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CVS * > S11 Haemodynamic Shock > Flashcards

S11 Haemodynamic Shock Flashcards

1
Q

What two things do you need to control to control arterial blood pressure?

A

Cardiac output and peripheral resistance

Mean arterial blood pressure = CO x TPR

(CO = SV x HR)
(Mean arterial BP = SV x HR x TPR)
(Mean arterial BP = diastolic pressure +1/3 pulse pressure) * pulse pressure is difference between diastolic and systolic pressures

TPR increase resistance by constriction

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2
Q

What is haemodynamic shock? What is is due to?

A

An acute condition of inadequate flow throughout the body.

Due to a catastrophic fall in arterial blood pressure leading to circulatory shock
Could be a fall in CO or a fall in TPR below the capacity the heart can cope with e.g. heart can increase CO enough

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3
Q

What can a fall in CO be due to?

A
  • ventricle can’t fill properly - mechanical shock (obstructive) -
  • pump failure, ventricle can’t empty properly - cardiogenic shock
  • loss of blood volume, poor venous return - hypovolaemic shock
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4
Q

What can a fall in TPR be due to?

A

Excessive vasodilation

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5
Q

What are the potential causes of carcinogenic shock?

A
  • after MI - damage to left ventricle
  • serious arrhythmias - e.g. heart block, low HR, bradycardia or tachycardia, not enough time for ventricles to fill in diastole so CO reduces (boarding on ventricular fibrillation)
  • acute worsening of heart failure
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6
Q

What is cardiogenic shock? What will CVP be like?

A

Acute failure of the heart to maintain CO - the heart fills but fails to pump effectively (so CVP may be normal or raised)

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7
Q

What does cardiogenic shock mean for tissue perfusion?

A

Poor perfusion e.g. coronary arteries which makes the problem worse or kidneys reduced urine production (oliguria)

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8
Q

What are two examples of mechanical shock?

A

Cardiac tamponade

Pulmonary embolism

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9
Q

What is a cardiac tamponade? What does it mean for CVP and mABP? Link it to CO and SV.

A

When blood or fluid builds up in the pericardial space and restricts the filling of the heart (limits the end diastolic volume). This affects the left and right sides of the heart.

Leads to high CVP and low mABP

Lower CO due to lower SV

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10
Q

What are the layers of the pericardium/heart?

A 
Serous pericardium:
* fibrous pericardium
* parietal layer 
* pericardial cavity 
* visceral layer
Heart:
* epicardium 
* myocardium 
* endocardium
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11
Q

How does a pulmonary embolism cause mechanical shock?

A

A very large PE that occludes a large pulmonary artery means that

  • pulmonary artery pressure is high
  • right ventricle can’t empty
  • CVP is high
  • reduced return to left side of heart
  • limits filling of left side of heart
  • left arterial pressure is low
  • mABP is low
  • shock
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12
Q

What symptoms does someone with a PE have?

A
  • chest pain
  • dyspnoea (difficulty breathing)
  • mechanical cardiovascular shock - haemodynamic shock
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13
Q

How might an embolus reach the lungs?

A

From a DVT, part breaks off, travels up venous system to right side of heart where it’s pumped out via the pulmonary artery to the lungs.

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14
Q

What is hypovolaemic shock? With how much blood loss is it likely to occur?

A

Reduced blood volume usually due to haemorrhage

  • if less than 20%, unlikely to cause shock
  • 20-30% some signs of shock
  • 30-40% substantial decrease in mABP and a serious shock response
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15
Q

What happens if there is a haemorrhage in terms of haemodynamics?

A
  • drop in venous pressure
  • CO drops as SV drops (as amount of blood returning to heart drops)
  • arterial pressure falls
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16
Q

What is the compensatory response to hypovolaemic shock due to haemorrhage?

A
  • drop in mABP is detected by baroreceptors
  • increased sympathetic stimulation (NA on beta-1 receptors)
  • tachycardia
  • increased force of contraction - steepens slope of Starling curve, for a given venous pressure, can get out same SV as before
  • peripheral vasoconstriction - to maintain arterial BP (CO drops, so TPR increases)
  • venoconstriction
17
Q

What change do you get in capillaries during hypovolaemic shock?

A
  • reversal of movement of fluid in capillaries e.g. small net movement of fluid out to tissues, which returns to the lymphatic drainage
  • reduced blood volume, so reduced hydrostatic pressure
  • net movement of fluid is into the capillaries (reabsorption rather than filtration)
18
Q

What signs and symptoms does someone with hypovolaemic shock have?

A
  • tachycardia
  • weak pulse
  • pale skin
  • cold, clammy extremities
  • low CVP
19
Q

What 3 things can hypovolaemic shock result from?

A
  • haemorrhage
  • severe burns
  • severe diarrhoea or vomiting and loss of Na+ (very severe, continued and persistent)
20
Q

What is a danger of hypovolaemic shock?

A

Danger of decompensation - when compensation fails

  • peripheral vasoconstriction impairs tissue perfusion
  • tissue damage due to hypoxia
  • release of vasodilator chemical mediators
  • TPR falls
  • blood pressure falls dramatically
  • vital organs no longer perfused
  • multi-system organ failure
21
Q

What are longer term responses to restore blood volume?

A
  • RAAS

* ADH release

22
Q

What is cardiac arrest?

A

When the heart ‘stops’ - unresponsiveness associated with a lack of pulse - the heart has stopped or has ceased to pump effectively

E.g. in asystole - loss of electrical and mechanical activity

23
Q

What is pulseless electrical activity

(PEA)?

A

When there’s electrical activity but no pulse
- if no pulse, no CO

Due to a dissociation between electrical and mechanical activity?
E.g. extreme hypovolaemia or extreme cardiac tamponade or ventricular fibrillation (uncoordinated electrical activity)

24
Q

When does ventricular fibrillation most commonly occur?

A

After an MI and is the most common form of cardiac arrest

Could also be caused by electrolyte imbalance e.g K+/Ca2+, drug interactions, congenital arrhythmia, long QT

25
Q

How do you treat/manage someone in cardiac arrest?

A
  • BSL - chest compression and external ventilation
  • ASL - defibrillation - electrical current delivered to the heart, depolarises all the cells at once (in refractory period) and allows coordinated electrical activity to restart
  • adrenaline - enhances myocardial function and increases peripheral resistance by acting on alpha-1 receptors leading to vasoconstriction
26
Q

What is distributive shock?

What can cause it?

A

Low resistance shock (normovolaemic shock)

Have profound peripheral vasodilation which leads to reduced TPR (the blood volume is constant but volume of circulation has increased)

Toxic shock or anaphylactic shock

27
Q

What is toxic shock? What are the haemodynamic effects?

A

Occurs due to sepsis which can lead to septic shock.

Endotoxins from circulation bacteria or chemokines and cytokines can result in profound vasodilation

  • fall in TPR
  • fall in arterial pressure
  • impaired perfusion of vital organs
  • capillaries become leaky so reduce blood volume
  • overtime, increased coagulation and localisation hypo-perfusion in extremities - ischaemia occurs
28
Q

What is the compensatory response to septic shock?

A
  • detection of decrease arterial pressure by baroreceptors
  • increased sympathetic output
  • vasoconstriction
  • HR and SV increase

However vasoconstriction is overridden by mediators of vasodilation

29
Q

How does a patient in septic shock present?

A
  • tachycardia

* warm, red extremities initially but later stages result in vasoconstriction and loacalised hypo-perfusion

30
Q

What is anaphylactic shock? And the haemodynamic effects? How is it so severe?

A

A severe allergic reaction due to histamine release from mast cells which leas to vasodilation leading to a fall in TPR

Vasodilation overrides vasoconstriction response, there cannot be impaired perfusion to vital organs

31
Q

How will someone with anaphylactic shock present?

A
  • difficultly breathing
  • collapse
  • rapid heart rate
  • red, warm extremities
32
Q

What is the treatment for anaphylactic shock?

A

Adrenaline which acts on alpha-1 adrenoceptors promoting vasoconstriction

  • when given pharmacologically activates alpha-1 receptors rather than the typical physiological activation of beta-2 receptors

CVS * (17 decks)

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