Advanced Heart Failure and Cardiogenic Shock

Introduction

The term shock first appeared in the English medical literature in a translation by John Clarke of a French treatise on gunshot wounds by Henry LeDran in 1740, Traité ou Reflexions Tirées de la Pratique sur les Playes d’armes à feu. In his translation, he used the English “shock” to translate the French word saisissement , which at that time might have meant “fright” or “violent emotion.” The description only slowly gained acceptance and described more the neurologic reaction, either torpor or agitation, to the trauma of violent injury rather than a physiologic response. The battlefield surgeons of the American Civil War were well acquainted with the condition, “Although the nervous shock accompanies the most serious wounds…. It is recognized by the sufferer becoming cold, faint and pale, with the surface bedewed with a cold sweat; the pulse is small and flickering; there is anxiety, mental depression, with at times incoherence of speech.” The measurement of blood pressure, at first invasively and then noninvasively, in the later part of the 19th century added reduced blood pressure to the syndrome.

In the late 19th and early 20th centuries, the etiology of shock was thought to be a neurologic reflex or a result of abnormal blood pooling in the mesenteric vessels. World War I led to an intensification of medical interest on the shock syndrome, with insights added from animal models used to scientifically test models for the initiation of shock.

In August 1917, George Crile led the Lakeside Unit from Cleveland into the war. These were the first US Army troops to enter the conflict. A base hospital was established to treat the wounded troops along the German-Allied lines near Rouen, France, and in Belgium’s Flanders Field. Several other units from academic medical centers were assembled, including the Harvard Unit, led by Harvey Cushing. Prior to the war, Crile developed an interest in hemorrhagic shock, developing during surgical procedures. He created a number of approaches to blood transfusion after visiting the labs of Alexis Carrel in 1902 and is sometimes credited with the first direct human blood transfusion. A poignant event is described in his autobiography when he was called by his dear friend Harvey Cushing to his outpost, also serving as a forward base hospital in the war. William Osler’s only child had been mortally wounded and Crile was called to assist with surgery and to arrange for blood transfusions in a desperate attempt to save his life. Sadly, Revere Osler died despite efforts to ameliorate his shock state, which was multifactorial in nature. Crile’s work subsequently led to development of “shock trousers,” which were used in the operating room when shock developed. It was also learned during this time that shock from blood loss could be reversed with lactated Ringer’s solution.

The current understanding, still incomplete, of cardiogenic shock moved forward in 1927, when Alfred Blalock, prior to the creation of his eponymous shunt with Vivien Thomas and Helen Taussig, began pivotal research on the origins and classification of shock. He was able to show experimentally that it often was not neurologically driven. He also classified its presentation into five clinical syndromes, which form the foundation for approaching shock today, including cardiogenic shock.

• 1.

  Shock due to volume loss

• 2.

  Neurogenic shock

• 3.

  Vasogenic shock, which includes sepsis and anaphylaxis

• 4.

  Cardiogenic shock

• 5.

  Unclassified conditions

What is described in the following is a current understanding of the pathophysiology of cardiogenic shock. This is by no means to suggest that cardiogenic shock is “understood,” a point that is underscored by the persistently high mortality of cardiogenic shock. We are standing on the shoulders of giants, but our vision is still woefully incomplete ( Table 2.1 ).

Definition

Shock is a clinical syndrome, much like heart failure, that is characterized by signs and symptoms recognized by the clinician. These can be horribly apparent, as when cardiac arrest initiates cardiogenic shock with complete absence of vital signs ( Fig. 2.1 ) or so subtle that the patient drifts into shock over the course of weeks or months and even skilled clinicians miss the transition (gradual-onset cardiogenic shock). In general, contemporary definitions of cardiogenic shock are eerily similar to battlefield depictions of severe trauma in the American Civil War, but with the addition of quantitative parameters of reduced urine output and blood pressure. Cardiogenic shock was defined in a recent trial evaluating percutaneous intervention in shock as “a systolic blood pressure of less than 90 mm Hg for longer than 30 minutes or the use of catecholamine therapy to maintain a systolic pressure of at least 90 mm Hg, clinical signs of pulmonary congestion, and signs of impaired organ perfusion with at least one of the following manifestations: altered mental status, cold and clammy skin and limbs, oliguria with a urine output of less than 30 mL per hour, or an arterial lactate level of more than 2.0 mm per liter.”

Etiology of cardiogenic shock

Acute myocardial infarction is a common, but by no means the only, cause of cardiogenic shock ( Box 2.1 ), and the infarction can result in shock in a number of ways. It can be the result of a catastrophically large infarct or a relatively small infarction in the setting of an ischemic cardiomyopathy. Infarction of the right ventricle with relative sparing of the left ventricle has unique clinical features, including shock. Severe ischemia even in the absence of myocardial injury can reduce cardiac output substantially with reduced blood pressure. Finally, infarction with tissue necrosis can result in papillary muscle rupture, acute ventricular septal defect, or free wall rupture with severe, often fatal, shock.

In the absence of coronary artery disease, acute myocarditis and especially giant cell myocarditis can result in profound cardiogenic shock such that almost cessation of myocardial contraction can be seen and/or incessant malignant arrhythmias requiring ECMO support. Takotsubo cardiomyopathy can mimic acute myocardial infarction in the emergency room and has a reported incidence of cardiogenic shock of 9%. Long-standing heart failure that has been stable for decades can devolve rapidly or insidiously into end-stage heart failure with hypotension and multiorgan dysfunction. Similarly, chronic valvular abnormalities, when they become severe, can profoundly impair hemodynamics and become life-threatening. Patients with adult congenital heart disease can sink later in life into a shock state with multiorgan failure after years of relatively normal cardiovascular status following early palliative surgery. Large pulmonary emboli can present with syncope and cardiogenic shock from right heart failure, as can end-stage pulmonary arterial hypertension. Finally, long-standing alcohol abuse and illicit drug use with methamphetamines or other sympathomimetic drugs can be responsible for profound cardiac dysfunction.

Hemodynamic effects of cardiogenic shock