L21: Shock Flashcards
What is the main controller of arterial blood pressure?
Cardiac output and total peripheral resistance
MAP= CO x TPR
Or
MAP= Diastolic pressure +1/3 pulse pressure
Or
MAP= 1/3 systolic + 2/3 diastolic
How do you calculate the cardiac output?
CO= SV x HR
How do you calculate pulse pressure?
Systolic pressure- diastolic pressure
What is haemodynamic shock?
Acute condition of inadequate blood flow throughout the body
Catastrophic fall in MAP–> circulatory shock
Insufficient perfusion of tissues/organs–> brain, kidneys, heart
What can cause shock?
Fall in CO
Fall in TPR beyond capacity of heart to cope
What can cause the CO to fall?
Mechanical –> ventricle cannot fill properly –> obstructive
Cardiogenic–> ventricle cannot empty properly –> pump failure
Hypovolaemic–> Reduced blood volume leads to poor venous return
What can cause cardiogenic shock?
Pump failure–> unable to maintain CO
- MI–> Damage to LV–> necrosis of tissue unable to contract and pump blood out properly
- Serious arrhythmias–> heart block, bradycardia or tachycardia (HR too fast, ventricles cannot fill properly so reduced CO)
- Acute worsening of HF–> if HF suddenly gets worse MAP pressure can suddenly decrease and lead to shock
What is the main prinicple behind cardiogenic shock?
Heart fills properly
Fails to pump it out effectively
CVP maybe raised or normal
–> raised due to back pressure, if heart doesn’t empty (ESP high), less can enter to fill it
Tissue poorly profused
–> coronary arteries–> worsens the problem
–> kidneys poorly perfused–> oligouria
What is cardiac arrest?
Lack on consciousness with lack of pulse
Heart stopped or has ceased to pump effectively
What can cause cardiac arrest?
- Asystole–> loss of electrical and mechanical activity
- -> heart stopped–> No CO–> shock - Pulseless electrical activity–> Electrical activity but no pulse, dissociation between electrical activity and mechanical activity, extreme hypovolaemia (blood loss), cardiac temponade, fast ventricular tachycardia
- Ventricular fibrillation–> uncoordinated activity
How does ventricular fibrillation lead to cardiac arrest?
Ventricular fibrillation usually follows MI or electrolyte imbalance or arrhythmias
Ventricular fibrillation–> heart unable to fill properly or eject blood properly reduced CO–> cardiac arrest
How is Cardiac arrest managed?
Basic life support
–> chest compression and external ventillation
Advance life support
–> defibrillation
–> electric current delivered to the heart
–> depolarises all the cells- puts them in the refractory period
–> allows coordinated electrical activity to restart
Adrenaline
–> enhances myocardial function
–> Increases peripheral resistance
What is cardiac temponade?
Compression of the heart
- -> blood or fluid fills up in pericardial space
- -> restricts filling of the heart–> limits end diastolic volume
- -> affects both left and right side of heart
What does cardiac temponade result in?
Increase CVP–> unable to fill properly
Low arterial BP–> less blood to pump out
Increase HR in attempt to compensate–> ↓ SV–> ↓ CO
How can a pulmonary embolism cause mechanical failure?
PE in pulmonary artery Pulmonary artery pressure is high Limited output from right ventricle Central venous pressure high Reduces blood return to left atrium and ventricle Reduced output from left ventricle Low arterial blood pressure Arterial blood pressure low Shock Chest pain, dyspnoea (difficulty breathing)
How does an embolus reach the lungs?
Usually deep vein thrombosis Portion break off--> emboli Travels in venous system to the heart Passes through right side of heart Pumped out via pulmonary artery Effect depends on the size of emboli --> Small--> block capillary so smaller area of lung affects --> Large--> block pulmonary artery prevents blood flow to lung
What is meant by hypovolaemic shock?
Reduced blood volume
Leads to decrease MAP–> shock
What causes hypovolaemic shock?
Commonly caused by haemorrhage
<20% blood loss–> shock unlikely
20-30% some signs
30-40% substantial decrease in MAP–> shock
Severity of shock related to amount and speed of blood loss
How does the body cope with a sudden loss of blood?
Haemorrhage–> venous pressure falls–> CO falls (Starlings law- less stretch, less contraction)–> arterial pressure falls–> detected by baroreceptors
Compensatory response–> increased sympathetic stimulation–> tachycardia (↑HR)–> ↑ force of contraction–> peripheral vasoconstriction (to ↑ TPR)–> ↑ venoconstriction (sympathetic system works on SM in veins too)
Attempt to increase CO and TPR
In hypovolaemic shock what changes are there in the formation of tissue fluid?
Normally in capillaries hydrostatic pressure is greater then the oncotic pressure–> net movement of water out of the capillaries
Returns to venous system via lymphatic drainage
Hypovolaemic shock–> decrease BP causes vasoconstriction–> less blood gets to capillary beds–> reduced hydrostatic pressure relative increase in oncotic pressure (more concentrated)–> net movement of fluid into the capillary
What are the clinical features of a patient in hypovolaemic shock?
Tachycardia
Weak pulse (BP dropped)
Pale skin (vasoconstriction–> reduced blood flow to skin)
Cold clammy extremities (vasoconstriction… and sympathetic system activates sweating)
Low CVP
What else can result in hypovolaemic shock? What also can change in these patients?
Severe burns
Severe diarrhoea and vomiting and loss of Na+
Severe burns–> increase proteins in blood–> increase oncotic presure
What does prolonged hypovolaemia lead to?
Decompensation Peripheral vasoconstriction (shutdown) impairs tissue perfusion --> Tissue damage due to hypoxia --> Release of chemical mediators--> vasodilators--> build up resulting in vasodilation --> TPR falls --> Blood pressure falls dramatically --> Vital organ no longer perfused --> Multi system failure
What is the long term response to hypovolaemia?
Attempt to restore blood volume
Renin-angiotensin-aldosterone system –> Increase BV
Anti-diuretic hormone –> promotes retention of water at the kidneys to increase blood volume
20% blood volume loss–> restoration of body fluid volume in about 3 days–> If Na+ and water intake are adequate
What is distributive shock?
Low resistance shock–> normovolaemic–> no change in BV
Profound peripheral vasodilation–> ↓ TPR
Increase in volume for circulation
Causes by toxic shock (sepsis) or anaphylactic shock
What is toxic (septic) shock?
Sepsis is a serious life threatening response to infection
Endotoxins released by circulating bacteria (chemokines and cytokines)
Profound vasodilation
Dramatic fall in TPR
Fall in arterial pressure
Impaired perfusion of vital organs
Capillaries become leaky –> reduced blood volume (change in hydrostatic pressure)
Increase coagulation and localised hypoperfusion
How does the body try to compensate for septic shock?
Decreased arterial pressure
Detected by baroreceptors–> increased sympathetic output
Vasoconstrictor effect over-ridden by mediator of vasodilation
Heart rate and stroke volume increase
What is the clinical presentation of a patient in septic shock?
Tachycardia
Warm, red extremities
Late stages of sepsis–> vasoconstriction–> localised hypo-perfusion
What is anaphylactic shock?
Severe allergic reaction
Release of histamine from mast cells and other mediators
Vasodilation–> fall in TPR
Drop in arterial pressure–> increase sympathetic response ↑CO can’t overcome vasodilation
Impaired perfusion of vital organs
Mediators also cause bronchoconstriction and laryngeal oedema –> difficulty breathing
What is the clinical presentation of a patient with anaphylactic shock?
Difficulty breathing
Collapsed
Rapid heart rate
Red, warm extremities –> vasodilation
What is the treatment for anaphylactic shock?
Acutely life threatening
Adrenaline–> pharmacological dose
–> Results in vasoconstriction by acting on the α1 adrenoreceptors (Gq–> IP3–> Ca2+ etc…)
–> Overcomes the preferential binding to the β2 adrenoreceptors
What is the outcome of all types of shock?
Decreased blood pressure
Decreased tissue perfusion
Multi-organ failure
