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                                                                          CHAPTER 1 / Cardiac Anatomy and Physiology   35

                     rate-related increase in force of contraction partially compensates for  ■ Is the patient already tachycardic, with a dilated left ventricle?
                     the lower end-diastolic filling. At rates exceeding about 180  ■ Is the patient’s heart already receiving a high level of endoge-
                     beats/min, diastole is shortened and the diastolic filling is decreased.  nous catecholaminergic stimuli?
                     Stroke volume is then decreased, as predicted by the Starling relation.  ■ How much of the patient’s reserve capacity is left? Of the re-
                     Furthermore, the coronary arteries are perfused during diastole, and  serve capacity left, how much can be used in planning the pa-
                     a fast heart rate decreases coronary blood flow, which may result in  tient’s care?
                     ischemia, and in turn decrease myocardial compliance and contrac-  ■ What is the cost of the patient’s current functional state in
                     tility. The stiff ventricle requires greater filling pressures to expand it  terms of myocardial oxygen consumption?
                     to the same diastolic volume and may operate at a smaller volume,
                     further decreasing stroke volume, as defined by the Starling relation.
                        During diastole, the heart can fill to a larger volume than  MYOCARDIAL METABOLISM
                     usual, thereby increasing its stroke volume. This is sometimes
                     called the diastolic cardiac reserve. Increases in diastolic volume are  The chemical energy of ATP powers myocardial contraction, ion
                     accompanied by increases in end-diastolic pressure. Left ventricu-  pumping, and many other activities. ATP is broken down (hy-
                     lar end-diastolic pressures beyond approximately 20 to 25 mm Hg  drolyzed) into adenosine diphosphate and inorganic phosphate.
                     typically result in pulmonary congestion. The more dilated the  With hydrolysis, chemical energy is transformed into mechanical
                     ventricle, the more oxygen it requires; this may be a limiting prob-  energy and heat. Because the heart is continuously active, ATP
                     lem in the patient with coronary artery disease.    must be continuously available. The usual intramyocardial cellu-
                        The heart also has systolic reserve, an ability to eject a larger per-  lar concentrations of ATP (estimated at 5 mM) are sufficient to
                     centage of the end-diastolic volume. Increased contractility and  power contraction mechanical activity for only a few beats.
                     decreased afterload increase stroke volume and cardiac output. In-  Creatine phosphate is a backup source of high-energy phos-
                     creases in velocity of contraction or contractility make extra de-  phate to replenish the ATP supply. However, energy stores in ATP
                     mands on the heart in terms of oxygen requirements and pose risk  and creatine phosphate together supply enough energy only for
                     for the patient with coronary artery disease.       several minutes of activity. Thus, the heart depends on ongoing
                        Factors involved in mechanical performance interact continu-  ATP synthesis. This occurs in a series of efficient, but complex,
                     ously. For example, an increase in afterload decreases the stroke  enzyme-dependent reactions. The bulk of myocardial ATP is syn-
                     volume. This in turn results in a larger volume of blood in the  thesized in an aerobic environment. Myocardial cells have large
                     heart at the end of systole. The addition of an unchanged amount  amounts of mitochondria, the sites of aerobic synthesis of ATP.
                     of blood during the subsequent diastole increases the end-diastolic  Free fatty acids are the preferred myocardial fuel, particularly
                     volume. The ensuing contraction is more forceful, and stroke vol-  when the patient is in the fasting state. Glucose or its storage form,
                     ume is increased owing to the Starling effect.      glycogen, can serve as an additional substrate for energy metabo-
                        In hemorrhage, the filling pressure may diminish; the stroke  lism. Whereas glucose contributes only 15% to myocardial ATP
                     volume decreases as predicted by the Starling relationship. How-  synthesis in the fasting patient, its role increases to nearly 50% in
                     ever, the afterload (ventricular wall tension) may also decrease.  the postprandial state. Amino acids play a minor role in energy
                     This tends to raise the stroke volume. Adrenergic outflow also  metabolism of the heart. In starvation, however, amino acid in-
                     contributes to increased stroke volume. The cardiac output may  termediates are metabolized to maintain energy stores.
                     increase despite decreased filling pressures.
                                                                           PHYSIOLOGY OF THE
                     Assessment of the Pump                                CORONARY CIRCULATION
                     Performance
                                                                         Under normal conditions at rest, the heart extracts a large amount
                     Assessment of the patient includes the evaluation of numerous in-
                     dices of overall pump performance as follows:       of oxygen from the blood perfusing the heart: the difference in
                                                                         oxygen content between coronary arterial and coronary sinus
                     ■ urine output, mental status, skin color, and temperature are indices  blood is approximately 11.4 mL O 2 /100 mL blood. 60  The total
                       of the adequacy of cardiac output to various organs and tissues;  oxygen content of arterial blood is normally approximately 20 mL
                     ■ cardiac output may be measured directly;          O 2 /100 mL blood, so this represents extraction of more than 50%
                     ■ left ventricular preload is estimated from the pulmonary artery  of the arterial oxygen content. It is difficult to extract much more
                       occlusion pressure;                               oxygen than this, yet the oxygen requirement of the heart may in-
                     ■ systemic vascular resistance (index of left ventricular afterload)  crease many fold. This additional oxygen can be supplied only by
                       is calculated; and                                increasing coronary blood flow. Coronary blood flow is propor-
                     ■ mean arterial blood pressure is the product of cardiac output  tionate to myocardial metabolism and oxygen consumption.
                       and vascular resistance.
                                                                         Determinants of Myocardial
                        These observations measure end products of many interacting
                     variables that together compose the reserve capacity of the cardio-  Oxygen Consumption
                     vascular system. In making these assessments, the nurse not only
                     should ask whether blood flow and pressure are adequate but also  Several factors contribute to the oxygen needs of the heart. A
                     should probe more deeply.                           small and relatively constant volume is used in the “housekeep-
                                                                         ing” activities of heart cells. “Housekeeping” activities are inde-
                     ■ How much of the patient’s reserve capacity must be used to  pendent of contraction and include repair or replacement of in-
                       maintain the current level of functioning?        tracellular proteins and maintenance of the ionic environment.
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