Cardiogenic shock. A humoral hemodynamic clinical picture resulting from a failure of the heart’s pump function to maintain tissue perfusion in accordance with the elemental organic needs at rest and can be considered the extreme degree of heart failure, so this definition includes low cardiac output.
Summary
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- 1 Causes of cardiogenic shock
- 2 Clinical diagnosis
- 3 Diagnostic criteria for cardiogenic shock
- 4 General measures
- 5 Symptoms
- 6 Exams
- 7 Treatment
- 8 Pathogenesis of cardiogenic shock
- 9 Moment of presentation of shock
- 10 Sources
Causes of cardiogenic shock
- Difficulty with cardiac filling
- Tension pneumothorax
- Positive pressure ventilation
- Cardiac tamponade
- Contractive pericarditis
- Alterations in myocardial compliance and change in ventricular geometry
- Loss of ventricular atrium synchrony
- Tachyarrhythmias
- Coarctation of the aorta
- Myxomas
- Afterload increase
- Severe aortic stenosis
- Pulmonary embolism
- Cardiac dysfunction
- Decreased contractility
- Acute Myocardial Infarction (AMI)
- Myocarditis
- Cardiomyopathies
- Toxic
- Regurgitant flow
- Ventricular septal defect
Clinical diagnosis
He usually finds a patient with an Acute Myocardial Infarction that is usually agitated, confused and sometimes comatose, with cold, sweaty skin, as well as distal cyanosis. The thermal gradient between the distal regions (less perfused) with the proximal ones (better prefused) is frequent.
The pulse is almost always fast and threadlike. As a rule, there is arterial hypotension, tachycardia unless it is associated with atrioventricular block, high arteriovenous oxygen difference (> 5.5 mL / dL). Low cardiac index (<2.2 L / min. / M2), high PCAP (> 18 mmHg), it is not unusual for different types of cardiac arrhythmias to occur. On auscultation, wet lung rales can be heard and the cardiac area must be listened to in detail to detect the presence of murmurs that indicate mechanical complications (rupture of the ventricular septum, rupture of the papillary muscle, etc.). Diuresis is low (less than 0.5 mL / kg / hour).
Diagnostic criteria for cardiogenic shock
- SBP <90 mmHg, or decrease> 50 mmHg from baseline (loss of peripheral or weak, filiform pulses)
- Tachycardia (except in that triggered by bradyarrhythmia)
- Oligoanuria: Diuresis <30 mL / hour
- Metabolic acidosis
- PVC: Increased (jugular engorgement, dyspnea)
- Changes in skin temperature and coloration (paleness, coldness, sweating and / or distal and perioral cyanosis)
- Neurological disorders (level of consciousness)
- Pulmonary congestion
- Heart rate <2.2 beats / min.
- Low temperature
- Weak heart sounds
- Fill capillary slow
General measures
- ABCD evaluation. This is a real medical emergency (Code Red)
- Lie in supine position with 15º of head elevation
- Adequate oxygenation. Nasal catheter or mask with reservoir at 4-5 L / min. (mechanical ventilatory assistance if necessary)
- Pulse oximetry
- Cardiac monitoring (rhythm, blood pressure, central venous pressure)
- Peripheral and then central venous access
- Measure PVC (PVC <6 cm low, normal between 6-12 cm H2O, high greater than 12 cm H2O)
- Strict management of hydration. It generally does not require the administration of serum therapy volumes, since PVC generally maintains values above 15 cm H20
- Correction of the basic acid balance if there is an imbalance
- Measure hourly urine output
- Pain management (with Meperidine, Morphine is not indicated)
- External pacemakers if necessary
- Platelet antiaggregants (ASA) if IAM
- These cases should always be referred to a Cardiac Intensive Care Unit for secondary care, ideally after obtaining at least a SBP of around 90 mmHg. If the cause is an AMI, it should be thrombolized independently of hypotension with prior vasoactive support
Symptoms
- Chest pain or pressure
- Profuse sweating, clammy skin
- Accelerated breathing
- Accelerated pulse
- Restlessness, agitation, confusion
- Difficulty breathing
- Skin that feels cold to the touch
- Pale or blotchy (mottled) skin
- Weak pulse (threadlike)
- Impaired mental state:
- loss of ability to concentrate
- loss of alertness
- Coma (loss of consciousness)
Exams
- Cardiac catheterization
- Chest x-ray
- Coronary angiography
- Echocardiography
- Electrocardiograph
- Scans
Treatment
This shock is a medical emergency. Her treatment requires hospitalization, usually in the Intensive Care Unit. The goal of treatment is to identify and treat the cause of the shock in order to save the patient’s life.
- Medicines to increase blood pressure and improve heart function, including:
Dobutamine
- Dose: 5-7.5 mcg / kg / minute. Due to its B1 agonist effect, it increases inotropism, cardiac output, heartbeat volume, left and right ventricular work. Decreases the pressure at the end of ventricular diastole without causing excessive tachycardia or hypotension. It is a pulmonary vasodilator. Doses greater than 7.5 mcg / kg / minute have a vasodilator effect, due to its B2 agonist effect, which can decrease systemic blood pressure.
Dopamine
- Dose: 5-10 mcg / kg / minute, looking for inotropic effect. 10-20 mcg / kg / minute as a vasoconstrictor. Presentation: 200 milligram jars.
Epinephrine
Norepinephrine
- When a disturbance of the heart rhythm (dysrhythmia) is severe, urgent treatment is needed to restore a normal heart rhythm. This may include:
Electro-shock therapy (defibrillation or cardioversion)
Implant of a temporary pacemaker
Medicines given through a vein (intravenous)
Pathogenesis of cardiogenic shock
Heart failure in SC patients is initiated by ischemia or myocardial infarction || myocardial infarction, generally of anterior, transmural and extensive location (35% -40% compromise of the myocardial mass). The ischemic or necrotic myocardium decreases the volume of the heartbeat and therefore the cardiac output. Myocardial perfusion, which depends on the pressure gradient between the coronary arterial system and the left ventricle and the duration of diastole, is compromised by hypotension and tachycardia, which increases ischemia. The increase in ventricular diastolic pressure caused by pump failure, decreases coronary perfusion, which increases the oxygen requirements by the myocardium, which further worsens ischemia. Decreased cardiac output also compromises perfusion, leading to lactic acidosis, which in turn affects systolic function.
When myocardial function is compromised, compensatory mechanisms such as increased heart rate, increased contractility and fluid retention are activated to increase preload, effects mediated by activation of the sympathetic system. These compensatory mechanisms worsen the situation when cardiogenic shock occurs, resulting in pulmonary edema and hypoxemia. Vasoconstriction to maintain adequate blood pressure increases the afterload, increasing the oxygen demand by the myocardium, which worsens ischemia, and if the cycle is not interrupted early, ends with the death of the patient. A rapid and adequate reperfusion intervention that improves ischemia is crucial once SC has been established.
Moment of presentation of shock
Of the total of patients who evolve with shock, only 15% present it at the time of hospital admission, the remaining 85% will develop it during their hospitalization.
The same trend was observed in the SHOCK study registry, regarding the time of presentation of cardiogenic shock. It can be summarized as follows: of the total number of patients with shock, 75% develop it in the first 24 hours, of this group 25% upon hospital admission, the remaining 3/4 between admission and the first 24 hours. the remaining 25% after 24 hours of hospital admission.
