What is Shock

Definition

Multifaktoren syndrome leading to systemic and/or localized tissue hypoperfusion which is subsequently celularna hypoxia and multi-organ dysfunction.

What is Shock

The anomalies in tissue perfusion may be a consequence of:

  • The inability of the heart to act as an effective pump
  • Mechanical barriers to blood flow
  • Loss of volume cirkolatoren
  • Abnormalities in the peripheral circulation

Types Of Shock And Etiology

  • Hypovolemic
  1.  Exogenous losses (heavy sweats, hemoragii, Burns)
  2.  Endogenous losses
  • Cardiogenic

Ischemic cardiac injury (often OMI)

  • Obstruktiven
  1. Obstruction in the course of the blood flow (pulmonary embolism)
  2. oReduced cardio (heart tamponade, tension pneumothorax)
  • Distributiven (sepsis, anaphylaxis)

the Vascular dilataciя

the Vascular sekvestraciя

the Шънтове АV

the Maldistribuciâ of blood flow

the Myocardial depression

Pathophysiology

Simpatico-adrenalen response: hypotension stimulates baroreceptorite, causing activation of simpotikusovata nervous system and separation of the original of the noradrenaline and adrenaline and later by nadb″brecite in circulation. That has the effect of increasing vakonstrikciâ miokardnia contractility and heart rate. Reduction of blood flow and stimulates kortest renalniâ ûkstraglomerularniâ to separate aparet Renin, which converts angiotenzinogena to angiotensin I, which is in the vaskularniâ endotelium of the lung is converted to angotenzin II which in turn stimulates the secretion of aldostron of adrenalniâ cortex, causing sodium and water retention. This helps to restore the cirkulatorniâ volume.

Neuron-endocrine response: is a release of pituitarni hormones such as ACTH, vasopressin (anti-diuretic hormone) and endogenous opioid peptides further stimulate the secretion of glucagon, which raises the level of blood sugar.

Separating Pro-and antiiflamatorni mediators: heavy infections, the presence of large areas with damaged tissue or prolongirane episodes of hypoperfusion induces the development of proinflamatorno State, the development of which we judge the system activation of leukocytes and the separation of many potentially harmful cells mediators. However, it is helpful in limiting the topical infections or necrotic tissue diseminaciâta of the proinflamatorniâ process in the body can lead to ‘ citokinen storm “and development of shock. It should be borne in mind that the initial activation and immune system is often followed by a period of immune suppression, which is a favorable factor for the development of secondary infections.

Micro-organisms and their toxins : in sepsis/septic shock inflamatornata cascade is activated by the presence in the blood circulation of the micro-organisms, parts of their cell wall (endotoxin) and/or ekzotoksini (antigenic proteins produced by bacteria, such as Streptococcus, Staphylococcus or psevdomonas). Endotoksinite are lipopolizaharidi, which are the parts of the cell wall of gram-negative microorganisms and their presence is a powerful incentive for the development of inflammatory response.

Activation of komplementnata system : one of the many features of the komplementnata system is activated leukocytes when they migrate to endoteliuma and begin to secrete inflamatorni mediators such as proteases and free radicals, as well as nitrogen-containing substances.

Haemodynamic and Microcirculatory changes the dominant feature of the hemodinamična: the shock is peripheral vascular insufficiency accompanied by: (1) vasodilation; (2) maldistribuciâ of the regional blood current; (3) the anomalies in the microcirculation: a micro AV shunts; “stop-flow” & “non-flow ‘ increased capillary permeability capillaries; with intestinal edema occurred centralization of blood circulation in order to maintain vitaleteta of žinenovažnite bodies.

Activation of the coagulation system : output of prostaglandin I2 from kapilârniâ endotelium may be impaired during the shock of ruga side cell death leads to the release of tissue factor, which launched the coagulation cascade in severe cases these changes are accompanied by elevated levels of inhibitor of plazminegonnata activation type 1, which affects fibrinolizata. shock upon establishing low levels of physiological inhibitors of coagulation (Antithrombin protein C & S).-regulated activation Ultimate coagulation can lead to the development of DICK syndrome, which is characterized by mikrovaskularna thrombosis, inadequate tissue perfusion and organ failure.

CLINICAL FEATURES OF SHOCK

Common clinical features of shock

  • Inadequate tissue perfusion

o Skin: cold, pale, blue, slow capillary filling

o CNS: changes in mental status

o Kidneys: oligo and anuriâ

  • Increased tonus of the sympathetic nervous system

o Tachycardia, close to border of systolic blood pressure and diastolnata

o Sweating

  • Metabolic acidosis: compensatory tahipneâ

Extreme hypovolemia can be accompanied by bradycardia.

Specific clinical features of shock

Hypovolemic shock

Cirkulatoren loss intravaskularen volume and reduced heart prednotavarvane. It should be borne in mind that all forms of shock have some element of reduced heart prednatovarvane.

This is the most common form of shock.

Classification of hipovolemičniâ shock is given below:

Indicator Class I Class Ii Class Iii Class Iv
Blood loss Up to 750 ml 750-1500 ml 1500-2000 ml Over 2000 ml
Blood volume in% Up to 15% 15-30% 30-40% Over 40%
Pulse Under 100 Over 100 Over 120 Over 140
Resp. frequency Normal 20-30 30-40 Disstres
Diuresis (ml/h) Over 30 20-30 5-15 Under 10

Cardiogenic shock

Signs of myocardial failure: elevated venous pressure ûgularno pulsus alternans;; glopen rhythm; Basal repitacii; pulmonary edema.

Shock Obstruktiven

Causes of mechanical obstruction of the normal heart ejection in reduced systemic perfusion.

The most common causes are: heart temponada and tension pneumothorax. Another common cause is pulmonary or air embolism.

Increased CVN; pulsus poss and paradoksus. signs of cardiac tamponade; signs of pulmnaren embolism.

Distribution shock (infection, anaphylaxis)

Anaphylactic shock

Signs of profundna vasodilatation:

  • Warm peripheries
  • Hypotension
  • Tachycardia

Erythema, urticaria, angioedema, pallor, cyanosis.

Bronchospasm, rhinitis.

Swelling of the face, pharynx, larynx.

Pulmonary edema.

Hypovolemia due to capillary collectors vasodilation.

Nausea, vomiting, abdominal cramps, diarrhea.

Septic shock

Pireksiâ, sweating, or rarely, hypothermia.

Nausea, vomiting.

Warm peripheries, vasodilation.

Fast capillary filling.

Hypotension.

Rare signs of cutaneous vasoconstriction.

Other signs:

  • Jaundice
  • Coma
  • Bleeding due to coagulopathy
  • Redness and meningiz″m
  • Hyper-or hypoglycemia in severe cases.

Monitoring Of A Patient In Shock

Vital signs

At 50-80% of patients in shock the vital signs are normal or close to normal.

  • Heart rate: tahikardiâta is an early sign of signifikantna volumetric loss in shock.It should be borne in mind that in young patients and those taking beta blockers heart rate may not increase. Bradycardia too after prolonged hypotension is the Herald of kardiovaskularen collapse.
  • Blood pressure: hypotension and sbliženite borders in blood pressure are common signs of heavy volume loss and shock.The mean arterial pressure is a better cue than blood pressure sistolnata therapy.
  • Temperature: Hyper-, norm-or hypothermia can occur in patients in shock.Hypothermia is a sign of severe hypovolemia or septic shock.
  • Diuresis: reflect and renalnoto blood supply.
  • Pulse oximetry: this is an early indicator of hypoxemia may be unenforceable in hipotermični patients.

Invasive monitoring hemodinamičen

  • Kateter arterial blood pressure monitoring
  • Central venous kateter monitoring of central venous pressure
  • With arterial kateter to measure: central venous pressure;dâsnopreds″rdno pressure; pulmonary arterial pressure okluzivno.

Gallery

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