NURS 5334 Study Questions Module 5. Complete Solution.

NURS 5334 Study Questions Module 5. Complete Solution.CV  What is cardiac output? o cardiac output is about 5 L/ minute. o Hence, every minute, the heart pumps the equivalent of all the blood in the body. o CO = HR ...

NURS 5334 Study Questions Module 5. Complete Solution.CV  What is cardiac output? o cardiac output is about 5 L/ minute. o Hence, every minute, the heart pumps the equivalent of all the blood in the body. o CO = HR x SV o an increase in HR or SV will increase CO, o whereas a decrease in HR or SV will decrease CO.  Stroke volume? o Stroke volume is determined largely by three factors:  (1) myocardial contractility,  (2) cardiac afterload, and  (3) cardiac preload. o Myocardial contractility is defined as the force with which the ventricles contract. o Contractility is determined primarily by the degree of cardiac dilation, which in turn is determined by the amount of venous return. o In addition to regulation by venous return, contractility can be increased by the sympathetic nervous system,  acting through beta1-adrenergic receptors in the myocardium.  Preload? o Preload is formally defined as the amount of tension (stretch) applied to a muscle before contraction. o In the heart, stretch is determined by ventricular filling pressure, that is, the force of venous return:  the greater filling pressure is, the more the ventricles will stretch. o Cardiac preload can be expressed as either end-diastolic volume or enddiastolic pressure. o As discussed later, an increase in preload will increase SV, o whereas a decrease in preload will reduce SV. o Frequently, the terms preload and force of venous return are used interchangeably— although they are not truly equivalent.  Afterload? o Afterload is formally defined as the load against which a muscle exerts its force (i.e., the load a muscle must overcome in order to contract). o For the heart, afterload is the arterial pressure that the left ventricle must overcome to eject blood. o Common sense tells us that, if afterload increases, SV will decrease. o Conversely, if afterload falls, SV will rise. o Cardiac afterload is determined primarily by the degree of peripheral resistance,  which in turn is determined by constriction and dilation of arterioles. 1 Study Questions Module 5  That is, when arterioles constrict, peripheral resistance rises, causing AP (afterload) to rise as well.  Conversely, when arterioles dilate, peripheral resistance falls, causing AP to decline.  What is Starling’s Law? - venous return is the primary determinant of SV o Starling's law states that the force of ventricular contraction is proportional to muscle fiber length (up to a point). o Accordingly, as fiber length (ventricular diameter) increases, there is a corresponding increase in contractile force (Fig. 34.5). o Because of this built-in mechanism, when more blood enters the heart, more is pumped out. o As a result, the healthy heart is able to precisely match its output with the volume of blood delivered by veins. o That is, when venous return increases, CO increases correspondingly. o Conversely, when venous return declines, CO declines to precisely the same extent. o Hence, under normal, nonstressed conditions, SV is determined by factors that regulate venous return.  What regulates artial pressure? o Arterial pressure is the driving force that moves blood through the arterial side of the systemic circulation. o The general formula for AP is: AP = PR × CO  where AP is arterial pressure,  PR is peripheral resistance, and  CO is cardiac output. o Accordingly, an increase in PR or CO will increase AP, o whereas a decrease in PR or CO will decrease AP. o Peripheral resistance is regulated primarily through constriction and dilation of arterioles. o Cardiac output is regulated by the mechanisms discussed previously.  AP is regulated primarily by three systems: o the ANS, o the renin-angiotensin-aldosterone system (RAAS), o kidneys. o These systems differ greatly with regard to timeframe of response. o The ANS acts in two ways:  (1) it responds rapidly (in seconds or minutes) to acute changes in blood pressure and  (2) it provides steady-state control. o The RAAS responds more slowly, taking hours or days to influence AP. o The kidneys are responsible for long-term control and hence may take days or weeks to adjust AP. 2 Study Questions Module 5 o Arterial pressure is also regulated by a fourth system: a family of natriuretic peptides.  These peptides come into play primarily under conditions of volume overload.  What are baroreceptors? o The baroreceptor reflex serves to maintain AP at a predetermined level. When AP changes, the reflex immediately attempts to restore AP to the preset value. o Baroreceptors (pressure sensors) in the aortic arch and carotid sinus sense AP and relay this information to the vasoconstrictor center of the medulla. o When AP changes, the vasoconstrictor center compensates by sending appropriate instructions to arterioles, veins, and the heart. o For example, when AP drops, the vasoconstrictor center causes  (1) constriction of nearly all arterioles, thereby increasing PR;  (2) constriction of veins, thereby increasing venous return; and  (3) acceleration of HR (by increasing sympathetic impulses to the heart and decreasing parasympathetic impulses). o The combined effect of these responses is to restore AP to the preset level. o When AP rises too high, opposite responses occur: the reflex dilates arterioles and veins and slows the heart.  What is the role of the natriuretic peptides? o Natriuretic peptides serve to protect the cardiovascular system in the event of volume overload,  a condition that increases preload, and thereby increases CO and AP. o Volume overload is caused by excessive retention of sodium and water. o Natriuretic peptides work primarily by  (1) reducing blood volume and  (2) promoting dilation of arterioles and veins. o Both actions lower AP. o The family of natriuretic peptides has three principal members:  atrial natriuretic peptide (ANP),  B- or brain natriuretic peptide (BNP), and  C-natriuretic peptide (CNP). o ANP is produced by myocytes of the atria; o BNP is produced by myocytes of the ventricles (and to a lesser extent by cells in the brain, where BNP was discovered); and o CNP is produced by cells of the vascular endothelium. o When blood volume is excessive, all three peptides are released.  (Release of ANP and BNP is triggered by stretching of the atria and ventricles, which occurs because of increased preload.)  ANP and BNP have similar actions.  Both peptides reduce blood volume and increase venous capacitance and thereby reduce cardiac preload. 3 Study Questions Module 5 o Three processes are involved.  First, ANP and BNP shift fluid from the vascular system to the extravascular compartment;  the underlying mechanism is increased vascular permeability.  Second, these peptides act on the kidney to cause diuresis (loss of water) and natriuresis (loss of sodium).  Third, they promote dilation of arterioles and veins, in part by suppressing sympathetic outflow from the central nervous system. o In addition to these actions, ANP and BNP help protect the heart during the early phase of heart failure by  suppressing both the RAAS and sympathetic outflow and  by inhibiting proliferation of myocytes. o Although CNP shares some actions of ANP and BNP, its primary action is to promote vasodilation. Diuretics  What are 3 basic functions of diuretics? o treatment of hypertension o mobilization of edematous fluid associated with heart failure, cirrhosis, or kidney disease. o prevent renal failure.  What are 3 basic functions of kidneys? o (1) filtration, o (2) reabsorption, and o (3) active secretion.  MOA of diuretics? o blockade of sodium and chloride reabsorption. o By blocking the reabsorption of these prominent solutes, diuretics create osmotic pressure within the nephron that prevents the passive reabsorption of water. o Hence diuretics cause water and solutes to be retained within the nephron and thereby promote the excretion of both. o The increase in urine flow that a diuretic produces is directly related to the amount of sodium and chloride reabsorption that it blocks. o Accordingly, drugs that block solute reabsorption to the greatest degree produce the most profound diuresis. o Because the amount of solute in the nephron becomes progressively smaller as filtrate flows from the proximal tubule to the collecting duct, drugs that act early in the nephron have the opportunity to block the greatest amount of solute reabsorption. As a result, these agents produce the greatest diuresis. o Conversely, because most of the filtered solute has already been reabsorbed by the time the filtrate reaches the distal parts of the nephron, diuretics that 4 Study Questions Module 5 act at distal sites have very little reabsorption available to block. Consequently, such agents produce relatively scant diuresis.