Cardiogenic shock is defined as a primary cardiac disorder that results in both clinical and biochemical evidence of tissue hypoperfusion. Clinical criteria include a systolic blood pressure of less than or equal to 90 mm Hg for greater than or equal to 30 minutes or support to maintain systolic blood pressure less than or equal to 90 mm Hg and urine output less than or equal to 30 mL/hr or cool extremities. Hemodynamic criteria include a depressed cardiac index (less than or equal to 2.2 liters per minute per square meter of body surface area) and an elevated pulmonary-capillary wedge pressure greater than 15 mm Hg.
Cardiogenic shock is a clinical entity characterized by a low cardiac output state of circulatory failure that results in end-organ hypoperfusion and tissue hypoxia. The most common cause of cardiogenic shock is acute myocardial infarction, though other disorders leading to impairment of the myocardium, valves, conduction system, or pericardium also can result in cardiogenic shock. Despite advances in reperfusion therapy and mechanical circulatory support treatments, morbidity, and mortality among patients with cardiogenic shock remain high.
The most common causes of cardiogenic shock include:
Risk of Cardiogenic shock after ST-elevation myocardial infarction (STEMI):
The incidence of cardiogenic shock is in decline, which can be attributed to increased rates of use of primary percutaneous coronary intervention (PCI) for acute MI. However, approximately 5% to 8% of STEMI and 2% to 3% of NON-STEMI cases can result in cardiogenic shock. This can translate to 40,000 to 50,000 cases per year in the United States.
Cardiogenic shock has a higher incidence in the following classes of patients:
The pathophysiology of cardiogenic shock is complex and not fully understood. Ischemia to the myocardium causes derangement to both systolic and diastolic left ventricular function, resulting in a profound depression of myocardial contractility. This, in turn, leads to a potentially catastrophic and vicious spiral of reduced cardiac output and low blood pressure, perpetuating further coronary ischemia and impairment of contractility. Several physiologic compensatory processes ensue. These include:
These compensatory mechanisms are subsequently counteracted by pathologic vasodilation that occurs from the release of potent systemic inflammatory markers such as interleukin-1, tumor necrosis factor a, and interleukin-6. Additionally, higher levels of nitric oxide and peroxynitrite are released, which also contribute to pathologic vasodilation and are known to be cardiotoxic. Unless interrupted by adequate treatment measures, this self-perpetuating cycle leads to global hypoperfusion and the inability to effectively meet the metabolic demands of the tissues, progressing to multiorgan failure and eventually death.
The presenting symptoms of cardiogenic shock are variable. The most common clinical manifestations of shock, such as hypotension, altered mental status, oliguria, and cold, clammy skin, can be seen in patients with cardiogenic shock.
History plays a very important role in understanding the etiology of the shock and thus helps in the management of cardiogenic shock.
The patient should also be assessed for cardiac risk factors:
Physical examination findings in patients with cardiogenic shock include the following:
Diagnostic evaluation of cardiogenic shock includes the following:
Cardiogenic shock is an emergency requiring immediate resuscitative therapy before the irreversible damage of vital organs. Rapid diagnosis with prompt initiation of pharmacological therapy to maintain blood pressure and to maintain respiratory support along with a reversal of underlying cause plays a vital role in the prognosis of patients with cardiogenic shock.
Early restoration of coronary blood is the most important intervention and is the standard therapy for patients with cardiogenic shock due to myocardial infarction.
The management of cardiogenic shock involves the following:
The goal of medical management is to restore cardiac output and prevent irreversible end-organ damage rapidly.
Percutaneous Coronary Intervention and Coronary Artery Bypass
SHOCK (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock) trial data confirmed an approach that combines early revascularization with medical management in patients with cardiogenic shock is optimal.
Mechanical Circulatory Support
Due to the poor prognosis associated with cardiogenic shock, medical therapy is often inadequate, and mechanical circulatory support (MCS) therapy to improve end-organ perfusion may be required. An experienced interprofessional team should evaluate MCS.
Short-term mechanical circulatory assist
IABP- Intra-aortic balloon pump
Some of the other indications apart from cardiogenic shock include intractable angina, adjunctive therapy in high risk or complicated angioplasty, refractory heart failure as a bridge to future therapy, intractable ventricular arrhythmias as a bridge to therapy.
Mechanism: Blood is displaced into the proximal aorta by inflation during diastole, during systolic, rapid balloon deflation occurs, creating a vacuum effect and reducing the afterload.
Contraindications include severe aortic regurgitation, aortic dissection, uncontrolled sepsis, uncontrolled bleeding disorders.
The patient needs to be on therapeutic anticoagulation to avoid thrombosis, and heparin is the most common anticoagulation used. Daily labs, including creatinine, platelet count, and hemoglobin, need to be checked. Uncommon events like cholesterol embolization and balloon rupture rare occurrence.
Limitations of IABP include variable effect on total coronary blood flow, no mortality benefit, modest hemodynamic support.
Non-IABP percutaneous mechanical devices
Left ventricular assist devices
1. Left ventricle to aorta- percutaneous transvalvular left ventricular assistance device (LVAD)
2. Left-atrium-to-aorta assist device-
3. Percutaneous cardiopulmonary bypass support with use of an extracorporeal membrane oxygenator (ECMO).
Right ventricular assist device
-The LVAD system is available in 2 different versions (2.5 and 5.0). The larger version needs surgical implantation, whereas the smaller motion could be placed percutaneously.
-This has an axial flow pump that revolves at a high-speed displacing blood from the left ventricle to proximal ascending aorta and works on the principle of Archimedes screw.
-Protective to trial compared to a 30-day incidence of major adverse events between intractable on the pump and the 2.5 LVAD. It showed no difference between the 2 groups; trends for improved outcomes were observed for the 2.5 supported patients at 90 days.
-Placement of the LVAD system takes a longer time compared to IABP and needs more experience. However, it provides a better improvement in cardiac index.
Left-atrium-to-aorta assist device
With a percutaneous left atrium to aortic assistive device, blood is pumped from the left atrium to the iliofemoral system. It is approved by the US FDA for 6 hours of support. A randomized control trial comparing this device with an IABP in 41 patients with cardiogenic shock after acute myocardial infarction. Hemodynamic and metabolic parameters were more effectively reversed with the left atrium to aorta assist device. Complications such as severe bleeding and acute limb ischemia are more common with this device, and there is no difference in 30-day mortality (VAT 43% versus balloon pump 45%). 
ECMO-venoarterial bypass configuration
Pulmonary circulation is bypassed, and oxygenated blood returns to the patient via an arterial or venous route. The extracorporeal pump is employed to support systemic perfusion. Cannulas are placed into the central vein and central artery. Blood from the venous catheter is pumped through a heat exchanger and oxygenator. Blood is returned to the systemic arterial circulation via arterial cannula. This is used in patients with circulatory and respiratory failure.
Palliative Care in Cardiogenic shock
Current Management Guidelines
Cardiogenic shock carries a poor prognosis and is the leading cause of death in patients with an acute MI. Close to 80% of patients die despite optimal treatment. Complications associated with cardiogenic shock include:
Cardiogenic shock is a life-threatening disorder and is the main cause of death after an acute MI. Even in the best of hands and the latest treatment, the condition carries a mortality rate in excess of 30%. The key to survival is to have prompt resuscitation with coronary artery revascularization. Unfortunately, even with revascularization, multiorgan failure is common, and long-term survival is not guaranteed. Because cardiogenic shock affects almost every other organ in the body, the condition is best managed by an interprofessional team that also includes ICU nurses.
Once cardiogenic shock has been diagnosed, patient monitoring is vital. The surgeon and cardiologist need to be notified right away. The cardiac catheterization nurses need to be informed of this emergency as the initial treatment of choice is PCI. The pharmacist should make sure that the patient is on no medications that depress the heart function like beta-blockers. If an IABP is contemplated, the perfusionist should be notified. Most patients require mechanical ventilation, and hence, respiratory therapists should be involved to ensure that positive pressure ventilation is avoided.
If the patient undergoes PCI or open-heart surgery, monitoring is required as complications are common in the post-operative period. The nephrologist, pulmonologist, and internist should be involved to ensure optional care. The nurse should monitor the patient for oliguria, coagulopathy, poor oxygenation, loss of pulses, abdominal pain (mesenteric ischemia), and stroke. Close communication is vital between the interprofessional team to improve outcomes.
Even though cardiogenic shock cannot be entirely prevented, clinicians should educate patients on reducing risk factors for heart disease. Patients should be urged not to smoke, lower the lipids, and ensure better control of blood sugars. In addition, enrollment in an exercise program can help lower body weight and help achieve better control of the blood pressure. [Level 5]
|||Rab T,Ratanapo S,Kern KB,Basir MB,McDaniel M,Meraj P,King SB 3rd,O'Neill W, Cardiac Shock Care Centers: JACC Review Topic of the Week. Journal of the American College of Cardiology. 2018 Oct 16 [PubMed PMID: 30309475]|
|||Maeda K,Takanashi S,Saiki Y, Perioperative use of the intra-aortic balloon pump: where do we stand in 2018? Current opinion in cardiology. 2018 Nov [PubMed PMID: 30303852]|
|||Kalmanovich E,Audurier Y,Akodad M,Mourad M,Battistella P,Agullo A,Gaudard P,Colson P,Rouviere P,Albat B,Ricci JE,Roubille F, Management of advanced heart failure: a review. Expert review of cardiovascular therapy. 2018 Oct 3 [PubMed PMID: 30282492]|
|||Ginwalla M,Tofovic DS, Current Status of Inotropes in Heart Failure. Heart failure clinics. 2018 Oct [PubMed PMID: 30266368]|
|||Saleh M,Ambrose JA, Understanding myocardial infarction. F1000Research. 2018 [PubMed PMID: 30228871]|
|||El Sibai R,Bachir R,El Sayed M, Outcomes in Cardiogenic Shock Patients with Extracorporeal Membrane Oxygenation Use: A Matched Cohort Study in Hospitals across the United States. BioMed research international. 2018 [PubMed PMID: 29789779]|
|||Mohananey D,Smilowitz N,Villablanca PA,Bhatia N,Agrawal S,Baruah A,Ali MS,Bangalore S,Ramakrishna H, Trends in the Incidence and In-Hospital Outcomes of Cardiogenic Shock Complicating Thyroid Storm. The American journal of the medical sciences. 2017 Aug [PubMed PMID: 28864374]|
|||Gaubert M,Resseguier N,Thuny F,Paganelli F,Cautela J,Pinto J,Ammar C,Laine M,Bonello L, Doppler echocardiography for assessment of systemic vascular resistances in cardiogenic shock patients. European heart journal. Acute cardiovascular care. 2018 Aug 20 [PubMed PMID: 30124051]|
|||Braile-Sternieri MCVB,Mustafa EM,Ferreira VRR,Braile Sabino S,Braile Sternieri G,Buffulin de Faria LA,Sbardellini BC,Vianna Queiroz CO,Braile DM,Zotarelli Filho IJ, Main Considerations of Cardiogenic Shock and Its Predictors: Systematic Review. Cardiology research. 2018 Apr [PubMed PMID: 29755623]|
|||Santucci A,Cavallini C, [Which role today for intra-aortic balloon counterpulsation?] Giornale italiano di cardiologia (2006). 2018 Oct [PubMed PMID: 30281041]|
|||Bonello L,Delmas C,Schurtz G,Leurent G,Bonnefoy E,Aissaoui N,Henry P, Mechanical circulatory support in patients with cardiogenic shock in intensive care units: A position paper of the [PubMed PMID: 29903693]|
|||Thiele H,Zeymer U,Neumann FJ,Ferenc M,Olbrich HG,Hausleiter J,Richardt G,Hennersdorf M,Empen K,Fuernau G,Desch S,Eitel I,Hambrecht R,Fuhrmann J,Böhm M,Ebelt H,Schneider S,Schuler G,Werdan K, Intraaortic balloon support for myocardial infarction with cardiogenic shock. The New England journal of medicine. 2012 Oct 4; [PubMed PMID: 22920912]|
|||Kar B,Adkins LE,Civitello AB,Loyalka P,Palanichamy N,Gemmato CJ,Myers TJ,Gregoric ID,Delgado RM 3rd, Clinical experience with the TandemHeart percutaneous ventricular assist device. Texas Heart Institute journal. 2006; [PubMed PMID: 16878609]|
|||Singh P,Lima FV,Parikh P,Zhu C,Lawson W,Mani A,Jeremias A,Yang J,Gruberg L, Impact of prior revascularization on the outcomes of patients presenting with ST-elevation myocardial infarction and cardiogenic shock. Cardiovascular revascularization medicine : including molecular interventions. 2018 Oct 15 [PubMed PMID: 30344055]|
|||Garan AR,Malick WA,Habal M,Topkara VK,Fried J,Masoumi A,Hasan AK,Karmpaliotis D,Kirtane A,Yuzefpolskaya M,Farr M,Naka Y,Burkhoff D,Colombo PC,Kurlansky P,Takayama H,Takeda K, Predictors of Survival for Patients with Acute Decompensated Heart Failure Requiring Extra-Corporeal Membrane Oxygenation Therapy. ASAIO journal (American Society for Artificial Internal Organs : 1992). 2018 Oct 9 [PubMed PMID: 30312208]|