Surgery SHOCK SGD LALALA-LALA

1. Define shock in general.

- Failure to meet the metabolic demands of cells and tissues and the consequences that ensue

o Inadequate tissue perfusion

o Inadequate removal of cellular waste products

o Hypoxic shift from aerobic to anaerobic metabolism (lactic acidosis)

- Inadequate tissue perfusion marked by decreased delivery of required metabolic substrates and inadequate removal of

cellular waste products

- Condition in which metabolic needs of the body are not met because of an inadequate cardiac output

- Initial cell injury is reversible BUT will become irreversible if tissue perfusion is prolonged or severe enough that

compensation is no longer possible

3 primary causes of shock:

a. Inadequate circulatory blood volume

b. Loss of autonomic control of the vasculature

c. Impaired cardiac function

Cellular Hypoperfusion

- Oxygen debt: deficit in tissue oxygenation over time; occurs during shock

- O2 needs > O2 consumption

- Usually repaid during reperfusion

- Changes in cellular gene expression

o DNA binding activity of a number of nuclear transcription factors

o Production of O2 radicals/N radicals

o Increased expression of gene products: HSP, vascular EGF, iNOS, heme oxygenase-1, cytokines

2. Phases of Shock

Initial physiologic response in shock are driven by tissue hypoperfusion and developing cellular energy deficit.

(Schwartz + Robbins)

PHASE 1: Compensated phase of shock

o Begins with mild hypotension, tachycardia, pallor, and cold clammy extremities (except in septic shock)

o Body can still compensate for initial loss of blood volume through neuroendocrine response to maintain

hemodynamics

PHASE 2: Decompensation phase of shock

o If circulatory insufficiency persists, compensatory mechanisms are overwhelmed with a decline in BP, rapid

pulse, respiratory difficulty, metabolic acidosis, a decline in renal function (output)

o With continued hypoperfusion (may be unrecognized), cellular death & injury are ongoing

o Microcirculatory dysfunction, parenchymal tissue damage, and inflammatory cell division can lead to

hypoperfusion

PHASE 3: Irreversible phase of shock

o If circulatory & metabolic defects are not corrected, a stage may develop when all therapeutic efforts are futile,

leading to coma and death.

o Persistent hypoperfusion results in further hemodynamic derangements and cardiovascular collapse

o Extensive parenchymal & microvascular injury that volume resuscitation fails to reverse the process -> death

However if underlying cause of shock can be controlled (ex. Sepsis) and patient electrolyte levels are

appropriately managed, shock up to terminal stages is still reversible with improvement in renal,

pulmonary & cerebral function

Full recovery is possible. But there is a high mortality in cardiogenic shock because of underlying

cardiac disease and with septic shock due to difficulty in controlling infection.

Physiologic responses:

a. Neuroendocrine/Inflammatory

o Magnitude is dependent on: volume of blood lost & rate at which it is lost

o Maintain perfusion in cerebral and coronary circulation (even at the expense of other organ systems) through:

Stretch receptors & baroreceptors in the heart and vasculature (carotid sinus & aortic arch)

Chemoreceptors

Surgery SHOCK SGD LALALA-LALA Cerebral ischemia responses

Release of endogenous vasoconstrictors

Shifting of fluid into intravascular space

Renal reabsorption + conservation of salt & water

b. Persistent hypoperfusion

o Hemodynamic derangement

o End organ dysfunction/failure

o Cell death -> patient death

3. Metabolic effect of shock

- Cellular metabolism is dependent on ATP hydrolysis (splitting of phosphoanyhydride bond of terminal or gamma

phosphate from ATP -> MAJOR source of energy)

- ATP availability depends on aerobic metabolism in the process of oxidative phosphorylation in mitochondria

o Oxidative phosphorylation is dependent on oxygen as final electron acceptor

o Thus, when O2 tension is low = low oxidative phosphorylation = low ATP generation

Dysoxia when O2 delivery is so severely impaired that O2 phosphorylation is not sustained

Cells shift to anaerobic metabolism + glycolysis to generate ATP

Glycogen -> Pyruvate: yields only 2mol ATP/1mol Glucose (compared to 38mol ATP/1mol Glucose)

If hypoxic, Pyruvate is converted to Lactate which can lead to intracellular metabolic acidosis

Consequences:

* No maintenance of cell membrane potential

* No synthesis of enzymes and proteins

* No cell signalling

* No DNA repair mechanisms

* Alteration in gene expression within the cell

* Alteration in Ca metabolism & signalling

- Epi, NE, ADH, Glucagon, Cortison = CATABOLISM

o Glu mobilization

o Protein breakdown

o Hyperglycemia

o Negative N balance

o Lipolysis

o Insulin resistance

o Relative underuse of Glu by peripheral tissues = preserved for brain and heart

4. Clinical manifestations of shock

Mild hypovolemic/ traumatic shock

Moderate H.S./T.S

Severe H.S./T.S.

Early septic shock

Late septic shock

Neurogenic shock

Cardiogenic shock

Obstructive shock

Skin perfusion Pale Pale Pale Pink Pale Pink* Pale Pale

Urine output Normal Low Low Low Low Low Low Low

BP Normal Normal Low Low Low Low Low Normal

Mental status Thirsty Restless Obtunded Abnormal Abnormal Normal** Normal normal

ECG Normal Normal Abnormal Normal Normal** Normal** Abnormal Abnormal

Neck veins Flat Flat Flat Flat Flat Flat Distended Distended

Cardiac output Low Low Low High Low Low Low Low

Systemic vascular resistance

High High High Low high Low High High

Mixed venous oxygen content

Low Low Low High Low Low Low Low

Oxygen consumption (in relation to needs)

Low Low Low Low Low Low Low Low

*in denervated areas ** will be abnormal if shock is severe

Surgery SHOCK SGD LALALA-LALA 5. Types of shock (see table)

6. Why do we have shock patients that are pale and cold patients that are pinkish and warm? Explain. Give example.

A patient in shock would usually appear pale or dusky, and their skin may be diaphoretic. One exception would be a patient

under septic shock.

Initial clinical manifestations of sepsis arise from the development of a hypermetabolic state. Heat production increases and

heat loss is done through the shunting of blood flow towards he skin through the opening of cutaneous arteriovenous shunts.

The capacitance of cutaneous vascular beds increases so that unless fluid volume is given simultaneously, other areas of the

body become deprived of blood flow. This is why a patient with septic shock, especially in its early stages, appear pinkish and

warm.

A patient with neurogenic shock may also appear pinkish and feel warm due to the loss of peripheral vasoconstriction,

mediated by the absence of SY discharge.