Acute cardiovascular insufficiency in shocks of infectious etiology.

Acute cardio – vascular insufficiency – the inability of the heart and blood vessels to provide adequate blood supply to tissues with metabolic disorders of the body, leading to dysfunction of cells and their death.

Acute vascular insufficiency occurs as a result of a violation of the relationship between the work of the heart, peripheral vascular resistance, the capacity of the arterial and venous vascular bed, the volume and speed of blood flow.

A large number of microbial toxins enter the blood

This leads to a sharp release of cytokines, adrenaline and other biologically active substances.

Under the action of biologically active substances, spasm of arterioles and postcapillary venules occurs, the opening of arterio-venous shunts.

The blood discharged through the shunts does not perform a transport function, which leads to tissue ischemia and metabolic acidosis, the release of histamine, and a decrease in the sensitivity of blood vessels to adrenaline.

Blood is deposited in the capillaries, which leads to the release of its liquid part into the intercellular space.

Paresis of arterioles occurs, while postcapillary venules are in a state of increased tone.

Violation of microcirculation exacerbates DIC syndrome.

Stages of acute cardiovascular insufficiency in children with shocks of infectious etiology:

4 phases (degrees):

· Early phase (grade 1) – compensated;

· The phase of severe shock (grade 2) – subcompressed;

Phase of decompensated shock (grade 3)

Late stage of shock (grade 4)

· Early phase (grade 1) – compensated;

– arterial hypotension may be absent
– tachycardia, decreased pulse pressure
– shock index up to 0.7 – 1.0
– signs of intoxication: muscle pain, abdominal pain without a specific localization, severe headache
– central nervous system disorders: depression, anxiety, or agitation and restlessness
– from the urinary system: decrease in the rate of urination: less than 25 ml / h

· The phase of severe shock (grade 2) – subcompressed;

– blood pressure drops critically (below 90 mm Hg)
– pulse is frequent (more than 100 beats / min), weak filling
– shock index up to 1.0 – 1.4
– the state of microcirculation, determined visually: the skin is cold, wet, acrocyanosis
– frequent breathing
– lethargy and apathy

Phase of decompensated shock (grade 3)
– further drop in blood pressure
– further increase in heart rate
– shock index about 1.5
– the state of microcirculation, determined visually: general cyanosis is growing
– there are signs of multiple organ failure: shortness of breath, oliguria, sometimes jaundice appears

Late stage of shock (grade 4)
– shock index over 1.5
– general hypothermia
– the state of microcirculation, determined visually: the skin is cold, earthy, cyanotic spots around the joints
– signs of multiple organ failure are aggravated: anuria, acute respiratory failure, involuntary defecation, impaired consciousness (coma)

Clinical symptoms of acute heart failure:

1) Tachycardia , which occurs initially as a compensatory reaction of the heart with a decrease in myocardial contractility and a decrease in the stroke volume of the heart, to maintain an adequate minute volume of blood circulation;

2) Shortness of breath, which also occurs as a compensatory reaction. The growth of heart failure, leading to a violation of pulmonary gas exchange, further increases shortness of breath with the involvement of accessory muscles in breathing;

3) Expanding the boundaries of the heart. It is practically important not only to determine the expansion of the heart, but also to establish whether this is a consequence of dilatation, compensatory or myogenic hypertrophy;

4) Cyanosis of the skin and mucous membranes, due to reduced blood supply to the tissues and their insufficient supply of oxygen. As a result, metabolic processes are disrupted in the tissues, the proportion of anaerobic glycolysis increases with the accumulation of products of incomplete cleavage and a shift in the reaction to the acid side;

5) Pastosity of the skin and swelling of the tissues. Of the various pathogenetic mechanisms for the development of these symptoms, stagnation of blood in the systemic circulation, changes in hydrostatic and colloid osmotic pressure, increased permeability of the vascular wall, slowing of renal blood flow, and electrolyte shifts due to increased secretion of aldosterone are important;

6 ) An increase in the liver, which indicates a violation of the venous outflow, stagnation of blood in the systemic circulation and is accompanied by an increase in CVP, expansion of the venous network on the face and chest;

7) Dyspeptic disorders.

With insufficiency of the left atrioventricular valve, the heart sounds are muffled, a systolic murmur is heard. The gallop rhythm indicates severe myocardial damage. Severe arrhythmias of various types appear, blood pressure decreases, acute cardiovascular insufficiency develops, which, as a result of depletion of myocardial contractility, can lead to death.
Changes appear on the ECG that reflect myocardial damage and disruption of its functions: a sharp flattening of the T wave, an increase in intraatrial and intraventricular conduction, depression of the ST segment, splitting of the QRS complex, and heart rhythm disturbance.

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