Session 11: Haemodynamic Shock Flashcards
Mean arterial BP
CO x TPR
SV x HR x TPR
DBP + 1/3 PP
or
2/3DBP + 1/3 SBP
Cardiac output
SV x HR
What is haemodynamic shock?
An acute condition of inadequate blood flow throughout the body.
Due to a catastrophic fall in arterial blood pressure.
This can either be due to a fall in cardiac output or a fall in total peripheral resistance (maBP = CO x TPR)
Reasons for fall in cardiac output.
(General)
Mechanical fault where the pump cannot fill
Pump itself fails
Loss of large amounts of blood
Reasons for fall in peripheral resistance.
(General)
Excessive vasodilation
Give three examples of shock due to a fall in cardiac output.
Briefly explain.
Cardiogenic shock - ventricles cannot empty properly
Mechanical shock - ventricles cannot fill properly
Hypovolaemic shock - reduced blood volume -> reduced venous return
Common causes of cardiogenic shock.
Following MIs where there is damage to left ventricle.
Due to serious arrhythmias (also following MIs)
Acute worsening of heart failure
Complications of cardiogenic shock.
(What happens to CVP and arterial BP?)
Central venous pressure may be normal or raised (heart is filling but not emptying properly)
There is a dramatic drop in arterial BP
This leads to poor perfusion
Coronary arteries can be poorly perfused making it even worse.
Kidneys may be poorly perfused as well leading to oliguria.
How does cardiogenic shock affect cardiac output?
(Think equation)
CO = HR x SV
SV is reduced however HR may be increased but not enough to combat the dramatic fall in SV
Explain cardiac arrest.
Unresponsiveness with lack of pulse
Heart stopped or not pumping effectively
Asystole meaning loss of electrical and mechanical activity
Can get pulseless electrical activity.
Usually due to ventricular fibrillation often following a myocardial infarction, electrolyte imbalance or some arrhythmias like long QTs.
Measure of QT interval.
Start of Q to end of T
Intervention of cardiac arrest.
Basic life support - chest suppression and external ventilation
Advanced life support - defibrillation
Adrenaline to enhance myocardial function (HR + SV) and increase TPR to increase aBP.
Common causes of mechanical shock.
Cardiac tamponade
Pulmonary embolism
What is cardiac tamponade?
How can it lead to mechanical shock?
Blood or fluid build up in pericardial space
This can lead to restriction of the filling of the heart limiting end diastolic volume. This affects stroke volume since SV = EDV - ESV
Affects both left and right side of heart
Indications of mechanical shock.
(CVP and maBP)
High central venous pressure
Low aBP
However the heart attempt to beat.
How can pulmonary embolism lead to mechanical shock? Explain events leading up.
Pulmonary embolism restricts blood flow in the pulmonary system.
This leads to increased pulmonary artery pressure.
This leads to the right ventricle not being able to empty correctly.
Leads to increase in CVP since venous return is still working.
However it limits filling of the left heart (mechanical shock)
Leads to low left atrial pressure and low aBP.
Signs of mechanical shock due to pulmonary embolism.
Chest pain and dyspnoea
How can an embolus reach the lung? (Common cause)
DVT in legs e.g. in e.g. deep femoral vein.
Thrombus breaks off and runs through common femoral to external iliac to common iliac into inferior vena cava.
It then runs through heart and gets stuck in arterioles of the pulmonary system.
Common cause of hypovolaemic shock.
A drastic reduction in blood volume. Most commonly due to haemorrhage.
Effects of loss of <20% blood volume.
Unlikely to cause shock.
Effects of loss of 20-30% blood volume.
Signs of shock response
Effects of 30-40% loss of blood volume.
Substantial decrease in aBP and serious shock response.
What is the severity of hypovolaemic shock related to?
Amount of blood loss and speed of blood loss.
What happens in hypovolaemic shock?
(CVP, CO, aBP)
CVP falls
CO falls
Arterial pressure falls
How does the body respond acutely to hypovolaemic shock?
A compensatory response detected by baroreceptors.
Baroreceptors send to the sympathetic nervous system to increased the sympathetic stimulation.
This leads to increased HR (tachycardia) and increased inotropy (SV).
Peripheral vasoconstriction and also venoconstriction.
How does vasoconstriction help in hypovolaemic shock?
(Think capillary)
It increased arterial pressure however it reduces pressure in capillaries. The reduction of pressure (hydrostatic pressure) in capillaries means that the amount of fluid going into tissue will be less.
Plasma oncotic pressure > Hydrostatic pressure + interstitial oncotic pressure
This means that there isn’t further loss of fluid worsening the hypovolaemic shock.
Signs of hypovolaemic shock.
Tachycardia
Weak pulse
Pale skin
Cold and clammy extremities
Low CVP (check jugular)
Other less common causes of hypovolaemic shock.
Severe burns
Severe diarrhoea, vomiting or loss of Na+.
Dangers of compensation in hypovolaemic shock.
(Think vasoconstriction)
The peripheral vasoconstriction will impair tissue perfusion.
This can lead to tissue damage due to hypoxia.
The tissue damage leads to release of chemical mediators causing vasodilation. This vasodilation leads to a fall in TPR and blood pressure falls dramatically so vital organs can no longer be perfused.
This can lead to multi system failure.
Longer term responses to restore blood volume in hypovolaemia.
RAAS
Anti-diuretic hormone (ADH aka vasopressin)
Time to restore a blood volume loss of 20%.
Around 3 days if salt and water intake is adequate.
What is distributive shock?
Low resistance shock meaning it is normovolaemic.
There is a dramatic fall in TPR due dramatic vasodilation.
Common types of distributive shock.
Toxic shock
Anaphylactic shock
Explain events of sepsis leading up to toxic (septic) shock.
Serious life-threatening response to infection
Endotoxins released by circulating bacteria leads to an excessive inflammatory response
This leads to profound vasodilation causing a dramatic fall in TPR.
There is also a fall in arterial pressure due to this.
Leads to impaired perfusion of vital organs and capillaries become leaky leading to hypovolaemia.
Sepsis can also cause increased coagulation and localised hypo-perfusion and DIC.
Compensatory responses due to septic shock.
Baroreceptors detect low arterial pressure so sympathetic output is increased.
Vasoconstriction is however still overridden by the mediators of the vasodilation due to the inflammatory response.
The increased sympathetic output leads to increased HR and SV.
Signs of septic shock.
Early vs. late stage
Tachycardia
Warm, red extremities (signs of inflammation)
In later stages of sepsis:
The vasoconstriction response of the baroreceptors lead to localised hypo-perfusion. This leads to pallor and cold extremities.
Explain events leading up to anaphylactic shock.
A severe allergic reaction to something results in the release of histamine from mast cells. Along with other mediatiors this leads to a drastic increase in vasodilation.
This results in an excessive fall in TPR and a rapid profound drop in arterial blood pressure.
This leads to an increased sympathetic response -> increase in CO due to increase in HR (chronotropy) and increase in SV (inotropy).
However this can’t compensate for the excessive vasodilation.
This leads to imparied perfusion of vital organs.
Other effects of anaphylactic shock.
Bronchoconstriction and laryngeal oedema leading to difficulty in breathing.
Signs of anaphylactic shock.
Difficulty breathing
Collapse
Rapid heart rate
Red and warm extremities
How do you treat anaphylactic shock?
Adrenaline
Why doesn’t giving fluid to a patient in septic shock work effectively?
Due to the leaky vessels. So all the fluids you give will leak out into interstitium.
