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Flashcards in Haemorrhage and Shock Deck (36)

What is shock?

An acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in cellular hypoxia


What are the four main types of shock?

Obstructive, distributive, hypovolaemic (haemorrhagic) or cardiogenic shock


What is obstructive shock? Give an example

Where there is a physical obstruction to the vessels that enter or leave the heart e.g. pulmonary embolism


What is distributive shock? Give two examples

This form of shock is due to the loss of vasoconstriction (vasodilation) in one or more end organs which leads to excess blood flow to these systems and poor in others

Causes include sepsis or anaphylaxis


What is hypovolaemic (haemorrhagic) shock? Give three examples

This type of shock is due to loss of blood volume and is associated with haemorrhage, burns and trauma


What is carcinogenic shock? Give three examples

This type of shock is due to failure of the heart to pump effectively and supply blood to the body, this can be caused by MI, heart failure or arrhythmia


What is cardiopulmonary obstructive shock?

This is a combination of carcinogenic and obstruction shock grouped together


What are the symptoms of hypovolaemic/haemorrhagic shock?

Symptoms are mainly due to the loss of blood volume and include low BP, increased HR, confusion, anxiety, cold and clammy skin


What are the common causes of hypovolaemic/haemorrhagic shock?

Haemorrhage, burns, surgery, trauma or loss of fluid/electrolytes from the gut


What is the immediate compensatory response for a venous bleed that leads to hypovolaemic shock?

A venous bleed causes a decreased venous return (preload) which reduces stroke volume and cardiac output. This reduced blood pressure is detected by baroreceptors and activates the nervous system to constrict the large veins to move blood out of the venous reservoir and increase/restore preload. in addition, the baroreceptors stimulate the vasomotor centre in the medulla to cause increase hypothalamic signalling to cause ADH release which slows urine flow and sodium excretion (which increases water reabsorption in order to increase blood pressure)


How does preload affect ANP production?

A reduced preload reduces the production of atrial natriuretic peptide


What is the immediate compensatory response to an arterial bleed that leads to hypovolaemic shock?

This decrease in blood pressure is detected by the baroreceptors and stimulates vasoconstriction by the sympathetic nervous system which then works to increase the BP


What are the long-term compensatory responses to hypovolaemia (hypovolaemic shock)?

- Increased renin release from the kidney
- Stimulating of albumin and protein synthesis
- Increased production of EPO from peritubular cells


Why is renin released in the long-term response to hypovolaemia?

- Renin release leads to the production of angiotensin II which can cause aldosterone release which causes sodium retention --> increase passive water reabsorption.
- Angiotensin II also binds to AT2 receptors in the subfornical organ of the brain to increase thirst to increase water intake to increase blood volume and BP


Why are albumin and other proteins synthesised in the long-term response to hypovolaemia?

Albumin and protein synthesis in the liver is stimulated in order to increase the osmolarity of the plasma and therefore reduce interstitial fluid deposition in order to increase circulating blood volume to restore blood pressure


Why do peritubular cells produce EPO in the long-term response to hypovolaemia?

The peritubular cells (fibroblasts in the extracellular space around the kidney tubules) detect hypoxia due to the shock which causes them to increase EPO production to stimulate red blood cell production to restore haematocrit levels which are reduced due to acute blood loss.


How can angiotensin II cause polydipsia?

Stimulates the subfornical organ above the hypothalamus in the brain by acting on AT2 receptors


What are the stages of hypovolaemic shock?

Class 1 - less than 15% of blood lost, this is fully compensated

Class 2 - 15-30% blood loss, they will fully compensate and recover without intervention

Class 3 - blood loss >30%

Class 4 - blood loss >40% (life-threatening)


What are the symptoms of cardiogenic shock?

Most patients with cardiogenic shock have an acute myocardial ischaemic attack and therefore their symptoms are related to those of cardiac dysfunction or failure e.g. chest pain, shortness of breath, syncope etc.


What are the symptoms of distributive (septic) shock?

Individual’s with this form of shock elicit the classic symptoms of low BP and tachycardia but the rest of the symptoms are non-specific and include fever, chills, rigor and fatigue.


What is the difference between sepsis and septic shock?

Sepsis is a systemic response to the presence of pathogens in the blood and other organs which causes temperature change, tachycardia and elevated WBCs. Septic shock is when this is accompanied by hypotension due to reduced systemic vascular resistance.


What is the role of LPS in sepsis?

Lipopolysaccharide (LPS) is present on the walls of gram-negative bacteria and this stimulates neutrophils and monocytes to release cytokines. The cytokines produced affect the endothelium and prevent normal vasoconstriction leading to reduced vascular resistance in implicated end-organs which may be severe enough to lower blood pressure and induce septic shock.


What are the symptoms of obstructive shock?

A tension pneumothorax is often implicated as the cause due to the mass effects with compression.

A patient with obstructive shock will present with tachycardia, anxiety, absent breath sounds on affected side, tracheal deviation and chest pain


How do cells respond to hypoxia?

1. Cells switch from aerobic to anaerobic metabolism
2. Lactate is produced as a result
3. The cell function begins to cease due to the lactate build up and the cell swells due to an increased osmotic gradient
4. The cellular membrane becomes more permeable
5. Electrolytes and fluid then begin to seep in and out of the cell in response to this damage
6. The Na+/K+ pump becomes impaired and this leads to further cell swelling
7. This further cell swelling leads to mitochondria damage and cell death


What factors control heart rate?

Baroreceptors - increased stretch leads to the parasympathetic innervation to cause vasodilation to decrease BP, or decreased stretch stimulates the sympathetic nervous system to cause vasoconstriction to increase BP

Environmental factors such as stress


What factors control stroke volume?

Preload (Starling mechanism) - increased preload increases SV

Contractility - catecholamines, sympathetic nervous system and inotropic drugs increase the force of contraction


What drugs can affect heart contractility?

Beta blockers and calcium channel blockers have negative ionotropic effects


What is prostacyclin?

A local vasodilator produced in endothelial cells from arachidonic acid in the conversion of prostaglandins


What is the role of prostacyclin in systemic vascular resistance?

This is a local vasodilator produced by the endothelial cells which prevents primary haemostasis by inhibiting platelet activation and reducing calcium entry into smooth muscle cells to reduce smooth muscle contractility --> vasodilation


How does the sympathetic nervous system affect systemic vascular resistance

Releases noradrenaline onto the tunica adventitia which then acts on local alpha-1 adrenoreceptors in the tunica media smooth muscle to cause vasoconstriction (contraction)


How does circulating angiotensin II affect systemic vascular resistance?

Angiotensin II acts on AT1 receptors on the endothelial lining of the arteriole as well as the smooth muscle


What is endothelin?

This molecule is released from the endothelial lining and causes local constriction or dilation depending on the receptors it binds to


How does endothelium affect systemic vascular resistance?

Can cause vasoconstriction or vasodilation depending on the subset of receptors it binds to; binding of endothelin to some receptors leads to NO release to decrease systemic vascular resistance


What are the two main physiologic causes of shock?

If the systemic vascular resistance is reduced (lack of arteriole vasoconstriction) or the preload decreases (due to blood volume loss or obstructed flow)


What is compensated shock?

This is where the body compensated for this by activating homeostatic mechanisms to allow sufficient tissue perfusion and prevent hypoxia


What is decompensated shock?

This is where the arterioles cannot maintain sufficient constriction or the reduction in preload is too great, and this leads to insufficient perfusion of end organs which then begin to fail; this process is fatal if allowed to continue