Structural heart disease (SHD) emergencies include acute deterioration of a stable lesion or development of a new critical lesion. Structural heart disease emergencies can produce heart failure and cardiogenic shock despite preserved systolic function that may not respond to standard medical therapy and typically necessitate surgical or percutaneous intervention. Comprehensive Doppler echocardiography is the initial diagnostic modality of choice to determine the cause and severity of the underlying SHD lesion. Patients with chronic SHD lesions which deteriorate due to intercurrent illness (eg, infection or arrhythmia) may not require urgent intervention, whereas patients with an acute SHD lesion often require definitive therapy. Medical stabilization prior to definitive intervention differs substantially between stenotic lesions (aortic stenosis, mitral stenosis, left ventricular outflow tract obstruction) and regurgitant lesions (aortic regurgitation, mitral regurgitation, ventricular septal defect). Patients with regurgitant lesions typically require aggressive afterload reduction and inotropic support, whereas patients with stenotic lesions may paradoxically require β-blockade and vasoconstrictors. Emergent cardiac surgery for patients with decompensated heart failure or cardiogenic shock carries a substantial mortality risk but may be necessary for patients who are not eligible for catheter-based percutaneous SHD intervention. This review explores initial medical stabilization and subsequent definitive therapy for patients with SHD emergencies.
Vasopressor and Inotrope Therapy in Cardiac Critical Care
Patients admitted to the cardiac intensive care unit (CICU) are often in shock and require hemodynamic support. Identifying and addressing the pathophysiology mechanisms operating in an individual patient is crucial to achieving a successful outcome, while initiating circulatory support therapy to restore adequate tissue perfusion. Vasopressors and inotropes are the cornerstone of supportive medical therapy for shock, in addition to fluid resuscitation when indicated. Timely initiation of optimal vasopressor and inotrope therapy is essential for patients with shock, with the ultimate goals of restoring effective tissue perfusion in order to normalize cellular metabolism. Use of vasoactive agents for hemodynamic support of patients with shock should take both arterial pressure and tissue perfusion into account when choosing therapeutic interventions. For most patients with shock, including cardiogenic or septic shock, norepinephrine (NE) is an appropriate choice as a first-line vasopressor titrated to achieve an adequate arterial pressure due to a lower risk of adverse events than other catecholamine vasopressors. If tissue and organ perfusion remain inadequate, an inotrope such as dobutamine may be added to increase cardiac output to a sufficient level that meets tissue demand. Low doses of epinephrine or dopamine may be used for inotropic support, but high doses of these drugs carry an excessive risk of adverse events when used for vasopressor support and should be avoided. When NE alone is inadequate to achieve an adequate arterial pressure, addition of a noncatecholamine vasopressor such as vasopressin or angiotensin-II is reasonable, in addition to rescue therapies that may improve vasopressor responsiveness. In this review, we discuss the pharmacology and evidence-based use of vasopressor and inotrope drugs in critically ill patients, with a focus on the CICU population.
Influence of cardiac arrest and SCAI shock stage on cardiac intensive care unit mortality
AbstractBackgroundPatients with concomitant cardiac arrest (CA) and shock are at increased risk of mortality, even when stratified according to shock severity. We sought to determine whether the presence of ventricular fibrillation (VF) modified the relationship between CA and mortality in cardiac intensive care unit (CICU) patients.MethodsWe retrospectively analyzed unique Mayo Clinic CICU patients admitted between 2007 and 2015. Society for Cardiovascular Angiography and Intervention (SCAI) shock stages A through E were classified at admission. Hospital mortality in each SCAI shock stage was stratified by the presence of CA, VF CA, or non‐VF CA.ResultsWe included 9,898 patients with a mean age of 68 years (38% females). CA was present in 12%, including 53% with VF CA and 47% with non‐VF CA. Hospital mortality was higher in patients with CA compared to patients without CA (34% vs. 6%; adjusted odds ratio [OR] = 3.1, 95% CI [2.4, 4.0],p < .001), and patients with non‐VF CA had higher hospital mortality than patients with VF CA (44% vs. 25%; adjusted OR = 2.1, 95% CI [1.4, 3.0],p < .001). After adjustment, patients with any CA or non‐VF CA had higher hospital mortality at each SCAI stage, except stage E (all otherp < .05), whereas patients with VF CA did not (allp > .1).ConclusionsCA rhythm modifies the relationship between CA and mortality in CICU patients, when accounting for coma, shock, and organ failure. Outcome studies examining CA in patients with cardiogenic shock need to account for important differences such as CA rhythm.
Early noncardiovascular organ failure and mortality in the cardiac intensive care unit
AbstractBackgroundNoncardiac organ failure has been associated with worse outcomes among a cardiac intensive care unit (CICU) population.HypothesisWe hypothesized that early organ failure based on the sequential organ failure assessment (SOFA) score would be associated with mortality in CICU patients.MethodsAdult CICU patients from 2007 to 2015 were reviewed. Organ failure was defined as any SOFA organ subscore ≥3 on the first CICU day. Organ failure was evaluated as a predictor of hospital mortality and postdischarge survival after adjustment for illness severity and comorbidities.ResultsWe included 10 004 patients with a mean age of 67 ± 15 years (37% female). Admission diagnoses included acute coronary syndrome in 43%, heart failure in 46%, cardiac arrest in 12%, and cardiogenic shock in 11%. Organ failure was present in 31%, including multiorgan failure in 12%. Hospital mortality was higher in patients with organ failure (22% vs 3%, adjusted OR 3.0, 95% CI 2.5‐3.7, P < .001). After adjustment, each failing organ system predicted twofold higher odds of hospital mortality (adjusted OR 1.9, 95% CI 1.1‐2.1, P < .001). Mortality risk was highest with cardiovascular, coagulation and liver failure. Among hospital survivors, organ failure was associated with higher adjusted postdischarge mortality risk (P < .001); multiorgan failure did not confer added long‐term mortality risk.ConclusionsEarly noncardiovascular organ failure, especially multiorgan failure, is associated with increased hospital mortality in CICU patients, and this risk continues after hospital discharge, emphasizing the need to promote early recognition of organ failure in CICU patients.