Session 11: Haemodynamic Shock

Question 1

Mean arterial BP

Answer 1

CO x TPR

SV x HR x TPR

DBP + 1/3 PP

or

2/3DBP + 1/3 SBP

Question 2

Cardiac output

Answer 2

SV x HR

Question 3

What is haemodynamic shock?

Answer 3

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)

Question 4

Reasons for fall in cardiac output.

(General)

Answer 4

Mechanical fault where the pump cannot fill

Pump itself fails

Loss of large amounts of blood

Question 5

Reasons for fall in peripheral resistance.

(General)

Answer 5

Excessive vasodilation

Question 6

Give three examples of shock due to a fall in cardiac output.

Briefly explain.

Answer 6

Cardiogenic shock - ventricles cannot empty properly

Mechanical shock - ventricles cannot fill properly

Hypovolaemic shock - reduced blood volume -> reduced venous return

Question 7

Common causes of cardiogenic shock.

Answer 7

Following MIs where there is damage to left ventricle.

Due to serious arrhythmias (also following MIs)

Acute worsening of heart failure

Question 8

Complications of cardiogenic shock.

(What happens to CVP and arterial BP?)

Answer 8

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.

Question 9

How does cardiogenic shock affect cardiac output?

(Think equation)

Answer 9

CO = HR x SV

SV is reduced however HR may be increased but not enough to combat the dramatic fall in SV

Question 10

Explain cardiac arrest.

Answer 10

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.

Question 11

Measure of QT interval.

Answer 11

Start of Q to end of T

Question 12

Intervention of cardiac arrest.

Answer 12

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.

Question 13

Common causes of mechanical shock.

Answer 13

Cardiac tamponade

Pulmonary embolism

Question 14

What is cardiac tamponade?

How can it lead to mechanical shock?

Answer 14

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

Question 15

Indications of mechanical shock.

(CVP and maBP)

Answer 15

High central venous pressure

Low aBP

However the heart attempt to beat.

Question 16

How can pulmonary embolism lead to mechanical shock? Explain events leading up.

Answer 16

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.

Question 17

Signs of mechanical shock due to pulmonary embolism.

Answer 17

Chest pain and dyspnoea

Question 18

How can an embolus reach the lung? (Common cause)

Answer 18

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.

Question 19

Common cause of hypovolaemic shock.

Answer 19

A drastic reduction in blood volume. Most commonly due to haemorrhage.

Question 20

Effects of loss of <20% blood volume.

Answer 20

Unlikely to cause shock.

Question 21

Effects of loss of 20-30% blood volume.

Answer 21

Signs of shock response

Question 22

Effects of 30-40% loss of blood volume.

Answer 22

Substantial decrease in aBP and serious shock response.

Question 23

What is the severity of hypovolaemic shock related to?

Answer 23

Amount of blood loss and speed of blood loss.

Question 24

What happens in hypovolaemic shock?

(CVP, CO, aBP)

Answer 24

CVP falls

CO falls

Arterial pressure falls

Question 25

How does the body respond acutely to hypovolaemic shock?

Answer 25

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.

Question 26

How does vasoconstriction help in hypovolaemic shock?

(Think capillary)

Answer 26

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.

Question 27

Signs of hypovolaemic shock.

Answer 27

Tachycardia

Weak pulse

Pale skin

Cold and clammy extremities

Low CVP (check jugular)

Question 28

Other less common causes of hypovolaemic shock.

Answer 28

Severe burns

Severe diarrhoea, vomiting or loss of Na+.

Question 29

Dangers of compensation in hypovolaemic shock.

(Think vasoconstriction)

Answer 29

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.

Question 30

Longer term responses to restore blood volume in hypovolaemia.

Answer 30

RAAS

Anti-diuretic hormone (ADH aka vasopressin)

Question 31

Time to restore a blood volume loss of 20%.

Answer 31

Around 3 days if salt and water intake is adequate.

Question 32

What is distributive shock?

Answer 32

Low resistance shock meaning it is normovolaemic.

There is a dramatic fall in TPR due dramatic vasodilation.

Question 33

Common types of distributive shock.

Answer 33

Toxic shock

Anaphylactic shock

Question 34

Explain events of sepsis leading up to toxic (septic) shock.

Answer 34

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.

Question 35

Compensatory responses due to septic shock.

Answer 35

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.

Question 36

Signs of septic shock.

Early vs. late stage

Answer 36

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.

Question 37

Explain events leading up to anaphylactic shock.

Answer 37

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.

Question 38

Other effects of anaphylactic shock.

Answer 38

Bronchoconstriction and laryngeal oedema leading to difficulty in breathing.

Question 39

Signs of anaphylactic shock.

Answer 39

Difficulty breathing

Collapse

Rapid heart rate

Red and warm extremities

Question 40

How do you treat anaphylactic shock?

Answer 40

Adrenaline

Question 41

Why doesn’t giving fluid to a patient in septic shock work effectively?

Answer 41

Due to the leaky vessels. So all the fluids you give will leak out into interstitium.