Shock. Etiology, pathogenesis, intensive therapy презентация

Terminology: The word shock ( "choc " in French and "shock " in English) is translated as stroke, shock. This term was used in the Middle Ages called the state of the armor-clad knights who fell into a stupor after impact of lance or spear. For the first time, both the medical term used a French military surgeon Le Dran in 1741. Widely implemented in practice by James Latta in 1743.

Shock - critical condition which develops as a result of impact on the body a factor (internal or external), the force and/or the duration of which exceeds the compensatory capacity of the organism.
A physiologic state characterized by
Inadequate tissue perfusion
Clinically manifested by
Hemodynamic disturbances
Organ dysfunction

Shock is not a disease entities, it decompensation syndrome, which is accompanied by a variety of pathological conditions.
The diagnosis is a shock - about the danger signal and the need for intensive care methods!
Basically, the shock is considered as hemodynamic syndrome, i.e. reduction in the systemic circulation, microcirculation disturbances and tissue perfusion with subsequent hypoxia and necrosis of cells

Physiological constants
Blood volume (CBV) - 70 ml / kg (males 70-75, 65-70 women).
Distribution of blood in the body:
Heart - 7%
Pulmonary circulation - 9%
The arteries of the systemic circulation - 15%
Capillaries of a large range of - 5%
Veins of large circle - 64%
Central venous pressure (CVP) - 60-120 mm H2O It reflects the blood return to the right ventricle.

Classification
According to the basic link of pathogenesis are 4 kinds of shock:
hypovolemic
cardiogenic
obstructive
distributive (vasogenic)

1.Hypovolemic- it is based on reduction of CBV. These include: hemorrhagic, traumatic shock, burn shock, dehydration shock
2. Cardiogenic - due to the failure of myocardial contractile function
3.Obstruсtive- due to cardiac dysfunction from extracardiac reasons (pulmonary embolism, cardiac tamponade, tension pneumothorax) - caused by vascular insufficiency.
4.Distributive (Vasogenic) - anaphylactic, endocrine (adrenal insufficiency), neurogenic (spinal), septic.

Keep in mind that, regardless of the primary cause, in the final phases of the shock pathophysiological mechanisms are the same.

Hypovolemic shock

Hypovolemic shock
Pathophysiology
Acute loss of more than 20% of the intravascular fluid due to blood loss or dehydration.
One possible mechanism of development - occlusion of the vein, thrombosis and embolism main veins, compression of the inferior vena cava
Etiology
External bleeding
Plasma loss from burn surface
Multiple injuries
Gastrointestinal bleeding
Diabetic ketoacidosis
Pancreatitis
Heavy, frequent vomiting
Profuse diarrhea

Blood loss
Fracture of pelvis in conjunction with damage to internal organs - 3-3.5 liters (60-70% BCV).
Fracture of the femur - 0.5-1 l.
Fracture of the tibia - 0,3-0,75 l.
Traumatic separation of the tibia - 1.8 liters.
Fracture of the humerus - 0.3-0.5 liters.
Traumatic amputation of shoulder - 1.5 liters.
Fracture of forearm bones - 0.25-0.4 l.
Traumatic amputation arm-1,0 l.

The clinical phase of development of a shock
erectile phase
excitation
heart rate acceleration
a transient increase of blood pressure
microcirculation disturbance
dyspnea

The pathogenesis of traumatic shock
pain
decrease in BCV and myocardial contractility
microcirculation disorders, blood cell aggregation occurs, which clog the capillary network;
disorders of pulmonary gas exchange, hypoxia, pulmonary shunts, the deterioration of the function of the alveolar-capillary membrane formed shock lung syndrome;
disorders tissue gas exchange due to reduction of blood flow volume of tissue
changes in metabolism towards anaerobic path to form an excess of lactate and other organic acids; acidosis, which results in deepening and paresis vascular circulatory decompensation-vicious circle
development of "shock kidney" (pre-renal and renal oliguria) as a consequence of renal hypoperfusion;
dysfunction of other organs (brain, liver, adrenal glands, intestine)
generalization of infection, and especially the intestinal flora;
the development of DIC;
breakdown of water-salt metabolism and protein balance.
long vasospasm also leads to the development of ulcers
stomach, hemorrhagic enteritis

Vasoconstriction occurs within 30-60 seconds after the injury.
Primarily reduced capacitance vessels (veins) and the resistance vessels (arterioles).
Venous return to the right heart increases due to contraction of the veins and narrowing of arterioles causes blood flow redistribution. Blood passes capillaries through arteriovenous anastomoses and immediately returned to the vein.
Thus, the volume of the blood goes to the vital organs (brain and heart) - developed circulatory centralization

Next compensation mechanism that develops within the first hour - interstitial fluid enters to the bloodstream. This increases the BCV, at the same time decreases the amount of interstitial fluid.
Temp fluid intake can be up to 1 l / hr. Further activation of the sympathoadrenal system causes releasing of other hormones. Primarily the level of vasopressin (ADH) increases and RAAS activation starts.

Total effects ADH and RAAS leads to a decrease in diuresis. Retention of water and salts increases BCV and volume of interstitial space, enhance circulatory centralization.
The next stage - the synthesis of red blood cells by the bone marrow begins within a few hours, but it takes a long time (up to 2 months)

Hemodynamics and survey data fizikalgo
low CVP
Low cardiac output
High peripheral vascular resistance
Jugular veins distansion
Cold sweat
Slow capillary refill of the nail

Shock index Algovepa
the ratio of heart rate to blood pressure.

"Small" signs of shock
pale skin
conjunctival pallor
cold sticky sweat
mouth dryness
thirst
a symptom of "white spots" - more than 2 seconds.
decreased urine output-less than 30 ml / h

Reduction of hemoglobin, hematocrit, red blood cells in peripheral blood does not develop immediately (the need for dilution of extracellular fluid), so that a proper evaluation requires dynamic control of these parameters

Stages of shock
I st- compensated - loss of 20% of BCV - systolic BP 90-100 mmHg, pulse rate 100 / min, Shock index of about 1.
RR = 20-22 / min. Consciousness is clear, oliguria is absent
II st subcompensated - loss of 25-30% of BCV - systolic BP 70-90 mmHg, pulse rate 120 / min. shock index of about 1.5, RR up to 30/min, CVP decreased, consciousness is not broken, oliguria

III st- decompensated reversible - loss of 30-40% of BCV - systolic BP 50-70 mmHg, pulse rate 120/min, shock index of 2 or more, RR over 30 / min, CVP negative, consciousness broken (stunning), significant oliguria or anuria.
IV st- refractory irreversible (terminal) - BCV loss of more than 40% -50% - BP lower than 50 mmHg, item or not is determined, the pulse on peripheral arteries "filiform" or not is determined, a heart rate more 140/min. Growing bradycardia is a sign of a quick stop of the heart, RR more than 40/min, profound disturbance of consciousness, anuria.

Treatment of hemorrhagic and traumatic shock

The main anti-shock activity
Hemostasis
Providing free airway patency
Anesthesia (drugs)
Installation of central venous access (subclavian vein catheterization)
infusion solutions (saline, colloid) and blood products (in the absence of signs of pulmonary edema)
vasopressors (dopamine to 10 mkg / kg / min, or epinephrine, or norepinephrine 0.01-0.1 mkg / kg / min).

Prehospital aid
Partially revised the tactics of infusion-transfusion therapy in the prehospital phase. If bleeding is not stopped, massive fluid therapy increases BP, it’і can lead to revival bleeding and prognosis.

Adequate consciousness, sufficient diuresis (30 ml / hr), the absence of a severe tachycardia and hyperventilation, stable BP (systolic of at least 80 mm Hg) - signs of adequate gas exchange, when the patient should be left alone in the literal and figurative sense. Working muscles require 20 times more blood than the muscle at rest.

When a shock is suspected:
identify the specific cause and severity of the condition
carry out the necessary treatment with the appropriate specialist
Urgent surgical intervention, including hemostasis, drainage of tension pneumothorax, cardiac tamponade liquidation carried out immediately simultaneously with intensive care

General principles of treatment
The basis of any treatment of hypovolemic shock is fluid resuscitation, i.e filling the BCV, which has the advantage over the administration of vasopressors.
When treating patients with any shocks is necessary to observe the principle of "three catheters" - a catheter into a vein, the introduction of nasogastric tube, a catheter into the bladder. It is also advantageous to use oxygen nasal catheter or mask

Following questions need to be decided before planning treatment
where
what
how much and in what order of entering into the bloodstream

Crystalloid infusion solutions or colloids and crystalloids simultaneously insert at the beginning. If rapid infusion in a volume of 800-1200 ml does not increase the BP, it is advisable to start introduction of sympathomimetics: dopamine in moderate doses, norepinephrine, mezaton.

Blood transfusion, especially red blood cell mass is advisable to begin only after the full recovery of BCV and microcirculation, otherwise it simply will not be able to perform its function.
Blood transfusion may be replaced or supplemented perfluorane infusions.

Classification of plasma substitutes

Crystalloid solutions:
drugs with low molecular weight
quickly leave the bloodstream and move into the interstitial space.
in the bloodstream leaves 1/3 - 1/4 of the administered volume.
duration of circulation in the bloodstream is about 30 minutes
Examples: isotonic sodium chloride solution, Ringer’s sol, Ringer-lactate sol, Trisol, Reosorbilact etc.

2. The colloid plasma expanders
This solution of high molecular weight, which for a long time (4-6 hours) are contained in the lumen of the vessel and thereby maintain the BCV
Examples:
a. dextran derivatives - Poliglyukin, Reopoligljukin
b. gelatin derivatives - Zhelatinol
c. hydroxyethyl starch derivatives - Refortan, Stabizol, Gekodez, Refordez, Voluven®
d. plasma expanders with the function of oxygen transport - Perftoran.
e. natural colloids - fresh frozen plasma, packed red blood cells, albumin

Hydroxyethyl starch derivatives:
low MW (130,000) It belongs to the pharmacological group "Tetrastarch "- Voluven®, Volyutenz
Average MW (200000) - to the group "Pentastarch “-Stabizol, Plazmasteril
High MW (450,000) - to the group "Hetastarch " - Refortan, Gekodez
Hetakrahmal compared with tetra and pentastarch causes a longer plasma-effect, but can sometimes have a negative impact on blood clotting

Algorithms infusion-transfusion therapy for different amounts of blood loss
1.Blood loss up to 10% VBC does not require replacement.
2. Loss 10-15% volume - crystalloid infusion solutions. The volume of crystalloid infusion should exceed 3 times the volume of blood loss (300% of the amount of blood loss).
3. Blood loss 15-20% VBC compensates by combination of synthetic colloids and crystalloids in a ratio of 1: 2.Volume infusion - 200% VBC loss.

4.Defitsit VBC 20-30% - synthetic colloids, crystalloids plasma expanders. The ratio of colloids - crystalloids 1: 1. Infusion Volume - 180-200% of deficit. According to current guidelines, blood loss up to 30% of VBC does not require blood transfusion therapy.
5. Deficit 30-40%BCC - the volume of the infusion 200-250% of deficit. Included crystalloids, synthetic colloids, fresh frozen plasma, packed red blood cells. The ratio is 1: 1: 1: 1

In the treatment of traumatic shock should not forget the need for adequate immobilization and full anesthesia. Anesthesia implements by narcotic, non-narcotic analgesics, ketamine and different types of local anesthesia.
The introduction of narcotic analgesics is contraindicated in patients with head injury and with suspected injury to the abdominal organs.

Clinic of shock depends on the reasons that cause shock and localization of the injury. Traumatic brain injury is often masks the shock clinic due to symptomatic hypertension. On the other hand significant hemodynamic disorders can lead to disturbance of consciousness.
Empirically, it is believed that when the systolic BP less than 70 mm, and the patient has consciousness, it does not have a serious head injury.

Criteria of efficiency antishock therapy
1. In patients without cardiac disease:
Mean blood pressure> 60 mm Hg;
CVP> 2 cm H2O;
Diuresis> 50 ml / h
2. In case of doubt:
Sample load volume with: for 15-20 min poured 400-500 ml crystalloid and observing the dynamics of CVP and diuresis
-Significant increased CVP without increasing urine output - suspected heart failure.
- CVP and diuresis remain low - most likely hypovolemia, requires a higher rate of re-infusion phase estimate.
- An increase of urine output - prerenal oliguria, renal hypoperfusion due to hypovolemia.
3. When a circulatory system is compromised :
Inotropic support (increased cardiac output)
Correct using of diuretics,
Manipulating of afterload

Pathophysiology
Reducing the stroke volume of the heart with the defeat: - violation of the contractile function
- failure or obstruction of valves,
- intracardiac reset from left to right
- arrhythmia
Etiology
Myocardial infarction,
Severe myocarditis
Acute mitral or aortic regurgitation
Significant aortic stenosis
Prosthetic valve thrombosis
Rupture of the interventricular septum
Cardiac tamponade
Myocardial insufficiency after cardiac surgery.
Cardiogenic shock

Hemodynamics and physical examination data
High CVP
Low cardiac output
High peripheral vascular resistance
Jugular venous distention
Cold sweat
Slow capillary refill of the nail
Possible pulmonary edema, chest pain, and heart murmur

Obstructive shock
Pathophysiology
Reduction in stroke volume due to the extracardiac causes.
Etiology
PE (pulmonary embolim)
Cardiac tamponade
Tension pneumothorax

Hemodynamics and physical examination data
High or Low CVP
Low cardiac output
High peripheral vascular resistance
Often - distention of the neck veins
Cold sweat
Slow capillary refill of the nail bed
Rarely - pulmonary edema

Distributive shock
Pathophysiology
A significant reduction in peripheral vascular resistance with redistribution intravascular volume due to the increase
capillary permeability or arterio-venous shunting
Etiology
acute adrenal insufficiency
anaphylaxis
sepsis
neurogenic shock
toxic shock

Hemodynamics and physical examination data
Low CVP
Increased cardiac output
Low resistance peripheral
vessels
Lack of the neck veins
distention
limbs warm
capillary of nail refill
normally

Symptoms of shock
Decreased blood pressure;
Increased heart rate >90 beats per minute, the pulse becomes weak, "filamentous";
Increased frequency of respiratory movements;
Severe weakness: a man unable to move, and sometimes - even to say the words;
Skin pallor:
The absence of urine (anuria)
Varying degrees of impairment of consciousness up to the loss; lack of response to pain.
Shock does not always lead to a quick death, he often develops gradually – during minutes, tens of minutes or even several hours. In this listed symptoms and progress in the above order.

The adult patients compensate state of shock principally by decrease systemic vascular resistance, increase cardiac contractility and increased heart rate.
The child's body compensates for this condition primarily an increase in heart rate and vasoconstriction. Vasoconstriction in children leads to the fact that hypotension becomes late sign of shock.

Anaphylactic shock or anaphylaxis - acute generalized allergic reaction of immediate type, the state dramatically increased sensitivity of the organism that develops due to repeated insertion of the allergen into the body, accompanied by damage to its own tissues, lower blood pressure and vital organs circulatory disturbance.

One of the most dangerous complications of drug allergy, ends in 10-20% of cases, lethal.
The appearance time of anaphylactic shock - from a few seconds or minutes to 2 hours from the start of contact with the allergen. In the development of anaphylactic reactions in patients with a high degree of sensitization dose or route of administration of the allergen does not play a decisive role. However, a large dose increases the severity and duration of shock.

Pathogenesis

Etiology
Medication.
The introduction of blood products.
Food products (eggs, coffee, cocoa, chocolate, strawberry, fish, milk, alcoholic drinks).
The introduction of vaccines and serums.
Insect bites (wasps, bees etc.).
Pollen allergens.
Chemical agents (cosmetics, detergents).
Animal dander.

Clinical symptoms
1. Initial period develops within 3-30 minutes after allergen exposure (medication, food, insect sting or bite, etc.).
Local reactions at the site of contact with the allergen into the body - an unusually sharp pain, swelling and hyperemia at the place of the sting or injection of the drug, a strong itching of the skin, quickly spreads all over the skin (generalized pruritus). After receiving the allergen per os the first symptom may be a sharp pain in the abdomen, nausea and vomiting, swelling of the mouth and larynx.

Clinical symptoms
2. The period of clinical manifestation characterized by loss of consciousness, decrease of blood pressure (less than 90/60 mm Hg), tachycardia, paleness of the skin, lips cyanosis, cold perspiration, dyspnea, involuntary urination and defecation, decreased urine output.

clinical symptoms
3. Output period of shock usually lasts 3-4 weeks. Patients have weakness, headache, memory impairment. During this period may develop acute myocardial infarction, cerebrovascular disease, allergic myocarditis, glomerulonephritis, hepatitis, lesion of the nervous system (meningoencephalitis, arachnoiditis, polyneuritis), hemolytic anemia and thrombocytopenia.

Form of anaphylactic shock
at Hemodynamic form the clinic with hypotonia dominated by pain in the heart, arrhythmias. Possibly the development of acute myocardial infarction and acute left ventricular failure.
Asphyxial form characterized by the appearance of dyspnea (bronchoconstriction, pulmonary edema) or hoarseness and stridor (laryngeal edema).
at Abdominal form patients is dominated by epigastric pain, symptoms of irritation of the peritoneum, involuntary defecation, melena
Cerebral form characterized by agitation, stunning, convulsions and meningeal symptoms which are caused by cerebral edema and meningitis.

Diagnostics
Diagnosis of anaphylaxis is based on specific clinic:
hypotension,
loss of consciousness,
peripheral signs of shock,
symptoms develop after administration of drugs, food intake, insect bites, etc.
Determination of serum tryptase (the single marker of acute allergic reactions in the international practice) three times: immediately, after 30-120 minutes and after 24 hours.

Cross-allergic reactions are observed between:
1. Natural and semi-synthetic penicillins (penicillin G, oxacillin, ampicillin, amoxicillin, and others).
2. Streptomycin and other aminoglycosides (neomycin, kanamycin, gentamycin, amikacin, etc.).
3. Cephalosporins and penicillin.
4. Tetracycline and its derivatives (doxycycline and others).
5. Iodine and iodinated all preparations (Lugol's solution, iodine-containing radiopaque agents and others).
6. Thiamine and cocarboksylase.
7. Barbiturates and derivatives (pentobarbital and others).
8. Non-steroidal and certain analgesic agents (e.g., drugs between pyrazolone (metamizole sodium), acetylsalicylic acid and between preparations from different subgroups of non-steroids.

Risk factors for the development of medicinal allergiesth

First aid
90% of allergic reactions developed within 10 minutes after drug application.

Tourniquet on the limb does not overlap!
The injection site is not pricked around!

Priority treatment
Epinephrine (adrenaline) may save the patient's life, therefore, should be immediately administered as first-line treatment of anaphylaxis.
Early introduction of epinephrine should be conducted on an individual basis, when the allergic reaction is likely to develop into anaphylaxis.
Epinephrine be administered intramuscularly in the outer surface of the middle third of the femur 0.01 mg / kg, dilution 1: 1,000 (1 mg / ml) of a maximum of 0.5 mg (adult) or 0.3 mg (child).
Patients who need repeated doses of epinephrine injection should be administered at least every 15 minutes.
In the case of an inadequate response to two or more doses of epinephrine intramuscularly, it is administered as an infusion (infusion) in the emergency department (emergency), intensive therapy with cardiac monitoring.

The second line of treatment
It should suspend trigger anaphylactic reactions
Providing the correct body position for aspiration prophylaxis (supine position with their tender limbs with unstable circulation, in the sitting position for respiratory failure in saving the situation on the side of the loss of consciousness.
Oxygen through a mask with 6-8 L / min
Recovery airway patency and aspiration prevention
Quickly enter 1-2 liters of 0.9% sodium chloride solution through the catheter (5-10 ml / kg in the first 5-10 minutes adult, 10 ml / kg child)
Inhaled beta-2 agonists
If necessary - the cardio-pulmonary resuscitation

In severe shock is necessary to transfer the patient on mechanical ventilation with increased concentration of oxygen in the inspired gas (50-60%).
epinephrine intravenously at a dose of 0.3-0.5 mg, if needed, i.e. for refractory hypotension, epinephrine infusion can be continued or dopamine (5-10 mkg /kg/ min) in order to maintain a value of BP 60 mmHg

In cases of a significant tachycardia (> 120 beats / minute) tachyarrhythmia or blood pressure may be maintained by norepinephrine or phenylephrine
In the treatment of severe anaphylactic shock observed significant loss of fluid due to a significant endothelial damage, so massive infusion fluid necessary to 2-4 liters.It is usually necessary to apply a solution of sodium chloride 0.9%.
In severe cases it is necessary to apply a solution of HES 130 000 / 0.4.

According to modern views the introduction of chloride or calcium gluconate, was widely practiced before can cause a negative impact on the patient's condition.

H1 blockers and systemic H2 receptor can alleviate the symptoms of cutaneous anaphylaxis (infusion - H1-receptor blockers (chlorpheniramine 10 mg (adults) 2.5-5 mg (children) or diphenhydramine 25-50 mg (adults) and 1 mg / kg, a maximum of 50 mg (children) H2 receptor blockers - ranitidine 50 mg (adults) or 1 mg / kg, a maximum of 50 mg (children)).
Systemic corticosteroids (glucocorticoids) can be used as they can reduce the risk of respiratory symptoms late phase and generalization process (infusion - Hydrocortisone 200 mg (adults), a maximum of 100 mg (children) or methylprednisolone 50-100 mg (adults) and 1 mg / kg up to 50 mg (children).

Patients who exhibit respiratory failure should be carefully inspected for at least 6-8 hours; patients who exhibit instability circulation should be inspected for 12-24 hours in reanimation department, followed by transfer to allergological department.
Before discharge should assess the risk of future reactions autoinjector with epinephrine should be assigned to persons who are at risk of relapse.

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