Cardiogenic shock has been difficult to define and is often misdiagnosed or diagnosed late. There was a significant increase in the incidence of cardiogenic shock over the last couple of decades which is thought to be due to an increase in diagnosis more than an actual increase in numbers. The mortality for cardiogenic shock remains around 50% despite multiple advances in medications and mechanical support devices (1-3). Due to this high mortality rate, There has been an increased focus over the last decade to try to improve the mortality level. There are several different hospitals and organizations that have tried and succeeded to tackle this difficult disease process.
In this series of blog posts, I am hoping to show how important it is to 1. diagnose cardiogenic shock; 2. have a method to diagnose cardiogenic shock early; 3. have a cardiogenic shock team with a treatment algorithm at your hospital.
Part 1: Early Diagnosis of Cardiogenic Shock
Part 2: Physiology of Cardiogenic Shock
Part 3: Management of Cardiogenic Shock
Part 4: Creating a Cardiogenic Shock Team/Protocol
Problems with Diagnosis:
The number of patients that have been admitted to the ICU for bilateral, multilobar pneumonia with no white blood cell count or fever that is actually in cardiogenic shock is unbelievable. Even with the knowledge that the patient has a history of heart failure, practitioners are so beaten down into not missing a sepsis diagnosis, or making sure they do not get in trouble for not giving 30mL/kg of crystalloid, they immediately go to sepsis even when a different diagnosis is screaming at them. This is very frustrating when working in a cardiac ICU. These patients will be sitting in the medical ICU getting the opposite treatment they need until they decompensate further and someone decides to look closer.
Also, even when the thought of a cardiogenic origin to the shock is entertained, there is a misconception going around that it does not matter because norepinephrine is the treatment for both septic shock and cardiogenic shock. It appears that this comes from the SOAP II trial. This trial looked at undifferentiated shock, compared norepinephrine and dopamine, and found no difference in outcomes, but more dysrhythmias in the dopamine group. In a subset analysis in cardiogenic shock patients, they found better outcomes with norepinephrine. People have taken this and said that norepinephrine is the first line for cardiogenic shock, which is just not true.
Another pitfall that I see is when hemodynamics are done on the patient, there is a focus on the wrong information or the interpretation of them is wrong. Systemic vascular resistance (SVR) is a calculation of a calculation, which makes it only as good as the original information. It should be low on the list of hemodynamic numbers when making a clinical decision. The circulatory system vasodilates for a lot of reasons, but the one that it gets most associated with is septic shock. This means more misdiagnosis of cardiogenic shock. Patients with a large acute myocardial infarction will almost all have a period of vasodilation (vasoplegia) due to the significant cytokine release with a large infarction. This vasoplegia can also be seen with acute on chronic heart failure exacerbation and if a mechanical circulatory device is placed in the patient. This vasoplegia usually lasts 12-24 hours and is not a sign of septic shock. This phenomenon can be supported with a brief stent of vasopressors added to the heart failure treatment.
Cardiogenic shock etiology:
One way to increase the success of accurately diagnosing cardiogenic shock is to know the etiology. Understanding the etiology will help keep cardiogenic shock in the differential and help aid diagnosis.
Table 1: Cardiogenic Shock Etiology
Defining Cardiogenic Shock:
Table 2: Different Ways of Defining Cardiogenic Shock
The difficulty of defining cardiogenic shock is that it varies in its presentation and, depending on the source, there is a lot of variability in its definition.
Diagnosing Cardiogenic Shock
Clinical definition:
The most well-known cardiogenic shock trials are the SHOCK and IABP-SHOCK II trials. The SHOCK trial used a systolic < 90mmHg or the use of inotropes/vasopressors or mechanical devices to maintain an SBP ≥ 90mmHg, whereas IABP-SHOCK II used systolic < 90mmHg despite fluid resuscitation. Both definitions included evidence of end-organ damage, which included decreased urine output, cool extremities, altered mental status, and elevated lactic acid.
The reason that I use mean arterial pressure (MAP) and not systolic pressure is that patients will often have a narrow pulse pressure with a low systolic and high diastolic and not be in shock. A patient with an EF 5-10% could have a blood pressure of 88/65 and not be in shock. I believe that MAP does a better job of capturing these patients.
A problem with the clinical definition is that it does not distinguish cardiogenic shock from other types of shock. All 4 groups of shock have low blood pressure and elevated lactic acid. Hypovolemic and obstructive will also have organ dysfunction and cool extremities. By just using the clinical definition, practitioners seem to consider other causes first and are less likely to diagnose cardiogenic shock.
Imaging definition:
This definition should improve the ability to diagnose cardiogenic shock. If you see someone with decreased cardiac function and high filling pressures on echo it should lead someone to cardiogenic shock, but often people with still default to saying they have heart failure but are in septic shock. The comfort level of practitioners to make a medical decision with point-of-care ultrasound (POCUS) is low and so they often do not attempt to look at the heart bedside. The imaging definition is often just not done. Besides a comfort level, right heart failure and valvular dysfunction leading to cardiogenic shock are much harder to diagnose with a basic POCUS skill level.
Hemodynamic definition:
The SHOCK trial also included hemodynamic compromise: cardiac index ≤ 2.2 L/min, pulmonary artery occlusion pressure (PAOP) ≥ 15 mmHg. This is a standard definition and is used most often for cardiogenic shock. I use a cardiac index < 2L/min because it is easier clinically for practitioners to visualize and understand. This is the gold standard for identifying cardiogenic shock, but it usually requires an invasive procedure. The pulmonary artery catheter will give you the most information including PAOP, which is difficult to objectively get otherwise. There are options for estimating cardiac index that are less invasive but do not include direct measurements of the left ventricle.
Another reason hemodynamic measurements are important is that it can be used to predict mortality. Clinical decision parameters and hemodynamic measurements were evaluated for mortality predictors in cardiogenic shock. Cardiac power was shown to be the strongest correlate to mortality in cardiogenic shock. Cardiac power is MAP x cardiac output (CO)/451 (11). It is used in prognosis at 12-24hrs post-intervention as shown below (12).
Figure 1: Cardiac power, lactic acid, and cardiogenic shock outcomes (1).
CPO = (MAP x CO)/451 (Normal Range: > 1 W)
CPI = [(MAP x CO)/451]BSA (Normal Range: 0.5-0.7 W/m2)
Table 3: Cardiogenic Shock Hemodynamics
Since 2019, with the increase in cardiogenic shock teams and treatment algorithms, it has been shown that pulmonary artery catheters in cardiogenic shock improve outcomes. This is a significant difference from the data from the previous decades that looked at PACs for all shock and found no improvement in outcomes and more adverse events (8). The previous studies included surgical and septic shock patients, whereas this was only looking at patients with heart failure.
Which identification method is best?
Are practitioners able to diagnose cardiogenic shock with a good physical exam? It was found that providers are very poor at estimating cardiac output clinically, with an accuracy of around 50%.
It is recommended that all patients with suspected cardiogenic shock receive imaging.
Most diagnoses and clinical decisions are based on hemodynamic parameters. Patients with a high suspicion of cardiogenic shock clinically or through imaging should get hemodynamic data.
Why early identification is important
Early identification and early intervention of cardiogenic shock have shown the best outcomes. The term “door to support” is being used to bring awareness to the early identification/treatment of cardiogenic shock (5,6). Also, early treatment with a mechanical circulatory support (MCS) device, if needed, was shown to improve outcomes in post-acute MI cardiogenic shock.
In one study (Figure 2), the time to MCS initiation was evaluated at < 75min, 75min - 4.25hrs, and > 4.25hrs. Survival was 66%, 37%, and 26% respectively (5). Every hour delay in the escalation of care from patient presentation there was a 10% increased mortality risk. Improved outcomes were able to obtained if intervened within 5 hours (5).
Figure 2: Door to Support Time & Survival
Why early identification of the severity of cardiogenic shock is important.
Being able to recognize that a patient is in cardiogenic shock is a great first step. What makes cardiogenic shock different from other forms of shock is that there are a large number of mechanical support devices that can improve mortality. Treatment with medications may not be adequate for a lot of patients. The heart needs to rest, inotropes increase cardiac output but increase stress and oxygen demand on the heart, whereas a mechanical support device can aid in the cardiac output and decrease cardiac demand. Delays in appropriately escalating care or not recognizing they need MCS was studied based on the number of inotropes started before initiation of MCS. Survival was 68%, 46%, 35%, 35%, and 26% for patients requiring 0, 1, 2, 3, and 4 inotropes before MCS respectively (5). Just because a patient's hemodynamics look better on two or three inotropes does not mean that is what is best for the patient.
Figure 3: Number of Inotropes & Survival
The main point to take away from this is that we as clinicians are not good at determining adequate cardiac output at the bedside with a success rate of 50%, or a coin flip. Additionally, the speed of diagnosing the type of shock is just as important as the accuracy of diagnosing the type of shock. If a patient presents with cardiogenic shock to the hospital their mortality can be 50% or be reduced to 20% by having a good algorithm and system in place to help with a quick accurate diagnosis. Make sure the emergency department, cath lab, and ICU know the different definitions of cardiogenic shock and know how to get imaging and hemodynamic data quickly to ensure an efficient accurate diagnosis.
In part 2 the physiology of cardiogenic shock will be discussed and how this knowledge can help improve mortality.
Part 2: Physiology of Cardiogenic Shock
Part 3: Management of Cardiogenic Shock
Part 4: Creating a Cardiogenic Shock Team/Protocol
REFERENCES:
Fincke R, Hochman JS, Lowe AM, Menon V, Slater JN, Webb JG, et al. Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic shock: a report from the SHOCK trial registry. J Am Coll Cardiol. 2004;44(2):340-8.
Jones TL, Nakamura K, McCabe JM. Cardiogenic shock: evolving definitions and future directions in management. Open Heart. 2019;6(1):e000960.
Vahdatpour C, Collins D, Goldberg S. Cardiogenic Shock. J Am Heart Assoc. 2019;8(8):e011991.
Basir MB, Kapur NK, Patel K, Salam MA, Schreiber T, Kaki A, et al. Improved Outcomes Associated with the use of Shock Protocols: Updates from the National Cardiogenic Shock Initiative. Catheter Cardiovasc Interv. 2019;93(7):1173-83.
Basir MB, Schreiber TL, Grines CL, Dixon SR, Moses JW, Maini BS, et al. Effect of Early Initiation of Mechanical Circulatory Support on Survival in Cardiogenic Shock. Am J Cardiol. 2017;119(6):845-51.
Esposito ML, Kapur NK. Acute mechanical circulatory support for cardiogenic shock: the "door to support" time. F1000Res. 2017;6:737.
Moghaddam N, van Diepen S, So D, Lawler PR, Fordyce CB. Cardiogenic shock teams and centres: a contemporary review of multidisciplinary care for cardiogenic shock. ESC Heart Fail. 2021;8(2):988-98.
Hernandez GA, Lemor A, Blumer V, et al. Trends in Utilization and Outcomes of Pulmonary Artery Catheterization in Heart Failure With and Without Cardiogenic Shock. J Card Fail. 2019;25(5):364-371. doi:10.1016/j.cardfail.2019.03.004
Thiele H, Ohman EM, Desch S, Eitel I, de Waha S. Management of cardiogenic shock. Eur Heart J. 2015;36(20):1223-30.
Combes A, Price S, Slutsky AS, Brodie D. Temporary circulatory support for cardiogenic shock. The Lancet. 2020;396(10245):199-212.
Levy B, Clere-Jehl R, Legras A, Morichau-Beauchant T, Leone M, Frederique G, et al. Epinephrine Versus Norepinephrine for Cardiogenic Shock After Acute Myocardial Infarction. J Am Coll Cardiol. 2018;72(2):173-82.