Session 11 Flashcards

1
Q

How do you calculate mean arterial blood pressure?

A

CO x TPR
SV x HR x TPR
diastolic pressure + 1/3 pulse pressure

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2
Q

How do you calculate cardiac output?

A

HR x SV

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3
Q

What is haemodynamic shock?

A

An acute condition of inadequate blood flow throughout the body - fall in arterial blood pressure leading to circulatory shock

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4
Q

What can cause haemodynamic shock?

A
  • Fall in cardiac output

- Fall in TPR beyond capacity of the heart to cope

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5
Q

What can cause shock due to fall in cardiac output?

A
  • Cardiogenic shock
  • Mechanical shock
  • Hypovolaemic shock
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6
Q

What is cardiogenic shock?

A

Pump failure where the ventricle cannot empty properly

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7
Q

What is mechanical shock?

A

An obstruction where the ventricle cannot fill properly - cardiac output drops (eg. cardiac tamponade)

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8
Q

What is hypovolaemic shock?

A

Loss of blood volume leading to poor venous return

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9
Q

What can cause cardiogenic shock?

A
  • Damage to LV during MI
  • Serious arrhythmias (heart block) - REDUCED HR
  • Profound tachycardia (not enough time to fill)
  • Acute deterioration of the heart
  • DECREASE IN STROKE VOLUME
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10
Q

What are the features of cardiogenic shock?

A
  • Normal or raised central venous pressure
  • Dramatic drop in arterial BP!!! (hallmark of haemodynamic shock)
  • Poor tissue perfusion
  • Poor kidney perfusion causing oliguria
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11
Q

What is the pulse pressure?

A

The difference between the diastolic and systolic pressure

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12
Q

How do you manage someone in cardiac arrest?

A
  • Basic life support (ventilation/compressions)
  • Advanced support
  • Adrenaline
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13
Q

What does defibrillation do?

A

Puts all cells into refractory period and allows coordinated activity to restart

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14
Q

What does adrenaline do in cardiac arrest?

A
  • Enhancing myocardial function

- Increasing peripheral resistance to manage cardiac output and therefore MABP

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15
Q

What is cardiac tamponade?

A

Blood or fluid buildup in pericardial space that will constrict the filling of the heart and limit EDV

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16
Q

What are the features of a cardiac tamponade?

A
  • High central venous pressure
  • Low arterial blood pressure
  • HR will increase to try and bring up BP
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17
Q

How can a pulmonary embolism cause mechanical shock?

A
  • Occludes a large pulmonary artery
  • High pulmonary pressure
  • Right ventricle unable to empty giving reduced blood return and filling to left heart (occlusion)
  • Left atrial pressure is low (less blood returned to the left side of the heart)
  • Arterial BP low
    = Shock due to low CO and SV
18
Q

How does an embolus reach the lungs?

A
  • DVT (most common)
  • Portion of thrombus breaks off and travels in venous system to the right side of the heart
  • Embolus is pumped out via the pulmonary artery to the lungs
  • Effect corresponds to the size of the embolus
19
Q

What is hypovolaemic shock?

A

Shock caused by reduced blood volume (20-30% of blood loss will cause some shocks signs, 30-40% serious shock), most likely due to HAEMORRHAGE

20
Q

How does haemorrhage cause hypovolaemic shock?*

A
  • Venous pressure falls
  • Cardiac output falls (Starling’s law)
  • Arterial BP falls as CO falls
  • Fall in arterial blood pressure detected by baroreceptors
21
Q

What is the compensatory response to hypovolaemic shock?*

A
  • Increased sympathetic stimulation to try and raise MABP
  • Therefore tachycardia
  • Increased force of contraction (steeper Starling’s curve)
  • Peripheral vasoconstriction (BP = CO x TPR)
  • Venoconstriction
22
Q

What else can cause hypovolaemic shock?

A
  • Severe diarrhoea/vomiting, loss of Na+

- Severe burns

23
Q

What are the signs and symptoms of hypovolaemic shock?

A
  • Tachycardia
  • Weak pulse (low SV)
  • Pale skin (peripheral vasoconstriction)
  • Cold and clammy extremities (peripheral vasoconstriction + sympathetic system)
  • Low central venous pressure (less blood in system)
24
Q

What are the complications of shock?*

A

Multi-organ failure due to severely reduced perfusion

25
Q

How do capillary pressures change in hypovolaemic shock?*

A

Normal: small net movement of fluid into tissues
- Re-enters via venous system by lymphatic drainage

REVERSED in SHOCK
- Very low hydrostatic pressure due to the hypovolaemia
- Arterioles constrict to maintain ABP = pressure in capillaries is therefore lower
= Net movement of fluid into capillary (reabsorption)

26
Q

What reduces hydrostatic pressure?

A
  • Hypovolaemia

- Arteriole constriction to maintain ABP causing a drop in capillaries as blood goes through the resistance

27
Q

What is an issue with peripheral vasoconstriction in hypovolaemic shock?

A

Impaired tissue perfusion = danger of DECOMPENSATION

  • Peripheral tissue damage due to hypoxia
  • Release of vasodilator chemical mediators that will overcome sympathetic nervous system - TPR falls
  • Blood pressure falls dramatically when TPR falls
  • Vital organs not perfused and so multi-system failure
28
Q

What are the longer-term responses to hypovolaemia?

A
  • Renin-angiotensin-aldosterone system
  • Anti-diuretic hormone that promotes water retention and rebuilding of the blood volume
  • Salt and water retention by kidneys promoted
29
Q

What is distributive shock?

A

Normovolaemic shock caused by low total peripheral resistance (blood volume stays constant but circulation volume has increased)

30
Q

What are examples of distributive shock?

A

Toxic shock and anaphylactic shock

31
Q

What is cardiac arrest?

A

Unresponsiveness associated with the lack of pulse due to the heart stopping or not pumping effectively

32
Q

What are the features of a cardiac arrest?

A
  • Asystole (no electrical and mechanical activity)
  • Pulseless electrical activity - no pulse, so no cardiac output (dissociation between electrical and mechanical activity)
  • Ventricular fibrillation (uncoordinated electrical activity, most common)
33
Q

What is toxic shock?

A

Sepsis: a life threatening response to infection that can lead to toxic shock

34
Q

How does toxic shock occur?

A
  • Endotoxins get released by circulating bacteria
  • Causes massive inflammatory response
  • Profound vasodilation so massive fall in TPR
  • Fall in arterial BP
  • Impaired organ perfusion
  • Leaky capillaries
  • Increased coagulation
35
Q

What is the definition of septic shock?

A

Persisting hypotension requiring treatment to maintain blood pressure despite fluid resuscitation

36
Q

What are the features of septic shock?

A
  • Decreased arterial blood pressure
  • Detected by baroreceptors and causing increased sympathetic output
  • Vasoconstriction effect > vasodilators
  • Higher HR and SV to increase CO
37
Q

What are the patient signs of septic shock?

A
  • Tachycardia
  • Warm, red extremities at first)
  • Then vasoconstriction so localised hypo-perfusion
38
Q

What is anaphylactic shock?

A

A severe allergic relation that causes the release of histamine from mast cells + other vasodilators

39
Q

How does anaphylaxis cause shock?

A
  • Inflammatory mediators are powerful vasodilators
  • Vasodilation = dramatic drop in TPR
  • Increased sympathetic response that cannot override vasodilators, so low arterial BP
  • Impaired vital organ perfusion
40
Q

Why do people in anaphylactic shock have difficulty breathing?

A

Local mediators also cause bronchoconstriction and laryngeal oedema

41
Q

What are the signs of anaphylactic shock?

A
  • Difficulty breathing
  • Collapse and syncope
  • Rapid heart rate (trying to get CO up)
  • Red and warm extremities due to vasodilation
42
Q

How is anaphylactic shock immediately treated?

A

Adrenaline (epipen)

  • Vasoconstriction via action of alpha 1 adrenoceptors
  • Builds the total peripheral resistance and therefore mean arterial blood pressure up