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changes in venous return and cause pulmonary edema. Diastolic heart failure results from a diverse group of causes, including valvular disease, restrictive or infiltrative cardiomyopathies, and hypertensive and hypertrophic cardiomyopathies.

disruption or dissection of coronary vessels. e most commonly injured chamber is the RV (40%) because of its anterior location underneath the sternum.9 As a result, RV systolic dysfunction may be seen aer injury.13 Echocardiography diagnoses the wall motion abnormalities from a cardiac contusion that can signicantly aect both

RIGHT HEART FAILURE

In contrast to the left ventricle (LV), the right ventricle (RV)— a thin- walled chamber with a complex three- dimensional shape— is not adapted for significant pressure generation. The RV can usually deliver adequate flow to the low- resistance pulmonary vasculature, but its performance is exquisitely sensitive to RV afterload, which can increase suddenly in the setting of acute pulmonary hypertension or pulmonary venous congestion from left ventricular failure. Approximately two- thirds of the force involved with right ventricular contraction is provided by the thickwalled intraventricular septum. Decreased contractility of the RV and/ or septum and changes in septal geometry can contribute to RV failure. When the RV begins to fail, it dilates, increasing myocardial wall tension, myocardial oxygen demand, and filling pressures.7 Unlike the LV, the RV receives its blood supply throughout the cardiac cycle. Increases in both systolic and diastolic RV intraventricular pressure coupled with the systemic hypotension of RV failure and increased myocardial oxygen demand, decreases myocardial blood flow and contractility.

5,8

Eventually, RV dilatation results in tricuspid insufficiency and an abrupt rise in central venous pressure (CVP). Failure of the RV causes systemic hypoperfusion via two mechanisms:decreased cardiac output with hypotension and increased CVP with venous congestion. An increased CVP effectively increases the outflow pressure to perfusion of vital organ systems to further decrease organ perfusion accelerating multiorgan system failure.

CARDIACTRAUMA

Blunt cardiac injury (BCI) accounts for 10%– 25% of trauma mortality.

9– 11

Direct impact of the chest wall, rapid deceleration, and abdominal visceral herniation from an injury below the diaphragm can compress the heart between the sternum and spine. e most common cause of death aer BCI is from rupture of one or more cardiac chambers.

Nonlethal injuries aer BCI include myocardial con-

tusion, valvular lesions, laceration of the pericardium, and

le and right ventricular function. Echocardiography identies dysfunctional walls and guides uid resuscitation as well as ionotropic support. Additionally, intramural hematomas (IMH) can result in cardiac irritability and conduction abnormalities. Intramural hematomas are relatively benign and will resolve in 4– 12 weeks with conservative management.9 e rhythm disturbances in the immediate postinjury period may require temporary intravenous pacing. Valvular injury can also be diagnosed by echocardiography and may require repair or replacement of the aected valve. Acute dissection of the coronary vessels due to BCI is oen successfully treated with percutaneous angioplasty and/ or stenting.13 e le anterior descending artery is the most common coronary artery to be injured, owing to its anterior location.

SPINALSHOCK

Spinal, or neurogenic shock is caused by transection of the spinal cord above the level of T6. Injuries above this level interrupt the outow of the sympathetic nervous system, leading to a form of distributive shock characteristically associated with bradycardia due to unopposed parasympathetic innervation of the heart.15 It is estimated that there are approximately 12,000 cases a year of spinal, or neurogenic shock.16 e most common cause of traumatic spinal cord injury includes motor vehicle accidents, falls from signicant heights, violence, and recreational activities. It disproportionately aects young adult males.17 In the immediate period of traumatic injury, it is important to assess other organ systems for injury, as spinal cord injury is usually not an isolated lesion and hypotension in these patients could be due to hemorrhagic shock or cardiogenic shock from blunt cardiac injury. Transection at level C3 results in complete loss of respiratory function.17 Patients need to have an airway device placed and be ventilated immediately. In- line neck stabilization or cervical spine immobilization is necessary while attempting to establish an airway in order to avoid potentiating the spinal cord injury. Antimuscarinics like atropine and chronotropes such as dopamine, norepinephrine, and epinephrine should be used to increase the heart rate and blood pressure; phenylephrine should be avoided because of its association with reex bradycardia.

15,17

76 PART III.SHOCK

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ASSESSMENT OFTHE PATIENT:PRESENTING SIGNS AND SYMPTOMS AND INITIAL INVESTIGATIONS

Preoperative evaluation of all patients with a history of HF includes a thorough history and physical examination. e cardiac history focuses on the etiolog y of HF, symptoms (such as orthopnea, dyspnea on exertion, and peripheral edema), functional capacity, current therapy— including medications as well as devices (such as pacemakers, debrillators, or circulatory assist devices), and history of surgical procedures.4 Physical examination includes an assessment of vital signs, auscultation of heart and lungs for rales, evaluation of jugular venous pressure, abdominal palpation for hepatomegaly and ascites, and extremity inspection for peripheral edema. Routine diagnostic evaluation includes electrocardiogram, chest radiography, complete blood count, electrolytes, creatinine, glucose, and liver function tests.

Further preoperative evaluation is guided by the degree of symptoms and the stage of the patient’s heart failure. ere are two major systems used to grade HF patients. Historically, the New York Heart Association (NYHA) has classied HF based on the degree of functional limitation due to symptoms. More recently, the American Heart Association and the American College of Cardiology (AHA/ ACC) have introduced a staging system for HF, which is meant to characterize HF as a “progressive, irreversible, syndrome caused by the interaction of risk factors and the development of structural cardiac abnormalities.”19 e two classication systems provide complementary information in risk assessment of HF patients (Table 10.1). While the degree of a patient’s functional limitation, and

thus NYHA class, can improve or deteriorate, the AHA/ ACC stages are progressive and irreversible— once a patient progresses to stage C, for instance, they cannot revert to a lower stage in the disease process.

For the purposes of perioperative risk stratication, asymptomatic patients (NYHA ClassI, AHA/ ACC stage A and B) do not require further cardiac evaluation, but attention is directed to optimize comorbid conditions and risk factors for the development of HF (hypertension, diabetes, hyperlipidemia, coronary artery disease). Symptomatic patients (NYHA classII- IV, AHA/ ACC stage C and D) are at an increased risk for developing major adverse cardiac events (MACE) in the perioperative period and may require further preoperative evaluation as well as invasive monitoring and specic interventions before elective surgical procedures.4 Elective surgery is contraindicated in patients with signs or symptoms of acute decompensated HF, and emergency procedures in these patients require specialized monitoring and therapy as described in the following sections.

20,21

Preoperative evaluation of symptomatic HF patients (NYHA II- IV, AHA/ ACC stage C- D) should include recent echocardiography and potentially stress testing along with evaluation of B- type natriuretic peptide. Echocardiography evaluates le- and right- systolic and diastolic function, wall motion, and valvular and pericardial abnormalities and estimates pulmonary artery pressures.

4,20

Reduced le ventricular ejection fraction (LVEF) has been associated with postoperative HF exacerbations and MACE.

2,22– 24

Noncardiologists can perform focused point of care echocardiographic exams to assess the HF patient who is undergoing an emergency procedure. In symptomatic HF patients presenting for emergency surgery, an

TABLE10.1 COMPARISON OFACC/ AHA AND NYHA CLASSIFICATION

ACC/ AHA HF Stage NYHA Classication

A High risk for HF but without structural heart disease or

symptoms

B Structural heart disease without signs or symptoms of HF I No symptoms with ordinary physical activity.

C Structural heart disease with prior or current symptoms

ofHF

D Refractory HF requiring specialized intervention IV Symptoms at rest.

Data from:Yancy CW, etal. 2013 ACCF/ AHA guideline for the management of heart failure:a report of the American College of Cardiology Foundation/ American Heart Association Task

Force on Practice Guidelines. Journal of the American College of Cardiology. 62(16):e147– 239.

American College of Cardiology/ American Heart Association Task Force on Practice, G., etal. ACC/ AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac

surgery:executive summary:a repor t of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines

on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). Anesthesia & Analgesia. 106(3):685– 712.

CARDIOGENICSHOCK 77

None

II Slight limitation of physical activity. Symptoms with exertion.

III Marked limitation of physical activity. Symptoms with minimal

exertion.

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abbreviated focused preoperative transthoracic echocardiography (TTE) exam, performed by a trained anesthesiologist, has been shown to change the cardiac diagnosis in 67% and the management plan in 44% of patients.

e role of preoperative stress testing and B- type natriuretic peptide (BNP) levels in symptomatic HF patients is unclear. Released by cardiac myocytes in response to stretch injury, BNP can stratify risk in symptomatic and asymptomatic HF patients. Among lower- risk HF patients (NYHA classIand II), a BNP greater than 189 was associated with a signicantly increased risk of MACE.26 A limitation of clinically using natriuretic peptides in preoperative risk assessment, however, is the wide range of reported cutos and the heterogeneity of the populations studied.2 Similarly, multiple reports have demonstrated that stress testing, when added to clinical risk stratication, can improve prediction of postoperative cardiac death and myocardial infarc-

2,27,28

tion.

Most of these studies, however, have not examined the role of preoperative stress testing in HF specic populations.2 Although BNP and stress testing may provide useful information for perioperative risk stratication and management in select HF patients undergoing elective surgical procedures, these tests should not be routinely ordered as part of the preoperative evaluation of HF patients.

Many patients with advanced symptomatic HF will have pacemakers for cardiac resynchronization therapy or AICDs for arrhythmia prophylaxis. ese devices can interact with surgical electrocautery, to either inhibit pacemaker device functions or cause an AICD to falsely detect an arrhythmia and deliver a therapy. e Heart Rhythm Society and the American Society of Anesthesiologists have published consensus guidelines for the perioperative management of AICDs and pacemakers.29 In general, all pacemakers should be interrogated within 12months; and all AICDs should be interrogated within 6months of elective surgical procedures; AICDs should be inactivated (and the patient should have external debrillator pads placed); and the pacemaker of dependent patients should be placed in an asynchronous pacing mode for all procedures employing monopolar electrocautery above the umbilicus. Procedures involving electrocautery below the umbilicus do not require adjustment of the device, because there is less potential for interference.

further progression of the HF syndrome. While the degree to which HF optimization is taken in order to reduce the risk of perioperative cardiac events has not been thoroughly evaluated, patients with newly diagnosed HF, should have elective procedures delayed in order to evaluate the etiology of their myocardial dysfunction and initiate appropriate interventions.2 Patients with refractory HF may require admission for preoperative optimization of their hemodynamic status with invasive monitoring, vasodilators, and inotropic therapy.

Some HF medications can have adverse eects during the perioperative period. e standard medical therapy administered to HF patients typically includes angiotensinconverting enzyme inhibitors (ACE- I), beta blockers, angiotensin receptor blockers (ARB), aldosterone blockers, diuretics and sometimes digoxin, anticoagulants, and antiarrhythmic medications.4 Chronic beta- blocker therapy is well known to reduce mortality in patients with HF, and acute beta- blocker discontinuation can precipitate withdrawal symptoms that can be life threatening, so patients should be maintained on these agents (e.g., bisoprolol, carvedilol, or metoprolol) unless they require vasopressor or inotropic support.

31– 33

e POISE trial demonstrated that initiating high- dose beta blockers on the day of surgery reduced cardiac mortality but increased all cause mortality, primarily from stroke.34 Consequently, initiation of highdose beta blockers in the perioperative period, without dose titration, is now contraindicated.

2,33

e preoperative administration of ACE- I and ARBs has been associated with severe hypotensive episodes aer induction of regional and general anesthesia. ere is some evidence that patients taking these drugs may be at risk for higher morbidity and mortality. In contrast to discontinuing beta blockers, preoperative discontinuation of ACE- Is or ARBs does not appear to cause rebound hypertension and should be considered prior to elective procedures.

4,35

ere does not however appear to be increased mortality associated with postoperative nonresumption of ACE- I, so these drugs should be restarted in the postoperative period when feasible.36 Preoperative digoxin should be discontinued if there is evidence of digoxin toxicity or bradycardia because of atrioventricular block. Digoxin has a half- life of 1.5days and, if

29,30

necessary, should be discontinued the day before surgery.4

Heart failure patients are oen taking chronic diuretic ther-

MANAGEMENT OFTHE PATIENT

PREOPERATIVE MANAGEMENT

Heart failure patients presenting for surgery can be on complex medication regimens for medical optimization and to limit

apy, and in these patients careful evaluation and management of intra- and postoperative volume status are needed to prevent volume overload. Management of perioperative anticoagulation for HF patients (especially those who have an intracardiac thrombus) should be done in consultation with the surgeon, cardiologist, and anesthesiologist.

78 PART III.SHOCK

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Patients with signicant right ventricular dysfunction, particularly those with pulmonary hypertension, are at extremely high risk for MACE and death aer noncardiac surgery. Symptomatic patients require a preoperative evaluation including the elements described above, and potentially may require preoperative admission for right heart catheterization to initiate or titrate inotropes and pulmonary vasodilators.4 Chronic pulmonary vasodilators should be continued throughout the perioperative period. Discontinuing intravenous prostacyclin therapy can precipitate a life- threatening pulmonary hypertensive crisis.

may be the drug of choice during induction of patients with end- stage HF because it does not produce signicant cardiovascular depression, but concerns over its potential for adrenal suppression limit its use. Induction with ketamine can preserve hemodynamic stability via its sympathomimetic eects. However, in patients with compensated and decompensated HF, induction doses of ketamine can blunt high levels of compensatory endogenous sympathetic tone, adversely aecting hemodynamics. Regardless of the agent used, induction doses should be carefully titrated with

decreased doses and adjusted dosing intervals to account for the increased circulation time of drugs in patients with

INTRAOPERATIVE MANAGEMENT:MONITORING, SURGICAL, AND ANESTHETIC PLANNING

Although minimally invasive surgical techniques that limit inammation, uid shis, or sympathetic activation in HF patients could potentially reduce morbidity and mortality, high- quality clinical evidence to support this notion is lacking. Randomized controlled trials that have reported short- term benets have not investigated HF populations, and have not been adequately powered to appropriately evaluate mortality or rates of MACE.37 Observational studies of minimally invasive surgery have shown a trend toward decreased cardiac and surgical complications as well as length of stay.

2,38

ere is little evidence to support a regional approach over general anesthesia in the high- risk HF patient. e anesthetic goals should include maintenance of hemodynamic stability and avoidance of abrupt changes in cardiac preload, inotropic state, or aerload.

2,39– 43

e eects of intravenous anesthetic drugs in patients with LV systolic dysfunction have been reviewed.44 Avoidance of drugs with substantial negative inotropic or vasodilatory eects, such as barbituates and high- dose propofol, is preferable in this patient population, because many patients with end- stage HF have xed low- stroke volumes, and cardiac output is dependent on compensatory increases in endogenous sympathetic response and baseline heart rate. Suppression of endogenous sympathetic tone during induction can cause hypotension and cardiac arrest even when medications do not have direct negative cardiac eects. Preparation, including invasive intraoperative monitoring

limited cardiac output.

Invasive hemodynamic monitoring is recommended for symptomatic HF patients (NYHA III- IV, AHA/ ACC C- D) who undergo major surgical procedures. Direct arterial pressure monitoring prior to the induction of anesthesia is preferable to facilitate the titration of anesthestic agents, vasopressors, and inotropes during this critical time. Central venous access, which can usually be placed aer induction, permits measurement of CVP and allows the administration of inotropes and vasopressors if necessary.4 e role of the pulmonary artery catheter (PAC) is less clear. Although the PAC indirectly measures le- sided lling pressures, directly measures pulmonary artery pressures, and allows calculation of cardiac output, cardiac index, and systemic vascular resistance, there is little high- quality data to support the assertion that even selective placement of a PAC for adjusting hemodynamic support improves outcomes in surgical patients. Some expert opinion, however, still favors PAC placement in select patients at high risk for hemodynamic disturbances undergoing major procedures involving large uid shis. transesophageal echocardiography (TEE), interpreted by a trained echocardiographer, can provide a valuable adjunct to invasive hemodynamic monitoring. Transesophageal echocardiography can provide a wealth of quantitative and qualitative information on le and right heart function and regional wall motion abnormalities, and serial assessment can help evaluate the response to therapies such as volume administration, vasopressors, inotropes, and systemic and pulmonary vasodilators.

4,44

2,45

Intraoperative

and the timely administration of vasopressors and inotropes can counteract this eect.4 High doses of benzodiazepines (such as midazolam) and opiates (such as fentanyl) have traditionally been used in cardiac anesthesia to maintain hemodynamic stability during induction, however prolonged eects can delay postoperative extubation and are strongly associated with postoperative delirum. Etomidate

INTRAOPERATIVE MANAGEMENT OFCARDIOGENICSHOCK

Cardiogenic shock is dened as a low cardiac output state leading to tissue hypoxemia with end- organ dysfunction in the absence of hypovolemia. It can be due to le- ,

CARDIOGENICSHOCK 79

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right- , or biventricular failure and is associated with a low cardiac index (<2.2 L/ min/ m2), low mixed venous saturation (<60%), and elevated lling pressures (pulmonary capillary wedge pressure >18mmHg for le heart failure, or CVP > 15mmHg for right heart failure).

46,47

e goals for intraoperative management of cardiogenic shock are to identify the cause and rapidly institute appropriate resuscitative measures (maximizing oxygen delivery and reducing oxygen demand) while treating any reparable lesions. If not placed already, invasive hemodynamic monitoring with an arterial line, central venous access, and potentially a PAC is essential for monitoring and administration of pharmacologic support for the patient in cardiogenic shock. Early echocardiography evaluates right and/ or le ventricular dysfunction, the presence of tamponade or regional wall motion abnormalities, and valvular dysfunction and indirectly assesses right- and le- sided preload.

Initial steps in the resuscitation of cardiogenic shock include correction of preload, aerload, heart rate, and rhythm; minimizing myocardial oxygen demand; and increasing oxygen- carrying capacity. Assessing volume status and optimizing preload can be one of the most challenging, yet essential, aspects of managing the patient in cardiogenic shock. Careful assessment of lling pressures, echocardiography, and dynamic assessments of volume responsiveness using techniques such as pulse pressure variation guide uid management to maintain an adequate preload and avoid peripheral or pulmonary edema.4 Maintenance of coronary and systemic perfusion pressure is important to manage cardiogenic shock, but acute

increases in aerload can reduce cardiac output in patients with HF. Careful titration of vasopressors to maintain coronary perfusion and initiation of peripheral or pulmonary vasodilators for elevated systemic vascular resistance (SVR) or pulmonary vascular resistance (PVR) in the setting of le- or right- sided cardiogenic shock, respectively, enhances cardiac output.

4,48

Nonperfusing ventricular or supraventricular arrhythmias require immediate cardioversion, and termination of atrial and junctional arrhythmias (whenever possible and safe) should be attempted in the patient with shock. Because of the association between LV and RV failure and annular dilation with MR or TR, higher heart rates (80– 100 beats per minute) can reduce end diastolic volume to optimize lling.

4,8

Correction of metabolic and respiratory acid/ base disturbances and optimization of oxygenation and ventilation either noninvasively or invasively can enhance oxygen utilization. Reducing myocardial oxygen demand by controlling fever, agitation, or pain; avoiding shivering; and optimizing oxygen- carrying capacity (transfusing to a hemoglobin of 10G/ dL) are important goals in the setting of reduced cardiac output.

Maintaining contractility and cardiac output with inotropic agents and vasopressors may become necessary for persistently low cardiac output aer optimization of preload, aerload, and heart rate. Abrief description of common inotropes and vasopressors is provided in Table 10.2. Because of the down- regulation of beta- adrenergic receptor density and sensitivity that occurs in patients with chronic HF, higher doses of beta agonists, such as epinephrine, norepinephrine, dobutamine, or dopamine, may be required

TABLE10.2 MECHANISM OFCOMMON VASOPRESSORS AND INOTROPES

Medication Receptor/ Mechanism Physiologic Effects

BP HR CO SVR

Epinephrine

Norepinephrine

Dobutamine

Moderate- Dose Dopamine

High- Dose Dopamine

Phenylephrine

Vasopressin V

Milrinone PDE- 3 inhibition (increases cAMP) − − + ++ − −

Levosimendan Calcium Sensitizer 0 0 ++ − −

80 PART III.SHOCK

β1=β2 > α

β1 > α > β

β1 > β2 > α

DA> β

DA > β > α

+ + ++ +

++ 0/ − 0/ + ++

− + ++ −

++ + ++ 0/ −

++ ++ + ++

++ − − ++

++ 0 0 ++

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to increase contractility in these patients.

49,50

Alternate

FOLLOW‐UP

inotropic agents that act downstream of the beta receptor, are oen helpful. Milrinone, a phosphodiesterase- 3 inhibitor that increases intracellular cyclic AMP levels, increases contractility; decreases both systemic and pulmonary vascular resistance; and potentiates the eects of other beta agonists.

48,51

Levosimendan is a newer agent that also acts downstream of adrenergic receptors with a complex mechanism resulting in its properties as an inodilator. It is a myolament Ca2+- sensitizer that promotes a conformational change in cardiac troponin C, increasing myocardial con-

Patients with symptomatic HF (ACC/ AHA stage C- D or NYHA Class II- IV) undergoing high- risk procedures or with complicated intraoperative courses will require postoperative placement in the intensive care unit. Recovery aer less complicated procedures in these patients can be accomplished in the postanesthesia care unit. For asymptomatic patients (ACC/ AHA stage A- B or some NYHA ClassI) recovery and postoperative monitoring should be based on the procedure performed.

4,44

tractility while causing vasodilatation through its interaction with ATP- sensitive K+ channels.52 In general, both retrospective and prospective analyses of many of these

CASE- BASED LEARNING DISCUSSION

agents have suggested increases in mortality and MACE with their acute and chronic use in HF patients, their use should be limited to patients in refractory cardiogenic shock despite optimization of all other parameters, or as a bridge to recovery, transplant, or institution of mechanical circulatory support.

When inotropic agents cannot maintain cardiac output,

short- term mechanical circulatory support can bridge to

46,48,53,54

and

e patient’s BiV AICD is interrogated in the pre- op area. He is 100% paced, and the pacemaker is currently set as DD 60– 120. His AICD is on and has not red in the past 12 months. Everything else is within acceptable limits. How would you choose to reprogram his pacemaker? What would you do with his AICD? Are there any precautions

that you shouldtake? either cardiac recovery or institution of a durable mechanical circulatory support device. Mechanical circulatory support includes the intra- aortic balloon pump (IABP), short- term ventricular assist device (VAD), or circulatory support with an arteriovenous extracorporeal membranous oxygenator (VA- ECMO).

4,46

Preoperative insertion of an IABP can prevent MACE and rescue patients with refractory cardiogenic shock who undergo high- risk noncardiac surgery.4 e IABP inates during diastole and is timed to rapidly deate just before the opening of the aortic valve and has two putative hemodynamic eects: counterpulsation, or augmentation of the diastolic blood pressure (and thus coronary blood ow) with balloon ination, and LV aerload reduction (with consequent reduction in myocardial oxygen demand) caused by systolic balloon deation. It can be placed percutaneously with uoroscopic or echocardiographic guidance.55 Percutaneous VAD therapy (e.g., impella or tandem heart) supports the le ventricle with a rotary pump connected to a cannula that drains either the LA (tandem heart, through a percutaneous atrial septostomy) or LV (impella) and ejects into the aorta.55 e IABP or percutaneous VADs primarily provide le- sided support. In right heart or biventricular failure, ECMO therapy rests the heart to promote recovery of heart function or bridges to a more permanent device,56 although there may be a role for newer temporary right- sided VADs such as the ImpellaRP.

1. You place a preinduction arterial line and perform a rapid sequence induction with etomidate and succinylcholine. Immediately upon induction, the patient’s MAP falls from 70 to 40 with a good waveform on the arterial line. He responds only modestly to phenylephrine and ephedrine boluses, and there are no signs of pneumothorax or tamponade. Could this be due to the interaction between any of his preoperative medications and the induction agents? In addition to investigating other causes of hypotension, are there any other agents that you would like to administer?

2. You stabilize the patient with additional vasopressor agents and place a PA catheter and TEE probe. Your TEE shows global hypokinesis with a LVEF of < 10% with a normal- sized RV with mildly reduced RV function. You obtain a set of hemodynamics:CI 1.5 L/ min/ m2, CVP 10, PA pressure 55/ 24 (mean 31), PCWP 24, MAP 65 on norepinephrine and vasopressin infusions. You send a mixed venous oxygen sample, and the oxygen saturation is 45%. Would you add inotropes at this point? What about inhaled nitricoxide?

3. You elect to start milrinone and epinephrine infusions, and initially see some improvement in oxygen delivery, however he goes into atrial brillation, which causes

CARDIOGENICSHOCK 81

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a signicant drop in his cardiac index and increasing pressor requirements. Would you cardiovert this patient? What anti- arrhythmic drugs would you consider?

4. He is loaded with amiodarone, and three attempts at direct current cardioversion (DCCV) are unsuccessful. His CI and mixed venous saturations stay low despite optimizing his volume status and hematocrit. His lactate begins to rise, and he becomes increasingly unstable. What additional strategies would you consider? Would this involve consultation with another physician?

REFERENCES

1. Go AS, etal. Heart disease and stroke statistics— 2014 update: a

report from the American Heart Association. Circulation, 2014;129(3):e28– e292.

2. Upshaw J, Kiernan MS. Preoperative cardiac risk assessment for

noncardiac surgery in patients with heart failure. Current Heart Fail Reports. 2013;10(2):147– 56.

3. Maile MD, etal. Worsening preoperative heart failure is associated

with mortality and noncardiac complications, but not myocardial infarction aer noncardiac surgery: a retrospective cohort study. Anesth Analg. 2014;119(3):522– 32.

4. Gelzinis TA, Subramaniam K. Systolic heart failure and anes-

thetic considerations. International Anesthesiology Clinics. 2012;50(3):146– 70.

5. McMurray JJ. Clinical practice:systolic heart failure. New England

Journal of Medicine. 2010;362(3):228– 38.

6. Clark JA, Subramaniam B. Diastolic heart failure: periop-

erative management. International Anesthesiology Clinics. 2012;50(3):171– 86.

7. Zarbock A, Van Aken H, Schmidt C. Management of right ventricu-

lar dysfunction in the perioperative setting. Curr Opin Anaesthesiol. 2014;27(4):388– 93.

8. Strumpher J, Jacobsohn E. Pulmonary hypertension and right ven-

tricular dysfunction:physiology and perioperative management. J Cardiothorac Vasc Anesth. 2011;25(4):687– 704.

9. Yousef R, Carr JA. Blunt cardiac trauma: a review of the cur-

rent knowledge and management. Annals of oracic Surgery. 2014;98(3):1134– 40.

10. Skinner DL, et al. Blunt cardiac injury in critically ill trauma

patients:a single centre experience. Injury. 2014;46(1):66– 70.

11. National Trauma Data Bank. 2014 Annual Report. https:// www.

facs.org/ ~/ media/ files/ quality%20programs/ trauma/ ntdb/ ntdb%20annual%20report%202014.ashx

12. Turan AA, etal. Cardiac injuries caused by blunt trauma:an autopsy

based assessment of the injury pattern. Journal of Forensic Sciences. 2011;55(1):82– 4.

13. El- Chami MF, Nicholson W, Helmy T. Blunt cardiac trauma.

Journal of Emergency Medicine. 2011;35(2):127– 33.

14. Sybrandy KC, Cramer MJ, Burgersdijk C. Diagnosing cardiac con-

tusion:old wisdom and new insights. Heart. 2003;89(5):485– 9.

15. Fox AD, Spinal shock. Assessment and treatment of spinal cord inju-

ries & neurogenic shock. Journal of Emergency Medical Services. 39(11):64– 7.

16. http:// www.cdc.gov/ traumaticbraininjury/ scifacts.html.

17. McDonald JW, Sadowsky C. Spinal- cord injury. Lancet. 359(9304):417– 25.

18. Bradic Z, et al. Preoperative preparation of patients with cardiomyopathies in non- cardiac surgery. Acta Chirurgica Iugoslavica. 2011;58(2):39– 43.

19. Yancy CW, etal. 2013 ACCF/ AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/ American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology. 2013;62(16):e147– 239.

20. American College of Cardiology/ American Heart Association Task Force on Practice G, et al. ACC/ AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: executive summary: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). Anesthesia and Analgesia. 2007;106(3):685– 712.

21. Fleisher LA, etal. ACC/ AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery:a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). Circulation. 2007;116(17):e418– 99.

22. Fletcher JP, et al. Risk of aortic aneurysm surgery as assessed by preoperative gated heart pool scan. British Journal of Surgery. 1989;76(1):26– 8.

23. Rohde LE, etal. Usefulness of transthoracic echocardiography as a tool for risk stratication of patients undergoing major noncardiac surgery. American Journal of Cardiology. 2001;87(5):505– 9.

24. Halm EA, et al. Echocardiography for assessing cardiac risk in patients having noncardiac surgery. Study of Perioperative Ischemia Research Group. Annals of Internal Medicine. 125(6):433– 41. [Erratum appears in Annals of Internal Medicine. 1997;126(6):494.]

25. Holm JH, et al. Perioperative use of focus assessed transthoracic echocardiography (FATE). Anesth Analg. 2012;115(5):1029– 32.

26. Dernellis J, Panaretou M. Assessment of cardiac risk before noncardiac surgery: brain natriuretic peptide in 1590 patients. Heart. 2006;92(11):1645– 50.

27. Boersma E, etal. Predictors of cardiac events aer major vascular surgery: role of clinical characteristics, dobutamine echocardiography, and beta- blocker therapy. JAMA. 2001;285(14):1865– 73.

28. L’Italien GJ, etal. Development and validation of a Bayesian model for perioperative cardiac risk assessment in a cohort of 1,081 vascular surgical candidates. Journal of the American College of Cardiology. 1996;27(4):779– 86.

29. Crossley GH, etal. e Heart Rhythm Society (HRS)/ American Society of Anesthesiologists (ASA) Expert Consensus Statement on the perioperative management of patients with implantable debrillators, pacemakers and arrhythmia monitors:facilities and patient management. Heart Rhythm. 2011;8(7):1114– 54.

30. Crossley GH, etal. e Heart Rhythm Society (HRS)/ American Society of Anesthesiologists (ASA) Expert Consensus Statement on the perioperative management of patients with implantable debrillators, pacemakers and arrhythmia monitors:facilities and patient management:executive summary. Heart Rhythm. 2011;8(7):e1– 18.

31. Anonymous. Eect of metoprolol CR/ XL in chronic heart failure: Metoprolol CR/ XL Randomised Intervention Trial in Congestive Heart Failure (MERIT- HF). Lancet. 1999;353(9169):2001– 7.

32. Anonymous. e Cardiac Insuciency Bisoprolol Study II (CIBISII):a randomised trial. Lancet. 1999;353(9146):9– 13.

33. Jessup M, etal. 2009 focused update:ACCF/ AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults:a report of the American College of Cardiology Foundation/ American Heart Association Task Force on Practice Guidelines: developed

82 PART III.SHOCK

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in collaboration with the International Society for Heart and Lung Transplantation. Circulation. 2009;119(14):1977– 2016.

34. Group PS, et al. Eects of extended- release metoprolol succinate in patients undergoing non- cardiac surgery (POISE trial): a randomised controlled trial. Lancet. 2008;371(9627):1839– 47.

35. Comfere T, etal. Angiotensin system inhibitors in a general surgical population. Anesthesia and Analgesia. 2005;100(3):636– 44, table of contents.

36. Lee SM, Takemoto, S, Wallace, A. Association between withholding angiotensin receptor blockers in the early postoperative period and 30- day mortality:a cohort study of the Veterans Aairs healthcare system. Anesthesiology. 2015;123(2):288– 306.

37. Cox MR, et al. Prospective randomized comparison of open versus laparoscopic appendectomy in men. World Journal of Surgery. 2005;20(3):263– 6.

38. Brunt LM. e positive impact of laparoscopic adrenalectomy on complications of adrenal surgery. Surgical Endoscopy. 2002;16(2):252– 7.

39. Christopherson R, et al. Perioperative morbidity in patients randomized to epidural or general anesthesia for lower extremity vascular surgery. Perioperative Ischemia Randomized Anesthesia Trial Study Group. Anesthesiology. 1993;79(3):422– 34.

40. Barbosa FT, et al. Neuraxial anaesthesia for lower- limb revascularization. Cochrane Database of Systematic Reviews. 2013; (1):CD007083.

41. Park WY, ompson JS, Lee KK. Eect of epidural anesthesia and analgesia in perioperative outcome: a randomized, controlled Veterans Aairs cooperative study. Annals of Surgery. 2001;234(4):560– 9; discussion 569– 71.

42. Stundner O, etal. Comparative perioperative outcomes associated with neuraxial versus general anesthesia for simultaneous bilateral total knee arthroplasty. Regional Anesthesia and Pain Medicine. 2012;37(6):638– 44.

43. Mauermann WJ, Shilling AM, Zuo Z. A comparison of neuraxial block versus general anesthesia for elective total hip replacement:a meta- analysis. Anesthesia and Analgesia. 2006;103(4):1018– 25.

44. Bovill JG, Intravenous anesthesia for the patient with le ventricular dysfunction. Seminars in Cardiothoracic and Vascular Anesthesia. 2006;10(1):43– 8.

45. American Society of Anesthesiologists Task Force on Pulmonary Artery C, Practice guidelines for pulmonary artery

catheterization: an updated report by the American Society of Anesthesiologists Task Force on Pulmonary Artery Catheterization. Anesthesiology. 2003;99(4):988– 1014.

46. Soussi S, Chatti K, Mebazaa A. Management of perioperative heart failure. Curr Opin Anaesthesiol. 2014;27(2):140– 5.

47. Denault AY, etal. Perioperative right ventricular dysfunction. Curr Opin Anaesthesiol. 2013;26(1):71– 81.

48. Nativi- Nicolau J, et al. Pharmacologic therapies for acute cardiogenic shock. Current Opinion in Cardiology. 2014;29(3):250– 7.

49. Fripp RR, Lee JC, Downing SE. Inotropic responsiveness of the heart in catecholamine cardiomyopathy. American Heart Journal. 1981;101(1):17– 21.

50. Beau SL, Tolley TK, Satz JE. Heterogeneous transmural distribution of beta- adrenergic receptor subtypes in failing human hearts. Circulation. 1993;88(6):2501– 9.

51. Prielipp RC, et al. Pharmacodynamics and pharmacokinetics of milrinone administration to increase oxygen delivery in critically ill patients. Chest. 1996;109(5):1291– 301.

52. Papp Z, et al. Levosimendan: molecular mechanisms and clinical implications: consensus of experts on the mechanisms of action of levosimendan. International Journal of Cardiology. 2012;159(2):82– 7.

53. Tacon CL, McCarey J, Delaney A. Dobutamine for patients with severe heart failure: a systematic review and meta- analysis of randomised controlled trials. Intensive Care Medicine. 2012;38(3):359– 67.

54. Bayram M, etal. Reassessment of dobutamine, dopamine, and milrinone in the management of acute heart failure syndromes. American Journal of Cardiology. 2005;96(6A):47G– 58G.

55. Mulukutla S, Schneider L, Cohen HA. Percutaneous mechanical assist devices. In: Feldman AM, ed., Heart Failure: Device Management. Chichester, West Sussex, UK:Blackwell;2010.

56. Tsuneyoshi H, Rao V. e role of extracorporeal membrane oxygenation (ECMO) therapy in acute heart failure. International Anesthesiology Clinics. 2012;50(3):114– 22.

57. Cheung A. TCT- 371 rst clinical evaluation of a novel percutaneous right ventricular assist device:the impella RP. Journal of the American College of Cardiology. 2012;60(17):B106– 7.

CARDIOGENICSHOCK 83

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11.

DISTRIBUTIVESHOCK

Angela Lee and Gebhard Wagener

CASE

familiar with the physiologic balance of vasoconstriction

and vasodilation as mediated by the autonomic nervous A 56- year- old male with a history of hepatitis C and cirrhosis presents to the emergency department with new- onset fever, chills, abdominal pain, and tense ascites. ere is concern for spontaneous bacterial peritonitis and sepsis. Aurinary catheter is placed and there is minimal urine output in the next hour aer admission.

BASIC PHYSIOLOGY

Shock is a circulatory state in which perfusion and oxygen delivery is inadequate to meet the metabolic demands of tissue at the cellular level leading to possible end- organ damage. e classications of shock as described by Weil and Shubin (cardiogenic, hypovolemic, obstructive, distributive), are dened by their mechanism of circulatory dysfunction.1 Distributive shock is dened by high cardiac output and low systemic vascular resistance (SVR). ere are multiple pathophysiologic processes that ultimately lead to this clinical picture, as evidenced by the various etiologies of distributive shock such as sepsis, liver failure, anaphylaxis, reperfusion injury, or adrenal insuciency.2 In a simplied view, the circulatory system can be analogous to an electrical circuit and therefore SVR can be derived from Ohm’s law:pressure=ow × resistance. In the setting of distributive shock, inammatory mediators cause microvascular dysfunction and regional vasodilation, thus compro-

system. Basal vascular tone is predominantly mediated by

the active sympathetic nervous system that innervates the

arterial and venous systems.3 Reduced activation of mecha-

noreceptors in the setting of low blood pressure leads to

increased sympathetic outow by mechanisms of venocon-

striction, vasoconstriction, increased cardiac contractility

and heartrate.

e splanchnic circulation is the largest blood reservoir in the body, containing 20%– 30% of total blood volume, and has signicant innervation by sympathetic bers.5 During conditions of circulatory compromise such as shock, the body diverts blood ow from nonessential organs to vital organs, maintaining cerebral, cardiac, and renal perfusion. In response to autonomic signals and regional vasoactive mediators, the venous component of the splanchnic bed venoconstricts for recruitment of blood volume in states of low arterial blood pressure in order to maintain normal cardiac output. is selective redistribution of blood ow can lead to ischemic injury of splanchnic organs.

Various vasoactive mediators of the splanchnic and systemic circulation have been identied in animal models and human studies of septic shock and include endotoxin, tumor necrosis factor, interleukin, endothelin, nitric oxide, and angiotensin. Angiotensin appears to play a large role in mesenteric/ portal vasoconstriction observed in anaphylactic and thermal shock animal models.

6,7

mising organ perfusion pressure. e extent to which the body can compensate with increased ow or cardiac output to sustain organ function depends on which end of the shock continuum the patient exists.

EVALUATION OFPERFUSION

e morbidity and mortality of shock is attributed to tissue hypoperfusion and multiorgan failure, and early detection

MAINTENANCE OFVASCULARTONE

To understand mechanisms underlying the regional alterations in vascular tone in distributive shock, one must be

and intervention of inadequate perfusion is central to the management of all types of shock. ere has been controversy regarding the utility of pulmonary artery catheters (PACs) in the management of critically ill patients over the

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last two decades, and their use has declined overall from

10.8% to 6.2% across intensive care units (ICUs) in the United States from 2001 to 2008.8 Based on results of several large studies, the general consensus is that they likely do not improve nor worsen patient outcomes and hospital length of stay.

9,10,11

Central venous pressure (CVP) has traditionally been used along with pulmonary artery occlusion pressure as a surrogate to estimate preload and volume status and to guide uid management in shock. However there is basically no meaningful correlation between CVP and circulating blood volume status or uid responsiveness.

12– 16

Central venous pressure is a static measurement that is altered by changes in intrathoracic pressure such as during mechanical ventilation, intra- abdominal pressure, patient positioning, pulmonary vascular resistance, and homeostatic mechanisms that lead to changes in venous tone that do not necessarily reect the patient’s volume status.17 Aretrospective study by Boyd etal. suggests that aggressive uid resuscitation based on CVP goals in septic shock is associated with a

subsequent organ dysfunction.33 Gastric tonometry allows for the assessment of splanchnic perfusion and potentially for the early detection of splanchnic tissue hypoxia by measuring the gastric mucosal partial pressure of carbon dioxide (PCO2) with a nasogastric or orogastric tonometer.

34,35

Lower gastric intramucosal pH correlates with splanchnic hypoperfusion and multiple system organ failure and has been shown to be a more sensitive and specic prognostic index of morbidity and mortality in critical illness and sepsis as compared to global indicators of oxygen delivery.

36– 40

Indocyanine green (ICG) is a dye eliminated exclusively by rst- pass eect and the biliary excretion of the liver. e measurement of its clearance can therefore estimate splanchnic and hepatic perfusion and hepatic function.

41– 3

e ICG is rst injected intravenously, and measurements of hepatic extraction are obtained via a hepatic vein catheter or less invasive systemic plasma measurements to calculate ICG clearance. Changes in ICG clearance are used as a surrogate for hepatic and splanchnic perfusion using the Fick principle.

higher mortality in patients with positive uid balance and higher CVP.18 ere are several dynamic measurements that are more predictive of uid responsiveness such as pulse pressure variation, stroke volume variation, passive leg raise test, and vena cava collapsibility.

19,20,21,22,23

Arterial lactate is a biomarker of tissue hypoperfusion and anaerobic metabolism in critically ill patients.24 Serum lactate is a prognostic factor for mortality in shock of any cause, and serial lactate measurements provide a good index for patient response to therapy and reversibility of global tissue hypoxia.

25,26

In patients with severe sepsis or septic shock, lactate clearance aer initial resuscitation was associated with improved survival compared to groups with persistently elevated serum lactate levels.

27,28

ese ndings emphasize the importance of early hemodynamic optimization in patients with severe sepsis and septic shock in order to improve global perfusion and survival.

e microcirculation is the site of tissue oxygen and nutrient exchange at the level of arterioles, capillaries, and venules and is altered in animal models of sepsis and in patients with septic shock.

29– 31

During septic shock, splanchnic perfusion is compro-

SYSTEMIC INFLAMMATORY RESPONSE SYNDROME/ SEPSIS

More than 1.1million hospitalized patients are diagnosed with sepsis every year in the United States with an estimated cost of more than $15 billion. Sepsis is a signicant contributor to death in the United States,44 and is the primary cause of mortality in ICUs.45 e incidence of sepsis increases by 8.7% annually and is more common in male, nonwhite patients based on an epidemiological study from 1979 to 2000.46 Patients admitted with the diagnosis of sepsis have signicantly longer hospital length of stays, and although mortality due to sepsis has continued to decrease from 30% to 18% over the last two decades, the absolute number of sepsis related deaths has risen.46 Based on estimates from the US Centers for Disease Control, 17% of in- hospital deaths in the United States were attributed to sepsis in 2008 and those patients surviving hospitalization were more likely to be discharged to short- or long- term care facilities.

mised due to regional alterations in blood ow and disproportionate metabolic demands of the splanchnic tissue that lead to gut ischemia.32 Intestinal ischemia has been postulated to be the driving force of multiple organ failure in septic shock due to the breakdown of gut barrier function resulting in the translocation of endogenous bacterial endotoxin, activation of inammatory mediators, and

DEFINITIONS

In order to standardize terminology, the American College of Chest Physicians and the Society of Critical Care Medicine proposed consensus- driven denitions of sepsis in 1991 that continue to be used and have served

DISTRIBUTIVESHOCK 85

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