdominal pressure which increases mean systemic venous pressure. In hypovolemic patients this increase in intra-abdominal pressure can cause collapse of intra-abdominal vein thus decreasing preload further and decreasing cardiac output. Conversely, in patients with acute congestive cardiac failure, the decreased preload may place them back on to a more efficient part of the Frank-Starling curve thus increasing cardiac output.
  • Effect on afterload
    • RV: increased intrathoracic pressure increases pulmonary artery pressure and pulmonary vascular resistance, therefore increasing right ventricular afterload. This increases right ventricular work and oxygen demand and may worsen RV dysfunction. However, the PEEP may improve lung volumes and reverse local hypoxia resulting in vasodilatation of previously constricted vessels. This may then decrease pulmonary vascular resistance and thus RV afterload.
    • LV: increased intrathoracic pressure will decrease LV transmural pressure which decreases LV afterload. This reduction in afterload can be especially beneficial in acute congestive cardiac failure by reducing myocardial oxygen demand, improving cardiac output and reducing pulmonary oedema.
  • Effect on myocardial oxygen consumption
    • PEEP generally decreases myocardial oxygen consumption.
  • Effect on cardiac output
    • The effect of PEEP on cardiac output generally depends on whether the patient is more preload or afterload dependent. Healthy patient’s without cardiovascular disease are generally more preload dependent and PEEP will either cause no significant change to cardiac output or will decrease cardiac output if they are hypovolemic
    • In patients with RV failure, PEEP may decrease cardiac output by decreasing preload and increasing RV afterload
    • Patients with LV failure are generally more afterload dependent and PEEP may therefore increase cardiac output by decreasing afterload

Outline the physiological responses to chronic anaemia

Anaemia is a condition in which the number or oxygen carrying capacity of red blood cells is insufficient to meet physiological needs. Oxygen carrying capacity is determined by the haemoglobin concentration multiplied by the saturation of haemoglobin multiplied by the oxygen binding capacity of haemoglobin plus the amount of dissolved oxygen in the blood. Therefore, a decrease in haemoglobin will significantly affect the oxygen carrying capacity of blood. Oxygen delivery is dependent on oxygen carrying capacity multiplied by cardiac output, therefore in order to maintain oxygen delivery in anaemia, cardiac output must increase. There are several responses that occur with chronic anaemia

  • Decreased peripheral vascular resistance due to decreased blood viscosity and decreased oxygen delivery which causes local vasodilatation
  • Increased cardiac output due to a decrease in total peripheral resistance which deceases afterload and an increase in preload due to decreased blood viscosity. The increased cardiac output helps to offset the reduced oxygen carrying capacity of the blood
  • Redistribution of blood flow to vital organs such as the brain and heart.
  • Increased oxygen extraction: the oxygen extraction ratio increases in the body and there is a decrease in mixed venous oxygen saturation. Coronary and cerebral circulations which already have high oxygen extraction ratios are unable to increase oxygen delivery via this mechanism but this does occur in the kidney, skeletal muscle and skin. 
  • increase in 2,3-DPG which causes a right shift of the haemoglobin oxygen dissociation curve
  • Stimulation of erythropoietin and angiogenesis

List the changes to cardiovascular physiology in a healthy elderly person

  • Myocardial
    • Structure:
      • Concentric ventricular hypertrophy causing an increase in cardiac size
      • Hypertrophy of myocytes but decrease in myocyte number
      • Increase in atrial size
      • Change in overall shape from elliptical to spheroid with an asymmetric increase in the intraventricular septum more than the free wall
      • Increase in valvular circumference
    • Systolic function
      • Overall resting systolic function does not change
    • Diastolic function
      • Decrease in diastolic compliance and ventricular filling, especially in the early or passive diastolic phase. As ventricular filling is more reliant on later or active filling it becomes more reliant on atrial contraction for filling.
      • Increase in isovolumetric relaxation time
    • Cardiac output
      • Decrease in cardiac output
      • Increased left ventricular afterload
    • Cardiac conduction system
      • Fat accumulation around the sinoatrial node and decrease in number of pacemaker cells
      • Increase in PR interval, leftward QRS shift, blunted respiratory sinus arrhythmia
    • Autonomic and integrated response
      • Decreased autonomic receptor number and density and therefore decreased sensitivity to catecholamines
      • Decrease in maximum heart rate
      • Decrease in maximum ejection fraction during exercise
      • Impaired baroreceptor reflex
  • Vasculature
    • Thickened intima and media of vasculature resulting in reduced distensibility, increased total peripheral resistance, increased pulse pressure and MAP
    • Decreased nitric oxide release
    • Increased diameter of aortic root

Outline the cardiovascular changes associated with morbid obesity

Morbid obesity is defined as a body mass index of over 40 or a BMI of over 30 and experiencing obesity related health problems. The cardiovascular effects of obesity are inter-related and complex but can be sub-divided into cardiac, vascular and hormonal changes.

  • Cardiac
    • LV hypertrophy secondary to increased afterload due to hypertension and/or volume overload.
    • RV hypertrophy secondary to LV diastolic failure and/or increased pulmonary vascular resistance from chronic hypoxia
    • Fatty infiltration of myocardium and cardiac conduction system which increases the risk of arrhythmias. This risk is also increased due to the increased incidence of hypoxia, hypercapnoea, coronary artery disease, increased circulating catecholamines and OSA in the obese population.
    • Impaired left ventricular systolic function, especially during exercise, with a slower and smaller rise in ejection fraction
    • Diastolic dysfunction secondary to myocardial fibrosis which impairs relaxation and LV dilatation which increases wall stress and reduces compliance.
    • Increased stroke volume, cardiac output and left ventricular end diastolic pressure
    • Heart rate is usually unchanged
  • Vascular
    • Increased total blood volume due to increased angiotensin 2 and aldosterone. Splanchnic blood flow is increased but renal and cerebral blood flow remains the same.
    • Increased oxygen consumption due to increased size
    • Endothelial dysfunction due to hormonal factors which increases the risk of atherosclerotic disease
    • Increased blood pressure
  • Hormonal:
    • Increased leptin secreted by fat which contributes to left ventricular hypertrophy
    • Increased angiotensinogen which increases angiotensin 2 and aldosterone and results in hypertension, sodium and water retention and LV hypertrophy
    • Increased plasminogen activator inhibitor 1 which reduces fibrinolysis and therefore increases the risk of thromboembolic disease
    • Increased catecholamines which increase contractility and systemic vascular resistance
    • Increased inflammatory adipokines which impair endothelial function and increase systemic vascular resistance

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