shock amr mohsen. what is shock? acute circulatory failure leading to inadequate tissue perfusion...

Shock

Amr Mohsen

What is shock?

Acute circulatory failure

leading to

Inadequate tissue perfusion

that results in

Generalized organ hypoxia

3 components

cardiovascular physiologic reserve

1. Heart Rate2. Stroke Volume [venous return (blood volume)

& myocardial contractility & peripheral resistance]

3. Peripheral Resistance

All exist in dynamic equilibrium. These interactions maintain blood pressure. If one of the three becomes abnormal, the other two compensate.

Compensatory mechanisms

Receptors Respond to ResultsSympatho-Adrenal Response

Carotid & aortic baro-receptors

Reduced baroreceptor stretch

++ HR

++ SV

= maintain CO

VC (selective)

= maintain ABP

Compensatory mechanisms

Receptors Respond to ResultsADH (VASOPRESSIN)

Osmoreceptors Increased osmolality

Water retention

VC

Compensatory mechanisms

Receptors Respond to ResultsRENIN(Angiotensin ii & AldosteronE)

Juxtaglomerular apparatus

Renal ischemia

VC

Salt & water retention

Compensatory mechanisms

Sympatho-adrenal Response

Hypotension is an indication of:

1) An abnormality of Heart Rate, Stroke Volume or Peripheral Resistance

2) Failure of the others to compensate.

Classification of shock

failure

=hypovolemia

maldistribution

loss

• Hypovolemic shock

blood loss, plasma loss (burns), fluid loss

• Cardiogenic shock (pump failure)

Arrhythmias, MI, tamponade

• Maldistribution shock– Septic shock– Spinal shock– Anaphylactic shock

Classification of shock

Pathophysiology

Disturbedconsciousness

LiverFailure

DICUlcers

Translocationileus

ATNARF

Hypotension

ARDS

MOF

………

ARDS

Impaired ventilation

•Stiff lungs (surfactant def.)

•Alveolar oedema

Impaired perfusion

•Shock

•Shunts

Impaired diffusion

•Oedema of alveolo-capillary membrane

ARDS

ARDS

Late findingNormal

Chest X-ray

DIC

DIC

Serious sign

•Low platelet count

•Low fibrinogen

•Prolonged PT & APTT

•Elevated Fibrin-degradation product

Management of Shock & MOF

Treat Cause

SupportBody

SystemsMonitoring

In ICU

Treat Cause

Examples

•Control bleeding

•Eradicate sepsis (pus drainage)

•Antibiotics

Monitoring

Clinical parametersPulseTemp (peripheral & core)Blood pressureRespiratory rate

Continuous

•ECG

•Pulse oxymetry

Monitoring

Urine output

Optimum output 0.5-1ml/kg/hour.

Monitoring(invasive)

(2) CVP

N= 0-8 cmH2O (3) Swan Ganz (PAWP)

(1) Arterial cannula for ABP

MonitoringLaboratory tests

•CBC

•Renal function tests (Urea & elect)

•Arterial Bl Gases (ABGs)

•Lactates

•Liver function tests

•PT, PTT & FDP

Monitoring

Normal Arterial Bl Gases (ABGs)

Normal serum electrolytes

pH ~ 7.4

PO2 ~ 100

PCO2 ~ 40

HCO3- ~ 25 mmol/L

Na+ ~ 142 mmol/L

K+ ~ 4 mmol/L

Cl- ~ 103 mmol/L

-- CVP

++ Lactate

-- Haematocrit

ABGs: --PO2

--pH

--PCO2

-- ABP

++ Pulse

-- Urine flow

Cold sweaty skin

SupportBody

Systems

Respiration

•Clear airway

- Suction of secretions

- Tracheal intubation or tracheostomy

•Oxygen (essential)

- Mask for respiratory distress

- Mechanical ventilation for respiratory failure

PO2 < 60mm Hg RR > 35/m

SupportBody

Systems

Correct acidosis

Careful use of IV sodium bicarbonate

SupportBody

Systems

Circulation

Correction of hypovolaemia (essential)

•Two peripheral venous lines

•One central venous line

•Crystalloids

•Blood

•Plasma

Medications (if the above fail to restore BP)

•Inotropes (e.g., dopamine & dobutamine)

•Vasopressors (noradrenaline)

SupportBody

Systems

Renal

•Adequate volume replacement

•Dopamine improves renal blood flow

•Dialysis in case of acute renal failure (K+ >7mmol/L), until the kidneys recover

SupportBody

Systems

GITRoutine acid suppression

IV H2 blockers or Omeprazole

SupportBody

Systems

Coagulation

Treatment of DIC

•Platelet transfusion

•Fresh Frozen Plasma (FFP) as it contains coagulation factors

Mortality of MOF

1.Renal failure only 8%

2.Renal + other organ failure70%

3.Three failing organs 90%