Introduction and pathogenetic basis
The development of acute vascular failure is based on the loss of adequate vascular wall tone. Blood is redistributed, accumulating in certain vascular beds, which deprives other organs of essential oxygen and nutrients. Traditionally, surgery and intensive care distinguish three severity degrees or forms of this condition:
- Syncope (mildest course);
- Collapse (severe hemodynamic disorders);
- Coma (extreme degree of CNS depression).
Syncope (Syncope)
Syncope is the mildest form of acute vascular insufficiency. The main clinical sign is transient (short-term) loss of consciousness, which occurs due to a sharp decrease in cerebral blood flow.
Pathogenesis The triggering mechanism is acute dilation of internal organ vessels (primarily those innervated by the splanchnic nerves). Blood is pooled in this dilated vascular network. As a result of this redistribution, there is a sharp shortage of blood volume for the brain—acute cerebral ischemia develops, and the patient loses consciousness.
Etiology Three main groups of factors can trigger syncope:
- Orthostatic and physical: prolonged standing or sudden standing up after a long bed rest.
- Iatrogenic (medical) causes: rapid evacuation of large fluid volumes from the abdominal cavity (in ascites) or early patient mobilization after administration of ganglion blockers.
- Cardiac: pathologies of the heart itself leading to pauses in blood circulation (extrasystole, atrioventricular blocks).
Clinical presentation and care The patient turns pale, the pulse becomes rapid and weak, and blood pressure drops. When syncope develops, it is necessary to immediately lay the patient horizontally and ensure a supply of fresh air. Medical and reflex measures include inhalation of ammonia vapors (ammonia spirit), hot drinks, and, if necessary, administration of vasopressors.
Collapse
Collapse is a more severe form of acute vascular failure caused by rapid blood pooling in organs.
Hemodynamics and pathogenesis The key link in pathogenesis is a catastrophic drop in circulating blood volume (CBV). Following this, arterial and central venous pressure (CVP), as well as cardiac output (minute volume), inevitably decrease. It is important to understand that the mechanisms of collapse development largely resemble shock, but in collapse, the damage is of an isolated vascular nature: changes in other organs and systems do not develop at the initial stages.
Causes of development
- Acute disruptions in heart function (marked myocardial weakness, blunt cardiac trauma/contusion).
- Severe acute infectious processes.
- Acute intoxications and poisonings.
Symptoms The patient's appearance in collapse is very characteristic: the skin becomes not just pale, but acquires a specific grayish tint. Breathing becomes rapid. Auscultation reveals muffled heart sounds. The pulse is rapid, of low volume, and rhythm disturbances are often detected against the background of pronounced arterial hypotension.
Treatment of collapse is always comprehensive: it should be aimed not only at supporting cardiovascular activity, but also at mandatory elimination of the etiological factor (combating infection, detoxification, etc.).
Briefly: answers to topical questions
What types of collapse are distinguished depending on the etiological factor?
Depending on the etiological factor and the initial link of pathogenesis, three main varieties of collapse are distinguished, including narrower forms.
- Cardiogenic — includes post-infarction, arrhythmic, and cardiomyopathic types.
- Hypovolemic — combines post-hemorrhagic, dehydrational, toxic-infectious, and orthostatic types.
- Vasodilatory — represented by hyperthermic, orthostatic, and toxic types.
Also, in clinical practice, according to the specific cause, infectious, radiation, pancreatic, and hypocapnic types of collapse are additionally distinguished.
What is the pathogenesis and clinical picture of coma as an extreme form of acute vascular failure?
The pathogenesis of coma includes hypoxia, microcirculatory disorders, and cerebral edema, leading to total and deep depression of central nervous system functions.
The clinical picture of this condition is determined by the classic triad of symptoms:
- Complete loss of consciousness — profound shutdown of the patient's consciousness.
- Extinction of reflex activity — manifested by hyporeflexia or areflexia.
- Disruption of vital functions — significant disorders of internal organ functions and physiological systems.
Additionally, focal symptoms of CNS damage may be observed.
What methods are used to measure central venous pressure (CVP) to assess the severity of hemodynamic disorders in collapse?
To measure central venous pressure (CVP), the method of catheterization of the superior or inferior vena cava is used.
Access to the central veins is achieved via the basilic vein or the great saphenous vein of the thigh. If surface veins collapse against the background of shock or collapse, when percutaneous puncture is impossible, venesection is performed. This method involves tissue dissection, isolation of the vein, opening its lumen, and catheter insertion with fixation by a central ligature.
Before placing a central venous catheter, it is recommended to perform chest radiography or CT, as well as ultrasound duplex scanning of upper extremity arteries. The normal CVP value is 50–150 mm H₂O.
To understand pathogenesis, remember the chain: "Splanchnic nerves relaxed → abdominal vessels dilated → blood flowed down → brain 'dried out' (ischemia) → syncope".
Class and exam questions
What is the main difference in the pathogenesis of collapse versus shock?
In collapse, hemodynamic disorders similar to shock are observed (blood pressure drop, decrease in CBV due to blood pooling), but this condition is not accompanied by the profound changes and multiple organ dysfunction in other organs and systems characteristic of shock.
Why can syncope develop upon removal of ascitic fluid?
Rapid removal of a large volume of fluid from the abdominal cavity leads to a sharp drop in intra-abdominal pressure, causing the vessels of internal organs to dilate rapidly, pooling blood and causing cerebral ischemia (iatrogenic factor).
What skin color is characteristic of collapse?
Collapse is characterized not just by pallor (as in syncope), but by pronounced pallor with a characteristic gray skin tint.
What else to study on this topic
- Pathogenesis of coma development as an extreme degree of acute vascular failure
- Mechanisms of action of ganglion blockers and management rules for patients after their intake
- Hemodynamic features in atrioventricular block
- Differential diagnosis of shock types and collapse
- Algorithm for pharmacological support in decreased CVP and cardiac output
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