Chapter 22. Patient in Cardiogenic Shock

A 62-year-old man presents to the emergency department by car complaining of chest pain, air hunger, and extreme weakness. He has a history of hypertension and an anterior wall myocardial infarction (MI) 2 years ago. His electrocardiogram shows a large anterolateral MI, and his chest radiograph shows vascular redistribution and mild interstitial edema. He is on beta blockers. His last echocardiogram was done 2 months ago and showed an ejection fraction of 25%.

His respiratory rate (RR) is 40 breaths per minute, heart rate (HR) 100 beats per minute (bpm), blood pressure 68/40 mm Hg, and his oxygen saturation is at 86% with a non-rebreather mask. He is intensely diaphoretic and has two-word dyspnea. He has a beard and a normal stature.

22.2.1 What Is This Patient's Physiological Reserve?

Many medications employed in airway management possess properties that affect cardiac and respiratory function. For this reason, it is critical that the practitioner evaluates the ability of these systems (physiological reserve) to withstand the effects of administered medications and procedures.

22.2.1.1 Cardiac Reserve

This patient is in cardiogenic shock with limited to no cardiac reserve. He has severe systolic dysfunction and almost certainly the same degree of diastolic dysfunction. It appears that his sympathetic nervous system is working at maximum ability just to sustain his present vital signs.

22.2.1.2 CNS Reserve

There is nothing to indicate that this patient will have any CNS problems with induction agents.

22.2.1.3 Respiratory Reserve

This patient is in pulmonary edema and will have limited respiratory reserve. Denitrogenation prior to intubation may help but is of questionable value. He is already maximizing his respiratory effort and induction may precipitate acute hypoxemia.

22.2.2 How Would You Evaluate the Airway of This Patient for Difficulty?

1. On MOANS-guided evaluation for difficult BMV (see Sections 1.6.1), you are uncertain that the patient can be ventilated by bag and mask. He has a thick beard and is likely to have gastric air distention due to his increased respiratory effort and air swallowing. His lungs will be stiff (reduced compliance) secondary to his interstitial pulmonary edema. This is of particular concern on initiating positive pressure ventilation following intubation with respect to a reduction in venous return.

2. On LEMON evaluation to predict difficult laryngoscopy and intubation (see Sections 1.6.2), looking externally his face and neck appear normal, although he has a beard and that may hide a small mandible. He cooperates for a Mallampati evaluation and appears to have a Grade II. He is not obese; his neck is freely mobile.

3. The mnemonic RODS can be used to guide the evaluation for difficulty in the use of extraglottic devices (EGD) (see Sections 1.6.3). His mouth opening is not restricted, upper airway obstruction is not anticipated, and his airway does not appear distorted or disrupted. However, as with bag-mask-ventilation, his lungs are stiff meaning that ventilation employing an EGD may be unsuccessful.

4. On SHORT evaluation for difficult surgical airway (see Sections 1.6.4), there is no history of previous neck surgery or evidence of anterior neck hematoma. He is not obese and there is no history of neck radiation or tumor.

In summary, this gentleman has little cardiac and respiratory reserve. Difficulty with oxygenation and ventilation via a bag-mask due to reduced lung compliance and poor mask seal secondary to his beard is predicted. However an EGD, endotracheal tube, or a surgical airway are not predicted to be difficult. Therefore, he is a reasonable candidate for rapid sequence intubation should one wish to employ that technique.

22.2.3 Are There Other Airway Management Concerns in the Patient with Cardiogenic Shock?

Most medications used for sedation or induction of anesthesia have the potential to produce hypotension, less so perhaps with etomidate and ketamine than others. This patient has limited to no cardiac reserve, and medications that reduce cardiovascular performance are contraindicated. Induction agents, in particular, must be chosen carefully and in reduced dosages. Some would say that amnesia in situations such as this, rather than induction of anesthesia, is the goal in an effort to preserve cardiac performance to the extent possible. The administration of an opioid in an individual exhibiting signs of maximal sympathetic stimulation may be contraindicated in the face of actual or incipient hypovolemia or hypotension. Finally, the onset times of medications administered intravenously may be delayed due to low cardiac output, a particular concern with the muscle relaxant in a situation where rapid-sequence intubation is desired. Under this circumstance, it is prudent to consider succinylcholine over nondepolarizing agents to achieve rapid muscle relaxation.

22.2.4 How Should We Medically Optimize This Patient Prior to Intubation?

22.2.4.1 Diuretics and Vasodilators

This patient is hypotensive, and the concern is that induction and intubation may acutely worsen his hypotension, as may therapies used to treat pulmonary edema such as diuretics and vasodilators. Small doses of nitroglycerine and furosemide may help to relieve some of the cardiac stress due to the pulmonary edema but may aggravate the hypotension. Consider delaying the administration of these drugs until the decision is made regarding airway control and stabilization.

22.2.4.2 Noninvasive Ventilatory Support

Numerous small studies have demonstrated a beneficial effect of using noninvasive ventilatory support (NIVS) in patients with cardiac pulmonary edema (CPE). However, it has been argued that larger prospective trials are needed before firm conclusions can be drawn. A randomized prospective study of 39 patients with pulmonary edema showed a significant decrease in need for intubation (p = .005) in patients receiving CPAP compared to patients receiving standard medical care. However, there were no significant differences in mortality and hospital length of stay between the study groups.1 An open, nonrandomized study involving 29 patients with NIVS showed that oxygen saturation increased from 73.8 ± 11% to 93 ± 5%, mean pH increased from 7.22 ± 0.1 to 7.31 ± 0.07 (p <0.01), and PaCO2 decreased from 62 ± 18.5 to 48.4 ± 11.5 mm Hg.2 A randomized, controlled, prospective clinical trial with 27 patients comparing nasal CPAP to nasal bi-level positive airway pressure (BL-PAP) against historical controls for intubation rates and MI found that BL-PAP improved ventilation and vital signs more rapidly than CPAP. However, intubation rates, hospital stay, and overall mortality between these two modes of NIVS showed no significant differences in this study. There was a higher rate of MI in patients treated with BL-PAP (71%) as compared to CPAP (31%) and that found in the historical controls (38%).3 A randomized prospective study of 40 patients comparing BL-PAP to high-dose isosorbide (HDI) reported that 80% of patients in the BL-PAP group required intubation as compared to 20% in the HDI group. In addition, there were more deaths (2 vs 0) and a higher MI rate (55% vs 10%) in the BL-PAP group compared to the HDI group. Unfortunately, this study was prematurely terminated.4 One subsequent study comparing BL-PAP with mask-ventilation in patients with CPE failed to demonstrate an increase in MI or mortality in the BiPAP-treated group.5 A meta-analysis of NIVS studies in pulmonary edema from 1983 through 1997 found that only 3 of 497 studies were sufficiently rigorous to fulfill study criteria. These three randomized control trials showed that NIVS patients had a decreased need for intubation (−26%, 95% CI, −13% to −38%), but the decrease in hospital mortality was not significant (−6.6%, +3% to −16%) as compared to standard therapy alone.6

In this case, it is necessary to carefully weigh the potential benefits of NIVS against the potential to increase mean intrathoracic pressure, which reduces venous return and cardiac output. Furthermore, it is apparent that intubation is indicated and therefore NIVS is unlikely to be a serious consideration.

22.3.1 Which Pharmacologic Agents Would You Select for This Case?

Drug selection in individuals who are moribund is particularly important, especially medications that have significant cardiopulmonary side effects.

22.3.1.1 Neuromuscular Blocking Agent

Recalling that circulation times in cardiogenic shock are prolonged, the muscle relaxant of choice for intubation is the one with the most rapid onset, succinylcholine, unless there is a contraindication. In the face of metabolic acidosis, as is almost certainly the case in this patient, the potassium may be elevated, but this ought not deter the use of succinylcholine. Longer-acting neuromuscular blocking agents, such as pancuronium, vecuronium, and rocuronium, may be employed postintubation to maintain paralysis. The relative sympathomimetic side effects of pancuronium may be of some benefit in this patient, although the degree of sympathetic activation that is evident indicates that this would be of marginal value.

22.3.1.2 Sedative/Induction Agent

The selection of an induction agent is more difficult. However, in this patient, one is more interested in amnesia than induction of anesthesia. Recognizing this as the goal, small doses of ketamine (10-20 mg) and midazolam (1-2 mg) are clearly preferable to the other induction agents. Small doses of etomidate may be used, although the amnestic effects of etomidate may be less intense than with those already mentioned. Agents such as thiopental or propofol may cause further deterioration in this patient's hemodynamic status and should not be used.

22.3.1.3 Cardiovascular Pressure Support

This patient is hypotensive, and it is likely that intubation and positive pressure ventilation will acutely worsen his hypotension. Therefore, vasopressors should be prepared and immediately available, recognizing that balanced α/β adrenergic agonists (epinephrine, norepinephrine, vasopressin) are preferable to α-agonists alone, particularly in a catecholamine-depleted heart, as in this patient.

Inotropic support should theoretically improve outcomes in patients who present with CPE. However, they can also cause tachycardia, dysrhythmias, increase myocardial oxygen demand, and myocardial ischemia, all of which may increase mortality. These medications should be used judiciously. There are two common inotropic classes, catecholamines and phosphodiesterase inhibitors (PDEIs). The catecholamine class includes dopamine, dobutamine, and norepinephrine. Dopamine and norepinephrine may provide blood pressure support by increasing systemic vascular resistance, which can actually worsen cardiac output. Dobutamine, while inducing some mild preload and afterload reductions, may also further lower the blood pressure. Catecholamines work through the adenoreceptors, which are often saturated with endogenous catecholamines due to the patient's condition. Therefore, higher than normal dosages may be needed in the CPE patient, and unfortunately these dosages are associated with a higher rate of adverse effects. Regarding vasopressin, one experimental study comparing dobutamine (DOB) to dobutamine-norepinephrine combination to arginine vasopressin (AVP) demonstrated that AVP further worsened shock by decreasing the cardiac output and systemic vascular resistance compared with DOB alone.7

PDEIs work by increasing intracellular cyclic-AMP, which produces a positive inotropic effect on the heart, induces peripheral vasodilation, and reduces pulmonary vascular resistance. Together, these effects produce preload, afterload, and cardiac output improvement.8 Studies comparing milrinone to dobutamine in patients with severe CPE did not show any improvement in hospital length of stay or mortality.9,10

"Calcium sensitizer" levosimendan has been suggested and studied recently as an alternative to dobutamine for CPE.11,12 In one study comparing the two agents, levosimendan produced greater improvement in cardiac output and pulmonary vascular pressures and a reduced 180-day mortality rate (26% vs 38%).13 However, in the SURVIVE trial there was no decrease in 180-day mortality. There was significant reduction in B-type natriuretic peptide in the levosimendan group.14

22.3.2 So, How Exactly Would You Handle the Entire Process?

1. Pre-procedure preparations:

   • Get the difficult airway devices ready
     • Tracheal introducer
     • Glidescope® or other video laryngoscopes
     • Intubating LMA™ (Fastrach-LMA)
   • Ketamine 10 to 20 mg in syringes or midazolam 1 to 2 mg
   • Succinylcholine at 1.5 to 2.0 mg·kg−1 in prefilled syringes
   • Sedation and paralytic agents for postintubation
   • Epinephrine 10 μg·mL−1 or vasopressin 0.4 U·mL−1 in 10 mL syringes

2. The patient is seated initially. The cardiac monitors are applied along with pulse oximetry. The patient is denitrogenated.

3. Ketamine or midazolam is administered IV followed immediately by succinylcholine. The patient is then placed supine with the head and neck in a sniffing position. The patient is observed for fasiculations.

4. Laryngoscopy is performed. The cords are visualized and the endotracheal tube is placed and secured.

5. Capnography and auscultation are performed to confirm tracheal intubation.

6. Postintubation drugs are administered for sedation and paralysis to permit mechanical ventilation.

7. Postintubation hypotension is managed by reevaluating ventilation parameters, volume infusion, repeated small doses of epinephrine (10 μg per dose), or vasopressin (0.4 U per dose). Postintubation hypertension may be managed with small doses of propofol (10 mg per dose) or a nitroglycerine infusion.

22.4.1 How Should the Patient Be Managed Following Tracheal Intubation?

The initial goal of ventilator management in this patient is to maximize oxygenation and relieve the work of breathing while at the same time being sensitive to the adverse effects of positive-pressure ventilation on venous return. It is important to realize that the air hunger exhibited by this patient is in large measure related to the metabolic acidosis associated with cardiogenic shock as he attempts to remove carbon dioxide. The ventilator should be set at tidal volumes of 8 mL·kg−1. PEEP should be started at about 5 cm H2O and then be increased depending on the cardiovascular effects and oxygenation status of the patient. Careful and immediate attention to the peak and plateau pressures should guide the ventilator settings thus maximizing oxygenation.

22.4.1.1 Cardiovascular Considerations

The blood pressure should be monitored immediately after intubation, expecting that the patient's hypotension may be acutely worsened. Agents that should be considered have been discussed earlier. If they have been started, they may need to be titrated depending on the patient's blood pressure in the early postintubation period.

Patients in cardiogenic shock are critically ill. Endotracheal intubation is often temporally associated with circulatory and cardiac arrest. Attention to detail is crucial. The maintenance of oxygenation, medication selection, dosage adjustments, and caution with respect to positive-pressure ventilation are exceedingly important in these patients.