Postoperative Vasodilatory Shock

This chapter discusses vasodilatory shock. The hallmark of vasodilatory shock is hypotension with normal or increased cardiac output. The hyperdynamic circulatory state of vasodilatory shock results in a tachycardia and an increased pulse pressure. Radiological and biochemical investigations can assist with determining the diagnosis of shock. The causes of vasodilatory shock are diverse; they include sepsis, surgical insult, anaphylaxis, and others such as trauma, burns, and pancreatitis. However, sepsis is by far the most common cause of vasodilatory shock. The pathophysiology of vasodilatory shock is also complex and multifactorial. Although still not fully understood, it is widely accepted that it includes activation of several intrinsic vasodilatory pathways and a vascular hyporesponsiveness to vasopressors. Early fluid resuscitation and appropriate antimicrobial therapy are the most crucial treatment interventions in septic shock. Meanwhile, noradrenaline is the first-line vasopressor of choice in septic shock.

Coagulopathy in Cardiac Surgery: Etiology and Treatment Options

This chapter reviews the causes and outlines an approach to the management of coagulopathy following cardiac surgery. Bleeding after cardiac surgery is common and expected up to a rate of 2 mL/kg/h for the first 6 hours. A more significant hemorrhage needs to be investigated and treated. Causes are often multifactorial. It is imperative that surgical causes be excluded early concomitant to providing resuscitation, investigating other medical causes for bleeding, and treating coagulopathy empirically until laboratory testing becomes available. The most frequent causes for coagulopathy post–cardiac surgery are excess heparinization, prolonged cardiopulmonary bypass time, hypothermia, acidosis, and preexisting bleeding diathesis. The management of coagulopathy implies maintenance of the normal physiological conditions for coagulation, reversal of excess heparinization, treatment of hyperfibrinolysis, maintaining normal levels of coagulation factors, and transfusion of platelets if thrombocytopenia or platelet dysfunction occurs. The chapter reviews what is involved in standard laboratory testing (complete blood count, prothrombin time, activated partial thromboplastin time, fibrinogen level, etc.) for coagulopathy. Also discussed is point-of-care testing and how the results from these tests should be interpreted. The chapter details the various blood products that are required in this scenario and suggests doses and transfusion thresholds.

Intra-aortic Balloon Pump

This chapter describes the intra-aortic balloon pump (IABP), which is the single most widely used mechanical circulatory assist device available today. Counterpulsation refers to balloon inflation in diastole and deflation in early systole: this results in increased coronary blood flow, left ventricular afterload reduction, and increased end-organ perfusion. Other uses of balloon counterpulsation include refractory ventricular arrhythmias, inability to wean from cardiopulmonary bypass, bridge to intervention in severe/critical aortic stenosis, and refractory pulmonary edema from decompensated heart failure. However, the absolute contraindications for IABP placement are aortic dissection, clinically significant aortic aneurysm, severe peripheral artery disease, significant aortic regurgitation, uncontrolled bleeding, and/or sepsis. The chapter then explains the optimal positioning for IABP. It also looks at complications associated with IABPs. These include thrombocytopenia and vascular complications, such as limb ischemia, bleeding, dissection, and hematoma/pseudoaneurysm formation. The presence of blood in the balloon tubing suggests the possibility of balloon rupture and gas embolism, an extremely uncommon but catastrophic event.

Left Ventricular Assist Device Implantation and Management

This chapter studies left ventricular assist device (LVAD) implantation. A thorough preoperative evaluation of a patient undergoing LVAD implantation is of utmost importance because of the confluence of associated medical problems patients can have secondary to heart failure. Knowledge of the indications and contraindications for LVAD implantation is needed to provide proper consultation. Indications for LVAD implantation include bridge to transplantation, destination therapy, bridge to decision, and bridge to recovery. Contraindications to LVAD implantation include neurological changes following implantation, pulmonary dysfunction, renal dysfunction, and hepatic dysfunction. Intraoperative management of LVAD implantation involves monitoring, anesthetic induction/maintenance, and device management. Echocardiography is an invaluable tool in the perioperative monitoring and diagnostic assessment of LVAD implantation. The chapter then looks at early complications such as hypovolemia, vasoplegia, and right ventricular failure.

Robotic Mitral Valve Surgery and Unilateral Pulmonary Edema

This chapter describes robotic or minimally invasive mitral valve surgery, which was pioneered in 1998 to be the less invasive approach to sternotomy-based mitral valve operations. Patients undergoing robotic valve surgery carry a similar risk of complications that may occur with traditional median sternotomy surgery, but minimally invasive valve surgery has its own inherent complications associated with cardiac access, perfusion, and ventilation methods used in robotic surgeries. Unilateral pulmonary edema (UPE) is an uncommon but potentially life-threatening complication of robotic mitral valve surgery. The incidence of unilateral lung injury, which commonly manifests as UPE, has been reported to be quite variable. The variation in incidence could be related to the difference in patient populations, diagnostic criteria, as well as management. Moreover, the pathophysiology of UPE associated with robotic mitral valve repair remains unclear. The current literature suggests that UPE can be prevented by shorter cardiopulmonary bypass times, avoiding barotrauma, limiting blood product transfusion, and minimizing lung isolation times. Lung preventive ventilation, such as low-level positive pressure and frequent alveolar recruitment, while on cardiopulmonary bypass may be beneficial. Meanwhile, treatment for UPE is dependent on the severity of symptoms.

Respiratory Acidosis in the Intensive Care Unit

This chapter explains that the interpretation of acid–base abnormalities is an essential skill required when caring for critically ill patients. The differential causes of respiratory acidosis include central nervous system depression, upper and lower airway obstruction, and hypermetabolic states with increased production of CO2, such as malignant hyperthermia and thyroid storm. The treatment for hypoxic and hypercarbic respiratory failure involves reversing the offending agents if applicable, treatment of the underlying cause, and mechanical ventilation. The 2 commonly used strategies for mechanical ventilation are non-invasive ventilation with a mask and endotracheal intubation. The selection of ventilation strategy is dependent on numerous patient factors. Clinicians must set respiratory rate, tidal volume, positive end-expiratory pressure, inspiratory flow, fraction of inspired oxygen, mode (volume versus pressure control), and the amount of assistance per breath. All need to be tailored toward each patient’s specific goals. In patients with severe acidosis, there may be a temptation to hyperventilate in order to treat the hypercarbia and hypoxia as quickly as possible. This can be deleterious as high tidal volumes may lead to ventilator-induced lung injury due to volutrauma, cytotrauma, and barotrauma.

Cardiac Surgery–Associated Acute Kidney Injury

This chapter on the topic of cardiac surgery–associated acute kidney injury (CS-AKI) examines the risk factors for and the prevention, diagnosis, and management of this serious and common consequence of cardiothoracic surgery. The chapter follows the clinical course of a patient with a moderate risk of CS-AKI undergoing an aortic valve replacement and coronary artery bypass grafting. The risk factors, both patient- and surgery-specific, are demonstrated in tabular form. Methods to mitigate against these risk factors are explained, including optimizing the timing of surgery. The most up-to-date diagnostic criteria for AKI are compared. It also recommends the most accurate formulae to evaluate the severity of CS-AKI. The value of medical therapies prior to renal replacement therapy (RRT) is examined. The clinical decisions regarding the mode of RRT, timing of RRT, anticoagulation methods, and vascular access are highlighted. Patients with already established end-stage renal disease are discussed as a separate cohort. The chapter concludes by discussing the short- and longer-term prognosis associated with CS-AKI.

Postoperative Cardiogenic Shock

Postoperative cardiogenic shock describes the management of a postoperative coronary artery bypass graft patient who develops early postoperative shock; after a brief discussion of the different potential causes, the chapter focuses on postoperative myocardial infarction due to graft failure. It reviews the assessment and treatment of patients with postoperative myocardial ischemia causing shock; it then outlines the immediate steps to take for diagnosis and patient stabilization, before discussing the definitive management strategy. A stepwise discussion covering fluids and pharmacological and mechanical support is provided to help guide management decisions. The chapter then outlines revascularization as the optimal treatment and fundamental goal.

Endocarditis

In this chapter we describe the case of a patient presenting with signs and symptoms of infective endocarditis following a recent mitral valve replacement. We describe the epidemiology of infective endocarditis and discuss its features including echocardiographic features. We discuss diagnosis, treatment (both medical and surgical), complications and prognosis with a focus and emphasis on the ICU patient. The clinical presentation of IE in the ICU setting may be atypical and classic features may be masked by critical care interventions and concomitant pathology. Echocardiography can be particularly challenging in the ICU setting. There should be a low threshold for TEE in critically ill patients with Staphylococcus aureus catheter-related bloodstream infection because of its high propensity to cause IE.

Left Ventricular Assist Device Troubleshooting: Hypotension

The differential diagnosis for postoperative hypotension after left ventricular assist device (LVAD) implantation is broad and is defined as a mean arterial pressure <60 mm Hg for continuous-flow LVADs. Etiologies to consider include vasodilatory shock from systemic inflammatory response syndrome or sepsis, hypovolemia, cardiogenic shock secondary to right ventricular dysfunction, cardiac tamponade, pulmonary embolus or tension pneumothorax, and device-related complications that obstruct flow through the pump. Clinical examination is an important component of the initial evaluation. Assessment of LVAD flows/cardiac output can help to differentiate between vasodilatory and non-vasodilatory shock. The cause of non-vasodilatory shock can be further narrowed with the aid of pulmonary artery catheter placement, transthoracic or transesophageal echocardiography, and chest radiography and guide specific treatments and interventions.