Forward movement of blood occurs when the arterial wall boundaries are pliable and compliant. These properties allow the arterial wall to distend when pressure increases, resulting in a pulse that can be detected by touch.
Exercise, environmental stress, or psychological stress can cause the heart rate to increase above the resting rate. The pulse is the most straightforward way of measuring the heart rate, but it can be a crude and inaccurate measurement when cardiac output is low. In these cases as happens in some arrhythmias , there is little pressure change and no corresponding change in pulse, and the heart rate may be considerably higher than the measured pulse.
Every single heartbeat includes three major stages: atrial systole, ventricular systole, and complete cardiac diastole. Throughout the cardiac cycle, the arterial blood pressure increases during the phases of active ventricular contraction and decreases during ventricular filling and atrial systole. Thus, there are two types of measurable blood pressure: systolic during contraction and diastolic during relaxation.
Systolic blood pressure is always higher than diastolic blood pressure, generally presented as a ratio in which systolic blood pressure is over diastolic blood pressure. Pressures higher than that range may indicate hypertension, while lower pressures may indicate hypotension. Blood pressure is a regulated variable that is directly related to blood volume, based on cardiac output during the cardiac cycle.
Cardiac output Q or CO is the volume of blood pumped by the heart, in particular by the left or right ventricle, in one minute. While there are many clinical techniques to measure CO, it is best described as a physiological and mathematical relationship between different variables. When one of the variables change, CO as a whole will change as a result. This can also be used to predict other regulated variables, such as blood pressure and blood volume.
The heart rate is determined by spontaneous action potential generation in the sinoatrial SA node and conduction in the atrioventricular AV node. It refers to the number of heartbeats over the course of a minute.
Sympathetic nervous system activation will stimulate the SA and AV nodes to increase the heart rate, which will increase cardiac output.
Parasympathetic nervous system activation will conversely act on the SA and AV nodes to decrease the heart rate, which will decrease cardiac output. Stroke volume refers to the amount of blood ejected from the heart during a single beat. Contractility of the heart refers to the variability in how much blood the heart ejects based on changes in stroke volume rather than than changes in heart rate. Additionally, another indicator known as the ejection fraction EF is used to evaluate stroke volume and contractility.
A higher EF suggests more efficient heart activity. Cardiac output is an indicator of mean arterial blood pressure MAP , the average measure of blood pressure within the body. TPR is a measure of resistance in the blood vessels, which acts as the force by which blood must overcome to flow through the arteries determined by the diameter of the blood vessels. The exact relationship is such that a twofold increase in blood vessel diameter doubling the diameter would decrease resistance by fold, and the opposite is true as well.
CO can also predict blood pressure based on blood volume. Essentially, this means that higher venous blood return to the heart also called the preload will increase SV, which will in turn increase CO. This is because sarcomeres are stretched further when EDV increases, allowing the heart to eject more blood and keep the same ESV if no other factors change.
The main implication of this law is that increases in blood volume or blood return to the heart will increase cardiac output, which will lead to an increase in MAP.
The opposite scenario is true as well. For example, a dehydrated person will have a low blood volume and lower venous return to the heart, which will decrease cardiac output and blood pressure. Those that stand up quickly after lying down may feel light-headed because their venous return to the heart is momentarily impaired by gravity, temporarily decreasing blood pressure and supply to the brain.
The adjustment for blood pressure is a quick process, while blood volume is slowly altered. Blood volume itself is another regulated variable, regulated slowly through complex processes in the renal system that alter blood pressure based on the Starling mechanism.
During a single cardiac cycle, the atria and ventricles do not beat simultaneously; the atrial contraction occurs prior to ventricular contraction. This timing delay allows for proper filling of all four chambers of the heart. Recall that the left and right heart pumps function in parallel. The diastolic phase of the cardiac cycle begins with the opening of the tricuspid and mitral valves atrioventricular valves. The atrioventricular valves open when the pressures in the ventricles fall below those in the atria.
This can be observed in here for the left heart, in which the mitral valve opens when the left ventricular pressure falls below the left atrial pressure. Expiration partially restricts blood flow into the left side of the heart and may amplify left-sided heart murmurs. Figure 4 indicates proper placement of the bell of the stethoscope to facilitate auscultation. Figure 4. Proper placement of the bell of the stethoscope facilitates auscultation.
At each of the four locations on the chest, a different valve can be heard. The cardiac cycle comprises a complete relaxation and contraction of both the atria and ventricles, and lasts approximately 0.
Beginning with all chambers in diastole, blood flows passively from the veins into the atria and past the atrioventricular valves into the ventricles. The atria begin to contract atrial systole , following depolarization of the atria, and pump blood into the ventricles. The ventricles begin to contract ventricular systole , raising pressure within the ventricles.
When ventricular pressure rises above the pressure in the atria, blood flows toward the atria, producing the first heart sound, S 1 or lub. As pressure in the ventricles rises above two major arteries, blood pushes open the two semilunar valves and moves into the pulmonary trunk and aorta in the ventricular ejection phase. Following ventricular repolarization, the ventricles begin to relax ventricular diastole , and pressure within the ventricles drops.
As ventricular pressure drops, there is a tendency for blood to flow back into the atria from the major arteries, producing the dicrotic notch in the ECG and closing the two semilunar valves. The second heart sound, S 2 or dub, occurs when the semilunar valves close. When the pressure falls below that of the atria, blood moves from the atria into the ventricles, opening the atrioventricular valves and marking one complete heart cycle. The valves prevent backflow of blood.
Failure of the valves to operate properly produces turbulent blood flow within the heart; the resulting heart murmur can often be heard with a stethoscope. Answer the question s below to see how well you understand the topics covered in the previous section. Skip to main content. Search for:. Critical Thinking Question Describe one cardiac cycle, beginning with both atria and ventricles relaxed. Show an Example Answer The cardiac cycle comprises a complete relaxation and contraction of both the atria and ventricles, and lasts approximately 0.
The atria begin to contract following depolarization of the atria and pump blood into the ventricles. The ventricles begin to contract, raising pressure within the ventricles.
When ventricular pressure rises above the pressure in the two major arteries, blood pushes open the two semilunar valves and moves into the pulmonary trunk and aorta in the ventricular ejection phase. Following ventricular repolarization, the ventricles begin to relax, and pressure within the ventricles drops.
Activation of the Heart and the ECG The drawings to the right in the table below show the main stages of activation of the heart, as well as the ECG recorded in lead II at those stages. The electrical activity of the heart originates in the sino-atrial node.
The impulse then rapidly spreads through the right atrium to the atrioventricular node. It also spreads through the atrial muscle directly from the right atrium to the left atrium. The P-wave is generated by activation of the muscle of both atria. The impulse travels very slowly through the AV node, then very quickly through the bundle of His, then the bundle branches, the Purkinje network, and finally the ventricular muscle.
The first area of the ventricular muscle to be activated is the interventricular septum, which activates from left to right. This generates the Q-wave. Next, the left and right ventricular free walls, which form the bulk of the muscle of both ventricles, gets activated, with the endocardial surface being activated before the epicardial surface.
This generates the R-wave. A few small areas of the ventricles are activated at a rather late stage.
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