HYPOVOLEMIC SHOCK

HYPOVOLEMIC SHOCK
DEFINITION
 syndrom characterized by decreased circulating blood volume (hypovolemia), which results in reduction of effective tissue perfusion pressure and generalized cellular dysfunctions.

Forms:

• Hemorrhagic shock • Nonhemorrhagic hypovolemic shock

HYPOVOLEMIC SHOCK
CAUSES: • Hemorrhagic:
 External blood loss (wounds)  Exteriorization of internal bleeding (hematemesis, melena, epistaxis, hemoptysis,etc.)  Internal bleeding (hemothorax, hemoperitoneum,etc. )  Traumatic shock

• Non-hemorrahagic:
 Digestive losses (vomiting, diarrhea, nasogastric suction, biliary, digestive fistulas, etc )  Renal losses (diabetes mellitus, polyuria caused by overdosing diuretics, osmotics substances, polyuric phase of acute renal failure, etc.)  Cutaneous losses (intense physical effort, overheating enviroment, burns, etc.)  Third space losses (peritonites, intestinal oclussion, pancreatits, ascite, pleural effusions, etc.)

PATHOPHYSIOLOGY
Primary pathophysiological event
(reduction of ventricular filling volumes and pressures)

compensatory phenomena time decompensatory phenomena

macrocirculatory reaction

microcirculatory reaction

Hypodynamic shock:

PATHOPHYSIOLOGY

 Macrocirculatory reaction:
• sympatho-adrenergic reaction + humoral reaction (ADH, cortizol, SRAA)
o EFFECTS: centralisation of the circulation (compensatory) worsening of tisular hypoperfusion (decompensatory)

 Microcirculatory reaction:
• Alterations of capillary exchanges
o EFFECTS: transcapilary filling (compensatory) capilary leak (decompensatory)

• Maldistribution of blood flow
o EFFECTS: preferential renal blood flow towards medular region (cortical vasoconstriction)

• Arterial-venous shunt
o EFFECTS: shunting of capilar territory (functional reality)

• Rheologic changes

• Endhotelial modifications

o EFFECTS: ↑ blood viscosity, ↓ blood flow, CID o EFFECTS: morpho-functional modifications proinflamatory and procoagulatory status, altered permeability

HYPOVOLEMIC SHOCK
CLINICAL SIGNS:
   –         + Intense thirst Tachycardia Tachypnea Positive orthostatic test Small pulse wave hTA Agitation, anxiety , confusion, coma Oliguria Cold extremities Profuse sweating Collapsed peripheral veins Delayed return of color to the nail bed History of hemorrhagic or non-hemorrhagic losses

CLASSIFICATION OF HYPOVOLEMIC SHOCK
Class I
Blood loss- ml Blood loss-% Pulse rate TA Plus wave amplitude Capillary refill Respiratory rate Urinary output Mental status < 750ml <15% <100/min N N N 14-20/min >30ml/oră Mild anxiety

Class II
750-1500ml 15-30% < 100/min N ↓ + 20-30/min Oliguria Anxiety

Class III
1500-2000ml 30-40% 120-140/min ↓ ↓ + 30-40/min Oligoanuria Confused

Class IV
>2000ml >40% >140/min ↓ ↓ + >40/min Anuria Lethargic

DIFFERENTIAL DIAGNOSIS WITH OTHER FORMS OF SHOCK
FC TA DC PVC PCPB RVP Da-vO2 SvO2

Hypovolemic shock Cardiogenic shock Septic shock

↑ ↑ ↑

↓ ↓↓

↓ ↓

↓ ↑

↓ ↑ N

↑ ↑ ↓

↑ ↑ ↓

↓ ↓ ↑

↓ ↑ N ↓N

HYPOVOLEMIC SHOCK
TREATMENT PRINCIPLES • Initial treatment of shock states • Causal treatment – stop losses • Volume repletion therapy • Inotropic therapy • Vasomotor therapy

TREATMENT OF HYPOVOLEMIC SHOCK

• Causative treatment – stop losses
– essential role – surgical treatment (when appropriate) – emergency surgery for ongoing hemorrhage

TREATMENT OF HYPOVOLEMIC SHOCK

• volume replacement
– Vascular access site – Solutions for volume replacement – Rhythm of administration

TREATMENT OF HYPOVOLEMIC SHOCK
• Volume replacement – vascular access site
– Peripheral vascular access
• Multiple access (2-4 veins) • Large peripheral catheters • External jugular vein Advantages:
– Short time of instalation – Requires basic knowledge and simple matherials – Minor complications (hematomas, cutaneous seroma, etc.)

Disadvantages:
– The diameter of peripheral catheter must be adapted for peripheral veins dimensions – Vascular access can be lost (restless patient, during transportation); must be changed at 24-48 hours; – no catecholamines administration (except in emergency for a short time period,until a central venous access is established)

Central venous access
• After peripheral vascular access is established and volume replacement is initiated Advantages:
– Reliable and long lasting venous access (7-10 days) – Allows CVP measuring and guiding of treatment – Allows the administration of catecholamines and hypertonic substances

Disadvantages:
– Risk of complication (at instalation – pneumothorax, cervical or mediastinal hematoma, cardiac dysrhytmias; during utilization – infection, gas embolism)

TREATMENT OF HYPOVOLEMIC SHOCK
• Volume replacement - Solutions for volume replacement
– – – – Isotonic crystalloid solutions Hypertonic crystalloid solutions Colloid solutions Whole blood and red blood cells

– Fresh-frozen plasma – Platelets

TREATMENT OF HYPOVOLEMIC SHOCK
Solutions for volume replacement
-Isotonic crystalloid solutions
• Normal saline (NaCl 0,9 %), Ringer solution, lactated Ringer solutions • Advantages:
– easy available – cheap – reduced risks

• Disadvantages:
– reduced capacity of volume replacement (for 1000ml infused – 250-300ml remain in vessel, the rest is distributed in interstitial space) – short duration of intravascular remanence – risk of interstitial edema, metabolic hyperchloremic acidosis

-Hypertonic crystalloid solutions
• hypertonic saline (NaCl 7,4%) • Advantages:
– resuscitation with small volume; water is atracted from interstitial space – avoid fluid loading and edema formation

• Disadvantages:
– may result in acute pulmonary edema

TREATMENT OF HYPOVOLEMIC SHOCK Solutions for vulume replacement
Colloid sollutions
• • • • Dextrans: Dextran 70, Dextran 40 Gelatines: Gelofusin, Haemacel, Eufusin Hetastarch: Haes, Voluven, Refortan Human albumin 5%, 20%

– Advantages:
• Good volume replacement • large duration of intravascular remanence

– Disadvantages:
• • • • expensive risk for anphylactic reactions interfere with blood groups determination can determine/ aggravate disorders of coagulation

TREATMENT OF HYPOVOLEMIC SHOCK

Solution for volume replacement
Blood and blood products
• Only izogroup izoRh blood • Only after restauration of intravascular volume with cristalloid /colloid solutions; • For correction of oxygen transport • When the patient presents posthemorragic anemia (after volume replacement) or when ongoing hemorrhage is present; • In case of massive blood transfusion – fresh-frozen plasma and platelets are administered

TREATMENT OF HYPOVOLEMIC SHOCK
• Volume replacement – Rhytm of administration
– Rhytm of administration depends on:
• Ongoing losses / stopped losses • Rhytm of losses – rapid (minutes, hours) or slow (days) instalation

– For the patient with hypotension – normal saline (2000 ml in the first 15-30 minutes) – after the first 15-30 minutes - volume replacement continues depending on the clinical and hymodinamic parameters (BP, HR, etc..)

TREATMENT OF HYPOVOLEMIC SHOCK
• Volume replacement – monitoring the efficiency of treatment
– Clinical parameters (normalisation of BP, HR, pulse amplitude, colour and temperature of teguments, mental status, urinary output) – Hemodynamic parameters (CVP, PCPB, DC, RVS, etc.) – Laboratory parameters ( acid-base ballance, Hb şi Ht)

TREATMENT OF HYPOVOLEMIC SHOCK

• Inotropic support
– Only after volume replacement – Used to improve cardiac output – Dobutamine ( inotropic positive support and peripheral arterial vasodilatation)

TREATMENT OF HYPOVOLEMIC SHOCK
• Vasopressor therapy
– Vassopressors
• unadvisable (aggravate peripheral hypoperfusion and metabolic acidosis) EXCEPTIONS • Only temporary • In case of ongoing hemorrhage, which outruns the possibilities of volume replacement • Only until surgical procedure stops the hemorrhage (emergency surgical treatment) • Noradrenaline, dopamine, adrenaline

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