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Blood Lungs and Heart > Shock (Week 5) > Flashcards

Shock (Week 5) Flashcards

1
Q

Define Shock

A

Shock: is present when blood pressure or circulating blood volume falls to a level that results in inadequate oxygen supply to the tissues leading to cellular hypoxia and irreversible tissue injury.

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2
Q

Define decompensation

A

When the body is no longer able to maintain equilbrium with adjustment to other centres.

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3
Q

What treatment approach do you use when treating a patient with suspected shock?

A
  • DR ABCDE:
    • Danger
    • Response
    • Airways- high flow O2
    • Breathing - resp rate, inspect/palpate/percuss/auscultate
    • Circulation: fluid recuscitation, and assess peripheral perfusion (cold clammy vs dry warm), pulse (weak and thready vs bounding)
    • Disability - concious level assess GCS or AVPU (alert/ voice/ pain/ unconcious) in acute environment
    • Exposure/ everything else - causes? trauma/ bleeds/ concealed bleeds/ peripheral oedema
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4
Q

What are some of the urgent assessments for shock?

A
  • GCS or AVPU (Alert, Voice, Pain, Unresponsive)
  • BP
  • HR
  • Urine output
  • JVP
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5
Q

What two systems control the Blood pressure?

A

Hormonal/Humoral regulation

Neural regulation

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6
Q

List three factors involved in neural and hormonal control of BP

A

Humoral:

  1. Renin- angiotensin system
  2. Aldosterone
  3. ADH

Neural:

  1. Aortic and Carotid bodies
  2. Medullary cardiac and vasomotor centres
  3. Peripheral NS- both somatic (contraction skeletal muscle) and autonomic - Para S and Symp.
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7
Q

Describe how the RAAS system controls BP

A
  • Renin released from juxtaglomerular cells in the afferent arteriole of glomerulus
  • Renin released when:
    • Decrease in afferent arteriole BP detected by stretch
    • Decrease in NaCl at macula densa
    • SNS stimulation
  • Renin converts angiotensinogen from liver into AT1
  • AT1 converted into AT11 by ACE in pulm. capillaries
  • AT11 has multiple effects:
    • Blood vessels- acts directly as vasoconstrictor- increase SVR and BP
    • Hypothalamus- stimulates thirst and ADH release from posterior pituitary
    • Aldosterone release from adrenal cortex
    • SNS- stimulates SNS, +ve feedback on renin release
  • Kidney: insertion AQP’s in collecting duct and aldosterone upregulates Na/K ATPase/Enac, increase Na+ and H2O reabsorption- increase circulating fluid volume - increase BP
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8
Q

Describe neural control of BP

A
  • Aortic and carotid bodies respond to BP by stretch in vessel walls.
  • Both signal to cardiac and vasomotor areas of medulla
  • Carotid bodies more important than aortic bodies, signal via CN IX
  • Aortic bodies signal via CN X

Sudden increase in BP:

  • increased stretch, increased firing rate by aortic and carotid bodies
  • Increased inhibition on SNS output reducing sympathetic tone
  • Stimulation of vagal output and tone
  • Bradycardia and -ve inotropy - decreased CO
  • Vasodilation - decreased SVR
  • ↓ SVR and ↓ CO = ↓MABP

Sudden decrease in BP:

  • Decreased stretch, decreased firing and output to medulla
  • Decreased inhibition (disinhibition) on SNS, inhibition vagal tone
  • Tachycardia and +ve inotropy = increased CO
  • Vasoconstriction = increased SVR
  • ↑ SVR and ↑CO = ↑ MABP
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9
Q

Describe autoregulation of blood flow and how this relates to shock

A
  • Autoregulation refers to the intrinsic ability of body tissues/organs to regulate their own blood flow in response to changes in perfusion pressure
  • ↑ in perfusion pressure leads to vasoconstriction and ↓ in flow.
  • ↓ in perfusion pressure leads to vasodilation and ↑ in flow.
  • Autoregulation can only occur over a certain range of perfusion pressures
  • Below a certain perfusion pressure cannot increase flow anymore as vessels are already maximally dilated
  • In shock- continued decline in perfusion pressure leads to decrease in flow and tissue hypoxaemia and injury.
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10
Q

What are the two equation for MABP?

Which one directly relates to shock?

A

MABP= CO x SVR (relates to shock)

MABP = 2/3 systolic P + 1/3 diastolic P

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11
Q

List three mechanisms of shock

A

MABP = CO X SVR

  1. Loss CO- pump failure- cardiogenic shock
  2. Loss of SVR- afterload failure- vasodilatory or distributive shock
  3. Loss of fluid volume- preload failure- Hypovolaemic shock
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12
Q

Define vasodilatory/ distributive shock

What can cause it?

What is its compensation?

A

Vasodilatory/ distributive shock is shock caused by the redistribution of body fluid

Generally caused by: Increase in vascular permeability leading to loss of intravascular fluid into the extravascular space OR extensive vasodilation leading to peripheral pooling of blood.

Causes:

1) Sepsis and SIRS - ↑ vasodilation and vascular permeability

2) Anaphylaxis- release histamine, ↑ vasodilation and vascular permeability

3) Loss SNS output (Neurogenic shock) - Loss symp tone, vasodilation and peripheral pooling of blood.

4) Drug overdose

Compensation: ↑ CO (tachycardia) and ↑ SVR (vasconstriction)

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13
Q

Define Cardiogenic Shock

What can cause it?

How is it compensated?

A

Cardiogenic shock is shock caused by inability of the heart to circulate blood.

Causes:

  • Cardiac tamponade (compression/ pericardial disease)
  • MI - myocardial damage ( muscle, valves, conduction system)
  • ACS -Insufficient blood supply O2
  • Arrhythmias
  • Outflow obstruction PE

Compensation: ↑ SVR , tachycardia

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14
Q

Define Hypovolaemic shock

What can cause it?

How is it compensated?

A

Hypovolaemic shock is shock caused by insufficient circulating blood volume. (Loss of more than 20%)

Causes:

  • Trauma: Blunt and Penentrating
    • External haemorrhage
    • Internal haemorrhage - Upper GI bleed/ liver/ spleen/ intrabdominal
  • Vomiting
  • Diarrhoea
  • Polyuria

Compensation: ↑ HR (tachycardia) ↑ Stroke volume

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15
Q

What are three phases of shock?

A
  1. Compensatory phase
  2. Progressing phase
  3. Decompensation/ irreversible phase
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16
Q

Describe initial compensation of shock

A
  • Activation of neurohormonal response to maintain vital organ perfusion
  • Sympathetic NS stimulation to increase HR (tachycardia) and vasoconstriction
  • Peripheral vasoconstriction to maintain blood flow to vital organs (brain and heart):
    • Constriction of precapillary bed to reduce hydrostatic pressure and favour reabsorption tissue fluid into circulation
17
Q

Describe how shock progresses

A
  • Worsening hypotension leads to worsened hypoperfusion of tissues and organs
  • Hypoxaemia in tissues leading to anaerobic respiration
  • Lactic acid production –> Acidosis
  • Worsening tachypnea (acidosis) and reversal of pre capillary constriction:
    • Loss of precapillary constriction, increase hydrostatic pressure and net filtration into tissues, less volume in blood
    • stasis blood in capillary bed
  • Cerebral hypoxia leads to altered mental status
18
Q

Describe decompensation in shock

A
  • With prolonged hypotension –> Loss of SNS activation and compensation:
    • Desensitisation of adreno Receptors and depletion neurotransmitters
    • Loss of vasoconstriction - decrease SVR worsens shock
    • Loss of constriction of precapillary bed- hydrostatic pressure increase and net filtration into tissue fluid, decreasing blood volume more.
    • Stasis of blood in capillary bed
  • Inadequate blood supply to heart:
    • ischaemia and decreased CO
    • Worsens shock
  • Inadequate blood supply to brain:
    • Autonomic dysfunction- loss of SNS output worsens shock
  • Hypoxia induced Cell necrosis:
    • Inflammation increasing vasodilation and permeability worsens shock
  • Multiple organ failure and death
19
Q

What blood pressure is seen in shock?

What issues are there with one of the definitions of shock BP?

A
  • systolic BP < 90 mmHg or MABP less than 65 mmHg
  • 20 mmHg less than normal
  • Issue is in young and fit may have normal BP
  • May not know normal if elderly, on medication, young, fit, pregnant
20
Q

Fill out blanks: Hypovolaemic Shock

Prime problem: ?

Compensation: ?

Consequence: ?

Clinical features: ? (8)

A

Hypovolaemic shock

Prime problem:

  • Inadequate circulating volume leading to
  • Fall in CO (↓ EDV and therefore SV)

Compensation:

  • SNS activation- tachycardia and ↑SVR via vasoconstriction

Consequence: Hypotension

Clinical features:

  • Weak thready pulse
  • Tachycardia
  • Tachypnoea
  • Peripheral vasoconstriction:
    • Cold, clammy peripheries
    • Empty veins
    • Slow cap refill
  • ↓ Pulse pressure in decompensation stage
21
Q

Fill out the blanks: Cardiogenic Shock:

Prime problem: ?

Compensation: ?

Further complications: ?

Clinical features:? (10)

A

Cardiogenic shock:

Prime problem: ↓ CO- inability of the heart to effectively circulate blood volume

Compensation: ↓ BP activates SNS, ↑SVR - vasoconstriction

Further complication: ↓ CO leads to back up into the heart, back up into venous system

Clinical features:

  • Pulse: Weak, thready
  • Tachycardia
  • Peripheral vasoconstriction:
    • Cold clammy peripheries
    • Poor capillary refill time
  • Bibasal crackles due to pulmonary oedema ( left sided back up)
  • Dysponea
  • Distended neck veins and ↑JVP
  • Hepatomegaly
  • Peripheral oedema
22
Q

Fill out blanks: Vasodilatory / Distributive shock

Primary problem: (2 methods)

Consequence:

Compensation:

Clinical features: (5)

Main 3 types:

A

Vasodilatory/ Distributive Shock:

Primary problem: Redistribution of intravascular fluid either by 1) vasodilation and pooling of blood 2) increased vascular permeability and movement of intravascular fluid to extravascular space

Consequence: Hypotension

Compensation: ↑ SNS activation ↑ HR (tachycardia)-↑ CO

Clinical features:

  • Tachycardia
  • Warm dry peripheries
  • fast capillary refill
  • Bounding pulse
  • full veins

Main 3 types:

1) Neurogenic- loss of SNS vasoconstriction
2) Septic shock - Systemic inflammatory response leading to ↑ vasodilation and ↑vascular permeability
3) Anaphylactic shock- Systemic inflammatory response to allergen leading to ↑ vasodilation and ↑vascular permeability

23
Q

Fill the blanks

A

Blood Lungs and Heart (24 decks)

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