Haemodynamic Shock Flashcards
Control of arterial BP
Control cardiac output and peripheral resistance to control arterial BP
Mean arterial BP = CO x TPR
CO = SV x HR
Mean arterial BP (maBP) = SV x HR x TPR
maBP = diastolic pressure + 1/3 pulse pressure
Haemodynamic shock
BP drops so far so that there is inadequate blood flow throughout the body - an acute condition
A catastrophic fall in arterial blood pressure leads to circulatory shock
For Mean arterial BP to drop there needs to be a drop in CO or TPR (beyond capacity of the heart to cope)
Shock due to fall in cardiac output
Cardiogenic (genesis of shock is heart) shock (pump failure) – ventricle cannot empty properly
Mechanical shock (obstructive) – ventricle cannot fill properly
Hypovolaemic shock – reduced blood volume leads to poor venous return
Cardiogenic shock:
Acute failure of the heart to maintain cardiac output - i.e. pump failure
Potential causes - following an MI - damage to the left ventricle - heart cant pump out sufficntyl well
- due to a serious arrythmia - could be heart block - would have a very low heart rate - profound bradycardia - e.g. have no info going through the AV node, so ventricles are depolarisation at their own rate
Could also be due to tachycardia - so ventricles don’t have enough time to fully fill - so heart not pumping enough blood around the body (decrease in stroke volume)
Could also be due to worsening heart failure - could be an acute worsening - arterial bp drops profoundly
Central venous pressure (CVP) may be normal or raised
Dramatic drop in arterial BP
Therefore tissues become poorly perfused
e.g. coronary arteries may be poorly perfused - exacerbates problem
Kidneys may be poorly perfused - reduced urine production - oliguria
Need to consider cardiac arrest
Unresponsiveness associated with lack of pulse
Heart has stopped or has ceased to pump effectively
Asystole (loss of electrical and mechanical activity)
Can also get Pulseless Electrical Activity (PEA)
Ventricular fibrillation (uncoordinated electrical activity)
– most common form of cardiac arrest
– often following MI
– or electrolyte imbalance
– or some arrhythmias (eg long QT and Torsades de Pointes)
Cardiac Arrest - need Basic life support
– chest compression and external ventilation
Advanced life support
– defibrillation
– electric current delivered to the heart
– depolarises all the cells – puts them into refractory period
– allows coordinated electrical activity to restart
Adrenaline
– enhances myocardial function
– increases peripheral resistance
Mechanical shock
Cardiac tamponade
blood or fluid build up in pericardial space
which restricts filling of the heart
which limits end diastolic volume
this affects left and right sides of heart
Patient will have a high central venous pressure - usually seen in neck veins (jugular)
Patient will also have Low arterial blood pressure - as heart cant fill, so cant pump blood out so decreasing SV and therefore decreaseing bp in aorta
Heart attempts to beat - may increase due to low bp in carotid sinus – continued electrical activity
Mechanical shock – pulmonary embolism Massive pulmonary embolism (PE) Embolus occludes a large pulmonary artery – Pulmonary artery pressure is high – Right ventricle cannot empty – Central venous pressure high – Reduced return of blood to left heart – Limits filling of left heart – Left atrial pressure is low – Arterial blood pressure low – Shock BP = CO x TPR – Also chest pain, dyspnoea
Hypovolaemic shock
Patient will present with - tachycardia, weak pulse, pale skin, cold extremities, and low central venous pressure
Reduced blood volume - Most commonly due to haemorrhage
< 20% blood loss unlikely to cause shock
20-30% some signs of shock response
30-40% substantial decrease in mean aBP and serious shock response
Severity of shock is related to amount and speed of blood loss
Haemorrhage – venous pressure falls – cardiac output falls (Starling
Distributive shock
Or Low resistance shock (normovolaemic) - no change (at first) to the volume of the blood
Occurs due to Profound peripheral vasodilation -
Toxic shock - sepsis
Serious life-threatening response to infection
Can lead to septic shock
Could be that Endotoxins are released by circulating bacteria
–causing a Profound inflammatory response (excessive)
– Causes profound vasodilation to allow for adhesion of WBC to the site of inflammation
– Dramatic fall in TPR
– Fall in arterial pressure
– Impaired perfusion of vital organs
– also - capillaries become leaky (which also reduces blood volume
– Increased coagulation and localised hypo-perfusion at fingers and toes - can get ischaemia
Septic shock -
Persisting hypotension requiring treatment to maintain blood pressure despite fluid resuscitation
Decreased arterial pressure
– Detected by baroreceptors – increased sympathetic output
– Vasoconstrictor effect overridden by mediators of vasodilation
– Heart rate and stroke volume increased
Patient has
– Tachycardia
– Warm, red extremities initially BUT
Later stages of sepsis – vasoconstriction due to localised hypo-perfusion
Anaphylactic shock
severe allergic reaction (anaphylaxis)
– release of histamine from mast cells
This has a powerful vasodilator effect – fall in TPR – dramatic drop in arterial pressure
Causes an increase sympathetic response -