Cardiogenic Shock Case File

Cardiogenic Shock Case File

Eugene C. Toy, Md, Michael d . Faulx, Md

Case 3

A 60-year-old Caucasian man is seen in the emergency department for confusion and lethargy. His wife states that he was in his typical state of good health until a week ago when he complained of an intense episode of nausea, diaphoresis. and epigastric pain. The patient attributed his symptoms to indigestion. He felt better until 3 days ago. when he experienced progressive fatigue and dyspnea with exertion. He has slept on a recliner for the past two nights because of recent-onset orthopnea. This morning his wife could not easily awaken him to go to work. His medical history is noteworthy for obesity. hypertension, and type 2 diabetes mellitus. He has no known heart disease, but he does not visit his primary care physician regularly. His medications include aspirin, metformin, simvastatin, hydrochlorothiazide,

and lisinopril, which he frequently forgets to take, He has a 40-pack/year smoking history and currently smokes. He drinks three to sex beers every weekend and does not use illicit drugs. Physical examination reveals an obese middle-aged man who is somnolent but arousable and voicing no complaints. His vital signs are: BP 90/75 mmHg. pulse 110 bpm. RR 22 breaths/min, body mass index (BMJ) 35 kg/m². and oximetry on room air 94%. His jugular veins are not easily seen secondary to obesity. Cardiac auscultation reveals a regular tachycardia with distant S1/S2 an S3 gallop. and a III/VI holosystolic murmur at the left sternal border that varies in intensity with breathing. He also has a higher-pitched II/VI holosystolic murmur in the 6th intercostal space along the midclavicular line that does not vary with respiration. This murmur is also audible posteriorly. Chest auscultation reveals poor inspiratory effort and diffuse end expiratory wheezes. His extremities are cool to touch with 2+ pretibial edema in both legs. His neurological examination is grossly nonfocal. A room air arterial blood gas shows: pH 7.25, pCO2, 36 mmHg, pO2, 90 mmHg. HCO3 19 mEq/L, and lactate 7 mEq/L.

c What is the most likely diagnosis?

c What is the most appropriate initial test?

c What is the most important initial therapeutic maneuver?

Answer to Case 3:

Cardiogenic Shock

Summary: This is a 60-year-old obese man with multiple risk actors or coronary artery disease who presents with progressive dyspnea, orthopnea, and somnolence that began several days after an episode of epigastric pain, nausea, and diaphoresis. These symptoms are suggestive of an unrecognized myocardial infarction. His vital signs reveal tachycardia, tachypnea, and relative hypotension, which would be unexpected in a noncompliant patient with a history of hypertension. His pulse pressure is narrow, suggesting reduced cardiac output. His physical examination is limited by obesity but suggests reduced perfusion of the peripheral musculature and brain. He also has peripheral edema and murmurs suggestive of tricuspid and mitral regurgitation. His arterial blood gas (ABG) is consistent with an incompletely compensated metabolic acidosis with increased serum lactate.

• Most likely diagnosis: Cardiogenic shock.
• Most appropriate initial test: ECG.
• Most important initial therapeutic maneuver: Aggressive hemodynamic support measures in an intensive care unit (ICU) setting in conjunction with prompt coronary revascularization if there is evidence of an acute myocardial infarction.

ANALYSIS

Objectives

1. To understand the de inition o shock as a global state o tissue hypoper usion.
2. To recognize the clinical and laboratory indicators o shock.
3. To identi y the three major types o shock and the di erential diagnoses or each.
4. To manage shock on the basis o its type and tailor treatment to the speci ic hemodynamic issues or an individual patient.

Considerations

This patient is presenting with signs and symptoms consistent with cardiogenic shock. Although the presentation of cardiogenic shock can be obvious in some patients, particularly those with profound hypotension and marked end-organ failure, many patients such as ours present with less obvious clinical evidence of shock. Shock is a pathophysiologic state defined by ineffective oxygen delivery to the cells and tissues of the body. In the case of cardiogenic shock, the reason for this is ineffective pump function. Clues to the presence of cardiogenic shock in our case include the patient’s physical examination findings that indicate poor tissue-level perfusion and his high underlying risk for ischemic heart disease and his description of what was likely an acute myocardial infarction 1 week prior to presentation.

Given the 1-week delay between his symptoms and his presentation with shock, one should think of mechanical complications of myocardial infarction as a precipitant of cardiogenic shock, including progressive left ventricular systolic dysfunction, right ventricular failure, severe mitral regurgitation, or ventricular septal rupture. His physical examination suggests the presence of significant mitral and tricuspid valve regurgitation. Early recognition of this patient’s shock state is of the utmost importance, as cardiogenic shock may be reversible when it is detected early. Untreated, his cardiogenic shock will invariably lead to tissue-cellular death. metabolic acidosis, failure of major organ systems. and death. Given that this patient is not presenting with an acute myocardial infarction, the next step in his management would be supportive care to improve global perfusion with pharmacological and mechanical support such as the use of inotropic agents, vasopressors, or mechanical support devices.

Approach To:

Shock

SHOCK: Pathophysiologic state characterized by reduced tissue-level oxygen delivery.

CARDIOGENIC SHOCK: Shock that is caused by failure o the heart as a pump to deliver adequate perfusion to peripheral tissues.

DISTRIBUTIVE SHOCK: Shock that is caused by failure o the arterial circulatory bed to maintain adequate perfusing pressure to peripheral tissues.

HYPOVOLEMIC SHOCK: Shock that is caused by significant reduction in circulating vascular volume, resulting in reduced perfusing pressure to peripheral tissues.

INVASIVE HEMODYNAMIC MONITORING: Use of an arterial pressure monitoring catheter and an indwelling pulmonary artery (Swan-Ganz) catheter to collect invasive hemodynamic information to facilitate the diagnosis and treatment of shock.

CARDIAC OUTPUT: Rate of delivery of oxygenated blood to the body by the heart; the product of the stroke volume and heart rate, normally 4.0 to 8.0 L/min Cardiac output is measured in liters per minute or in liters per minute indexed to body surface area [cardiac index (CI); normal, 2.5–3.5 L/min/m²].

PULMONARY CAPILLARY WEDGE PRESSURE (PCWP): Mean pressure detected by the tip of the pulmonary artery catheter when the catheter is “wedged” in a distal pulmonary artery branch with the balloon inflated. This is a reflection of left atrial pressure and used to gauge left ventricular filling pressure as a surrogate for preload; normal 8–15 mmHg

SYSTEMIC VASCULAR RESISTANCE (SVR): Measure of arterial resistance calculated by data obtained from invasive hemodynamic monitoring; a surrogate for afterload. Measured in dynes; normally 800–1200 dyn.

MIXED VENOUS SATURATION (SVO2): Oxygen saturation taken in the pulmonary artery. SVO2 is subtracted from the systemic arterial saturation to calculate the cardiac output using the Fick equation. Reflects degree of oxygen extraction by body tissue and is a surrogate for oxygen delivery. Normal SVO2 is 70%.

CLINICAL APPROACH

Pathophysiology

To understand the pathophysiology of shock states, one must irst understand normal cardiovascular physiology. Perfusion pressure (ΔP) is de ined by the pressure difference between the arterial and venous vascular beds: [mean arterial pressure (MAP)] – [mean right atrial pressure (RAP)]. The perfusion pressure is dependent on cardiac output and systemic vascular resistance, and this relationship is explained by Ohm’s law (ΔP = Q × R), where Q is flow and R is resistance. Thus, for the perfusion pressure ΔP = CO × SVR, where CO is cardiac output and SVR is systemic vascular resistance. This equation can be juxtaposed to determine the cardiac output (CO = ΔP/R) or systemic vascular resistance (SVR = ΔP/CO). Relative values for these basic hemodynamic elements can be estimated from the physical examination, whereas invasive hemodynamic monitoring provides a means for more quantitative measurement.

Figure 3-1 is a flowchart illustrating how heart rate, stroke volume, and systemic vascular resistance are influenced by other determinants of cardiovascular performance. Heart rate is regulated by the autonomic nervous system. Stroke volume is influenced by left ventricular preload, afterload, and myocardial contractility. Systemic vascular resistance is governed by arterial tone, arterial volume, and the structural integrity of the vessels themselves. There is a fair degree of overlap between these determinants that allows for broad adaptation to physiologic changes or needs. For example, in response to running up a steep hill a jogger will experience a surge in serum catecholamines and increased sympathetic nerve output. This will result in increased heart rate and increased myocardial contractility that will raise cardiac output. At the same time arteriolar tone will increase as a result of the vasoconstrictor effects of catecholamines. The net result is an increase in perfusion pressure that matches physiologic demand and allows for adequate blood flow to the jogger’s lower extremity muscles and diaphragm. Shock occurs when there is massive perturbation of one or more of these processes that cannot be compensated for by adaptations in other areas.

Shock is classified as cardiogenic, distributive, or hypovolemic with respect to the inciting event or events that precipitate the shock state. In cardiogenic shock the primary problem is failure of the heart to adequately pump blood to the peripheral tissues. Cardiogenic shock can be caused by any disease state that alters cardiac performance, but it most commonly occurs as a consequence of myocardial infarction. In distributive shock the primary problem is failure of the arterial system to maintain adequate tissue perfusion secondary to loss of vascular tone or increased vascular permeability. Distributive shock is most commonly associated with systemic inflammatory states such as sepsis or systemic inflammatory response syndrome (SIRS). Common triggers include bloodstream bacterial infections,

Figure 3-1. determinants of myocardial performance.

pancreatitis, and major burns. Hypovolemic shock occurs as a result of inadequate intravascular volume. The most common cause of hypovolemic shock is acute blood loss, often secondary to traumatic injury or gastrointestinal bleeding.

Although the hemodynamic derangements that define each subtype o shock are fairly well described (see Table 3-1), these abnormalities are not static, nor are they mutually exclusive. For example, a patient with a history of heart failure may present with distributive shock due to sepsis, but over time the metabolic derangement and acidosis related to sepsis may result in progressive pump failure and secondary

cardiogenic shock. These cases of “mixed shock” are not uncommon and can be extremely challenging to manage. These patients o ten require a multidisciplinary approach to their care.

In cardiogenic shock the principal issue is loss of effective pump unction. This can be caused by virtually any cardiovascular disease state, but most commonly cardiogenic shock occurs as a consequence of acute myocardial infarction. The hemodynamic hallmarks of cardiogenic shock include low cardiac output with a related

Abbreviations: CI, cardiac index; HR, heart rate; PCWP, pulmonary capillary wedge pressure; RAP, right atrial pressure; SVO2, mixed venous oxygen saturation; SVR, systemic vascular resistance.

decrease in SVO2 (Table 3-1). The PCWP and central pressures proximal to the left atrium are typically elevated secondary to congestion and loss of adequate forward ejection. The heart rate is usually increased (unless there is an issue with intrinsic conduction) as a result of a compensatory increase in sympathetic tone. SVR is usually high for the same reason, but it can be reduced in certain settings (post–cardiac surgery vasoplegia, cardiogenic shock with sepsis).

In distributive shock the primary issue is loss ofarterial tone and increased capillary leak due to bacterial endotoxin or profound systemic in flammation. The hemodynamic hallmarks of distributive shock include low SVR and increased cardiac output and SVO2. Heart rate is typically increased in an effort to maintain a high cardiac output. Central filling pressures may be low or relatively normal.

In hypovolemic shock the principal problem is a dramatic decrease in intravascular circulating volume. The hemodynamic hallmarks of hypovolemic shock include low central filling pressures with low cardiac output and SVO2 secondary to suboptimal preload with a subsequent reduction in stroke volume. Heart rate and SVR is typically increased as a result of compensatory increases in systemic tone, and the increased SVR can further limit stroke volume.

Clinical Presentation

Shock patients may present in a number of ways depending on the type of shock. Most patients will have some sort of inciting event (myocardial infarction, infection, trauma, etc.) followed by a period of hemodynamic compensation be ore progression to overt shock. The length of time between the inciting event and the onset of shock is variable, and depends mostly on the general health and condition of the patient prior to the event. Regardless of the type, patients with shock will eventually develop clinical evidence of tissue-level hypoperfusion.

The major clinical features suggestive of end-organ hypoperfusion include depressed mental status, diffuse weakness, reduced urine output, metabolic acidosis, and hypotension (in most cases). In cardiogenic and hypovolemic shock the extremities may be cool or cold to touch due to profound peripheral vasoconstriction, but patients presenting with distributive shock typically feel warm because of pathologic vasodilation. Hypotension is a cardinal feature for most patients with shock, but the absence of hypotension does not exclude shock; patients with normal blood pressure or even hypertension can also present with shock. For example, a patient with a history of critical aortic stenosis and poor left ventricular systolic function may be able to maintain a systolic blood pressure of 105 mmHg due to extreme compensatory vasoconstriction but still be in cardiogenic shock due to profoundly reduced stroke volume and markedly increased afterload. A patient with a history of nonischemic cardiomyopathy and polysubstance abuse might present after 3 days of cocaine abuse with no food or water intake with a systolic blood pressure of 240 mmHg but have evidence of shock due to extremely high afterload and extremely low preload and reduced intravascular volume.

Laboratory features o shock include abnormal markers of end-organ function, including increased serum blood urea nitrogen (BUN) and creatinine, increased hepatic transaminases, and elevated serum lactate. The rise in lactate indicates a switch from aerobic to anaerobic metabolism and is a cardinal feature of shock. Lactic acidosis is a poor prognostic indicator in patents presenting with all forms of shock, and the degree of lactate elevation generally correlates with overall mortality.

Diagnosis

Shock is a clinical diagnosis that can typically be made at the bedside following a thorough history and physical examination with an emphasis on the features described in the previous section. However, these findings may be subtle, particularly in the early stages of shock where the patient may still be compensated, so a high index of suspicion and frequent reassessment is required. Pay particular attention to unexplained sinus tachycardia because this is often the first sign of trouble in a patient with shock.

Laboratory data can confirm the presence of end-organ dysfunction and may also provide insight into the etiology of shock. An arterial blood gas and lactate levels should be obtained early in patients with suspected shock. Appropriate laboratory testing will vary between patients but generally includes a comprehensive metabolic panel; complete blood count with differential; blood cultures (when bloodstream infection is suspected); serum cardiac biomarkers, including troponin and creatinine kinase; coagulation studies; and serum or urine toxicology if drug abuse is on the differential. An ECG and chest x-ray should be obtained on presentation, and an early echocardiogram is an important component of the workup for cardiogenic shock. As mentioned previously, invasive hemodynamic monitoring can be immensely helpful with respect to clarifying the type of shock and monitoring response to therapy. Although there are no data clearly demonstrating that invasive hemodynamic monitoring improves survival in patients with shock, when performed by experienced ICU staff using imaging guidance for vascular access, invasive hemodynamic monitoring can be performed safely and with few major complications.

The mortality associated with shock is variable but high, ranging between 30% and 80% depending on the cause. The morbidity of shock is also enormous; patients presenting with shock face lengthy ICU stays, prolonged recovery, and risk for permanent disability from end-organ injury. The annual cost of caring for patients with shock is measured in tens of billions of US dollars.

Management of Shock

The management of shock is dictated by the type of shock and by the patient’s unique hemodynamic and medical needs. However, there are a few fundamental principles that apply to all patients presenting with shock. The first is prompt recognition of the shock state and management in an intensive care setting that is properly equipped to handle critically ill patients. Another principle of shock management is the aggressive support of end-organ function. Initial support measures and diagnostic investigation should occur simultaneously in patients with shock. Interventions such as endotracheal intubation and mechanical ventilation, renal replacement therapy, and mechanical hemodynamic support can be life-sustaining as the cause of shock is determined and ultimately treated. Finally, aggressive preventive measures should be instituted to avoid dangerous complications that can befall critically ill patients such as deep-vein thrombosis (DVT), decubitus ulcers, and gastrointestinal hemorrhage. Appropriate nutritional support should begin on arrival at the ICU, preferably via the enteric route.

Management of Cardiogenic Shock The goals for management of cardiogenic shock include immediate measures to improve cardiac output with simultaneous investigation to determine a treatable cause for the cardiogenic shock. Exclusion of acute myocardial infarction is a top priority. Data from the landmark SHOCK Trial suggest that early revascularization in patients presenting with myocardial infarction (mostly anterior STEMI) complicated by cardiogenic shock was associated with a trend toward improved 30-day survival and a statistically significant increase in survival at 6 months. For this reason shock, even in the presence of a non-ST-segment elevation myocardial infarction (NSTEMI), is an indication for early coronary angiography and prompt revascularization.

The approach to cardiogenic shock is dictated by the cause of the shock and the most pressing hemodynamic insult facing the patient. Since most patients with cardiogenic shock have reduced stroke volume and high systemic vascular resistance, primary medical therapy is directed at reversing these abnormalities. In rare circumstances patients with cardiogenic shock will present with vasoplegia (reduced arterial vascular tone), heralded by hypotension and low SVR. Cautious intravenous fluid management and use of vasopressor agents such as norepinephrine may be required. In patients without profound hypotension (SBP < 90 mmHg), the use of intravenous sodium nitroprusside often produces significant hemodynamic improvement. Nitroprusside is a potent direct vasodilator that can dramatically reduce left ventricular afterload. Although nitroprusside also reduces SVR, its effect on afterload (which is determined by both systemic blood pressure and LV wall tension) is generally greater, leading to increased stroke volume and improved perfusion pressure. Cardiac output can also improve with the use of positive inotropes such as dobutamine or milrinone. Inotropes improve stroke volume by directly increasing ventricular contractility. However, the use of these agents is also associated with a greater risk for ventricular and atrial tachyarrhythmias and greater overall mortality. In patients with shock that is refractory to vasoactive medical therapy, the use of mechanical hemodynamic support such as an intraaortic balloon pump (IABP) may be beneficial. IABP therapy involves the use of a large (30–50 mL) balloon advanced percutaneously via the femoral artery into the descending thoracic aorta. The balloon is gated to the ECG or arterial pressure waveform and inflates during diastole, augmenting diastolic coronary flow and raising diastolic blood pressure. The balloon deflates during systole, creating a “vacuum” effect that effectively

lowers afterload and promotes forward ejection. IABP therapy can be used in conjunction with nitroprusside or inotrope therapy to facilitate hemodynamic recovery. Select patients with cardiogenic shock that proves refractory to IABP and vasoactive medical therapy sometimes respond to more advanced mechanical support such as percutaneously or surgically placed extracorporeal membrane oxygenation (ECMO) or ventricular assist devices (VADs).

Preload optimization is another key feature in the management of cardiogenic shock. Patients with left ventricular dysfunction typically require higher-thannormal LV filling pressures (PCWP 18–20 mmHg) for adequate preload. Most patients with cardiogenic shock have markedly increased biventricular filling pressures (PCWP > 25 mmHg with high RAP) that results in suboptimal ventricular preloading, pulmonary congestion, hypoxemia, and venous congestion of the liver and kidneys. Therapy with intravenous loop diuretics such as furosemide can reduce central filling pressures, optimize preload, and improve perfusion pressure (remember that perfusion pressure = MAP – RAP). Alternatively, lower-than-ideal filling pressures can also result in reduced preload and reduced stroke volume. In these patients cautious volume resuscitation (normal saline 250-mL bolus at a time) can both increase and improve stroke volume.

One often overlooked variable in the management of cardiogenic shock is the heart rate. Although tachyarrhythmias in the setting of shock typically demand immediate attention (usually by electrical cardioversion as rate-controlling drugs such as beta-blockers or diltiazem are negative inotropes and contraindicated in shock), relative bradycardia can be equally problematic. Tachycardia is a relatively uniform response to shock; patients in shock with bradycardia or lower normal heart rates may benefit from some attempt at increasing heart rate (catecholamine therapy, transvenous pacing, etc).

Addressing the primary cardiac insult is also an essential element of cardiogenic shock management. Patients presenting with acute myocardial infarction should receive immediate revascularization if appropriate. Patients with acute valvular regurgitation (aortic or mitral regurgitation) or a mechanical complication from a recent myocardial infarction (ventricular septal rupture, papillary muscle rupture) should have emergent consultation with a cardiothoracic surgeon, as shock in the setting of acute valvular regurgitation is considered a surgical emergency. Patients with severe valvular stenosis should be evaluated for urgent surgical or percutaneous management. Patients presenting with arrhythmias complicated by shock should receive prompt cardioversion, antiarrhythmic drug treatment, and possible consultation with a cardiac electrophysiologist. Extracardiac causes of cardiogenic shock such as massive pulmonary embolism or pericardial tamponade may also need to be diagnosed and treated.

Management of Distributive Shock The treatment of distributive shock involves immediate goal-directed management of reduced intravascular tone and capillary leak along with management of the inciting event. Common early (within the first 6 hours of presentation) management goals include maintaining central venous pressure (CVP) (RA pressure) >10 mmHg, SVO2 ≥70%, MAP ≥65 mmHg, and urine output >0.5 mL/kg/h. Management includes intravenous crystalloid or colloid volume

resuscitation, along with vasopressor infusions such as norepinephrine or dopamine, which should be titrated to the lowest possible dose to achieve the target MAP. Although dopamine is commonly used as a vasopressor in patients with shock, there are data supporting improved outcomes with norepinephrine in both distributive and cardiogenic shock.

In cases where sepsis is suspected, blood and urine cultures are obtained prior to the use o broad-spectrum antimicrobial agents to cover infective etiologies. Laboratory data to exclude other causes of distributive shock such as pancreatitis, adrenal failure, toxin ingestions, and thyroid disease should also be obtained.

Management of Hypovolemic Shock Hypovolemic shock is managed in a fashion similar to distributive shock, namely, goal-directed volume resuscitation (or transfusion in the setting of known or suspected bleeding) and judicious vasopressor support. Addressing the underlying cause for the hypovolemia is also key.

CASE CORRELATION

• See also Case 1 (acute coronary syndrome/STEMI) and Case 2 (acute coronary syndrome/NSTEMI).

COMPREHENSION QUESTIONS

3.1 A 75-year-old man with a history of hypertension, diabetes, and complete heart block that was treated with a permanent pacemaker several years ago arrives at the ICU from the orthopedic surgery service for shock management. He is one day removed from an elective right total hip replacement, and his surgery was reportedly uncomplicated. His preoperative dobutamine echocardiogram revealed normal ventricular function and no evidence of ischemia. On arrival he is pale and somnolent but arousable. Vital signs: blood pressure (BP) 80/40 mmHg, heart rate (HR) 50 bpm, respiratory rate (RR) 18/min, temperature 37.9°C, and oxygen saturation 96% on room air. On examination his neck veins are flat at 45°. His cardiopulmonary examination is normal. His extremities are cool and without edema. Laboratory rate includes the following: BUN 50, creatinine 1.8 mg/dL, hemoglobin 6.0 g/dL, mean corpuscular volume (MCV) 89, and white blood cells (WBC) 12,000 with normal differential. Cardiac biomarkers are normal. ECG reveals a paced ventricular rhythm. Two units of blood are ordered, and 2 L of normal saline is infused rapidly. After fluid resuscitation his examination is unchanged and his blood pressure is now 84/45 mmHg.

Which of the following is the most appropriate next step?

A. Infusion of sodium nitroprusside

B. Infusion of norepinephrine

C. Infusion of milrinone

D. Pacemaker reprogramming to a heart rate of 90 bpm

E. Placement of an intraaortic balloon pump

3.2–3.6 Match the hemodynamic profile with the most appropriate patient. Each answer (A–E) can be used more than once or none at all.

3.2 A 55-year-old woman with breast cancer who presents to the emergency department (ED) with dyspnea and syncope following an episode of sharp right-sided chest pain.

3.3 A 19-year-old man with no medical problems who was found unconscious following a gunshot wound to the abdomen.

3.4 A 77-year-old man with ischemic heart disease and an indwelling Foley catheter admitted from his nursing home with 3 days of confusion and hypoxemia.

3.5 A 17-year-old woman presenting to the ED with confusion, fever, and abdominal pain attributed initially to menstrual cramps. She has a diffuse erythrodermic rash.

3.6 A 65-year-old man presents from the regular nursing floor 3 days after undergoing PCI to treat an anterior STEMI.

3.7 A 67-year-old woman with advanced systolic heart failure is admitted for altered mental status and dyspnea after running out of her heart failure medications one week ago. Vital signs are BP 92/70 mmHg (MAP 77 mmHg), HR 100 bpm, RR 18/min, O2 saturation 92% on 4 L nasal cannula (NC) oxygen. She has 20 cm JVP at 90°, S3 gallop, wet bibasilar pulmonary rales, and cold lower extremities with 1+ edema.

All of the following would be expected to improve her perfusion pressure except…

A. Intra-aortic balloon pump placement

B. Intravenous furosemide

C. Intravenous normal saline

D. Intravenous milrinone

E. Intravenous nitroprusside

ANSWERS

3.1 D. This patient has evidence for hypovolemic shock that has not responded to initial volume resuscitation. His clinical picture is most consistent with acute blood loss following surgery. We would expect him to mount a compensatory tachycardia, but he is likely pacemaker-dependent and pacing in a programmed backup rate since surgery (device sensing is often programmed off for surgeries). Thus, increasing his device rate to 90 bpm would be the most reasonable next step. Pressor support with norepinephrine (B) is not an unreasonable choice, but it would be more appropriate to see if faster pacing solves the problem first. Dopamine at moderate doses (5–10 μg/kg/min) is not a bad choice in patients with bradycardia as the β1 effects can increase heart rate, although that may not help in this pacemaker-dependent man. The remaining options are all reasonable for patients with pure cardiogenic shock, but this patient’s profile is more consistent with hypovolemic shock that cannot be compensated because of his fixed slow heart rate. Improving the heart rate should eliminate the “cardiogenic component” of his shock.

3.2 E. This patient likely has cardiogenic shock and right ventricular failure due to acute pulmonary embolism.

3.3 C. This patient has hypovolemic shock due to blood loss from a gunshot wound.

3.4 D. Mixed distributive and cardiogenic shock triggered by severe urinary tract infection–related sepsis.

3.5 A. This patient has distributive shock secondary to toxic shock syndrome.

3.6 B. This patient has cardiogenic shock following an acute myocardial infarction.

3.7 C. This patient has examination evidence of  florid central volume overload. Although she is hypotensive, additional fluid resuscitation will not help because her preload is suboptimal (overloaded; on the far right of his Starling curve). Reducing preload with furosemide would actually improve ventricular loading conditions with expected improvement in stroke volume and perfusion pressure

(remember, ΔP = MAP – RAP). IABP therapy and nitroprusside both improve perfusion pressure by reducing afterload and optimizing cardiac output. Milrinone improves perfusion pressure by increasing stroke volume due to increased contractility.

CLINICAL PEARLS

C Most patients with shock present with sinus tachycardia. If you see a patient with unexplained sinus tachycardia and hypotension, think of shock. If you see a patient with shock who has bradycardia or a lower than expected heart rate, consider ways to increase the heart rate.

C Check arterial blood gases an lactate levels early and often in patients with suspected shock. It will give you important prognostic information and help you gauge response to therapy .

C Exclude acute myocardial infarction immediately in patients presenting with cardiogenic shock; early revascularization is associated with better outcomes.

References

De Backer D, Biston P, Devriendt J, et al. SOAP II Investigators. Comparison o dopamine and norepinephrine in the treatment o shock. N Engl J Med. 2010;362(9):779. 

Dellinger RP, Levy MM, Rhodes A, et al.. Surviving Sepsis Campaign Guidelines Committee including the Pediatric Subgroup. Crit Care Med. 2013;41(2):580. 

Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial in arction complicated by acute cardiogenic shock. SHOCK Investigators. Should we emergently revascularize occluded coronaries or cardiogenic shock. N Engl J Med. 1999;341(9):625. 

Mueller HS, Chatterjee K, Davis KB, et al.. ACC expert consensus document. Present use o bedside right heart catheterization in patients with cardiac disease. American College o Cardiology. J Am Coll Cardiol. 1998;32(3):840. 

Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon support or myocardial in arction with cardiogenic shock. IABP-SHOCK II Trial Investigators. N Engl J Med. 2012;367(14):1287.

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