The Physiologically Difficult Airway: Hemodynamics

Jarrod M. Mosier

Franz Rischard

DEFINITION OF THE PHYSIOLOGICALLY DIFFICULT AIRWAY

Critically ill patients present a unique danger during airway management. Despite the technologic devices available to us to overcome anatomic difficulty with laryngoscopy or mask ventilation, there are still unsettlingly high rates of desaturation, hypotension, and cardiac arrest during airway management. Although difficult intubations dramatically increase the risk of these complications, a recent study showed half of all critically ill patients had complications despite only a 5% difficult intubation incidence.¹ This risk of cardiopulmonary decompensation during intubation from physiologic disturbances despite the presence or absence of anatomic challenges to intubation is the definition of the physiologically difficult airway.²

The next three chapters are devoted to the physiologically difficult airway. This chapter is devoted to hemodynamics, whereas Chapter 7 explores oxygenation and Chapter 8 discusses apnea, induction drugs, and positive pressure ventilation (PPV). Chapter 9 describes how to incorporate the physiologically difficult airway into the airway assessment and strategy.

HEMODYNAMICS

Hemodynamic challenges have risen as the pinnacle source of danger to patients requiring intubation in the ED or ICU. The INTUBE study showed that, across 29 countries, almost half of critically ill patients developed hemodynamic instability as a result of intubation despite fewer than 10% of patients being intubated for hemodynamic instability.¹ Other studies have shown that peri-intubation hypotension is also an independent predictor of death. With 1 in 3 patients suffering cardiovascular collapse with intubation and nearly 1 in 30 a cardiac arrest,¹^,³^,⁴^,⁵ emergency airway management must include peri-intubation management of hemodynamics. Unlike the other major intubation-related complications that increase with successive attempts, cardiovascular collapse starts high and remains high throughout all attempts.¹^,⁶^,⁷^,⁸ Thus, just as preoxygenation is important for providing a safe apnea time, preintubation management of patients’ hemodynamics is as important to provide a safe transition to life support. Unfortunately, hemodynamic disturbances can be quite complex and there is no single intervention to make them less so.

Optimizing hemodynamics is a huge knowledge gap with limited data, not the first of which is a lack of standardized definitions regarding vital sign thresholds or what specific time interval is the peri-intubation period. Despite these limitations, observational data show that preintubation shock index (SI, heart rate/systolic blood pressure), older age, hypotension, shock, intubation for respiratory failure, and a higher severity of illness (APACHE) score are all factors associated with a higher likelihood of postintubation cardiovascular collapse.⁹^,¹⁰^,¹¹

Various methods to reduce hypotension rates have been attempted or debated for as long as critically ill patients have required intubation. Early on, patient positioning was altered to overcome hypotension associated with thiopental. Etomidate and ketamine have been debated for 20 years. Bolus-dose vasopressors and fluid resuscitation strategies have been proposed, and debated, without definitive evidence for either of these interventions. Resuscitation, however, when used as a part of a bundle in the perioperative period has been shown to reduce complications.¹² Blood products prior to intubation in trauma patients have also been shown to improve outcomes.¹³ Unfortunately, none of these findings have been consistently reproducible, illustrating the complex pathophysiologic disturbances that require personalization for each patient.¹⁴^,¹⁵^,¹⁶

The reason for this is that hemodynamic instability is a syndrome with many causes where we observe the end result-hypotension. What causes hypotension in critically ill patients may, and likely does, differ from patient to patient. Consider a patient with severe ARDS from viral pneumonia (e.g., COVID-19, Influenza). There is significant airspace disease resulting in the loss of functional residual capacity. That worsens ventilation/perfusion mismatch and increases hypoxic vasoconstriction, increasing the pulmonary vascular resistance and right ventricular (RV) strain. Any hypercapnia or desaturation with induction can further challenge an already compromised right ventricle. Any induction agent-induced venodilation or myocardial depression, or positive pressure-induced reduction in preload, can lead to precipitous cardiovascular collapse and cardiac arrest. Similar physiology occurs in patients with massive pulmonary embolism or decompensated pulmonary arterial hypertension. However, treating every hemodynamically compromised patient the same will likely harm some patients and improve others.

Septic patients, for example, lie on a spectrum from vasodilation and high cardiac output to high systemic vascular resistance and myocardial depression. Patients with heart failure with preserved ejection fraction (EF) have high left ventricular (LV) filling pressures and high pulmonary venous pressures leading to pulmonary edema, whereas patients with heart failure with reduced EF have poor contractility leading to high pulmonary venous pressures and pulmonary edema. Although these patients may present with hypoxemia, respiratory failure, and hypotension, the management for each of them needs to be tailored to attenuate the physiologic weakness (Fig. 6.1). Vasoplegia is a major factor contributing to the negative hemodynamic effects seen in the peri-intubation period and
may not be easily measured or adequately addressed. In addition, the choice of induction agents and vasoactive medications further adds to these myriad factors. Any of these factors may be responsible for cardiovascular collapse in a fragile, critically ill patient. As such, these dynamic cardiopulmonary changes are challenging to predict, understand, and optimize. We suggest a stepwise strategy to peri-intubation hemodynamics.

Figure 6.1: Factors affecting hemodynamics during intubation.

Respiratory factors include the effects of positve pressure ventilation (PPV), desaturation, or hypercapnia which all increase pulmonary vascular resistance and RV afterload, whereas inhaled nitric oxide (iNO) vasodilates the pulmonary circulation and decreases RV afterload. Fluids can often increase stressed volume, whereas sedatives have varying effects. Propofol and midazolam can decrease the stressed volume, thereby increasing the unstressed volume and decreasing the preload. Etomidate can decrease arterial elastance causing hypotension. Propofol can cause arterial dilation and depression of left ventricular (LV) contractility, whereas ketamine can cause arterial constriction and increased LV contractility through its indirect sympathomimetic effect, or LV suppression through its myocardial depressant effect. Vasopressors affect the cardiovascular system dependent on their potency and receptor profile.

(From Mosier JM, Natt B. The physiologically difficult airway. In: Brown CA III, ed. The Walls Manual of Emergency Airway Management. 6th ed. Wolters Kluwer; 2023:21-33. Figure 3.1.)

STEPWISE HEMODYNAMIC APPROACH

Not every patient requires an extensive hemodynamic evaluation and planning. Patients presenting without hypotension and hemodynamic instability are less dangerous than patients with instability before the intubation. The SI can be a good indicator of trouble lurking where it is unexpected. A SI (heart rate/systolic blood pressure) ≥0.8 is at high risk of developing postintubation hypotension and can alert you to the need for resuscitation prior to induction.¹⁷^,¹⁸^,¹⁹^,²⁰^,²¹^,²²^,²³ For example, vital signs that are not alarming in isolation, such as a heart rate of 100 and systolic blood pressure of 100 mm Hg, can be very concerning when viewed through the lens of the SI. This is a SI of 1 and alerts you to very high risk of decompensation in the peri-intubation period that should be attenuated with fluid resuscitation where appropriate and in-line vasopressors prior to induction. Patients that are unstable prior to intubation, however, require a more thoughtful approach.

There is no one-size-fits-all approach to hemodynamic assessment or resuscitation prior to intubation because there are many factors that can collude to cause postintubation cardiovascular collapse. There is no single induction agent that can eliminate concern of the underlying pathophysiology and no vasopressor that can eliminate peri-intubation deterioration. Volume depletion, vasoplegia, ventricular performance, hemodynamic effects of induction agents, and the effects of positive pressure ventilation (PPV) are all important factors that need to be carefully considered. It is important to do an underlying hemodynamic assessment, and there are many ways to assess for things like volume responsiveness. However, the near ubiquitous availability of point-of-care ultrasound equipment and training provides an excellent opportunity for rapid assessment of hemodynamics to better understand opportunities for targeted interventions (Fig. 6.2, Chapter 11, Applied Ultrasonography).

Figure 6.2: Not every patient needs a full echocardiogram but answering a series of questions can help phenotype the underlying pathophysiology and guide management during airway management.

While these measurements are not diagnostic alone, they can alert to underlying physiology that may change the resuscitation. The first question is with a simple parasternal long-axis view—Is this a primary LV problem, a primary RV problem, or an external problem such as pericardial effusion and tamponade? In this view, the LV function can be easily seen qualitatively and can be estimated quantitatively with E-point septal separation (EPSS) or fractional shortening (FS%). A patient with poor function and a dilated left ventricle may need an inotrope compared to a patient with a hyperdynamic LV with complete cavity obliteration during systole. Still, a patient with thick myocardial wall and a dilated left atrium may need a separate approach. In this view, the LV outflow tract diameter can be measured and recorded for estimating stroke volume when combined with the VTI on the apical view if desired*. If a pericardial effusion is present**, m-mode can be used to assess for diastolic collapse, in addition to retrograde flow in the hepatic vein and IVC on subxiphoid view. The RV in this view should be minimally visible^#, so if the RV is large on the long-axis view, there may be a primary RV problem. The next step is a parasternal short-axis view— Is the RV pressure and/or volume overloaded? Pressure and volume overload can be qualitatively evaluated by looking at septal flattening on the short-axis view. The next view is the apical view and further evaluation can be guided toward the appropriate ventricle. In the setting of a normal RV, the LV pathway is chosen. If the LV is dilated and contractility is poor, it is more likely LV dysfunction is the primary problem. If the RV is normal and the LV is hyperdynamic, it is likely LV/vasoplegia is the primary problem. The next question in the LV assessment is—Is the patient likely to be fluid responsive? This can be assessed with variability of the LVOT VTI. Volume responsiveness is followed by—Is the patient likely to be volume intolerant? Volume intolerance occurs when a fluid bolus ends up worsening pulmonary congestion or edema. This can occur if there is restrictive physiology and high left atrial pressure, which is assessed with the e′ and EA, or if there is wide-open mitral or aortic valve regurgitation, which is assessed with color flow Doppler. If the RV is dilated, and there is septal flattening on the parasternal short axis view, in the setting of a normal appearing or hyperdynamic LV, there is likely RV dysfunction as the primary problem and an RV-focused assessment should be performed in the apical view. The key questions are—Is the right ventricle under strain (TAPSE), what is the contractility (IVV), and is there uncoupling leading to failure and cardiogenic shock (***,****see text)?

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