The pulmonary circulation is the blood flow within the lungs that is involved in the exchange of gases between the blood and alveoli. The systemic circulation is comprised of all the blood vessels within and outside of organs excluding the lungs. The right side of the heart comprises the right atrium and the right ventricle. The right atrium receives venous blood from the systemic circulation, and the right ventricle pumps it into the pulmonary circulation where oxygen and carbon dioxide are exchanged between the blood and alveolar gases.
The left side of the heart comprises the left atrium and the left ventricle. The right side of the heart, pulmonary circulation, left side of the heart, and systemic circulation are arranged in series.
Blood then flows from the left atrium into the left ventricle. The left ventricle ejects the blood into the aorta, which then distributes the blood to all the organs via the arterial system. Within the organs, the vasculature branches into smaller and smaller vessels, eventually forming capillaries, which are the primary site of exchange. Blood flow from the capillaries enters veins, which return blood flow to the right atrium via large systemic veins the superior and inferior vena cava.
As blood flows through organs, some of the fluid, along with electrolytes and small amounts of protein, leaves the circulation and enters the tissue interstitium a process termed fluid filtration. The lymphatic vessels, which are closely associated with small blood vessels within the tissue, collect the excess fluid from within the tissue interstitium and transport it back into the venous circulation by way of lymphatic ducts that empty into large veins subclavian veins above the right atrium.
It is important to note the overall arrangement of the cardiovascular system. First, the right and left sides of the heart, which are separated by the pulmonary and systemic circulations, are in series with each other see Fig. Therefore, all of the blood that is pumped from the right ventricle enters into the pulmonary circulation and then into the left side of the heart from where it is pumped into the systemic circulation before returning to the heart.
This in-series relationship of the two sides of the heart and the pulmonary and systemic circulations requires that the output volume of blood ejected per unit time of each side of the heart closely matches the output of the other so that there are no major blood volume shifts between the pulmonary and systemic circulations. Second, most of the major organ systems of the body receive their blood from the aorta, and the blood leaving these organs enters into the venous system superior and inferior vena cava that returns the blood to the heart.
Therefore, the circulations of most major organ systems are in parallel as shown in Figure 1. The liver also receives blood from the aorta via the hepatic artery. Therefore, most of the liver circulation is in series with the intestinal circulation, while some of the liver circulation is in parallel with the intestinal circulation see Chapter 7.
The parallel arrangement has significant hemodynamic implications as described in Chapter 5. Briefly, the parallel arrangement of major vascular beds prevents blood flow changes in one organ from significantly affecting blood flow in other organs. In contrast, when vascular beds are in series, blood flow changes in one vascular bed significantly alter blood flow to the other vascular bed.
While this is true, it is more accurate to view the heart as a pump that receives blood from venous blood vessels at a low pressure, imparts energy to the blood raises it to a higher pressure by contracting around the blood within the cardiac chambers, and then ejects the blood into the arterial blood vessels.
It is important to understand that organ blood flow is not driven by the output of the heart per se, but rather by the pressure generated within the arterial system as the heart pumps blood into the vasculature, which serves as a resistance network. Organ blood flow is determined by the arterial pressure minus the venous pressure, divided by the vascular resistance of the organ see Chapters 5 and 7.
Pressures in the cardiovascular system are expressed in millimeters of mercury mm Hg above atmospheric pressure. One millimeter of mercury is the pressure exerted by a 1-mm vertical column of mercury 1 mm Hg is the equivalent of 1. Vascular resistance is determined by the size of blood vessels, the anatomical arrangement of the vascular network, and the viscosity of the blood flowing within the vasculature.
The right atrium receives systemic venous blood venous return at very low pressures near 0 mm Hg Fig. This venous return then passes through the right atrium and fills the right ventricle; atrial contraction also contributes to the ventricular filling.
Right ventricular contraction ejects blood from the right ventricle into the pulmonary artery. This generates a maximal pressure systolic pressure that ranges from 20 to 30 mm Hg within the pulmonary artery.
As the blood passes through the pulmonary circulation, the blood pressure falls to about 10 mm Hg. As the left ventricle contracts and ejects blood into the systemic arterial system, a relatively high pressure is generated to mm Hg maximal or systolic pressure.
Therefore, the left ventricle is a high-pressure pump, in contrast to the right ventricle, which is a low-pressure pump. Details of the pumping action of the heart are found in Chapter 4.
The pumping activity of the heart is usually expressed in terms of its cardiac output, which is the amount of blood ejected with each contraction i. Any factor that alters heart rate or stroke volume will alter the cardiac output.
The heart rate is determined by specialized cells within the heart that act as electrical pacemakers, and their activity is increased or decreased by autonomic nerves and hormones see Chapter 2.
The action potentials generated by these pacemaker cells are conducted throughout the heart and trigger contraction of cardiac myocytes see Chapter 3. This results in ventricular contraction and ejection of blood. The heart has other important functions besides pumping blood. The heart synthesizes several hormones. One of these hormones, atrial natriuretic peptide, plays an important role in the regulation of blood volume and blood pressure see Chapter 6.
Sensory nerve receptors associated with the heart play a role in regulating the release of antidiuretic hormone from the posterior pituitary, which regulates water loss by the kidneys. Vascular System Blood vessels constrict and dilate to regulate arterial blood pressure, alter blood flow within organs, regulate capillary blood pressure, and distribute blood volume within the body. Changes in vascular diameters are brought about by activation of vascular smooth muscle within the vascular wall by autonomic nerves, metabolic and biochemical signals from outside of the blood vessel, and vasoactive substances released by endothelial cells that line the blood vessels see Chapters 3, 5, and 6.
Blood vessels have other functions besides distribution of blood flow and exchange. The endothelium lining blood vessels produces substances that modulate hemostasis blood clotting and inflammatory responses see Chapter 3. Interdependence of Circulatory and Organ Function Cardiovascular function is closely linked to the function of other organs. For example, the brain not only receives blood flow to support its metabolism but also acts as a control center for regulating cardiovascular function.
A second example of the interdependence between organ function and the circulation is the kidney. The kidneys excrete varying amounts of sodium, water, and other molecules to maintain fluid and electrolyte homeostasis.
Blood passing through the kidneys is filtered, and the kidneys then modify the composition of the filtrate to form urine. Furthermore, renal dysfunction can lead to large increases in blood volume, which can precipitate cardiovascular changes that can lead to hypertension or exacerbate heart failure. In summary, organ function is dependent on the circulation of blood, and cardiovascular function is dependent on the function of organs.
For example, when a person exercises, increased metabolic activity of contracting skeletal muscle requires large increases in nutrient supply particularly oxygen and enhanced removal of metabolic by-products e. To meet this demand, blood vessels within the exercising muscle dilate to increase blood flow; however, blood flow can only be increased if the arterial pressure is maintained.
Arterial pressure is maintained during exercise by increasing cardiac output and by constricting blood vessels in other organs of the body see Chapter 9. If these changes were not to occur, arterial blood pressure would fall precipitously during exercise, thereby limiting organ perfusion and exercise capacity.
Therefore, a coordinated cardiovascular response is required to permit increased muscle blood flow while a person exercises. Another example of adaptation occurs when a person stands up. Gravitational forces cause blood to pool in the legs when a person assumes an upright body posture see Chapter 5. In the absence of regulatory mechanisms, this pooling will lead to a fall in cardiac output and arterial pressure, which can cause a person to faint because of reduced blood flow to the brain.
To prevent this from happening, coordinated reflex responses increase heart rate and constrict blood vessels to maintain a normal arterial blood pressure when a person stands. As described in Chapter 6, neural and hormonal neurohumoral mechanisms regulating cardiovascular function are under the control of pressure sensors located in arteries and veins i. These baroreceptors, through their afferent neural connections to the brain, provide the central nervous system with information regarding the status of blood pressure in the body.
A decrease in arterial pressure from its normal operating point elicits a rapid baroreceptor reflex that stimulates the heart to increase cardiac output and constricts blood vessels to restore arterial pressure Fig.
These cardiovascular adjustments occur through rapid changes in autonomic nerve activity particularly through sympathetic nerves to the heart and vasculature. Negative feedback control mechanisms, as this example illustrates, can be defined as a process in which a deviation from some condition e. In contrast to the rapidly acting autonomic mechanisms, hormonal mechanisms acting on the kidneys require hours or days to achieve their full effect on blood volume.
Hormonal mechanisms include secretion of catecholamines chiefly epinephrine by the adrenal glands; release of renin by the kidneys, which triggers the formation of angiotensin II and aldosterone; and release of antidiuretic hormone vasopressin by the posterior pituitary. Hormones such as angiotensin II, aldosterone, and vasopressin are particularly important because they act on the kidneys to increase blood volume, which increases cardiac output and arterial pressure. In summary, arterial pressure is monitored by the body and ordinarily is maintained within narrow limits by negative feedback mechanisms that adjust cardiac function, systemic vascular resistance, and blood volume.
This control is accomplished by changes in autonomic nerve activity to the heart and vasculature, as well as by changes in circulating hormones that influence cardiac, vascular, and renal function.
Chapter 2 describes the electrical activity within the heart, both at the cellular and whole organ level. Chapter 3 builds a foundation of cellular physiology by emphasizing intracellular mechanisms that regulate cardiac and vascular smooth muscle contraction. These cellular concepts are reinforced repeatedly in subsequent chapters. Chapter 4 examines cardiac mechanical function. Chapter 5 summarizes concepts of vascular function and the biophysics of blood flow in the context of regulation of arterial and venous blood pressures.
Neurohumoral mechanisms regulating cardiac and vascular function are described in Chapter 6. Electrical changes within the myocytes initiate this contraction.
This chapter examines 1 the electrical activity of individual myocytes, including resting membrane potentials and action potentials; 2 the way action potentials are conducted throughout the heart to initiate coordinated contraction of the entire heart; and 3 the way electrical activity of the heart is measured using the electrocardiogram ECG. This potential can be measured by inserting a microelectrode into the cell and measuring the electrical potential in millivolts mV inside the cell relative to the outside of the cell.
By convention, the outside of the cell is considered 0 mV. This resting membrane potential Em is determined by the concentrations of positively and negatively charged ions across the cell membrane, the relative permeability of the cell membrane to these ions, and the ionic pumps that transport ions across the cell membrane.
Although chloride ions are found inside and outside the cell, they contribute relatively little to the resting membrane potential. Figure 2. The concentration differences across the cell membrane for these and other ions are determined by the activity of energy-dependent ionic pumps and the presence of impermeable, negatively charged proteins within the cell that affect the passive distribution of cations and anions.
The equilibrium potential is the potential difference across the membrane required to maintain the concentration gradient across the membrane.
Sodium ions also play a major role in determining the membrane potential. The net driving or electrochemical force acting on sodium and each ionic species has two components.
Although the number of ions moving across the sarcolemmal membrane in a single action potential is small relative to the total number of ions, many action potentials can lead to a significant change in the extracellular and intracellular concentration of these ions. To prevent this change from happening i. By pumping more positive charges out of the cell than into it, the pump creates a negative potential within the cell. Two primary mechanisms remove calcium from cells Fig.
The exchanger can operate in either direction across the sarcolemma depending on the Em. The opposite occurs in depolarized cells. As described in Chapter 3, this can lead to an increase in the force of myocyte contraction.
Ion Channels Ions move across the sarcolemma through specialized ion channels in the phospholipid bilayer of the cell membrane.
These channels are made up of large polypeptide chains that span the membrane and create an opening in the membrane. Conformational changes in the ion channel proteins alter the shape of the channel, thereby permitting ions to transverse the membrane channel or blocking ion movement.
Ion channels are selective for different cations and anions. For example, there are ion channels selective for sodium, potassium, and calcium ions Table For example, several different types of potassium channels exist through which potassium ions can move across the cell membrane. Two general types of ion channels exist: voltage-gated voltage-operated and receptorgated receptor-operated channels. Voltagegated channels open and close in response to changes in membrane potential.
Examples of voltage-gated channels include several sodium, potassium, and calcium channels that are involved in cardiac action potentials. Receptor-gated channels open and close in response to chemical signals operating through membrane receptors.
For example, acetylcholine, which is the neurotransmitter released by the vagus nerves innervating the heart, binds to a sarcolemmal receptor that subsequently leads to the opening of special types of potassium channels IK, ACh.
Ion channels have both open and closed states. Ions pass through the channel only while it is in the open state. The open and closed states of voltage-gated channels are regulated by the membrane potential. Fast sodium channels have been the most extensively studied, and a conceptual model has been developed based upon studies by Hodgkin and Huxley in the s using the inside squid giant axon. In this model, two gates regulate the movement of sodium through the channel Fig.
In this configuration, the m-gate activation gate is closed and the h-gate inactivation gate is open. These gates are polypeptides that are part of the transmembrane protein channel, and they undergo conformational changes in response to changes in voltage. The m-gates rapidly become activated and open when the membrane is rapidly depolarized. This permits sodium, driven by its electrochemical gradient, to enter the cell.
As the m-gates open, the h-gates begin to close; however, the m-gates open more rapidly than the h-gates close. The difference in the opening and closing rates of the two gates permits sodium to briefly enter the cell. After a few milliseconds, however, the h-gates close and sodium ceases to enter the cell. The closing of the h-gates therefore limits the length of time that sodium can enter the cell.
This inactivated, closed state persists throughout the repolarization phase as the membrane potential recovers to its resting level. Near the end of repolarization, the negative membrane potential causes the m-gates to close and the h-gates to open. In the resting closed state, the m-gates activation gates are closed, although the h-gates inactivation gates are open.
Rapid depolarization to threshold opens the m-gates voltage activated , thereby opening the channel and enabling sodium to enter the cell. Shortly thereafter, as the cell begins to repolarize, the h-gates close and the channel becomes inactivated. Toward the end of repolarization, the m-gates again close and the h-gates open. This brings the channel back to its resting state. Full recovery of the h-gates can take milliseconds or longer after the resting membrane potential has been restored.
The response of the fast sodium channel, however, is different when the resting membrane potential is partially depolarized or the cell is slowly depolarized. For example, when myocytes become hypoxic, the cells depolarize to a less negative resting membrane potential.
This partially depolarized state inactivates sodium channels by closing the h-gates. The more a cell is depolarized, the greater the number of inactivated sodium channels. If a myocyte has a normal resting potential but then undergoes slow depolarization, more time is available for the h-gates to close as the m-gates are opening. This causes the sodium channel to transition directly from the resting closed state to the inactivated closed state.
The result is that there is no activated, open state for sodium to pass through the channel, effectively abolishing fast sodium currents through these channels. As long as the partial depolarized state persists, the channel will not resume its resting, closed state. As described later in this chapter, these changes significantly alter myocyte action potentials by abolishing fast sodium currents during action potentials.
A single cardiac cell has many sodium channels, and each channel has a slightly different voltage activation threshold and duration of its open, activated state. The amount of sodium the sodium current that passes through sodium channels when a cardiac cell undergoes depolarization depends upon the number of sodium channels, the duration of time the channels are in the open state, and the electrochemical gradient driving the sodium into the cell.
For example, slow calcium channels have activation and inactivation gates although they have different letter designations than fast sodium channels. Although this conceptual model is useful to help understand how ions transverse the membrane, many of the details of how this actually occurs at the molecular level are still unknown.
Nevertheless, recent research is helping to show which regions of ion channel proteins act as voltage sensors and which regions undergo conformational changes analogous to the gates described in the conceptual model. Action Potentials Action potentials occur when the membrane potential suddenly depolarizes and then repolarizes back to its resting state. The two general types of cardiac action potentials include nonpacemaker and pacemaker action potentials.
Nonpacemaker action potentials are triggered by depolarizing currents from adjacent cells, whereas pacemaker cells are capable of spontaneous action potential generation.
Both types of action potentials in the heart differ considerably from the action potentials found in nerve and skeletal muscle cells Fig. One major difference is the duration of the action potentials. Cardiac action potentials are much longer in duration than nerve cell action potentials. In skeletal muscle cells, the action potential duration is approximately 2 to 5 milliseconds.
In contrast, the duration of ventricular action potentials ranges from to milliseconds. These differences among nerve, skeletal muscle, and cardiac myocyte action potentials relate to differences in the ionic conductances responsible for generating the changes in membrane potential.
By convention, the action potential is divided into five numbered phases. ERP, effective refractory period. These two conductance changes very rapidly move the membrane potential away from the potassium equilibrium potential and closer to the sodium equilibrium potential see Equation L-type calcium channels are the major calcium channels in cardiac and vascular smooth muscle.
They are opened by membrane depolarization they are voltageoperated and remain open for a relatively long duration. These channels are blocked by classical L-type calcium channel blockers e. During phases 0, 1, 2, and part of phase 3, the cell is refractory i. During the ERP, stimulation of the cell does not produce new, propagated action potentials because the h-gates are still closed. The ERP acts as a protective mechanism in the heart by limiting the frequency of action potentials and therefore contractions that the heart can generate.
Unlike most other cells that exhibit action potentials e. Praised for its concise coverage, this highly accessible monograph lays a foundation for understanding the underlying concepts of normal cardiovascular function and offers a welcome alternative to a more mechanistically oriented approach or an encyclopedic physiology text. Clear explanations, ample illustrations and engaging clinical cases and problems provide the perfect guidance for self-directed learning and prepare you to excel in clinical practice.
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