LEARNING OUTCOMES
After completing this module the paramedic will be able to:
Cardiogenic shock is caused by a decrease in left ventricular function—this leads to persistent hypotension resulting in systemic end-organ hypoperfusion (Thiele et al, 2015; van Diepen et al 2017). It is associated with signs of organ hypoperfusion such as cool, clammy skin, altered mental status, oliguria and raised serum lactate in the presence of persistent hypotension despite adequate circulating volume. Acute ST-segment elevation myocardial infarction (STEMI) causing left ventricular dysfunction is the most common cause, accounting for approximately 80% of cases (Reynolds and Hochman, 2008).
Part one of this series outlined the pathophysiology, patient outcomes and diagnostic criteria associated with cardiogenic shock (O'Donovan, 2019). In part two, goals of care, evidence-based treatment strategies and the role of the paramedic will be discussed.
Treatment goals and strategies
Van Diepen et al (2017) recommend that treatment goals for cardiogenic shock should focus on restoring and maintaining end-organ perfusion but acknowledges that there are no published evidence-based treatment targets. While a mean arterial pressure of 65–70 mmHg is essential for end-organ perfusion, Vincent and De Backer (2013) advocate adjusting the mean arterial pressure goal based on mental status, skin appearance, serum lactate level, oxygen saturations and hourly urinary output, as these are reliable indicators of tissue perfusion status.
General supportive measures such as maintaining oxygenation and ensuring adequate circulating volume are intended to stabilise patient haemodynamics and prevent or halt the onset of multi-organ dysfunction syndrome (MODS). Reynolds and Hochman (2008) recommend achieving optimal arterial oxygenation and near normal pH to minimise tissue ischaemia.
A cardiovascular and respiratory assessment may demonstrate symptoms of respiratory distress, use of accessory muscles, cyanosis and an oxygen saturation of <94%. Increasing oxygen delivery to the patient may be achieved by non-invasive or mechanical ventilation. Mechanical ventilation is considered for those with respiratory fatigue, acidosis or distress (Hasdai et al, 2000). The prevalence of mechanical ventilation in the ‘SHould we emergently revascularise Occluded Coronaries for cardiogenic shocK (SHOCK)’ trial (Hochman et al, 1999) was in the 78–88% range. The benefits of non-invasive and invasive ventilation to patients are a reduction in respiratory workload and a decrease in preload and afterload, which reduce the workload of the failing left ventricle (Wiesen et al, 2013). Other benefits include improved gas exchange, alveoli recruitment and airway patency (Tobin, 1994). An integral aspect of mechanical ventilation is the use of sedation. A potential adverse effect associated with sedation agents is vasodilation; therefore, in the author's clinical practice, the lowest therapeutic dose is administered to avoid further reductions in cardiac output and blood pressure.
The European Society of Cardiology (ESC) Guidelines on the management of STEMI (Ibanez et al, 2017) recommend intravenous fluid is administered to patients with hypovolaemia, those with drug-induced hypotension or where there is no evident cause for cardiogenic shock. The aim is to increase circulating volume, raise systemic arterial pressure, decrease heart rate and increase urinary output. Fluid administration must be observed closely for the development of pulmonary oedema or fluid overload, which present as an increase in respiratory rate and heart rate and a decrease in oxygen saturation.
Other general principles of care include avoiding negative inotropes and vasodilators as they cause preload and afterload to fall further, decreasing cardiac output while increasing mortality risk. Van Diepen et al (2014) demonstrated that approximately 25% of patients with cardiogenic shock were administrated beta-blockers or renin–angiotensin–aldosterone system (RAAS) inhibitors within the first 24 hours of shock diagnosis. These patients had a higher 30-day mortality than those who did not receive these therapies. Van Diepen et al (2017) recommend starting these therapies when the patient is euvolaemic and has been off supportive therapies for at least 24 hours.
Revascularisation
From a prehospital perspective, Ibanez et al (2017) highlights the following steps to achieve a positive patient outcome with the goal being to reduce the delay between first medical contact and STEMI diagnosis to ≤10 minutes and that the patient is transferred directly to the cardiac catheterisation laboratory, bypassing the emergency department. According to Bagai et al (2013), bypassing the emergency department is associated with a 20-minute reduction in the time from first medical contact to wire crossing.
For patients who present to non-cardiac catheterisation facilities, Ibanez et al (2017) recommends a standard where the time from arrival of the patient to discharge of the patient to a cardiac catheterisation laboratory should be <30 minutes.
Primary percutaneous coronary intervention (PCI) is considered the gold standard treatment for those experiencing STEMI. The pivotal SHOCK trial (Hochman et al, 1999) randomised 302 patients with STEMI complicated with cardiogenic shock to an early revascularisation strategy within 12 hours of shock onset or initial medical stabilisation. Findings demonstrated that, although all-cause mortality reduction at 30 days was not significant (revascularisation 46% vs medical strategy 56% P=0.11), there was a significant mortality reduction at follow-up at 6 months, 1 year and 6 years (Hochman et al, 2001; 2006; Thiele et al, 2015). Reynolds and Hochman (2008) translated these findings into a 13% absolute increase in 1 year survival in those treated with early revascularisation. The current ESC guidelines on the management of STEMI (Ibanez et al, 2017) consider revascularisation within 120 minutes of first medical contact best practice. Therefore, in patients where reperfusion is expected to be outside this timeframe, immediate fibrinolysis and transfer to a PCI facility is recommended so that emergent angiography can be performed.
Complementary to revascularisation is the administration of dual antiplatelet therapy to reduce ischaemia and atherosclerotic thrombus perpetuation. The ESC STEMI guidelines (Ibanez et al, 2017) emphasise that dual antiplatelet therapy should not differ from that provided to any patients with STEMI. However, there is a paucity of scientific evidence of the impact of antiplatelet therapy in this patient population. Thiele et al (2015) caution that, in patients with cardiogenic shock, there is a risk of impaired intestinal absorption because of gut hypoperfusion. For some patients, dual antiplatelet therapy may be delayed until the coronary anatomy is known because coronary artery bypass grafts (CABG) may be necessary if coronary stenoses identified are not amenable to PCI. In addition to dual antiplatelet therapy, glycoprotein IIb/IIIa inhibitors such as abciximab are recommended for patients who have a high intracoronary thrombus burden or slow coronary blood flow following PCI (Ibanez et al, 2017).
Approximately 70–80% of patients with cardiogenic shock have multivessel disease, which is associated with a higher mortality rate. The ESC STEMI guidelines (Ibanez et al, 2017) advocate complete multivessel revascularisation with PCI or CABG. Although this is recommended, it is implemented in fewer than 5% of CABG and approximately 25% of PCI procedures (Thiele et al, 2012). Patient outcomes in relation to the multivessel versus culprit artery only revascularisation are unknown. To address this uncertainty, the CULPPRIT-SHOCK trial (Culprit Lesion Only PCI versus Multivessel PCI in Cardiogenic Shock) (Thiele et al, 2016), a prospective randomised trial, is currently enrolling patients.
Pharmacological therapy
Pharmacological therapy in cardiogenic shock aims to improve contractility, preserve end-organ perfusion and relieve fluid overload. Therapeutic strategies are guided by the patient's haemodynamic status and the state of end-organ perfusion.
Inotropes and vasopressors are the most commonly administered agents. They are used to improve organ perfusion by increasing cardiac output and blood pressure. They are indicated for persistent hypotension despite adequate circulating volume and evidence of end organ hypoperfusion (Teerlink et al, 2013). Although it is recognised that these agents temporarily improve cardiac output, they do not interrupt the compensatory mechanisms associated with cardiogenic shock, nor correct the cause (Reynolds and Hochman, 2008). A disadvantage of these agents in STEMI, where myocardial blood flow is compromised, is that they increase myocardial oxygen consumption, potentially exacerbating myocardial injury. Other potential adverse effects include excessive vasoconstriction and arrhythmias through beta 1 stimulation. Therefore, it is recommended that the lowest therapeutic dose possible is used (Werden et al, 2014).
Inotropes are beta agonists in that they stimulate the beta receptors, resulting in stronger contractility as well as increasing blood pressure and causing vasoconstriction. Two inotropes used in clinical practice are dobutamine and dopamine. Dobutamine is the agent of choice because of its low risk for arrhythmias. Dobutamine works by strengthening contractility via beta 1 receptor stimulation and causing mild vasodilation through beta 2 receptor enhanced activity (Teerlink et al, 2013). This translates in clinical practice as primarily strengthening contractility with some reduction in afterload. Other effects include mild pulmonary vasodilatory effects, which reduce pulmonary vasoconstriction and make it easier for blood to pass from the right ventricle to the pulmonary system for oxygenation.
Vasopressors are alpha receptor agonists that chiefly promote vasoconstriction with very little effect on contractility. Their effects include increased vascular tone and blood pressure, so they can help maintain adequate end-organ perfusion. The disadvantage of vasopressor therapy is its potential to impair hepatosplanchnic, cutaneous and renal perfusion by redirecting blood to more vital organs (Werden et al, 2014). Norepinephrine is the vasopressor of choice as it has predominantly alpha adrenergic stimulation properties while its modest beta adrenergic effects help maintain cardiac output.
In clinical practice, the question is: which is the best agent for the patient in cardiogenic shock? A multicentre, randomised controlled trial (RCT) conducted by De Backer et al (2010) enrolled 1679 patients with shock of various aetiologies. The objective of the trial was to determine the rate of death at 28 days after randomisation. Secondary endpoints included rates of death in the intensive care unit (ICU), in the hospital, at 6 months, and at 12 months. Other secondary endpoints included the duration of stay in the intensive care unit, the number of days without needing organ support, the time to haemodynamic stability and the occurrence of adverse outcomes. Adverse outcomes included arrhythmias, myocardial necrosis, skin necrosis, ischaemia in the limbs or distal extremities, or secondary infections.
The study period lasted a maximum of 28 days after randomisation to allow maximum exposure to the study drug. Following randomisation, 858 patients were assigned to dopamine and the remaining 821 to norepinephrine infusions. Cardiogenic shock was present in 280 patients, accounting for 16.7% of the total. Study drug doses were similar in both groups. Results demonstrated that there were no significant differences between the groups regarding death rate at 28 days (52.5% in the dopamine group and 48.5% in the norepinephrine group), nor in death rates in the ICU, in the hospital, at 6 months or at 12 months. There were no significant differences in the cause of death between the two groups, although death from refractory shock occurred more frequently in the group receiving dopamine (P=0.05).
In relation to adverse effects, 18.4% of patients experienced an arrhythmia. The most common arrhythmia was atrial fibrillation (AF), which occurred in 86.1% of these patients. This was seen more frequently in the dopamine group. The drug was discontinued in 65 patients because arrhythmias were severe—6.1% in the dopamine group and 1.6% of those receiving norepinephrine.
Following subgroup analysis, the rate of death was found to be higher in those with cardiogenic shock who were treated with dopamine than in those treated with norepinephrine (P=0.03). The exact cause of this greater mortality cannot be determined but the early difference in the rate of death suggests that the higher heart rate associated with dopamine may have contributed to the occurrence of ischaemic events.
Although this trial demonstrates the safety of norepinephrine over dopamine, it is acknowledged that there is a paucity of data on the use of agents in cardiogenic shock and, according to Thiele et al (2015), there are no RCTs demonstrating prognostic benefit.
The ESC guidelines on the management of STEMI (Ibanez et al, 2017) recommend dobutamine as the initial therapy for patients with predominantly low cardiac output and norepinephrine as the agent of choice for cardiogenic shock with severe refractory hypotension unresponsive to other therapies. Combination therapy with dobutamine and norepinephrine may be used to improve contractility and peripheral perfusion in patients who are unresponsive to inotropes alone.
Mechanical circulatory support
The disadvantage of vasopressors and inotrope therapy is that they increase myocardial oxygen demand in an already compromised coronary blood supply. Mechanical circulatory support (MCS) overcomes this by lowering the left ventricular workload by either preload or afterload reduction or by mechanically assuming the workload of the left ventricle, which in turn increases stroke volume and cardiac output. It is indicated when pharmacological therapy fails to improve patient haemodynamics and/or maintain adequate end-organ perfusion and there is risk of MODS.
Mechanical support can be provided to the left ventricle, to the right ventricle or can be biventricular. There are several modes of support including intra-aortic balloon pump (IABP) counterpulsation, percutaneous and surgically implanted ventricular assist devices, and extracorporeal membrane oxygenation.
Van Diepen et al (2017) broadly classify mechanical support into temporary or durable. Temporary devices are inserted either percutaneously or surgically and are indicated as firstline therapy when prompt stabilisation is required to prevent irreversible end-organ hypoperfusion or in high-risk patients undergoing a procedure such as revascularisation. Durable devices are inserted surgically and are indicated as a bridge to transplantation, a bridge to recovery or destination therapy.
There is a lack of evidence addressing patient selection, timing of insertion and type of device but the device should be inserted before the onset of multi-organ dysfunction. Werden et al (2014) note that mechanical circulatory support has limited ability to change the patient outcome if multi-organ dysfunction is already established, even if cardiac output improves.
In the author's clinical setting, patient assessment for insertion of mechanical support is undertaken by a multidisciplinary team with expertise in patient and device selection, implantation and device management.
The IABP is the most common form of circulatory support used in cardiogenic shock and will be the focus of mechanical support in this article. The IABP consists of a balloon catheter, which is inserted into the femoral artery and placed in the descending aorta 2 cm below the left subclavian artery and proximal to the renal arteries. The catheter has an internal arterial line that is attached to a pressurised flush system, similar to that of an arterial line, and to the IABP console. Helium is shuttled in and out of the catheter to inflate and deflate the balloon in synchrony with diastole and systole respectively.
Two benefits associated with IABP therapy are improved coronary perfusion achieved by inflation at the beginning of diastole and a reduction in afterload as the balloon deflates just before systole. The main patient benefits, outlined by Thiele et al (2015), are a reduction in left ventricular workload and myocardial oxygen demand, and a rise in mean arterial pressure.
Before the IABP II Shock trial (Thiele et al, 2012), this form of support was a class I recommendation in clinical guidelines for patients with STEMI complicated by cardiogenic shock. The IABP II SHOCK trial (Thiele et al, 2012) is the largest RCT in cardiogenic shock to date. In this study, 600 patients with STEMI and cardiogenic shock who underwent revascularisation were randomly assigned to IABP insertion (301 patients) or conventional therapy (299 patients). The primary endpoint was 30–day mortality and this was achieved by 39.7% in the IABP group and 41.3% in the conventional therapy group (P=0.69); there was no significant difference between the two groups. Thiele et al (2012) concluded that the use of IABP did not significantly reduce 30-day mortality.
Long-term follow-up at 12 months was reported by Thiele et al (2013), which demonstrated a 52% mortality rate in the patients who received an IABP and 51% in the conventional therapy group. There were no significant differences in reinfarction rates, recurrent revascularisation or stroke between the two groups. At 12 months, there was no comparable difference in relation to functional capacity, quality of life, or levels of anxiety or depression. Because of these findings, routine use of IABP in this patient population has been downgraded to a class III recommendation (Ibanez et al, 2017) but remains a therapeutic option in cardiogenic shock caused by mechanical complications such as acute mitral incompetence or ventricular septal defect.
Ventricular assist devices are another means of circulatory support; these offload the left ventricle and redirect volume into the aorta for systemic circulation. Insertion of these devices can be percutaneous or surgical. Percutaneous temporary devices such as the Impella (Abiomed, Danvers MA) are used for patients requiring short-term support or as a bridge to a more definitive form of therapy. Their aim is to stabilise patients and preserve end-organ perfusion. Although evidence on this mode of support is limited, a meta-analysis by Cheng et al (2009) demonstrated that patients receiving percutaneous circulatory support achieved an increased cardiac output and mean arterial pressures but at the expense of increased bleeding risk, continued inflammatory response and no difference in mortality rates.
More permanent devices are implanted surgically and are indicated for long-term support. They are indicated for patients with cardiogenic shock who are unlikely to recover without the aid of long-term mechanical support. Other indications for permanent devices are as a bridge to transplantation or destination therapy
Extracorporeal life support systems are another form of temporary mechanical support that may be deployed in patients with potentially reversible cardiogenic shock or as a bridge to a more definitive form of therapy (Vincent and De Backer, 2013). The advantage of these devices is that they can be inserted at the bedside as there is no need for fluoroscopy to guide their insertion. As with other percutaneous devices such as the Impella, Cheng et al (2013) identified potential complications such as limb ischaemia, bleeding, stroke, infection, compartment syndrome and aortic valve incompetence.
Patient care and monitoring
Paramedics play a pivotal role in the assessment of patients with cardiogenic shock, providing evidence-based treatment strategies and evaluating therapies administered such as non-invasive ventilation or pain relief. Goals include preservation of organ perfusion, anticipating and identifying clinical deterioration and provision of psychological care to the patient and family.
Integral to prehospital care is the cardiovascular and respiratory assessment. Findings from this assessment may identify patients who are at high risk of developing cardiogenic shock. Clues to impending shock include a higher heart rate and a lower blood pressure on initial assessment. For those with a diagnosis of cardiogenic shock, the cardiovascular and respiratory assessment provides information on end-organ perfusion and function and serves as a guide when evaluating the effect of therapies administered.
As reflected in part one, clinical presentation includes tachycardia, hypotension, oxygen saturations <94%, tachypnoea, and signs of decreased organ perfusion such as oliguria, altered mental status and cool clammy skin. The majority of these signs and symptoms are a result of compensatory mechanisms and acute left ventricular dysfunction.
Adjunctive to physical assessment is the role of monitoring. Van Diepen et al (2017) note that there is a high incidence of arrhythmias, respiratory failure and pulmonary odema in cardiogenic shock so continuous cardiac monitoring for atrial and ventricular arrhythmias, as well as pulse oximetry to monitor oxygen saturation and ensure it is maintained at 94% or above is undertaken. For patients being transferred from one hospital to another, they may have an arterial line monitoring arterial blood pressure and a central line. Invasive monitoring is essential in this patient population to provide information on haemodynamics and to assess the effectiveness of therapies which may be adjusted to achieve haemodynamic targets. According to Ponikowski et al (2016), arterial blood pressure monitoring will suffice in this patient population. Arterial blood pressure monitoring guides vasopressor and inotropic therapies while a central line allows measurement of the central venous pressure, but is also required for administration of vasopressors and inotropes. Both allow blood sampling to be reserved. For the patient who has a positive response to therapies, a mean arterial pressure (MAP) of 65–70 mmHg is evident in conjunction with the patient being warm to touch and well perfused. Patients who are not responding to supportive therapies will remain hypotensive with a MAP <65 mmHg and have signs and symptoms of hypoperfusion such as cool to touch, tachycardia and increased respiratory effort.
Patients who have received antiplatelet and antithrombotic agents are at increased risk of bleeding. In cardiogenic shock, liver hypoperfusion occurs, which impairs metabolism of antiplatelet and antithrombotic agents, further increasing risk. The patient is monitored for haematuria, increased bleeding following venepuncture and cannulation or blood in vomit.
Patients in cardiogenic shock are critically ill. Patients and their significant others are frightened, vulnerable and unsure of what is happening. Paramedics can provide psychological care and alleviate some of this stress by being present, answering concerns and queries simply in a language the patient and others can understand, as well as outlining the plan of care.
Is there a role for palliative care?
Palliative care is defined by the World Health Organization (WHO) (2009) as ‘an approach that improves quality of life of patients and their families facing the problems associated with life-threatening illness, through the prevention and relief of suffering by means of early identification and impeccable assessment, treatment of pain and other problems physical, psychosocial and spiritual’.
The objective of palliative care in cardiogenic shock is to reduce physical and emotional symptoms and should be perceived as complementary to curative therapy. Kavalieratos et al (2014) highlight several challenges around when to start palliative care. These include the unpredictable trajectory of the disease and the variability in patient response to therapies, which influence the timing of referral to the palliative service. Another barrier to referral is that cardiogenic shock presents acutely and the patient and significant others have little or no time to discuss the ceiling of care, patient wishes, quality of life, care transitions, and treatments to prevent and manage symptoms.
In relation to cardiogenic shock, the timing, assessment and the experience of palliative care is not well studied but van Diepen et al (2017) propose that palliative care in this patient cohort is perceived as a philosophy of care that blends with curative therapies.
Conclusion
Cardiogenic shock is an extreme form of left ventricular dysfunction and is associated with increased mortality. The objective of pharmacological and mechanical support is to prevent the onset of irreversible multi-organ dysfunction and to prolong survival.
Despite its high incidence, cardiogenic shock remains underinvestigated from a therapeutic perspective with strategies based on consensus expert opinion rather than RCT findings. Paramedics have an essential role in providing holistic care to this patient population from a physical, spiritual and psychological perspective.