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Cardio Vascular Physiology

SRI LANKA COLLEGE OF PAEDIATRICIANS; EDUCATION & TRAINING 1

Cardiovascular system

Function is:Delivery of oxygen and nutrientsRemoval of waste products

Flow is important


The cardiovascular system allows blood to circulate through the body to transport and deliver:-Oxygen-Nutrients to the tissues such as electrolytes and amino acids It also removes C02 and waste products from the tissues (so the body can then eliminate them)In order to achieve those functions, we have to maintain good blood FLOW to these organs and tissues

Direction of blood flow


Your heart works as a pump that in which arteries carry oxygen rich blood away from the heart to the organs, tissues, and cells of your body. After the oxygen has been delivered this now deoxygenated blood is returned back to heart and into the pulmonary circuit to become oxygenated again.

Flow requires pressure

Autoregulation

Flow

Pressure


For most healthy individuals, the body will "autoregulate" the blood flow to the tissues within a wide range of blood pressures, meaning that even at somewhat low or somewhat high pressures, the tissues will receive a relatively stable blood flow. For a healthy person, the blood pressure usually has to drop VERY low for us to lose adequate blood flow to the tissues, or to be VERY high for us to get too much. In the middle, the body maintains a balance.

Flow requires pressure

AutoregulationFl

ow

Pressure


In critically ill patients, thisautoregulation becomes lesseffective, meaning that the body isless able to maintain stable bloodflow in the lower or the higherblood pressure ranges. Becauseof this, critically ill patients requiremore tight regulation of bloodpressure to maintain blood flow toorgans and tissues.

Determinants of blood pressure

MAP=CO x TPR


So, in critically ill patients, it becomes more important to avoid low or high pressures. In order to understand how to do this, we first have to look at the components that make up blood pressure – how do we break it down?Blood pressure is determined by two main components:• Cardiac output – the amount of blood pumped out by the heart in one minute• Total peripheral resistance – the squeeze or relaxation of the blood vesselsThink of this as a simple system of water delivery to a village with a pump and flexible hoses - when we have a problem with blood pressure, is it a problem with the pump (cardiac output)? Or is it a problem with the hoses (peripheral resistance)?

CO=HR x SV

Cardiac output


Cardiac output is made up of • Heart rate – the number of beats per minute• Stroke volume – the volume of blood pumped

out by the heart with each contraction

Heart rate

Sino-atrial node

Atrio-ventricular node

Specialized conduction

fibres


What controls how fast the heart beats?The specialized electrical system in the heart haspacemaker cells that discharge in a chain reaction thatcauses the heart muscle to contract. How fast or slowthese cells discharge is affected by neurotransmitterslike adrenaline and our own sympathetic andparasympathetic nervous systems. (think of the fight orflight response, for example)

The electrical impulse starts with the sino-atrial (SA)node, spreads across the atria to cause them to contract,then the impulse travels to the atrio-ventricular (AV) nodeand down specialized conduction fibres to the ventricles,causing them to contract. So the SA node is the primarypacemaker (it controls how quickly the heart beats), butif this fails, then the AV node may take over, or even theelectrical fibers in the ventricles.

Stroke volume

Preload

Afterload

Contractility


So, we've talked about one part of Cardiac Output – the heart rate (CO=HR x SV)Now, about the stroke volume (volume of blood ejected in one beat)This breaks down more specifically the variables that affect the heart pumping action.

Preload


Preload is the end diastolic volume that stretches the ventricle of the heart to its greatest dimensions under variable physiologic demand. Or put more simply preload – is the degree to which the ventricle is stretched prior to contraction.

The filling of the heart with blood volume during diastole stretches the heart muscle in a way that prepares it to contract, like a rubber band – when it is stretched, it will snap back more forcefully.

Preload

Volume loading

Card

iac

outp

ut


So, if there is a problem with preload, suchas with hypovolemia, the preload can beincreased by infusing fluid volume. As weinfuse more fluid, the stretch on the heartincreases – the preload goes up. At first,this causes the stroke volume and cardiacoutput to increase, but eventually, the heartreaches a plateau point where infusingmore fluid no longer helps to increasecardiac output. In addition, further fluidloading of the patient can causecomplications.

Pulmonarycapillary

Lymphaticduct

Alveolar space

Interstitium



One of the main adverse effects of excessive fluid loading is pulmonary edema.

When too much fluid loading occurs, the volume and the pressure inside the left ventricle begin to rise. The heart has been attempting to pump the volume out forward, but once it cannot keep up, this excess pressure is translated backward

• from the left ventricle, to the left atrium• from the left atrium back to the pulmonary vasculature• eventually affecting the pulmonary veins and pulmonary capillary bed

As the pressure inside the pulmonary capillaries increases, this upsets the fluid balance in the alveolar walls

Normally, the body maintains a fluid balance in the pulmonary capillaries by two different pressure systems. Hydrostatic pressure – the pressure created inside the capillary from the blood flow and resistance. An increased greater pressure here has the effect of pushing fluid out into the tissues. Oncotic pressure – the pressure exerted by large molecules in the blood that pulls fluid toward them. This pressure tries to keep fluid inside the capillaries.

Normally these balance each other. There is a slightly greater push of fluid out than the pull of fluid in, so some fluid goes into the interstitium, but…


Normally these balance each other. There is a slightly greater push of fluid out than the pull of fluid in, so some fluid goes into the interstitium, but……this is drained by the lymphatic systemUp to a certain point…

pulmonarycapillarypressure



The balance is lost after a certain point when the hydrostatic pressure in the capillaries increases because of the increased pressure translated back from the left ventricle.

• fluid moves out into the alveolar tissue• the lymphatic system can no longer keep up with the drainage• so the fluid builds up within the alveolar interstitium and also leaks into the alveolus

What happens to gas exchange when alveoli and surrounding tissues are full of fluid?

Exactly – gas exchange will be impaired or nonexistent, creating a shunt (blood flow but no gas exchange), and a fall in oxygen saturation.

So remember, adequate preload is important, and we give volume to achieve it, but we must be aware of the complications – especially pulmonary edema, if we give too much.

When fluid present within the alveoli, it prcoduces the SHUNT effect leading to fall in oxygen saturation.

Afterload

Measure of the resistance to ejection of blood

by vasoconstriction

by vasodilatation


So basically, this is the resistance that the heart has to pump against in order to get the blood flow out of the heart and to the tissues. Recognize that an increase in afterload will decrease cardiac output. If we increase the resistance against which the heart has to pump, it becomes harder to eject blood. The opposite, of course, is also true. If we decrease our afterload (we vasodilate, opening up more space for the blood to flow out), this will increase our cardiac output. So, remember the effects that vasodilators and vasoconstrictors can have on your afterload, and therefore, your cardiac output. This is especially important to remember in patients who have a weakened heart muscle, such as those with heart failure or after a myocardial infarction. Those patients cannot tolerate hypertension well because their heart cannot handle the increase in afterload.


Contractility

by sympathetic activation and inotropes

by drugs (eg β blockers), hypoxia, acidosis, sepsis


Now we come to the last component of stroke volume – the contractility. "How well does this muscle function as a pump?"

Contractility can be increased by activation of our own sympathetic nervous system (think "fight or flight"), and by certain drugs such as inotropes

Contractility can be decreased by many factors, including drugs (such as beta blockers), acute factors such as hypoxia and sepsis, or by a damaged or weakened heart muscle itself, as is the case for those with heart failure.

Effect of mechanical ventilation

-ve pressure +ve pressure



Now that we've discussed all the components that affect blood flow, let's discuss the effect of mechanical ventilation on cardiac output.

Normal spontaneous breathing is based on a negative pressure system – the chest wall moves out, the diaphragm moves down, and this pulls the lungs open and sucks air inward. This negative pressure also helps to pull blood into the chest, another factor that helps to increase the return of blood to the heart (increases preload).

If the patient is mechanically ventilated, is this a negative pressure system or a positive pressure system?

Positive pressure now is pushing air into the lungs and chest. There is no longer a negative pressure in the chest to pull blood back to the heart. The positive pressure makes the blood work harder to return to the heart and decreases the preload.

Effect of mechanical ventilation

Afterload also reduced

afterload cardiac output

preload cardiac output

Net effect depends on LV. In general:Normal LV, cardiac output Failing LV, cardiac output



So will a patient who is intubated and started on mechanical ventilation likely have a decrease in cardiac output? It depends…

The positive pressure system of mechanical ventilation decreases the preload, but it also decreases the afterload.

Remember that a decrease in preload will usually decrease cardiac output…But an decrease in afterload will usually increase cardiac output

So there are two opposing forces at work and the way the patient is affected will usually depend on the condition of the patient's heart muscle before intubation.

If the patient has a normal left ventricle, the heart can effectively pump blood out and does not need a decrease in afterload, but a decrease in preload can be enough to cause a decrease in cardiac output, especially if the patient is already hypovolemic.

If the patient has a failing left ventricle, that ventricle already has difficulty pumping blood out, so it will respond well to a decrease in the afterload because this decreases the workload on the heart. These patients may show an increase in cardiac output.

The haemodynamic effects of PPV are more prevalent in the patient that is hypovolemic, patients with poor cardiac reserve and when PEEP is applied.

Response to hypovolaemia


Cardiovascular response to intravascular hypovolaemia.

It is important to understand this response, appreciate that considerable intravascular depletion is required before the blood pressure falls and understand how to detect signs of hypovolaemia at an early stage.

What are some signs of hypovolaemia?

-tachycardia-low CVP-Oliguria or anuria-Low BP


Venous capacitance vessels

Arterioles

Carotid bodies


Key components in this system include the carotid bodies, venous capacitance vessels, arterioles, sympathetic system and the heart



Hypovolaemia causes a fall in cardiacpreload which reduces cardiac outputand produces a small fall in bloodpressure. This is immediately detectedby the carotid bodies and theinformation is relayed to thevasomotor center in the brainstem



Resulting in an activation of the sympathetic system causing release of adrenaline from the adrenals



A direct effect, via the sympathetic nervous system, on the venous capacitance vessels (which act as a reservoir of blood)


Constriction of venous capacitance vessels


Causing venoconstriction. This restores the preload to normal and thus restores cardiac output and blood pressure. At this stage the hypovolaemia is undetectable.If the intravascular fluid loss continues the preload can no longer be maintained


Heart rate

Arteriolar constriction

Low JVP


If further volume loss occurs peripheral arterioles constrict to maintain blood pressure and flow to vital organs and the heart rate rises. Again this is mediated by the sympathetic nervous system.

At this stage the compensation is manifest as what?

Tachycardia, cold peripheries, skin mottling, slow capillary refill and low JVP., increased lactate


BP only falls if all these mechanisms are insufficient

Hypotension is a late feature of hypovolaemia



Summary

Homeostatic mechanisms to maintain CO and MAP

Mechanical ventilation reduces preload and afterload

MAP=CO x TPR

HR x SV

Preload, afterload, contractility


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