Cardiogenic shock: causes, symptoms, risks, diagnosis, treatment, prognosis, death
About cardiogenic shock: in medicine, ‘shock’ refers to a syndrome, i.e. a set of symptoms and signs, caused by reduced systemic perfusion with an imbalance between oxygen availability and oxygen demand at the tissue level
Shock is classified into two major groups
- decreased cardiac output shock: cardiogenic, obstructive, haemorrhagic hypovolaemic and non-haemorrhagic hypovolaemic;
- distributive shock (from decreased total peripheral resistance): septic, allergic (‘anaphylactic shock’), neurogenic and spinal shock.
Cardiogenic shock (in English ‘cardiogenic shock’) is due to a reduction in cardiac output secondary to a primitive deficit in the heart’s pumping activity or resulting from hyperkinetic or hypokinetic arrhythmias.
The critical depression of cardiac function determines the changes that lead to peripheral hypoperfusion associated with ischaemia, dysfunction and cellular necrosis, with altered organ and tissue function that may even result in the death of the patient.
This form of shock complicates 5-15% of all heart attacks and has a very high intra-hospital mortality rate (around 80%).
One of the possible classifications of cardiogenic shock is as follows:
A) Myogenic cardiogenic shock
- from myocardial infarction
- from dilated cardiomyopathy;
B) Mechanical cardiogenic shock
- from severe mitral insufficiency
- from interventricular septal defects;
- from aortic stenosis;
- from hypertrophic cardiomyopathy;
C) Arrhythmic cardiogenic shock
- from arrhythmia.
Causes and risk factors
Ventricular filling pressures and volumes are increased and mean arterial pressure is reduced.
Events follow this ‘pathway’:
- cardiac output decreases;
- blood pressure decreases (arterial hypotension);
- hypotension leads to decreased tissue perfusion (hypoperfusion);
- hypoperfusion leads to ischaemic suffering and tissue necrosis.
The upstream causes of cardiogenic shock, which can lead to and/or promote a reduction in cardiac output, are:
- acute myocardial infarction
- heart failure;
- rupture of the interventricular septum;
- mitral insufficiency from ruptured chordae tendineae;
- right ventricular infarction;
- rupture of the free wall of the left ventricle;
- dilated cardiomyopathies;
- end-stage valvulopathies;
- myocardial dysfunction from septic shock;
- obstructive pericardial effusion shock;
- cardiac tamponade;
- massive pulmonary embolism;
- pulmonary hypertension;
- coarctation of the aorta;
- hypertrophic cardiomyopathy;
- myxoma (tumour of the heart);
- hypertensive pneumothorax;
- hypovolaemic shock from haemorrhage.
Signs and symptoms of cardiogenic shock
The main manifestations of cardiogenic shock are arterial hypotension and tissue hypoperfusion, which in turn leads to various other symptoms and signs.
Typically, the subject’s systolic (maximum) blood pressure decreases by 30 or 40 mmHg from what it usually is.
Possible signs of cardiogenic shock are:
A) in the central nervous system:
- general malaise;
- loss of strength;
- motor deficit (difficulty walking, paralysis…);
- sensory deficit (blurred vision…);
- loss of senses;
B) affecting the skin:
- bluish-purple lips;
- cold sweat;
- feeling of coldness.
C) affecting the gastrointestinal system:
- paralytic ileus;
- erosive gastritis;
- cholecystitis alithiasis;
- gastrointestinal haemorrhages;
- hepatic suffering.
D) affecting the blood:
- DIC (disseminated intravascular coagulation);
- microangiopathic haemolytic anaemia;
- coagulation abnormalities.
E) affecting the heart:
- arterial hypotension;
- reduced carotid pulse;
- various types of arrhythmia;
- cardiac arrest.
F) affecting the kidneys:
- signs of acute renal failure.
G) affecting the immune system
- altered leucocyte function;
- fever and chills (septic shock).
H) affecting the metabolism:
- hyperglycaemia (early phase);
- hypoglycaemia (advanced phase);
- metabolic acidosis;
I) affecting the lungs:
- dyspnoea (air hunger)
Stenosis of the coronary arteries, which became apparent during the autopsy of subjects who died of irreversible shock, mainly affects the common trunk of the left coronary artery, which supplies two/thirds of the heart muscle.
The diagnosis of cardiogenic shock is based on various tools, including:
- objective examination;
- laboratory tests;
- blood count;
- CT SCAN;
- pulmonary angiography;
- chest X-ray;
- echocardiogram with colordoppler.
Anamnesis and objective examination are important and must be performed very quickly
In the case of an unconscious patient, the history can be taken with the help of family members or friends, if present.
On objective examination, the subject with shock often presents pale, with cold, clammy skin, tachycardic, with a reduced carotid pulse, impaired renal function (oliguria) and impaired consciousness.
During diagnosis, it is necessary to ensure airway patency in patients with impaired consciousness, place the subject in the anti-shock position (supine), cover the casualty, without making him sweat, to prevent lipotimia and thus further aggravation of the shock state.
In cardiogenic shock this situation occurs:
- preload: increases;
- afterload: reflexively increases;
- contractility: decreased;
- central venous satO2: decreased;
- Hb concentration: normal;
- diuresis: decreased;
- peripheral resistance: increased;
- sensorium: normal or confusional state.
We remind the reader that systolic output depends by Starling’s law on preload, afterload and contractility of the heart which can be monitored clinically indirectly by various methods:
- preload: by measuring the central venous pressure through the use of the Swan-Ganz catheter, bearing in mind that this variable is not in linear function with preload, but this also depends on the rigidity of the walls of the right ventricle;
- afterload: by measuring systemic arterial pressure (in particular diastolic, i.e. the ‘minimum’);
- contractility: by echocardiogram or myocardial scintigraphy.
The other important parameters in the case of shock are checked by:
- haemoglobin: by haemochrome;
- oxygen saturation: by means of a saturation meter for the systemic value and by taking a special sample from the central venous catheter for venous saturation (the difference with the arterial value indicates oxygen consumption by the tissues)
- arterial oxygen pressure: via haemogasanalysis
- diuresis: by bladder catheter.
During diagnosis, the patient is observed continuously, to check how the situation evolves, always keeping the ‘ABC rule’ in mind, i.e. checking
- patency of the airways
- presence of breathing;
- presence of circulation.
These three factors are vital to the patient’s survival, and must be checked – and if necessary re-established – in that order.
Once the process triggering the syndrome has begun, tissue hypoperfusion leads to a multi-organ dysfunction, which increases and worsens the state of shock: various substances are poured into the circulatory stream from vasoconstrictors such as catecholamines, to various kinins, histamine, serotonin, prostaglandins, free radicals, activation of the complement system and tumour necrosis factor.
All these substances do nothing but damage vital organs such as the kidney, heart, liver, lung, intestine, pancreas and brain.
Severe cardiogenic shock that is not treated in time has a poor prognosis, as it can lead to irreversible coma and death of the patient.
Course of cardiogenic shock
Three different phases can generally be identified in shock:
- initial compensatory phase: the cardiovascular depression worsens and the body triggers compensation mechanisms mediated by the sympathetic nervous system, catecholamines and production of local factors such as cytokines. The initial phase is more easily treatable. Early diagnosis leads to a better prognosis, however it is often arduous as symptoms and signs may be blurred or non-specific at this stage;
- progression phase: the compensation mechanisms become ineffective and the perfusion deficit to vital organs worsens rapidly, causing severe pathophysiological imbalances with ischaemia, cellular damage and accumulation of vasoactive substances. Vasodilatation with increased tissue permeability can even lead to disseminated intravascular coagulation. On this subject, read: Disseminated intravascular coagulation (DIC): causes and therapies
- irreversibility phase: this is the most severe phase, where marked symptoms and signs facilitate diagnosis, which, however, performed at this stage, often leads to ineffective therapies and poor prognosis. Irreversible coma and reduced cardiac function may occur, up to cardiac arrest and death of the patient.
Therapy: in patients with cardiogenic shock, treatment is often very complex
The treatment for arrhythmias is synchronised electrical cardioversion in tachyarrhythmia and transcutaneous pacing or isoprenaline infusion in bradyarrhythmias.
Pump deficiency due to structural heart disease, necrosis/ischemia, dilated heart disease, myocardiopathy requires the infusion of amines (dobutamine or dopamine) and, in the presence of myocardial infarction, the mechanical reopening of the occluded coronary artery by angioplasty.
Initial clinical stabilisation is followed by monitoring with a Swan-Ganz catheter, which will make it possible, by checking cardiac output and pulmonary wedge pressures, to modulate drug administration according to haemodynamic responses.
Vasodilating substances such as sodium nitroprusside and nitroglycerin may be used in forms with depressed systolic function or myocardial infarction.
In the majority of cases, however, sympathomimetic substances such as dopamine and dobutamine are used, which, by supporting arterial pressure, improve organ perfusion and thus reduce peripheral resistance, by reducing the production of local vasoconstrictive substances.
The mechanical support that the use of the aortic counterpulsator can provide is used in forms involving the ischaemic heart muscle: acute mitral insufficiency and ischaemic rupture interventricular defect. This support allows for a bridging solution, which will enable surgery to be performed in the best possible condition.
Surgical intervention is a must in mechanical defects, as reported, and one benefits from short latency periods between the start of medical therapy and eventual mechanical support.
The pathology unfortunately has a poor prognosis in almost 80% of untreated hospital cases (in some cases this figure approaches 100%).
The prognosis improves with diagnosis and treatment undertaken very quickly.
It is especially important to stabilise the patient with initial treatment, so that there is time for more specific diagnostic tests and more specific therapies.
In case of cardiogenic shock, the survival rate three years after diagnosis is about 40%, which means that out of 10 patients suffering from cardiogenic shock, 4 are still alive 3 years after diagnosis.
What to do?
If you suspect that someone is suffering from shock, contact the Emergency Number.
In the meantime, place the person in the anti-shock position, or Trendelenburg position, which is achieved by placing the casualty lying on the floor, supine, tilted 20-30° with the head on the floor without a pillow, with the pelvis slightly elevated (e.g. with a pillow) and the lower limbs raised.