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The cardiac output is equal to the volume of blood ejected from the heart with each contraction multiplied by the number of contractions per minute (i.e., the heart rate).
Cardiac Output = Stroke Volume x Heart Rate
Let’s look at stroke volume and heart rate separately, then put them together.
Heart Rate
The heart has the very important property of automaticity, which means that the heart spontaneously contracts, even if it is isolated from all neural and hormonal inputs. This is an essential feature because it means that under conditions in which the external inputs to the heart are lost, the intrinsic activity of the heart will allow it to continue to pump blood into the vasculature.
The physical source of automaticity in the normal heart is the sino-atrial (SA) node, a small cluster of specialized cells located in the right atrium. These cells spontaneously depolarize and produce action potentials, which are then propagated throughout the heart.
The rate at which action potentials are spontaneously generated by the SA node can be influenced by the autonomic nervous system (ANS). Input from the parasympathetic branch slows the spontaneous activity, whereas input from the sympathetic branch speeds up the spontaneous activity. The relative activity in the parasympathetic versus the sympathetic inputs depends on need: when a high level of cardiac output is needed the sympathetic activity increases, and, when we are resting, the parasympathetic activity is predominant.
The autonomic nervous system (Figure 1), in turn, is regulated by the central nervous system (CNS). The CNS receives information from baroreceptors (pressure-sensitive receptors in the vasculature) that monitor the blood pressure. This information enables the CNS to make adjustments to the heart rate to keep the blood pressure at a proper level. The CNS also includes control centers and pathways that can link the emotional state of a person to the control of the autonomic inputs to the heart. That is the reason that a frightening stimulus can rapidly increase our heart rate in preparation for a strenuous response to a stimulus, or, alternatively, eating a meal and relaxing on the couch can produce a slow heart rate.
Stroke Volume
Determinants of stroke volume
It is easy to define stroke volume as the volume of blood ejected from each ventricle of the heart with each contraction, but it is a more difficult task to identify all of the factors that can influence it. We will begin with a few basic features, and then give a more complete view at a later date.
Let’s begin by focusing on two phases of the cardiac cycle:
(1) the filling of the heart with blood when the cardiac muscle is relaxed (diastole) and
(2) the ejection of blood during ventricular contraction (systole).
Thinking back to our general model, the blood that is pushed out of the heart and into the arteries travels through the vasculature and is returned to the heart through the veins. Under normal conditions, the volume of blood that is ejected (pushed out) of the heart must be equal to the volume that is returned to the heart (i.e., it is a closed system). Although the pressure of the blood at the entrance to the upper chambers of the heart (the atria) is much lower than the pressure in the arteries, it is sufficient to push blood through the atria and into the lower chambers of the heart (the ventricles). This passive flow of blood into the heart during diastole begins a process of preloading the heart with blood, in which the prefix “pre-“ refers to the pressure in the ventricle produced by blood filling and stretching the heart before the beginning of systole. The volume of blood preloaded into the heart during diastole is the end-diastolic volume. Contraction of the heart can only eject a fraction of the end-diastolic volume. It is important, therefore, that the end-diastolic volume be large enough to produce a sufficient stroke volume.
During systole, blood is pushed from the atria into the ventricles, which, after a brief delay, begin to contract. When the pressure in the ventricles rises above the pressure in the aorta, blood can flow out of the ventricles and into the vasculature. Contraction of the ventricles cannot squeeze all of the blood out of the ventricles, and the residual volume of blood left in the ventricles is the end-systolic volume. We can calculate the stroke volume as the difference between the volume of blood loaded into the heart during diastole (the end-diastolic volume) and the volume of blood remaining at the end of systole (the end-systolic volume).
Stroke volume = end-diastolic volume – end-systolic volume
The extent to which blood can be squeezed out of the ventricles during systole is related to the contractility of the cardiac muscle. The more forcefully the muscle contracts, the greater the fraction of preloaded blood that can be ejected. Therefore, one mechanism for controlling stroke volume is to control contractility. The sympathetic input to the heart does this, with increased sympathetic activity increasing contractility and stroke volume (your pounding heart when frightened!).
There are several additional factors that influence stroke volume, but focusing on preload and contractility will be sufficient for now.
Putting Heart Rate and Stroke Volume together in a model of Cardiac Output
We can combine the two models described above (Figure 3), recognizing that the sympathetic input to the heart plays a role in controlling both heart rate and stroke volume, whereas parasympathetic input only significantly affects heart rate.
Resource
Now that you have explored some determinants of blood pressure, this video (see the WLM on JiT) will help you look more closely at how the body manipulates those determinants. It will also prepare you for the Key Concepts that follow.
We will discuss the treatment of hypertension in detail next week, but let’s introduce a few basic approaches now that will help bring together many of the key concepts in this Weekend Learning Module. The important relationships to remember are:
Mean Arterial Pressure = Cardiac Output * Systemic Vascular Resistance
and
Cardiac Output = Stroke Volume x Heart Rate
With these relationships in mind, it is clear that we can lower blood pressure by decreasing cardiac output and/or decreasing systemic vascular resistance. And, we can decrease cardiac output by decreasing heart rate or stroke volume. Therefore, the three parameters of primary interest are heart rate, stroke volume, and systemic vascular resistance. Let’s take a closer look at how we can decrease each of these parameters:
- Heart Rate: Drugs that block ß1 receptors will decrease the stimulation of the SA node pacemaker cells and slow the heart rate.
- Stroke Volume: This is a little more complicated. We can decrease the contractility of the heart by using drugs that block ß1 receptors. A less direct, but equally important approach is to decrease blood volume. By decreasing blood volume, we decrease the central venous pressure and the preloading of the heart during diastole. One approach to decreasing blood volume is to use drugs to inhibit the formation of Angiotensin II—these include the ACE inhibitor drugs. A second approach is to use drugs that increase the formation of urine (i.e., diuresis). These drugs are diuretics.
- Systemic Vascular Resistance: The systemic vascular resistance is primarily dependent on the “tone” of the arterioles, and our goal is to relax (vasodilate) the arterioles. Drugs that block \alpha1 receptors will decrease the vasoconstriction produced by norepinephrine and epinephrine. We can also use drugs that decrease the size of the calcium signals required to stimulate contraction of vascular smooth muscle. These include the calcium channel blockers.
This is a very brief overview of four basic mechanisms for lowering blood pressure: (1) decreasing heart rate; (2) decreasing contractility which decreases stroke volume; (3) decreasing blood volume which can also decrease stroke volume; and (4) decreasing systemic vascular resistance. We will discuss these mechanisms in much greater detail next week.