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With CAD, Faster Is Never Better
PATHO CORNER
With CAD, Faster Is Never Better Kim A. Noble, PhD, RN, CPAN YOU REALIZE it is another busy day in the Phase I PACU as you admit 88-year-old PC from the OR after a total hip arthroplasty. You receive the following report from anesthesia: PC is female, 5=2==, weighs 112 pounds, and has a past medical history of an old anterior myocardial infarction on electrocardiogram (ECG), coronary artery disease (CAD), and osteoarthritis. PC’s procedure was cancelled four weeks ago because her hemoglobin (Hgb) was 8.7 on preadmission testing. She has been taking an iron supplement and, although she was unable to autodonate blood, her repeat Hgb reading was 10.1 this morning. PC received a planned regional anesthesia epidural with lidocaine and 6 mg of duramorph, but after a late failure of the epidural block, she had general anesthesia with propofol and received the remaining 4 mg of duramorph intravenously. During the procedure, PC had episodic hypotension that was treated with a total of 25 mg of ephedrine given in 5-mg incremental doses intravenously. Her blood loss for the procedure was 450 mL and she was give 2200 mL of lactated Ringer’s solution. A cell saver was used for the procedure, but not enough blood was obtained to be given back to PC. PC arrives agitated and slightly confused. She reports pain in her right hip area as a 6 on a 10-point pain scale. Her vital signs are: blood pressure (BP) 164/104, heart rate (HR) 122, respiration rate (RR) 24, temperature 96.4° F, and oxygen saturation 96% on 4 L of nasal oxygen. She has decreased sensation from T4 bilaterally, reporting a “weird” feeling to stimulation application to T12 bilaterally. She has bilateral sensation on her feet with gross motor movement present with the right more than the Journal of PeriAnesthesia Nursing, Vol 22, No 1 (February), 2007: pp 47-50
left. She has a urinary catheter with adequate clear yellow urine. She has a right-sided hip dressing that is dry and intact, an abduction pillow in place and compression boots bilaterally. You notice occasional multifocal premature ventricular contractions (PVCs) on her ECG and she is holding her chest and reports being so hungry “it hurts.” Her lungs are clear to auscultation and there is no change in the duration or character of chest discomfort with deep breathing. She denies nausea and has active bowel sounds. You call the attending anesthesiologist for additional evaluation and a 12lead ECG is ordered. You give PC a loading dose of 4 mg of morphine and start her patientcontrolled analgesia as ordered. Ten minutes later PC reports slight improvement in her pain, now 5/10 on the pain scale, her BP is 158/98, HR 118 with continued multifocal PVCs, and her RR remains 24 per minute. The ECG is completed and read by anesthesia, who notes acute inferior wall changes. Intravenous nitroglycerin and an intensive care bed are ordered.
Sympathetic Nervous System Activation of the Cardiovascular System To fully understand the interactions that result in increases in heart rate and the myocardial oxygen requirements, one must begin with a brief review of the mechanism(s) that increase
Kim A. Noble, PhD, RN, CPAN, is an Assistant Professor at Temple University, Philadelphia, PA. Address correspondence to Kim A. Noble, PhD, RN, CPAN, Department of Nursing, Temple University, 3307 N. Broad St, Philadelphia, PA 19140; e-mail address:[email protected]. © 2007 by American Society of PeriAnesthesia Nurses. 1089-9472/07/2201-0007$35.00/0 doi:10.1016/j.jopan.2006.12.003 47
KIM A. NOBLE
48
cardiovascular (CV) functioning. Although to some extent CV control may be initiated by metabolic or humoral components, the most rapid forms of increases or decreases in CV functioning are mediated through the activity of the autonomic nervous system (ANS).1 There are two branches of the ANS, the parasympathetic nervous system (PSNS) and the sympathetic nervous system (SNS), which work in direct opposition to manipulate systemic function to meet the minute-to-minute changes in systemic needs. The SNS and the PSNS are on opposite ends of the spectrum in terms of mechanism of action and physiologic responses. The PSNS exerts an effect through the interaction of the neurotransmitter acetylcholine, and the muscarinic and nicotinic cholinergic receptors. The SNS uses the neurotransmitters norepinephrine and epinephrine, working through the autonomic alpha (␣) and beta () receptors. The autonomic receptors are further subdivided based on their location of effect, with the ␣-receptors residing in vascular smooth muscle, the -1 receptors found primarily in cardiac muscle, and the -2 receptors found in the conducting airways of the lungs. Activation of the SNS, as would be seen in a fight-or-flight response, leads to a rapid and dramatic increase in CV performance. SNS fibers innervate multiple areas of the atria and ventricles and trigger the release of norepinephrine, which binds to -adrenergic receptors on the cardiac cell membranes, causing an increased metabolic activity,1 which can be further divided into four separate events. First, -adrenergic receptors are present on the sinoatrial (SA) node and conduction system of the heart, leading to an increase in heart rate and conduction velocity. Second, norepinephrine increases the movement of calcium into the cardiac cells, leading to an increase in contractility of the cardiac myocytes. The third and fourth events are in response to SNS stimulation of the ␣-adrenergic receptors, leading to contraction and increased resistance in the vascular smooth muscle of the blood vessels. The third
event results from the contraction of the venous system, causing an increased venous return to the right atrium and increased preload or stretch of the ventricle. The fourth and final event is in response to the contraction of the arterial system and leads to an increase in the peripheral vascular resistance, arterial blood pressure, and the afterload or work required by the ventricle to eject blood. Each of these events independently increases myocardial oxygen requirements, but their summation significantly increases the demand for oxygen by the heart.1 Inequalities are encountered when the supply of oxygen via the coronary arteries is diminished by disease such as the partial coronary occlusion seen with PC.
Tachycardia and CAD Increasing the HR forces the events that take place during depolarization (systole) and repolarization (diastole) to increase in frequency, causing a higher demand for oxygen. With depolarization, ion channels open and electrically charged ions move across the cell membrane, allowing the interaction between actin and myosin and contraction of the myofibrils. During repolarization, ion concentration gradients are re-established through the activity of adenosine triphosphate-dependent, energy-burning pumps, and the resting membrane potential for the next contraction is reset. Because of the nature of myocardial contraction, very little blood is delivered to the contracting myocardial cells; instead a majority of blood flow to the muscle takes place during diastole, or repolarization. In a patient with a normal HR of 70 beats per minute, depolarization or systole accounts for one-third of the cardiac cycle, whereas diastole or repolarization represents twothirds of the cycle. The time of systole is relatively fixed and increases in HR predominantly affect the time of diastole, or filling. Because this is the only time the myocardium receives its blood supply, decreasing the time of filling reduces the supply of
PATHO CORNER
oxygen to the working heart. As an increase in HR simultaneously increases the demand for oxygen by myocardial cells, tachycardia creates a double-edged sword for the patient with pre-existing CAD: an increase in oxygen demand with a decrease of oxygen flow and nutrients to the contracting myocytes.
Implications for the PACU Patient CAD affects approximately 13 million Americans, leading to a coronary event every 26 seconds and a coronary-related death every minute.1 The chances of having a patient with CAD in your PACU are good and the prevention of coronary complications is a priority. A brief summary of the implications of CAD for the awakening PACU patient follow. Alteration in Gas Exchange
Every patient emerging from general anesthesia requires the maintenance of a patent airway and adequate respiration is priority one. The provision of supplemental oxygen is imperative but an even higher priority for the patient with CAD and increased myocardial oxygen requirements. Because the administration of more than 2 L of intravenous fluid and an increased workload on PC’s heart may lead to a new onset of heart failure, diligent monitoring of pulse oximetry and frequent auscultation of breath sounds is vital. The reason for PC’s admission agitation must be explored and a careful evaluation of her epidural level completed. The origination of PC’s increased respiratory rate should be determined too because this also indicates an increase in the work of breathing. The administration of opioids requires diligent monitoring for physiologic response and, as with any patient emerging from a surgical procedure, PC should be encouraged to breathe deeply and cough at intervals. Alteration in Cardiovascular Functioning
As discussed previously, the effect of heightened sympathetic nervous system activity in-
49
creases the workload and myocardial oxygen requirements of the myocardium. This is especially problematic for myocardial tissue that is not receiving an adequate supply of oxygen and nutrients. Control of PC’s pain is important through the administration of opioids and the initiation of a nitroglycerin infusion. Nitroglycerin rapidly dilates the coronary and systemic vasculature, leading to an increased blood supply to the myocardium and a reduction in the preload or venous return to the heart.2 Vasodilation of the arterial system will also decrease the afterload, or the amount of pressure or work that must be completed by the left ventricle to eject blood through the aortic valve. An optimal blood pressure goal based on preoperative readings should be received from the attending anesthesiologist, and diligent monitoring of systemic blood pressure and the titration of the nitroglycerin drip completed to maintain the target blood pressure. An ongoing nursing assessment of the epidural level should be conducted at intervals. Residual blockade from epidural injection may lead to a loss of sympathic tone, venous pooling, and blood pressure reduction. Caution should be used for any changes in position until the level is below T12.3 Lab work should be ordered and obtained from the attending anesthesiologist; these include cardiac isoenzymes and troponin levels, as well as hemoglobin and hematocrit (H&H) and serum electrolytes. Continuous cardiac monitoring is needed because PC is having frequent multifocal PVCs. These PVCs may be attributed to the myocardial ischemia, hypoxemia, or electrolyte imbalance, and they may require the administration of an antiarrhythmic if they persist. PC’s baseline H&H was low (10.1) and it should be expected to decrease further with the surgical procedure, administration of intravenous fluids, and blood losses. If it was not already completed, an order for a blood type and screen should be obtained for a possible transfusion because anemia will further complicate PC’s ischemic myocardium.
KIM A. NOBLE
50
Finally, as the cardiovascular effects of the SNS are mediated primarily through the  receptors which innervate the myocardium, the perianesthesia nurse must be prepared for the administration of a -antagonist or -blocker if PC remains tachycardiac because these pharmacologic interventions will decrease myocardial oxygen requirements and increase the time of diastole and blood supply to the myocardial cells.
Because of the significance of CAD in Americans, the chance of recovering a patient with CAD is very good and the perianesthesia nurse must be prepared to intervene should complications develop. With an understanding of the physiologic consequences of SNS activity on the cardiovascular system, the nurse caring for the patient with CAD emerging from anesthesia can be anticipated, identified, and treated rapidly.
References 1. McCance KL, Huether SE. Pathophysiology: The Biologic Basis for Disease in Adults and Children. Ed 5. St. Louis, MO: Mosby; 2006. 2. Aschenbrenner DS, Venable SJ. Drug Therapy in Nurs-
ing. Ed 2. Philadelphia, PA: Lippincott Williams & Wilkins; 2006. 3. Drain CB. PeriAnesthesia Nursing: A Critical Care Approach. Ed 4. St. Louis, MO: Saunders; 2003.
With CAD, Faster Is Never Better Kim A. Noble, PhD, RN, CPAN YOU REALIZE it is another busy day in the Phase I PACU as you admit 88-year-old PC from the OR after a total hip arthroplasty. You receive the following report from anesthesia: PC is female, 5=2==, weighs 112 pounds, and has a past medical history of an old anterior myocardial infarction on electrocardiogram (ECG), coronary artery disease (CAD), and osteoarthritis. PC’s procedure was cancelled four weeks ago because her hemoglobin (Hgb) was 8.7 on preadmission testing. She has been taking an iron supplement and, although she was unable to autodonate blood, her repeat Hgb reading was 10.1 this morning. PC received a planned regional anesthesia epidural with lidocaine and 6 mg of duramorph, but after a late failure of the epidural block, she had general anesthesia with propofol and received the remaining 4 mg of duramorph intravenously. During the procedure, PC had episodic hypotension that was treated with a total of 25 mg of ephedrine given in 5-mg incremental doses intravenously. Her blood loss for the procedure was 450 mL and she was give 2200 mL of lactated Ringer’s solution. A cell saver was used for the procedure, but not enough blood was obtained to be given back to PC. PC arrives agitated and slightly confused. She reports pain in her right hip area as a 6 on a 10-point pain scale. Her vital signs are: blood pressure (BP) 164/104, heart rate (HR) 122, respiration rate (RR) 24, temperature 96.4° F, and oxygen saturation 96% on 4 L of nasal oxygen. She has decreased sensation from T4 bilaterally, reporting a “weird” feeling to stimulation application to T12 bilaterally. She has bilateral sensation on her feet with gross motor movement present with the right more than the Journal of PeriAnesthesia Nursing, Vol 22, No 1 (February), 2007: pp 47-50
left. She has a urinary catheter with adequate clear yellow urine. She has a right-sided hip dressing that is dry and intact, an abduction pillow in place and compression boots bilaterally. You notice occasional multifocal premature ventricular contractions (PVCs) on her ECG and she is holding her chest and reports being so hungry “it hurts.” Her lungs are clear to auscultation and there is no change in the duration or character of chest discomfort with deep breathing. She denies nausea and has active bowel sounds. You call the attending anesthesiologist for additional evaluation and a 12lead ECG is ordered. You give PC a loading dose of 4 mg of morphine and start her patientcontrolled analgesia as ordered. Ten minutes later PC reports slight improvement in her pain, now 5/10 on the pain scale, her BP is 158/98, HR 118 with continued multifocal PVCs, and her RR remains 24 per minute. The ECG is completed and read by anesthesia, who notes acute inferior wall changes. Intravenous nitroglycerin and an intensive care bed are ordered.
Sympathetic Nervous System Activation of the Cardiovascular System To fully understand the interactions that result in increases in heart rate and the myocardial oxygen requirements, one must begin with a brief review of the mechanism(s) that increase
Kim A. Noble, PhD, RN, CPAN, is an Assistant Professor at Temple University, Philadelphia, PA. Address correspondence to Kim A. Noble, PhD, RN, CPAN, Department of Nursing, Temple University, 3307 N. Broad St, Philadelphia, PA 19140; e-mail address:[email protected]. © 2007 by American Society of PeriAnesthesia Nurses. 1089-9472/07/2201-0007$35.00/0 doi:10.1016/j.jopan.2006.12.003 47
KIM A. NOBLE
48
cardiovascular (CV) functioning. Although to some extent CV control may be initiated by metabolic or humoral components, the most rapid forms of increases or decreases in CV functioning are mediated through the activity of the autonomic nervous system (ANS).1 There are two branches of the ANS, the parasympathetic nervous system (PSNS) and the sympathetic nervous system (SNS), which work in direct opposition to manipulate systemic function to meet the minute-to-minute changes in systemic needs. The SNS and the PSNS are on opposite ends of the spectrum in terms of mechanism of action and physiologic responses. The PSNS exerts an effect through the interaction of the neurotransmitter acetylcholine, and the muscarinic and nicotinic cholinergic receptors. The SNS uses the neurotransmitters norepinephrine and epinephrine, working through the autonomic alpha (␣) and beta () receptors. The autonomic receptors are further subdivided based on their location of effect, with the ␣-receptors residing in vascular smooth muscle, the -1 receptors found primarily in cardiac muscle, and the -2 receptors found in the conducting airways of the lungs. Activation of the SNS, as would be seen in a fight-or-flight response, leads to a rapid and dramatic increase in CV performance. SNS fibers innervate multiple areas of the atria and ventricles and trigger the release of norepinephrine, which binds to -adrenergic receptors on the cardiac cell membranes, causing an increased metabolic activity,1 which can be further divided into four separate events. First, -adrenergic receptors are present on the sinoatrial (SA) node and conduction system of the heart, leading to an increase in heart rate and conduction velocity. Second, norepinephrine increases the movement of calcium into the cardiac cells, leading to an increase in contractility of the cardiac myocytes. The third and fourth events are in response to SNS stimulation of the ␣-adrenergic receptors, leading to contraction and increased resistance in the vascular smooth muscle of the blood vessels. The third
event results from the contraction of the venous system, causing an increased venous return to the right atrium and increased preload or stretch of the ventricle. The fourth and final event is in response to the contraction of the arterial system and leads to an increase in the peripheral vascular resistance, arterial blood pressure, and the afterload or work required by the ventricle to eject blood. Each of these events independently increases myocardial oxygen requirements, but their summation significantly increases the demand for oxygen by the heart.1 Inequalities are encountered when the supply of oxygen via the coronary arteries is diminished by disease such as the partial coronary occlusion seen with PC.
Tachycardia and CAD Increasing the HR forces the events that take place during depolarization (systole) and repolarization (diastole) to increase in frequency, causing a higher demand for oxygen. With depolarization, ion channels open and electrically charged ions move across the cell membrane, allowing the interaction between actin and myosin and contraction of the myofibrils. During repolarization, ion concentration gradients are re-established through the activity of adenosine triphosphate-dependent, energy-burning pumps, and the resting membrane potential for the next contraction is reset. Because of the nature of myocardial contraction, very little blood is delivered to the contracting myocardial cells; instead a majority of blood flow to the muscle takes place during diastole, or repolarization. In a patient with a normal HR of 70 beats per minute, depolarization or systole accounts for one-third of the cardiac cycle, whereas diastole or repolarization represents twothirds of the cycle. The time of systole is relatively fixed and increases in HR predominantly affect the time of diastole, or filling. Because this is the only time the myocardium receives its blood supply, decreasing the time of filling reduces the supply of
PATHO CORNER
oxygen to the working heart. As an increase in HR simultaneously increases the demand for oxygen by myocardial cells, tachycardia creates a double-edged sword for the patient with pre-existing CAD: an increase in oxygen demand with a decrease of oxygen flow and nutrients to the contracting myocytes.
Implications for the PACU Patient CAD affects approximately 13 million Americans, leading to a coronary event every 26 seconds and a coronary-related death every minute.1 The chances of having a patient with CAD in your PACU are good and the prevention of coronary complications is a priority. A brief summary of the implications of CAD for the awakening PACU patient follow. Alteration in Gas Exchange
Every patient emerging from general anesthesia requires the maintenance of a patent airway and adequate respiration is priority one. The provision of supplemental oxygen is imperative but an even higher priority for the patient with CAD and increased myocardial oxygen requirements. Because the administration of more than 2 L of intravenous fluid and an increased workload on PC’s heart may lead to a new onset of heart failure, diligent monitoring of pulse oximetry and frequent auscultation of breath sounds is vital. The reason for PC’s admission agitation must be explored and a careful evaluation of her epidural level completed. The origination of PC’s increased respiratory rate should be determined too because this also indicates an increase in the work of breathing. The administration of opioids requires diligent monitoring for physiologic response and, as with any patient emerging from a surgical procedure, PC should be encouraged to breathe deeply and cough at intervals. Alteration in Cardiovascular Functioning
As discussed previously, the effect of heightened sympathetic nervous system activity in-
49
creases the workload and myocardial oxygen requirements of the myocardium. This is especially problematic for myocardial tissue that is not receiving an adequate supply of oxygen and nutrients. Control of PC’s pain is important through the administration of opioids and the initiation of a nitroglycerin infusion. Nitroglycerin rapidly dilates the coronary and systemic vasculature, leading to an increased blood supply to the myocardium and a reduction in the preload or venous return to the heart.2 Vasodilation of the arterial system will also decrease the afterload, or the amount of pressure or work that must be completed by the left ventricle to eject blood through the aortic valve. An optimal blood pressure goal based on preoperative readings should be received from the attending anesthesiologist, and diligent monitoring of systemic blood pressure and the titration of the nitroglycerin drip completed to maintain the target blood pressure. An ongoing nursing assessment of the epidural level should be conducted at intervals. Residual blockade from epidural injection may lead to a loss of sympathic tone, venous pooling, and blood pressure reduction. Caution should be used for any changes in position until the level is below T12.3 Lab work should be ordered and obtained from the attending anesthesiologist; these include cardiac isoenzymes and troponin levels, as well as hemoglobin and hematocrit (H&H) and serum electrolytes. Continuous cardiac monitoring is needed because PC is having frequent multifocal PVCs. These PVCs may be attributed to the myocardial ischemia, hypoxemia, or electrolyte imbalance, and they may require the administration of an antiarrhythmic if they persist. PC’s baseline H&H was low (10.1) and it should be expected to decrease further with the surgical procedure, administration of intravenous fluids, and blood losses. If it was not already completed, an order for a blood type and screen should be obtained for a possible transfusion because anemia will further complicate PC’s ischemic myocardium.
KIM A. NOBLE
50
Finally, as the cardiovascular effects of the SNS are mediated primarily through the  receptors which innervate the myocardium, the perianesthesia nurse must be prepared for the administration of a -antagonist or -blocker if PC remains tachycardiac because these pharmacologic interventions will decrease myocardial oxygen requirements and increase the time of diastole and blood supply to the myocardial cells.
Because of the significance of CAD in Americans, the chance of recovering a patient with CAD is very good and the perianesthesia nurse must be prepared to intervene should complications develop. With an understanding of the physiologic consequences of SNS activity on the cardiovascular system, the nurse caring for the patient with CAD emerging from anesthesia can be anticipated, identified, and treated rapidly.
References 1. McCance KL, Huether SE. Pathophysiology: The Biologic Basis for Disease in Adults and Children. Ed 5. St. Louis, MO: Mosby; 2006. 2. Aschenbrenner DS, Venable SJ. Drug Therapy in Nurs-
ing. Ed 2. Philadelphia, PA: Lippincott Williams & Wilkins; 2006. 3. Drain CB. PeriAnesthesia Nursing: A Critical Care Approach. Ed 4. St. Louis, MO: Saunders; 2003.