3. Distribution of cardiac output and its disorders in the young and the elderly

Last updated on May 24, 2019 at 11:40


Heart failure is the condition where the heart is unable to pump enough blood to meet the needs of the body. People with failing hearts must redistribute their cardiac output from less important organs like the intestines and kidneys to their muscles.

Most failing heart can maintain a 5 L/min resting cardiac output. Only when the demand for CO increases will the failing heart cause symptoms.

People with heart failure utilize three compensatory mechanisms to try to increase their CO:

  • Activation of RAAS -> increased salt and water retention
  • High sympathetic activity -> increased heart rate
  • Hypertrophy of the left ventricle

These compensatory mechanisms manage to increase the CO, but they cause other problems.

Cardiac output distribution

In rest is the cardiac output distributed as follows:

  • Veins have 75-80%, arteries have 15% and the capillaries have 5-10% of the blood volume
  • The brain receives 15% of CO
  • The splanchnic organs receive 30%
  • The skin receives 10%
  • The kidneys receive 25%
  • The coronaries receive 5%

Along with the table in topic 2.

As we saw in the previous topic, the hearts of healthy people have a capacity to increase their cardiac outputs significantly when needed. They have a large reserve capacity. This reserve capacity is reduced in old age but is still considerable. However, sick and failing hearts don’t have a lot of reserve capacity; the most failing hearts may even be unable to uphold the resting cardiac output of 5 L/min!

Note that “Sick” here means a severely failing heart, not a patient with a flu. Also, most heart failures have some reserve capacity, unlike what’s seen here.
Heart failure

When the heart is unable to pump sufficiently to maintain the CO to meet the body’s needs, there is heart failure. In most cases when we talk about heart failure we mean chronic heart failure, which the patient cannot be cured of. Many forms of heart failure exist, as we will see.

Heart failure is not an etiology; it’s a clinical syndrome. There are many causes of heart failure. Almost all cases are caused either by hypertension or ischaemic heart disease like heart attacks.

The left ventricle and the right ventricle may fail separately, but the failure of one ventricle usually leads to the failure of the other. More about this in later topics.

When a person with a failing heart needs to increase the cardiac output due to activity is the increase mostly accomplished by tachycardia. This is not ideal due to the impaired coronary blood flow. The heart will therefore try to increase the EDV to increase the CO.

Failing hearts often have hypertrophied ventricles. When ventricles are hypertrophied do they lose some of their compliance, meaning that they are not as easily distensible. When ventricles are less compliant does it become more difficult to fill them up. Because of this can’t the EDV be increased without a higher end-diastolic pressure (EDp). This increased pressure will increase wall tension in the ventricle and impair the subendocardial blood flow. More about this here.

The serum levels of brain natriuretic peptide (BNP, which is produced in the ventricles despite the name) correlates closely with the degree of heart failure.

Compensatory mechanisms

In heart failure will these three compensatory mechanisms try to compensate for the insufficient cardiac output:

  • Decreased stimulation of baroreceptors -> sympathetic activity ↑ -> Heart rate ↑, contractility ↑
  • Low CO -> GFR ↓ -> RAAS activation -> salt and water retention ↑ -> preload ↑
  • EDp ↑ -> Hypertrophy of ventricles

The cardiac output increase by these mechanisms is significant, which enables patients with heart failure to maintain a 5 L/min CO in rest, despite their failing heart. However their reserve capacity is always smaller than in healthy individuals.

Patients with heart failure are mostly well-compensated while resting and doing nothing. However, once they do anything that increases the body’s need for cardiac output, like walking up stairs, experiencing heat or do light exercise will the compensatory mechanisms be unable to keep up with the required cardiac output. Most patients with heart failure are in this subcompensated state, meaning that they are compensated in rest, and so they only experience symptoms during exercise when the heart becomes decompensated. The worse the degree of heart failure, the less activity can the patient do before experiencing symptoms.

Decompensation is the state where a patient with heart failure starts to experience symptoms of temporary cardiac output insufficiency, like early fatigue and tiredness, dyspnoea and nocturia, or when the compensatory mechanisms themselves produce symptoms, like tachycardia or venous congestion. It’s called decompensation because there are no further compensatory mechanisms that can increase the cardiac output. Most patients only get decompensated during activity so that the symptoms will improve with rest. 

In end-stage (severe) heart failures will it be difficult to maintain cardiac output even in rest with these compensatory mechanisms. In these cases will blood be redistributed between organs, to keep the vital organs (brain, heart) perfused sufficiently while the other organs go hypoperfused. This will lead to cardiogenic shock. In end-stage chronic heart failure will every organ except the brain receive less than normal blood perfusion because the CO can be as low as 3.5 L/min!

The amount of exercise a patient can do before becoming decompensated obviously depends on the degree of heart failure. The New York Heart Association (NYHA) has created a classification system for heart failure that is widely used. It’s very simple:

  • NYHA I – Heart failure with no clinical symptoms
  • NYHA II – Heart failure symptoms occur after walking 2-3 flights of stairs
  • NYHA III – Heart failure symptoms occur after walking on flat ground
  • NYHA IV – Heart failure symptoms occur during rest or minimal activity

Previous page:
2. Cardiovascular adaptation in health and disease

Next page:
4. Causes and forms of heart failure

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