Cardiogenic shockR57.0

The French surgeon Le Dran was the first to describe the image of a shock (choc) in 1737. He referred to the shock as a vibration of the organism caused by an impacting bullet in the form of a blow or jolt (Erdmann 2011). It was not until 1967 that von Lasch published fundamental studies on microcirculation disturbances in the context of a shock event. In 1969, Loeb referred to the symptoms of hypovolemia (dry skin, elevated hematocrit, increased albumin concentration in the serum) in order to distinguish cardiogenic shock from hypotension of another cause with well perfused skin and normal urine excretion. Gunnar et al. limited the term cardiogenic shock in 1976 to a primary pump failure of the left ventricle in the context of a myocardial infarction. In 1977, Blau pointed to infectious, autoimmunological, uremic or carcinomatous pericarditis, which can trigger a cardiogenic shock via pericardial tamponade (Riecker 1984).

Cardiogenic shock (CS) is an acutely life-threatening situation in which severe systematic hypoperfusion occurs. (Kasper 2015). Cardiogenic shock is defined as:

• arterial hypotension (RR systolic < 90 mmHg)
• Heart index < 2.2 l/min/m2 (standard value: > 2.5 l/min/m2)
• PCW- pressure > 15 mmHg (standard value: 8 - 12 mmHg)

Killip classification: The Killip I - IV classification determines the severity of heart failure after an acute myocardial infarction. The cardiogenic shock corresponds to the classification in Killip IV.

Forrester Classification : The Forrester Classification I - IV was also developed for the further prognosis of patients after myocardial infarction. It mainly takes into account clinical signs of peripheral perfusion disturbance and pulmonary capillary pressure values (Siegenthaler 2006).

Cardiogenic shock (CS) corresponds to class IV:

• PCWP > 18 mmHg
• CI < 2.2 l / min / m2

Both congestion of the lungs and a peripheral reduced blood flow can be demonstrated (Böhm 2000).

In the 1960s, cardiogenic shock occurred in about 20% of patients during an acute myocardial infarction. With the early reperfusion therapy that is used today, this number could be reduced to approx. 5 % - 7 %.

Cardiogenic shock occurs predominantly in:

• older patients
• Women
• C. M. Myocardial infarction
• acute anterior myocardial infarction
• More frequent in STEMI than in NSTEMI (incidence 10.7 % vs. 5.2 % [Erdmann 2011])
• extensive stenoses of the coronary arteries (Kasper 2015)

In about 59% of patients with acute myocardial infarction, cardiogenic shock occurs within the first 48 h, in 11% on days 3 - 4 and in about 30% after day 4 (Pinger 2019).

Cardiogenic shock can be induced:

• myogenic through:
  • Myocardial infarction
  • Cardiomyopathies
  • Myocarditis
  • Myocardial contusion
  • Pharmacotoxicity due to e.g. cytostatics, calcium channel blockers, beta-receptor blockers, antiarrhythmics etc.
• mechanically through:
  • Diseases of the heart valves
  • hypertrophic cardiomyopathy
  • intracavitary flow obstruction such as atrial thrombi, myxoma etc.
• rhythmogenic:
  • severe bradycardia
  • severe tachycardia (Erdmann 2011)

In the majority of cases (78.5 % [Erdmann 2011]) CS leads to left ventricular dysfunction in the context of

• acute myocardial infarction (with an infarction from about 40%)
  • by pump failure of the left ventricle (at approx. 80 %)
  • mechanical complications such as papillary muscle dysfunction (6.9 %)
  • infarction-related ventricular septal defect ( 3.9 %)
  • Rupture of the ventricular wall (1.4 %) (Stierle 2017)
• less often by:
  • Cardiomyopathy
  • Myocarditis
  • Cardiac tamponade
  • Heart valve defect (Kasper 2015).

In cardiogenic shock, ischemia of the myocardium leads to a reduction in cardiac pumping function.

Left ventricular dysfunction leads to

• Reduction of the heart index (<2.2 l / min / m², standard value 2.2 - 4.5 l / min / m²)
• persistent systolic arterial hypotension (<90 mmHg)
• an increased pulmonary capillary occlusion pressure [PCWP] of > 18 mmHg, standard value: 5 to 18mmHg) (Kasper 2015 / Dick 2001)

This leads to a reduction in cardiac output with consecutive hypoperfusion and thus inadequate oxygen supply to all organs - including those of the heart, which leads to further ischemia in the myocardial region. This leads to a vicious circle (Kasper 2015 / Pinger 2019).

The following symptoms may occur with a CS:

• the systolic blood pressure is < 90 mmHg (most important symptom [Werdan 2019])
• initial hypotension is absent in about 25 % (Werdan 2019)
• clinical signs of centralization with
• cold beetles
• marbled cold sweaty skin
• Oliguria or anuria
• pulmonary congestion
• clouding of consciousness (Stierle 2017)
• Dyspnea (Kasper 2015)

Inspection and palpation

• Tachycardia with 90 - 120 beats / min
• Bradycardia in the presence of a heart block
• Tachypnea
• Cheyne- Stokes respiration (Kasper 2015)

Auscultation

• characteristic systolic sounds in:
  • heavy mitral regurgitation
  • Rupture of the ventricular septum
• Rales in left heart failure (Kasper 2015)

ECG: In most cases there are signs of an acute myocardial infarction with direct (caused by a tap directly above the infarction site) and indirect (mirror-inverted changes in the opposite leads) infarction signs (Herold 2020).

It is also possible:

• tachycardia
• Bradycardia (Erdmann 2011)

Chest X-ray

A chest X-ray should be taken at an early stage. It should be evaluated:

• Heart size
• Heart shape
• central vessels
• signs of pulmonary oedema
• indications of infiltrates / pneumothorax / pleural effusions
• Control of central venous access (Werdan 2019)

Echocardiography: Echocardiography is an important form to clarify the causes of CS. In particular, the following should be assessed:

• Pump function of the ventricles
• Function of the flaps
• evidence of ventricular rupture, ventricular septal defect, papillary muscle dysfunction or tearing

Pulmonary catheter: With the pulmonary catheter the following pressures can be determined:

• right atrium
• right ventricle
• Pulmonary artery pressure (PA)
• pulmonary capillary pressure (PCWP), also known as wedge pressure
• cardiac output (HZV)
• peripheral and pulmonary vascular resistance (Stierle 2017)

Cardiac catheterization: In case of CS caused by a myocardial infarction, immediate recanalization (class I according to ESC) is the preferred strategy (Pinger 2019).

• Leukocytosis with left shift
• Creatinine initially mostly inconspicuous, in the further course progressive increase
• Transaminases significantly increased by hypofusion of the liver
• Troponins I and T increased
• Creatine phospokinase increased
• CK- MB increased
• Blood gas analysis:
  • metabolic acidosis
  • possible respiratory alkalosis to compensate (Kasper 2015)

The initial stabilization of the heart, circulation and lungs should take place immediately after diagnosis. Hemodynamic monitoring is also recommended (Wolff 2020).

Intubation followed by controlled ventilation is necessary in most cases. As a rule, drug treatment to stabilize the heart and circulation takes place before coronary intervention. In individual cases, however, coronary intervention may also be necessary in unstable patients (Werdan 2019).

• Catecholamines: In emergency care, norepinephrine with positive ionotropic and vasopressor effect should be used, in the clinic dobutamine with positive ionotropic effect and norepinephrine with positive ionotropic and vasopressor effect (Werdan 2019).

Adrenalin or levosimendan should be used in cases of dominant forward failure with pronounced hypotension (Wolff 2020).

• Nitroprusside sodium / nitroglycerin perfusor: In rare cases, a pronounced peripheral vasoconstriction may occur. In this case, a nitroprusside sodium perfusor with an initial 0.3 µg / kg / KG / min and a subsequent increase to the maximum desired effect of 1 - 6 µg / kg / KG / min should be used primarily for vasodilatory reduction of the preload and postload. A Nitroglycerin Perfusor is the second choice of medication. It should be administered in a dosage of 0.3 - 6.0 mg / h (Wolff 2020).

• Volume administration: If the patient cannot be sufficiently haemodynamically stabilised under the above-mentioned drugs, echocardiographically monitored volume administration is recommended (Werdan 2019).

With a mean arterial pressure (MAP) of:

• MAP < 50 mmHg With a MAP < 50 mmHg no reduction in afterload is possible. Circulatory support should be provided with dobutamine for inotropy (contractility) and noradrenaline for vasoconstriction.

• MAP 50 - 70 mmHg: With a MAP between 50 - 70 mmHg a further reduction of the afterload should be carried out with a systemic or peripheral resistance (SVR) > 1.000 dyn x sec x cm-5. Levosimendan (inotropic agent) is available as an alternative. An increase in inotropy and vasoconstriction is necessary with an SVR of < 800 dynes x sec x cm-5.

• MAP > 79 mmHg: At values > 79 mmHg there is already scope for reducing the afterload with nitroprusside sodium. Should a blood pressure drop occur below this level, first evaluate whether an additional volume administration is necessary. If this is not the case, a low dose of dobutamine is usually sufficient (Wolff 2020).

A cardiatic power output (CPO) of > 0.6 W should be aimed for. This corresponds to a MAP of 65 mmHg and an SVR of 850 dyn x sec x cm-5 (Wolff 2020).

• Coronary revascularization: In case of cardiogenic shock due to myocardial infarction, PCI with or without stent implantation is the procedure of choice, not thrombolysis (for more details see coronary angiography and myocardial infarction) (Wolff 2007).

According to the Killip Classification (classification for the determination of heart failure in acute myocardial infarction, for details see Myocardial infarction), the lethality rate in the event of cardiogenic shock is up to 90% (Herold 2020).

The SHOCK study and the CathPCI Registry have shown the following favourable factors for one-year survival:

In acute revascularization, 13 patients out of 100 were saved. An advantage was shown for:

• Patients of younger age. Hazard ratio (HR) 1.56 per 10 year increase
• Patients with higher heart index (HR for death 0.51 per 0.5 unit increase)
• male patients with infarction-related cardiogenic shock had a 6.35 times lower risk than female patients
• a high TIMI flow rate (thrombolysis in myocardial infarction classification) was associated with a higher survival benefit
• if systolic blood pressure was low during treatment, mortality was higher

In the CULPRIT-SHOCK study published in 2017, it was shown that an immediate revascularization of all stenoses, including those not relevant for myocardial infarction, is prognostically disadvantageous within the first 30 days (55.4 vs 45.9).

However, the rate of hospital admissions in patients with immediate multi-vessel PCI was significantly lower (1.2 vs 5.2) (Thiele 2018).

However, the COMPLETE study published in 2019 showed that the risk of cardiovascular death including myocardial infarction was relatively 26% lower in patients undergoing complete revascularization than after revascularization of the infarction artery alone (Overbeck 2019).

According to a recent report from April 2020, a Covid-19 patient experienced cardiac shock with severe necrotizing myocarditis. Histoogically, a low-grade inflammation of the myocardium and the absence of myocyte necrosis were shown. Virus particles themselves could not be detected in the heart muscle cells. It is most likely to be due to transient viremia or migration of infected macrophages from the lung tissue into the myocardium (Tavazzi 2020).

1. Böhm M et al (2000) Reference Series Cardiology: Heart Failure. Georg Thieme Publisher S 38
2. Dick W et al (2001) Emergency and intensive care medicine. Walter de Gruyter Publisher S 332
3. Erdmann (2011) Clinical Cardiology: Diseases of the heart, the circulation and the vessels close to the heart. Springer publishing house S 181 - 184
4. Herold G et al (2020) Internal medicine. Herold Publisher S 253 - 254
5. Kasper D L et al (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education S 1608, S 1759 - 1760
6. Overbeck P (2019) The importance of complete revascularization in ST elevation myocardial infarction more firmly established. CardioVasc 19: 12 - 13
7. Pinger S (2019) Repetitorium Kardiologie: For clinic, practice, specialist examination. German publisher for physicians S 143 - 144, 544
8. Riecker G et al (1984) Manual of Internal Medicine: Shock. Springer Publishing House S 15 - 16
9. Siegenthaler W et al (2006) Clinical pathophysiology. Georg Thieme Publisher S 599
10. Stierle U et al (2014) Clinical Guide to Cardiology. Elsevier Urban and Fischer S 81 - 82
11. Tavazzi G et al (2020) Myocardial localization of coronavirus in COVID-19 cardiogenic shock. European Journal of Heart Failure https://doi.org/10.1002/ejhf.1828
12. Thiele H et al (2018) One-Year Outcomes after PCI Strategies in Cardiogenic Shock. N Engl J Med 379: 1699 - 1719
13. Werdan (2019) German-Austrian S3 Guideline "Infarction-induced Cardiogenic Shock - Diagnosis, Monitoring and Therapy" AWMF Guidelines - Register No. 019/013
14. Wolff H P et al (2007) Internal Medicine Therapy 2006 / 2007 Elsevier Urban und Fischer Verlag S 69 - 70
15. Wolff H P et al. (2020) Internistic Therapy 2020 / 2021 Elsevier Urban und Fischer Verlag S 113 - 115