Therefore, increased venous pressure or decreased right atrial pressure, or decreased venous resistance leads to an increase in venous return. P RA is normally very low fluctuating a few mmHg around a mean of 0 mmHg and P V in peripheral veins when the body is supine is only a few mmHg higher. Because of this, small changes of only a few mmHg pressure in either P V or P RA can cause a large percent change in the pressure gradient, and therefore significantly alter the return of blood to the right atrium.
For example, during lung expansion inspiration , P RA can transiently fall by several mmHg, whereas the P V in the abdominal compartment may increase by a few mmHg. These changes result in a large increase in the pressure gradient driving venous return from the peripheral circulation to the right atrium.
Although the above relationship is true for the hemodynamic factors that determine the flow of blood from peripheral veins abdominal venous cava in the figure back to the right atrium of the heart, it is important not to lose sight of the fact that blood flow through the entire systemic circulation can be represented by either the cardiac output or the venous return, because these are equal in the steady-state owing to the circulatory system being closed.
Strikingly, at the same time that arterial resistance to the splanchnic bed increased, the venous resistance draining this bed decreased. This decreased the time constant of drainage from the splanchnic bed. In this two-compartment model the time constants of flow into and out of each region become important because they affect the distribution of flow and emptying of the regions with changes in heart rate and blood pressure and this adds a further complexity to the analysis. These factors are likely important for the responses to vasopressors and inotropic agents.
The change in capacitance was an important part of the reflex response but this only can occur if there is adequate unstressed volume to recruit. Unfortunately, unstressed volume cannot be measured in an intact person and thus clinicians must think about the potential unstressed reserves. The existence of unstressed volume and the ability to adjust stressed volume by changes in capacitance introduces a role for volume infusions that is not simply to increase cardiac output but rather to ensure reserves.
Patients who have had volume losses and whose MSFP is being supported by a reduction in vascular capacitance by recruitment of their unstressed reserves no longer can use this mechanism to rapidly adjust stressed volume as needed. Volume infusion could potentially restore these reserves without producing much change in cardiac output, although there might be some decrease in heart rate because of a decrease in sympathetic activity. However, the response to the next stress would be very different.
Note that this would likely not produce much change in any measureable hemodynamic values, including ventilation-induced variations in arterial pressure or stroke volume. Although use of volume boluses to increase cardiac output is one of the most common clinical interventions in patients in shock, increasing preload is not the major way that the body normally produces large changes in cardiac output [ 42 ].
Under normal conditions the Frank—Starling mechanism primarily provides fine adjustment to cardiac function by making sure that the same volume that fills the ventricles on each beat leaves them.
For example, during peak aerobic exercise there is very little change in right atrial pressure with the very large increases in cardiac output [ 43 ]. The increase in cardiac output occurs by increases in heart rate, contractility, and peripheral mechanical adaptations that allow more venous return.
This is not to say that fluids should not be used for resuscitation of patients in shock. Use of fluids can avoid the need for central venous cannulation and the need for drug infusion but it is necessary to understand the limits of what fluids can do.
In a 70 kg man with a stressed volume of ml and a MCFP of 10 mmHg, an infusion of a fluid that increased stressed volume by 1 L would increase MCFP to 17 mmHg and likely produce a significant increase in vascular leak. More than likely the liter of fluid would not stay in the vasculature and the effect would be transient. If there is left ventricular dysfunction or non-West zone 3 conditions in the lungs, a greater than normal proportion of the fluid would be distributed to the pulmonary compartments [ 37 ].
When the two-compartment Krogh model is considered, the effect of the volume becomes even more complicated. The effect of the increase in stressed volume will be much greater if a greater fraction of the blood flow goes to the fast time constant muscle bed because this region is much less compliant and the increase in volume produces a greater increase in the regional elastic recoil pressure.
However, this also means that the equivalent of MSFP in the muscle region will be even higher than the estimate given above and be an even greater force for capillary filtration. The study on the effect of the baroreceptor response to hypotension discussed above [ 9 ] gives insight into the response of the peripheral circulation to infusions of norepinephrine.
Besides the expected increase in systemic arterial resistance, norepinephrine constricts the splanchnic venous compartment and increases stressed volume. It potentially dilates or at least does not constrict the venous drainage from the splanchnic bed. This is because activation of alpha-adrenergic receptors constricts the venous drainage of the splanchnic vasculature whereas beta-adrenergic receptors dilate it [ 41 ].
Through its beta-adrenergic activity norepinephrine increases cardiac function and has little effect on pulmonary vessels [ 44 ]. The increase in precapillary resistance vessels and the decrease in right atrial pressure with the improvement in cardiac function could potentially decrease capillary filtration and thus could reduce edema formation.
However, it is possible that very high levels of norepinephrine compromise the normal distribution of flow and compromise organ function. Epinephrine likely works in the same way [ 26 ] except that it generally produces a greater increase in heart rate, which could produce problems by shortening diastole and producing unexpected changes in distribution of flow due to the limits of time constants in different vascular beds, on both the arterial and venous side.
The response of the circuit to phenylephrine is very different from the response to norepinephrine because it only has alpha-adrenergic activity [ 45 , 46 ]. Although phenylephrine can constrict the splanchnic capacitance vessels, it increases the venous resistance draining this region and the net effect on venous return depends upon how much volume is recruited versus how much the downstream resistance increases.
In most critically ill patients capacitance reserves are reduced so that the net effect with phenylephrine is decreased splanchnic drainage and decreased venous return. Phenylephrine also does not increase cardiac function so that cardiac output most often falls [ 47 ]. Besides increasing cardiac contractility, an effective inotrope must also alter circuit properties to increase venous return. The circuit properties of dobutamine have not been well studied but we observed in dogs unpublished data that dobutamine decreased the resistance draining splanchnic vessels as observed with isoproterenol [ 41 ] and also increased MSFP.
The latter likely occurred because the d-isomer of dobutamine has alpha-adrenergic activity and thus could constrict capacitance vessels. This also would predict that the effect of dobutamine would be best when there are adequate reserves in unstressed volume to be recruited so that volume infusions could potentially augment its action.
The circulation starts with a potential energy which is due to the stretching of the elastic walls of all its components by the volume it contains even when there is no blood flow. This volume and the consequent potential energy is constant under steady state conditions but can be changed by recruitment of unstressed volume into stressed volume through what is called a decrease in capacitance, reabsorption of interstitial fluid into the vascular compartment, ingestion and absorption of fluid through the gut, or parenteral fluid administration by health care personnel.
A basic principle is that the heart cannot put out more than what it gets back from the large reservoir of volume in the systemic circulation. The time-varying elastance of the ventricles transiently raises the pressure in the volume they contain. This creates a volume and a pressure wave that are dependent upon the downstream resistance.
This pulse wave progresses through the vasculature from compliant region to compliant region at a rate dependent upon the resistance and compliance of each region. Limits to flow around the system are produced by the diastolic volume capacity of the ventricles, the flow limitation to venous drainage that occurs when the pressure inside the floppy veins is less than the pressure outside the vessels, and the time limits imposed by time constants of drainage on the movement of the volume wave due to the fixed cycle time determined by heart rate.
These mechanical factors can have a much larger impact than actual changes in blood volume. Finally, clinical responses to treatments can only be in the realm of the physiologically possible. On the mechanical factors which determine the output of the ventricles. J Physiol. Venous return at various right atrial pressures and the normal venous return curve. Am J Physiol. Effect of epinephrine on pressure, flow, and volume relationships in the systemic circulation of dogs. Circ Res.
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Bethesda: American Physiological Society; Changes in afterload affect the ability of the ventricle to eject blood and thereby alter ESV and SV.
For example, an increase in afterload e. It is important to note, however, that the SV in a normal, non-diseased ventricle is not strongly influenced by afterload because of compensatory changes in preload. In contrast, the SV of hearts that are failing are very sensitive to changes in afterload. Changes in ventricular inotropy contractility alter the rate of ventricular pressure development, thereby affecting ESV and SV.
In healthy young individuals, HR may increase to bpm during exercise. SV can also increase from 70 to approximately mL due to increased strength of contraction. This would increase CO to approximately Top cardiovascular athletes can achieve even higher levels. At their peak performance, they may increase resting CO by 7—8 times. Since the heart is a muscle, exercising it increases its efficiency.
The difference between maximum and resting CO is known as the cardiac reserve. It measures the residual capacity of the heart to pump blood. HRs vary considerably, not only with exercise and fitness levels, but also with age. Newborn resting HRs may be bpm. HR gradually decreases until young adulthood and then gradually increases again with age.
Maximum HRs are normally in the range of — bpm, although there are some extreme cases in which they may reach higher levels. As one ages, the ability to generate maximum rates decreases. So a year-old individual would be expected to hit a maximum rate of approximately , and a year-old person would achieve a HR of For an adult, normal resting HR will be in the range of 60— bpm.
Bradycardia is the condition in which resting rate drops below 60 bpm, and tachycardia is the condition in which the resting rate is above bpm. Trained athletes typically have very low HRs. If the patient is not exhibiting other symptoms, such as weakness, fatigue, dizziness, fainting, chest discomfort, palpitations, or respiratory distress, bradycardia is not considered clinically significant.
However, if any of these symptoms are present, they may indicate that the heart is not providing sufficient oxygenated blood to the tissues.
The term relative bradycardia may be used with a patient who has a HR in the normal range but is still suffering from these symptoms. Most patients remain asymptomatic as long as the HR remains above 50 bpm. Bradycardia may be caused by either inherent factors or causes external to the heart.
While the condition may be inherited, typically it is acquired in older individuals. Inherent causes include abnormalities in either the SA or AV node. If the condition is serious, a pacemaker may be required. Other causes include ischemia to the heart muscle or diseases of the heart vessels or valves.
External causes include metabolic disorders, pathologies of the endocrine system often involving the thyroid, electrolyte imbalances, neurological disorders including inappropriate autonomic responses, autoimmune pathologies, over-prescription of beta blocker drugs that reduce HR, recreational drug use, or even prolonged bed rest. Treatment relies upon establishing the underlying cause of the disorder and may necessitate supplemental oxygen.
Tachycardia is not normal in a resting patient but may be detected in pregnant women or individuals experiencing extreme stress. In the latter case, it would likely be triggered by stimulation from the limbic system or disorders of the autonomic nervous system. In some cases, tachycardia may involve only the atria.
Some individuals may remain asymptomatic, but when present, symptoms may include dizziness, shortness of breath, lightheadedness, rapid pulse, heart palpations, chest pain, or fainting syncope. While tachycardia is defined as a HR above bpm, there is considerable variation among people.
Further, the normal resting HRs of children are often above bpm, but this is not considered to be tachycardia Many causes of tachycardia may be benign, but the condition may also be correlated with fever, anemia, hypoxia, hyperthyroidism, hypersecretion of catecholamines, some cardiomyopathies, some disorders of the valves, and acute exposure to radiation. Elevated rates in an exercising or resting patient are normal and expected. Resting rate should always be taken after recovery from exercise.
Treatment depends upon the underlying cause but may include medications, implantable cardioverter defibrillators, ablation, or surgery. Initially, physiological conditions that cause HR to increase also trigger an increase in SV. During exercise, the rate of blood returning to the heart increases. However as the HR rises, there is less time spent in diastole and consequently less time for the ventricles to fill with blood. Even though there is less filling time, SV will initially remain high.
However, as HR continues to increase, SV gradually decreases due to decreased filling time. CO will initially stabilize as the increasing HR compensates for the decreasing SV, but at very high rates, CO will eventually decrease as increasing rates are no longer able to compensate for the decreasing SV. Consider this phenomenon in a healthy young individual. Initially, as HR increases from resting to approximately bpm, CO will rise. As HR increases from to bpm, CO remains stable, since the increase in rate is offset by decreasing ventricular filling time and, consequently, SV.
So although aerobic exercises are critical to maintain the health of the heart, individuals are cautioned to monitor their HR to ensure they stay within the target heart rate range of between and bpm, so CO is maintained. The target HR is loosely defined as the range in which both the heart and lungs receive the maximum benefit from the aerobic workout and is dependent upon age. Figure 2. Cardioaccelerator and cardioinhibitory areas are components of the paired cardiac centers located in the medulla oblongata of the brain.
They innervate the heart via sympathetic cardiac nerves that increase cardiac activity and vagus parasympathetic nerves that slow cardiac activity. Nervous control over HR is centralized within the two paired cardiovascular centers of the medulla oblongata Figure 2. The cardioaccelerator regions stimulate activity via sympathetic stimulation of the cardioaccelerator nerves, and the cardioinhibitory centers decrease heart activity via parasympathetic stimulation as one component of the vagus nerve, cranial nerve X.
During rest, both centers provide slight stimulation to the heart, contributing to autonomic tone. This is a similar concept to tone in skeletal muscles. Normally, vagal stimulation predominates as, left unregulated, the SA node would initiate a sinus rhythm of approximately bpm. Both sympathetic and parasympathetic stimulations flow through a paired complex network of nerve fibers known as the cardiac plexus near the base of the heart.
The cardioaccelerator center also sends additional fibers, forming the cardiac nerves via sympathetic ganglia the cervical ganglia plus superior thoracic ganglia T1—T4 to both the SA and AV nodes, plus additional fibers to the atria and ventricles.
The ventricles are more richly innervated by sympathetic fibers than parasympathetic fibers. Sympathetic stimulation causes the release of the neurotransmitter norepinephrine NE at the neuromuscular junction of the cardiac nerves. NE shortens the repolarization period, thus speeding the rate of depolarization and contraction, which results in an increase in HR.
It opens chemical- or ligand-gated sodium and calcium ion channels, allowing an influx of positively charged ions. NE binds to the beta-1 receptor. Some cardiac medications for example, beta blockers work by blocking these receptors, thereby slowing HR and are one possible treatment for hypertension.
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