There was delay in proceeding with diagnostic testing and treatment and finally an abdominal CT done 3 hours ago revealed a fluid collection and obvious perforation in the region of her sigmoid colon.

Over the past several hours she has become progressively more hypotensive and oliguric. Antibiotics have been instituted, a nasogastic tube and Foley catheter placed, and she has received 1,500 mL of normal saline over the past 3 hours. Her current vital signs are blood pressure 80/30 mm Hg, pulse (P) 110 per minute and full, respirations (R) 22 per minute and temperature 38.4°C. She is experiencing some shortness of breath although her lungs sound clear to auscultation. Her heart sounds are normal and her abdominal exam is as described above. Her airway also appears normal.

Her past medical history is significant for a myocardial infarction 3 years ago at which time she was in mild congestive heart failure. Angiography was performed at that time which revealed a 100% left anterior descending coronary artery (LAD) lesion with <50% lesions in her right main and circumflex coronary arteries. An angioplasty of the LAD was performed without stent placement. Since that time she has been asymptomatic. She is very active without any limitations.

Her medications have included atenolol 50 mg twice daily, which has not been administered since her admission, and furosemide 20 mg once daily with potassium supplementation. Available laboratory studies performed 24 hours ago showed a hemoglobin of 11 gm/dL, white blood count of 16,000 with a left shift and normal appearing platelets. Her electrolytes were sodium 145 mEq/L, potassium 4.2 mEq/L, chloride 104 mEq/L, and CO₂ 18 mEq/L. Additional findings were a BUN of 25 mg/dL, creatinine 1.4 mg/dL, and glucose 98 mg/dL. Her chest x-ray on admission was normal without any evidence of infiltrates or failure and her EKG showed a sinus rhythm at 72 per minute with evidence of an old inferior myocardial infarction, but no signs of acute ischemia.

Preoperative Evaluation and Preparation

Although in acute distress with signs consistent of septic induced shock, necessitating a surgical procedure for drainage of a likely abscess with bowel resection and diversion, the urgent, not emergent, nature of this procedure should allow for some stabilization prior to induction of anesthesia. Such must be discussed with the surgeon along with the offer to provide whatever assistance is necessary for this preoperative management. As antibiotic therapy has been instituted along with gastrointestinal drainage and urinary catheterization, the therapy now should be directed at stabilization of her hemodynamic dysfunction with the goal of improved tissue perfusion.

A definition of shock indicates that regardless of etiology this state is a manifestation of failure of the heart to pump blood into the aorta in sufficient quantity and under sufficient pressure to maintain the pressure-flow relationship for adequate tissue perfusion and aerobic metabolism. As such the clinician must first be aware of normal hemodynamic physiology, have the ability to assess existing pathophysiology and the therapeutic acumen to correct the abnormalities minimizing the adverse sequelae of both disease and therapy induced major organ dysfunction.

Controversy may exist as to the best monitoring approaches and the preferred pharmacologic manipulations to optimize tissue perfusion in shock, however, whatever options are taken should focus on the physiologic principles outlined by awareness of the models created by Starling with the ventricular function curves identified in Figure 70-1 and those of Otto Frank with the pressure volume loop diagram in Figure 70-2.

A full physiologic discussion is both beyond the scope of this presentation and is also assumed to be well understood by clinicians involved in the perioperative care of critically ill patients.

The most important assessment is to develop an initial hypothesis based on an understanding of the underlying disease and the information gained from selected laboratory and monitoring data. In the patient under consideration here, it is recognized that the principle etiology of her hemodynamic compromise is septic (likely gram-negative bacteremic) induced, but one must also be cognizant of the potential complicating role of her underlying ischemic cardiac disease.

As shown in Figure 70-3 using the pressure volume loop diagram, the patient’s initiating pathophysiology would be a dramatic fall in vascular resistance as a result of likely endotoxin and other cytokine-induced vasodilation. Accompanying this drop in resistance as shown by the decreasing slope of the effective arterial elastance (EAE) will be a profound decrease in preload—ventricular end-diastolic volume (EDV)—both as a result of vascular dilation but also an increase in endothelial permeability resulting in a loss of intravascular volume to the adjacent interstitium.

Options that exist for the assessment of her intravascular volume include central venous pressure (CVP), pulmonary artery occlusive pressure (PAOP) and echocardiography. Each clinician will have her/his preference based on experience, concerns over complications of the invasive procedure and awareness of the evidence in peer reviewed scientific literature.

Where the experienced echocardiographer can gain useful information in evaluating the volume status of the left ventricle, it should be recognized that the assessment of central venous or pulmonary arterial pressure provides the added benefit of minimizing the risk of development of hydrostatic pressure induced pulmonary edema from over aggressive fluid administration.

In recent years, there has been increasing reluctance to place the flow-directed pulmonary artery (PA) catheter based on concerns for complications and lack of scientific data in support of its benefits. As a result, increasing reliance on the central venous pressure (CVP) attained from catheters placed in the superior vena cava has developed. It must be recognized, however, that reliance on right-sided filling pressures may provide insufficient information regarding the optimization of left ventricular preload particularly in a patient such as the one presented here with underlying cardiac disease.

The availability of both end-diastolic related pressure assessment of the left ventricle measuring the pulmonary artery occlusive or wedge pressure (PAOP) and direct measurement of thermal dilution cardiac output (CO) and, thus calculation of stroke volume (SV) and systemic vascular resistance (SVR) are advantages of the PA catheter. The absence of some means to accurately assess the adequacy of CO is a limitation of the use of most commonly placed CVP catheters.

More recently the addition of oximetry to both PA and CVP catheters permits the clinician to assess mixed venous (S^vO₂) or central venous (S_cvpO₂) oxygen saturation as a means to evaluate the effectiveness of treatment to improve tissue oxygen delivery. If CVP measurement is to be the choice to assess the adequacy of preload in a patient such as the one here, the availability of direct measurement of central venous oxygen saturation (S_cvpO₂) either using a CVP catheter with oximetry or repeated measurement of central venous blood samples for oxygen saturation must be considered.

Assessment of the patient presented here shows her to be hypotensive, tachycardic, tachypneic, and oliguric. These findings along with her history and presentation indicate that she is suffering from septic shock likely with insufficient tissue perfusion. Steps to be considered at this time would be added oxygen by face mask and placement of an arterial catheter for blood pressure assessment and withdrawal of blood for evaluation of arterial blood gases (ABG) and other laboratory studies.

While awaiting the results of her ABG, central venous cannulation should be done using ultrasound guidance. For the purposes of this discussion, initial placement of a CVP catheter with oximetry will be used. Once accomplished, the following results are attained—mean arterial pressure (MAP) 50 mm Hg, P 110, CVP 3 mm Hg, and S_cvpO₂ 58%. An ABG reveals a PaO₂ 95 mm Hg (receiving 4 lpm oxygen), PaCO₂ 32 mm Hg, and pH 7.29. She remains anuric.

The results of the initial assessment following scheduling of her surgery demonstrate her to have insufficient perfusion as evidenced by her anuria, metabolic acidosis, and low central venous oxygen saturation (normal = 70%). Given her low CVP, further volume administration remains the principal means for resuscitation.

At this point one may consider temporizing with a vasoconstrictor—phenylephrine or norepinephrine; however, reliance on such a pharmacologic approach in the presence of insufficient preload would only aggravate her tissue hypoperfusion. Pending assessment of her hemoglobin, fluid therapy using either crystalloid or colloid would be acceptable. Should crystalloid be chosen, lactated ringer may be preferable to normal saline to avoid aggravating her acidosis by making her hyperchloremic.

Although her pH is low, the hazards of bicarbonate administration, including left shift of the oxyhemoglobin dissociation curve and decreased ionized calcium, should cause hesitation while observing to see if correction of her tissue hypoperfusion improves her apparent lactic acidosis. A reasonable goal for fluid administration would either be a return of reasonable blood pressure (MAP > 65 mm Hg) in the absence of vasopressor agents, or a CVP of 12 mm Hg whichever comes first. Once either goal is reached the S_cvpO₂ should be reassessed.

As one proceeds with treatment there should be anticipation for moving to the operating room (OR) as surgery will obviously be required to remove the offending etiology. The goal of preoperative stabilization should be to enhance the ability of the patient to withstand anesthesia induction and surgery and to allow the anesthesiologist to become more aware of the patient’s pathophysiology and ability to withstand the anesthesia and surgery.

After about 1 hour of therapy with fluid and vasopressor administration the patient remains hypotensive (MAP = 55 mm Hg) and anuric. At this point having received 2.5 liters of lactated ringer solution and a current infusion of phenyleprine at 120 μg/min, her CVP is 12 mm Hg and her S_cvpO₂ is 65%. Her arterial oxygen saturation is 95% and she is not showing signs of worsening respiratory function although she remains tachypneic and her ABG shows a PaCO₂ of 33 mm Hg and a pH of 7.26.

With her CVP having reached a reasonable level and her blood pressure remaining below acceptable levels the clinician must determine if the patient’s CO is inadequate requiring inotropic support or if further increase in SVR is necessary. This is the most common dilemma faced by clinicians in evaluating patients in septic shock, particularly in the older population with decreased cardiac reserve.

The questions to be answered are (1) Does the patient have sufficient CO to provide satisfactory perfusion or will the vasopressor while normalizing blood pressure further decrease perfusion through profound vasoconstriction? (2) Is mixed venous oxygen saturation a reliable indicator of satisfactory vital organ perfusion and oxygen delivery in a state of septic shock known to be accompanied by peripheral shunting?

Finally, to complicate matters further, caution must be exercised in evaluating the response to various vasoconstrictor and inotropic agents in the presence of reduced adrenergic receptor responsiveness known to be present in patients with bacteremic septic shock. Figure 70-4 demonstrates an algorithm that might be considered in treating patients with hemodynamic instability regardless of etiology. In reviewing this approach the author has indicated examples of data to be considered; however, the clinician must individualize each patient as to the values to assign for the parameters described. The influences of preexisting hypertension, coexisting cardiac disease, influence of current processes on mixed venous oxygen saturation and adverse responses to therapy must all be considered.

Accompanying any decision to institute pharmacologic support in the form of vasoconstrictors agents to increase SVR or inotropes to increase CO, the clinician must consider both the side effects of these agents and their mechanisms of action. Table 70-1 outlines expected responses to these agents and groups them by their mechanisms of action. The importance of the mechanism relates to reduced responsiveness of the adrenergic receptors—alpha and beta—with resultant decrease in adenyl cyclase production and thus decrease in cyclic-AMP. It is the cyclic-AMP that increases the availability of ionized calcium facilitating muscle contractility. Should responsiveness to adenyl cyclase stimulation be impeded, agents with alternative mechanisms should be considered.

Further consideration in evaluating the response to these agents must include the ionized calcium level as all agents ultimately cause their desired effect by increasing intracellular ionized calcium to facilitate the bond between the actin and myosin protein units for increasing muscular contractility be it the myocardium or the smooth muscle of the media layer of arteries. A decision to directly treat the patient’s acidosis may be influenced by the failure of responsiveness to adrenergic agents in an acidotic environment.

In the patient considered here, a decision is made to place a flow-directed PA catheter using the existing CVP site. With placement it is found that the patient’s PAOP is 14 mm Hg and CO is 3.6 lpm. As a result an infusion of epinephrine is selected to provide inotropic support while attempting to decrease the phenylephrine and maintaining the PAOP and CVP at current levels. Over the next 20 minutes with epinephrine now at 80 ng/kg/min and phenylephrine at 30 μg/min, the patient has attained a MAP of 72 mm Hg, P 92, PAOP 13 mm Hg, and CO of 6.2 lpm. The patient appears stable with satisfactory arterial oxygen saturation and she is brought to the OR for her procedure.

Figure 70-5 demonstrates the pathophysiology indicated by the data attained from the PA catheter demonstrating normalized EDP with persistent vasodilation and decreased myocardial contractility.

Although a favorable result has been described with this choice of therapy, it must be recognized that alternative choices regarding both the vasopressor and inotropic agents could have been made. Norepinephrine and vasopressin have been demonstrated to provide satisfactory increases in SVR. Dobutamine has been recommended as the preferable inotrope although one has to recognize that it is a far weaker beta-adrenergic stimulant when compared to epinephrine and has associated vasodilator effects that may be undesirable in this patient.

As one proceeds, careful attention to acid-base balance, lactic acid levels, urine output and clinical assessment of capillary filling must be continually evaluated as indicative of adequate tissue perfusion. The added benefit of echocardiography in assessing EDV as well as observing for any indications of myocardial ischemia should also be considered. Reliance on end-diastolic pressure as indicative of adequate EDV can be misleading in patients with cardiac disease manifested by diastolic dysfunction and altered ventricular compliance. Certainly, once under anesthesia should trans-esophageal echocardiography be available, it should be considered.

Finally, prior to anesthetic induction a repeat hemoglobin measurement should be attained as administration of crystalloid may have induced hemodilution and transfusion may be indicated. A hemoglobin level of at least 10 g/dL should be considered to minimize cardiac work and provide tissue oxygenation in the face of increased tissue demands in this hypermetabolic state. Blood availability and that of coagulation products should be assured prior to anesthetic induction and surgery.

Intraoperative Management

As the patient is brought to the OR the anesthesia caregiver must determine how best to induce anesthesia. The hemodynamic instability of this patient and the likelihood of coagulopathy would make a regional technique a poor choice. Thus, induction of general anesthesia must be considered.

With all of the monitoring in place and therapy satisfactorily applied the choice of induction agents is not as critical as the method of administration. Slow careful titration should be considered regardless of the agents selected. Gastric evacuation with the nasogastric tube should have decreased the risk of aspiration and made a rapid sequence induction (RSI) less necessary. If a RSI is planned than choice of induction agent may be more crucial with avoidance of propofol or thiopental, as a bolus of either could lead to profound hypotension and instability. In such a situation etomidate or even ketamine may be desirable.

The patient is transported to the OR with full monitoring and oxygen administration while continuing to administer the hemodynamic agents selected. Upon arrival in the OR the patient is moved to the operating table and monitors transferred. Availability of CO and venous saturation monitoring in addition to all pressures should be present upon arrival.

After re-establishment of the monitors and insuring continued stability the anesthesiology care proceeds with induction of general anesthesia. After preooxygenation, the choice is made to slowly titrate doses of intravenous midazolam and fentanyl until loss of lid reflex followed by intravenous administration of rocuronium. During induction the patient’s MAP decreases to 58 mm Hg and 100 μg of phenylephrine is administered. Following satisfactory muscle relaxation the patient is intubated and placed on mechanical ventilatory support. Anesthetic maintenance commences with titration of further intravenous opioid and inhalation of sevoflurane as tolerated. The surgical procedure then commences.

Although an example of anesthetic management is provided it must be acknowledged that multiple possibilities exist. Rather than focusing on the choices of anesthetic agents for induction and maintenance it is of far more importance to emphasize the continued monitored physiologic approach to therapy instituted in the preoperative period.

Now complicated by the application of surgical and anesthetic procedures and the stress accompanying those interventions, the anesthesia clinician must remain attentive to the existing monitors, assessing blood samples for acid base balance, hemoglobin levels, electrolytes, ionized calcium and coagulation factors, and responding to changes that can be expected to occur aggravated by the surgical manipulations including fluid shifts and hemorrhage. During the surgical procedure attention must also be focused on expected sequelae of the hemodynamic compromise and resuscitation that has taken place.

The development of respiratory insufficiency in the form of acute respiratory distress syndrome (ARDS), renal and hepatic ischemia and failure, cardiac ischemia and infarction, or coagulopathy must all be anticipated. Dependent on the magnitude of the surgery and its duration, one cannot underestimate the implications of intraoperative management on the postoperative course and eventual outcome. The role of the anesthesia caregiver in this patient goes far beyond that of providing insensibility to pain, lack of awareness and muscle relaxation. Barring a surgical catastrophe and a reasonable intraoperative time the patient should be expected to tolerate the procedure with minimal further disruption of hemodynamics.

Postoperative Management

The surgical procedure has taken about 90 minutes during which time incision and drainage of an abscess cavity, resection of the sigmoid colon and a descending colostomy has been performed with minimal blood loss. The patient has remained stable and trans-esophageal echocardiography (TEE) used during the procedure has not indicated any evidence of myocardial ischemia and has verified adequacy of ventricular EDV.

The agents used for hemodynamic support have been epinephrine now at 70 nanog/kg/min and phenylephrine at 50 μg/min. A recent ABG while receiving 50% oxygen showed a PaO₂ 105 mm Hg, PaCO₂ 37 mm Hg and a pH of 7.31. Ionized calcium was 0.98 and 1,000 mg of CaCl₂ was administered. During the surgery a hemoglobin of 8.8 gm/dL was noted and she received 2 units of packed cells. Her coagulation profile was acceptable and there was not excessive bleeding. She also received 2,200 mL of crystalloid keeping her CVP and PAOP at presurgical levels. Her urine output during the procedure remained scant. The decision is made to leave her intubated and sedated and to transport to the ICU with full monitoring and manual ventilation with oxygen.

The decision to leave the patient intubated and sedated for the early postoperative period provides the opportunity to maintain stability during the transport and reestablishment of intensive care while transitioning to a new nursing and medical team. This is not the time to add the potential development of respiratory insufficiency and effects of pain and anxiety while attempting to maintain a stable environment dealing with hemodynamic, renal, cardiac, and other system dysfunction.

In most clinical environments the anesthesia caregiver will provide a full and complete report to both the accepting nursing and medical teams who will be assuming further management. However, the knowledge gained and the experience with this patient over that last 3 to 5 hours provides a substantial amount of accumulated information that is invaluable to the physicians and nurses assuming care.

The postoperative period will present tremendous challenges in continuing to provide proper hemodynamic support with the hoped for restitution of vital organ function most notably splanchnic and renal. What has been demonstrated in this patient thus far is that proper management resulting in provision of satisfactory central hemodynamic function as evidenced by SVR, CO, indices of preload, mixed venous oxygen saturations and acid base status do not insure that those most sensitive tissues to ischemia—splanchnic and renal—will be preserved. Current monitoring technology is limited in provided evidence of perfusion and tissue oxygenation of these vascular compartments. Thus, continued management to avoid further insults is critical.

It must also be recognized that although the primary insult has been addressed and proper antibiotics will be provided based on results of microbial culture assessment, the progress of the septic process with its concurrent systemic inflammatory response syndrome will likely continue. Should decreasing responsiveness to inotropic and vasopressor agents be noted, in addition to consideration for agents with alternative mechanisms of action as described above, the possibility for adrenal suppression should be addressed with either the assessment of baseline cortisol levels or a corticotropin stimulation test. Should adrenal suppression be identified replacement therapy should ensue with recommended dosing of 125 mg of hydrocortisone IV every 8 hours.

Once the patient is stabilized with satisfactory hemodynamics, weaning from ventilatory support and extubation should be considered. This assumes that no evidence of ARDS has appeared and the patient has satisfactory oxygenation and acid-base equilibrium is evident.

Suggested Reading

1. Dellinger RP, Carlet GM, Masur H, et al. Surviving sepsis campaign guidelines for management of severe sepsis and septic shock. Crit Care Med 2004;32:858–873.

2. Doyle CA, Rosenthal MH. Hypotension and shock states. In: Gravenstein N, Kirby R, Lobato E, eds. Complications in Anesthesiology. Philadelphia, PA: Lippincott-Raven; 2007.

3. Gilbert EM, Hershberger RE, Weichmann RJ, et al. Pharmacologic and hemodynamic effects of combined beta-agonist stimulation and phosphodiesterase inhibition in the failing heart. Chest 1995;108:1524–1532.

4. Moran JL, O’Fathartaigh MS, Peisach AR, et al. Epinephrine as an inotropic agent in septic shock: a dose-profile analysis. Crit Care Med 1993;21:70–77.

5. Rivers E, Nguyen B, Havsted S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001;345:1368–1377.

6. Rozenfeld V, Cheng JW. The role of vasopressin in the treatment of vasodilation in shock states. Ann Pharmacotherap 2000;34:250–254.

7. Silverman HJ, Penaranda R, Orens JB, et al. Impaired beta-adrenergic stimulation of cyclic adenosine monophosphate in human septic shock: associated with myocardial hyporesponsiveness to catecholamines. Crit Care Med 1993;21:31–39.

Part C: Respiratory Diseases

Chronic Obstructive Pulmonary Disease

Binbin Wang, MD • Linda L. Liu, MD

1) Epidemiology

    a) COPD is the fourth leading cause of chronic morbidity and mortality in the United States (1).

    b) Prevalence can be as high as 5% to 10% in the age-matched general surgery population, and up to 40% of thoracic surgery patients (2).

2) Pathophysiology

    a) Pathological changes consist of chronic inflammation seen in the proximal and peripheral airways, lung parenchyma, and pulmonary vasculature.

  i) The gas exchange abnormalities of severe COPD depends on whether the inflammation leads to emphysema with alveolar wall and pulmonary capillary destruction or chronic bronchitis with airway obstruction and cough/sputum production.

    b) “Pink puffers” have emphysematous lung destruction and they tend to have PaO₂ > 65 mm Hg, with a normal to slightly decreased PaCO₂.

    c) “Blue bloaters” more often meet criteria for chronic bronchitis and have:

  i) Hypoxia from V/Q mismatch and

  ii) Hypercapnia from increased dead space ventilation, and impairment of ventilatory muscles (3).

Related posts:

Fiberoptic Intubation Obstructive Sleep Apnea Malignant Hyperthermia Local Anesthetics Pulmonary Artery Catheter Adult Cardiac Surgery

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