Cardiac Output (CO) is the amount of blood pumped by the ventricles each minute. It is the product of Heart Rate (HR) and Stroke Volume (the amount of blood ejected by the ventricle with each contraction).
CO=HR x SV
Normal C.O. = 4-8 L/min
* These values are relative to size*- What may be normal for a 5ft tall 80 yo 40 kg woman may be totally inadequate for a 6 ft 100kg man. So we use Cardiac Index to adjust to individual body size.
Cardiac Index = CO/the person's Body Surface Area
One of the first things you will see with a decreased cardiac output is a decrease in Urine Output. Never ignore a patient who has a sudden decrease in urine output! It is the poor man's predictor or cardiac output.
Increased Heart Rate effects on CO
In a normal, healthy individual, an increase in heart rate can lead to an increase in CO.
However, in a person with cardiac dysfunction or disease, increases in heart rate can lead to a decreased CO and sometimes even ischemia. Why?
Increased heart rate decreases the ventricular filling time, by reducing preload, which decreases stroke volume and leads to decreased CO - in other words....
The faster the heart beats the less time it has to fill with blood before it pumps it out.
Decreased Heart Rate effects on CO
A lower heart rate does not necessarily result in a lower CO. Decreased heart rates are often found in athletes or healthy individuals and they have a normal CO. Their heart muscle is strengthened and it causes an increase in the amount of blood pumped out with each beat (Stroke Volume).
In individuals with Left Ventricular dysfunction, a slow heart rate can produce a decrease in CO. This is caused by a decrease in contractility (the muscle is weaker and not able to contract as well as it should). Also fewer heart contractions every minute causes decreased cardiac output simply because the heart is squeezing less often. Fewer squeezes = less blood pumped.
Since CO is a product of Stroke Volume and Heart Rate, changes in HR can affect SV and changes in SV can affect HR.
Stroke Volume increases - heart rate can decrease (as seen in athletes)
Stroke Volume falls - heart rate increases (to try and compensate)
Evaluating the cause of the tachycardia becomes an essential component of hemodynamic assessment. Bradycardia and tachycardia are potentially dangerous because they may result in a decrease in CO if adequate stroke volume is not maintained. Sudden onset bradycardia is almost always reflective of a falling Cardiac Output. The cause of tachycardia on the other hand must be determined because it may not reflect a low output state but rather a normal physiologic response (ex tachycardia due to fever).
Stroke Volume is the amount of blood ejected from each ventricle with each heart beat. The right and left ventricle eject nearly the same amount, which is normally from 50-100 ml/ heart beat.
Ever see SVI and wonder what that means? Well it is the Stroke Volume Index. Just like Cardiac Index it takes into account the patient's size.
Normal SVI = 35-60 ml/beat
Stroke Volume is affected by Preload, Afterload, and Contractility.
Preload is the volume of blood that exerts a force or pressure (stretch) on the ventricles during diastole.
It may also be described as the filling pressure of the ventricles at the end of diastole or the amount of blood that fills the ventricles during diastole.
Preload is determined primarily by the amount of venous return to the heart. Venous constriction or dilation,and alterations in the total blood volume all affect preload. Preload decreases with volume change.
Decreased preload can occur in hemorrhage, diuresis, vomiting and diarrhea, third spacing, redistribution of blood flow and profound diaphoresis. Venous dilation also results in diminished preload. Etiologies that increase venous pooling and decreased venous return to the heart can include hyperthermia septic shock, anaphylactic shock, and drug administration.
Increased preload includes excessive fluid resuscitation and renal failure. Venous constriction results in teh shunting of peripheral blood to the central organs The increased venous return results in an increased preload. This may happen in hypothermia, some forms of shock, and with drugs that stimulate alpha receptors.
Frank Starling's Law of the heart states that the greater the stretch (preload) the greater the force of contraction.... to a point....
Think of it like a rubber band, the further you stretch the rubber band the farther it shoots when you let go. That is until you stretch the rubber band out so far that is can not bounce back. The same principle applies to the heart. The more amount of blood that fills before contraction (preload) the better cardiac output, until the heart becomes so stretched out it can't contract well anymore, like in some cardiomyopathies.
So increasing preload helps improve cardiac output, but only to a certain point.
Afterload is the resistance to the ventricles emptying during systole (contraction). It is the pressure or resistance that the ventricles must overcome to open the aortic and pulmonic valves and to pump blood into the systemic and pulmonary vasculature.
Vascular resistance is determined by three things:
1. the length of a vessel
2. the diameter or radius of that vessel
3. the viscosity (the measure of a fluid's resistance to flow) of the blood
As afterload increases (vasoconstriction or obstruction)the heart must work harder to eject the volume. With increased afterload the heart works harder to eject contents leading to increased myocardial oxygen demand.
Increased afterload causes: Decreased Afterload causes:
- pulomonic stenosis - hyperthermia
- hypothermia - distributive shock (septic, anaphylactic,etc)
- hypertension - vasodilating drugs (nitro. Beta Blockers, CA -
- classic shock states channel blockers, nipride)
- drugs that stimulate alpha receptors
(epi, levo, dopamine, phynelephrine)
- the body's compensatory response to hypotension and decreased CO