CVS 11 Flashcards

(81 cards)

1
Q

What is the definition of shock?

A

acute circulatory failure with inadequate or inappropriately distributed tissue perfusion

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2
Q

What defines the mean arterial pressure?

A

the average pressure driving blood into tissues throughout the cardiac cycle - reflects tissue perfusion pressure, not just the “average” of systolic and diastolic values

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3
Q

How is the mean arterial pressure calculated?

What is the normal MAP value and what is the minimum required value for vital organ perfusion?

A

normal MAP: 70-100
minimum required: >60 mmHg

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4
Q

What are the 4 types of shock?

A

hypovolaemic

mechanical

cardiogenic

distributive

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5
Q

What are the different types of hypovolaemic shock?

A
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6
Q

How does loss of blood volume lead to hypovolaemic shock?

A
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7
Q

What is the compensatory mechanism for hypovolaemic shock?

A
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8
Q

What causes hypovolaemic shock?

A

a loss of blood or fluid volume e.g haemorrhages, burns, dehydration - leading to decreased mean arterial pressure and poor tissue perfusion

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9
Q

What initially happens when MAP decreases?

A

the body detects the drop in pressure via baroreceptors and chemoreceptors, triggering sympathetic nervous system activation

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10
Q

What are the main physiological responses to decreased MAP?

A
  • increase in sympathetic activity
  • increase in renin release (RAAS activation)
  • increased ADH release
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11
Q

Following a detection in reduced MAP, what does increased sympathetic activity do?

A

causes vasoconstriction -> increases TPR

increases HR and contractility

stimulates renin release from the kidneys

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12
Q

What is the main role of renin in hypovolaemic shock?

What occurs after?

A

renin converts angiotensinogen -> angiotensin I which is later converted to angiotensin II by ACE

angiotensin II:
- causes systemic vasoconstriction which increases TPR
- stimulates aldosterone release from the adrenal cortex

aldosterone:
- promotes sodium and water reabsorption and potassium excretion in the kidneys -> increases blood volume and pre-load

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13
Q

What triggers ADH release in hypovolaemia? What does ADH then do?

A

baroreceptors in the carotid sinus and aortic arch sense low pressure -> stimulate ADH secretion from posterior pituitary

ADH then causes water retention in the kidneys and increases blood volume and preload

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14
Q

During compensation for hypovolaemic shock, what factors help with water retention - what does this do?

What helps with vasoconstriction - what does this do?

A

water retention: ADH released after low MAP is detected via carotid sinus and aortic sinus baroreceptors = INCREASES PRE-LOAD

vasoconstriction: ANGIOTENSIN II after renin was released due to low MAP detection via JGA baro/chemoreceptors = INCREASE TPR

sodium and water retention: ALDOSTERONE from RAAS = increase PRE-LOAD

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15
Q

How can hypovolaemic shock lead to multi-system organ failure?

A

via DECOMPENSATED SHOCK

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16
Q

What happens during the initial compensatory stage of hypovolaemic shock?

A

sympathetic nervous system and angiotensin II cause widespread vasoconstriction, maintaining blood pressure and perfusion to vital organs

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17
Q

What is the main effect of prolonged vasoconstriction?

A

peripheral organs receive less blood flow, leading to tissue hypoxia and metabolic acidosis due to anaerobic metabolism

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18
Q

Why does metabolic vasodilation occur in shock?

A

Hypoxic tissues release metabolic vasodilators (like adenosine, CO₂, lactic acid), causing vasodilation and a reduction in total peripheral resistance (TPR)

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19
Q

What happens to total peripheral resistance (TPR) during metabolic vasodilation?

A

TPR falls, which reduces mean arterial pressure (MAP) and compromises perfusion to vital organs

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20
Q

What is meant by circulatory collapse?

A

When TPR and MAP drop, blood flow to vital organs (like the brain and heart) becomes inadequate, leading to decompensated shock

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21
Q

What marks the transition from compensated to decompensated shock?

A

the loss of vasoconstrictor control and onset of metabolic vasodilation, causing falling MAP and organ hypoperfusion

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22
Q

What causes irreversible shock?

A

prolonged hypoxia and acidosis damage capillaries and endothelium, leading to fluid leakage, tissue injury, and organ failure that persist even if BP is restored

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23
Q

Can tissue damage in irreversible shock be reversed by restoring blood pressure?

A

No. By this stage, cell death and metabolic derangement are too severe to recover from, even with normalised BP

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24
Q

How can a prolonged reduced MAP lead to irreversible shock? Explain the steps.

A
  1. INITIAL COMPENSATION
    - sympathetic NS and angiotensin II = widespread vasoconstriction
  2. PROLONGED VASOCONSTRICTION
    - peripheral organs receive less blood flow -> tissue hypoxia -> met acidosis
  3. METABOLIC VASODILATION
    - hypoxic tissues release metabolic vasodilation -> vasodilation -> reduced TPR
  4. CIRCULATORY COLLAPSE
    - TPR falls -> MAP falls -> inadequate vital organ perfusion -> decompensated shock
  5. IRREVERSIBLE SHOCK
    - prolonged hypoxia -> capillary damage, endothelial damage -> even if BP is restored, tissue injury and acidosis may prevent recovery
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25
List the signs and symptoms of hypovolaemic shock.
26
What is the management for hypovolaemic shock?
27
How are mechanical shocks caused? What do they lead to?
they are caused by physical obstruction to blood flow in the heart or great vessels, leads to reduced venous return or cardiac output, despite normal myocardial contractility
28
What are the two types of mechanical shock? List 2 examples of each.
obstruction to filling - PE - tension pneumothorax - SVC obstruction restriction to filling - cardiac tamponade - constrictive pericarditis
29
A PE can lead to what kind of shock? Explain the steps/pathophysiology.
MECHANICAL SHOCK
30
How does a PE cause a reduction in pre-load? What does that then lead to?
PE blocking pulmonary artery so RV cannot empty properly so it builds up on the right side of the heart = causes increased right sided pressure and reduced forward flow in pulmonary circulation less blood leaves the RV = less blood reaches the lung -> less blood returns to the left ATRIUM LV receives less venous return = EDV aka pre-load DECREASES LESS EDV -> LESS SV -> LESS MAP -> INADEQUATE PERFUSION OF VITAL ORGANS
31
List the signs and symptoms of PEs.
32
List 3 things which you would do in the management of PEs.
1. ABCDE assessment 2. oxygen 3. thrombolysis - anticoagulation long term
33
What kind of shock would a cardiac tamponade cause? Explain the pathophysiology.
MECHANICAL
34
What is a cardiac tamponade?
a life-threatening condition where fluid, blood or air accumulates in the pericardial sac - because the pericardium is stiff and inelastic, even a small volume increase causes a rise in intra-pericardial pressure = this pressure compresses all cardiac chambers especially during diastole = HEART CANNOT FILL PROPERLY
35
How would a cardiac tamponade lead to multi-organ failure if left untreated? Explain it step by step.
1. CARDIAC TAMPONADE = fluid/blood builds up in the pericardial space 2. RISE IN INTRA-PERICARDIAL PRESSURE 3. COMPRESSION OF ALL CARDIAC CHAMBERS 4. REDUCED VENTRICULAR FILLING = REDUCED EDV = REDUCED SV = REDUCED MAP 5. LOW MAP = REDUCED PERFUSION OF VITAL ORGANS -> MULTI-ORGAN FAILURE IF UNTREATED
36
What are the causes of cardiac tamponades?
37
What types of fluid can end up in the pericardial sac and result in a cardiac tamponade?
serous: from HF or low albumin serosanguinous: trauma or malignancy inflammatory: pericarditis, infection
38
How can blood end up in the pericardial sac and cause a cardiac tamponade?
trauma e.g stab wound, surgery aortic dissection e.g rupture post-MI ventricular wall rupture
39
What is the name for air in the pericardial sac? How can this occur?
pneumopericardium rare but can occur in trauma, mechanical ventilation
40
What are chronic causes of cardiac tamponades?
post-MI (dressler's syndrome) post radiation pericarditis hypoproteinaemia
41
What is Beck's triad and what are its components?
medical term referring to a collection of three signs that indicate cardiac tamponade: - low blood pressure - distended neck veins (jugular venous distension) - muffled or distant heart sounds
42
List 4 symptoms and 4 signs of a Cardiac Tamponade.
43
What is the name of the set of three classic signs of cardiac tamponade?
beck's triad
44
What 2 things would you do in the management of a cardiac tamponade?
1. ABCDE assessment 2. pericardiocentesis
45
What type of shock is caused by a fall in contractility which results in the ventricles not being able to empty properly?
cardiogenic shock
46
What is cardiogenic shock? What two things cause it?
shock caused by a fall in contractility so the ventricles are unable to empty properly: - reduced stroke volume i.e pump failure - veinous congestion IMPAIRED CONTRACTILITY - muscle failure IMPAIRED ELECTRICAL CO-ORDINATION - rhythm failure
47
In regards to cardiogenic shock, list 3 causes of impaired contractility and 3 causes of impaired electrical co-ordination.
48
How can cardiogenic shock lead to a decrease in tissue perfusion?
49
Explain what occurs as a mechanism of compensation in cardiogenic shock.
low MAP detected: 1. increase in SYMPATHETIC nervous system activity -> NORADRENALINE released -> acts on b1 adrenoreceptors = increased HR and contractility + acts on a1 adrenoreceptors = increase vasoconstriction - INCREASE HR + INCREASE CONTRACTILITY = INCREASE CO - INCREASED SYSTEMIC VASOCONSTRICTION = INCREASES TPR 2. RAAS activated (JGA cells sensed low perfusion) -> water and sodium retention -> increases PRE-LOAD 3. ADH RELEASED (carotid and aortic sinus arch sensed low perfusion) -> water retention -> INCREASES PRE-LOAD
50
How can decompensated cardiogenic shock lead to multi-system failure?
INCREASED DEMAND + IMPAIRED FILLING = INADEQUATE PERFUSION OF VITAL ORGANS -> MULTI-SYSTEM FAILURE
51
List 4 symptoms and 4 signs of cardiogenic shock.
52
List 4 things you would do in the management of cardiogenic shock.
1. ABCDE assessment 2. oxygen if hypoxaemic 3. aid perfusion pressure i.e specialist care; vasopressor - noradrenaline, inotrope - dobutamine 4. fix underlying cause e.g PCI, pacing, surgery
53
What shock is caused by severe, inappropriate vasodilation and loss of vascular tone?
distributive shock
54
What is distributive shock caused by? There is a marked reduction in __1__ and circulating volume is __2__.
caused by severe, inappropriate vasodilation and loss of vascular tone 1. TPR 2. maldistributed
55
List 3 things which can cause distributive shock.
sepsis anaphylaxis neurogenic
56
Sepsis and anaphylaxis are what kind of shocks?
distributive shocks
57
What is the pathophysiology of septic shocks?
58
List 4 signs of septic shock.
tachycardia hypotension warm peripheries: early sign, progresses to cold later pyrexia
59
How would you manage septic shock?
ABCDE assessment early recognition: sepsis 6 bundles
60
What is the pathophysiology of anaphylactic shocks?
61
List 5 signs of anaphylactic shock. How would you manage this? List 2 things.
1. ABCDE assessment 2. IM adrenaline
62
List 2 rhythms which are shockable. List 2 rhythms which are non-shockable.
shockable: - pulseless VT - VF non-shockable: - asystole - PEA
63
What is this rhythm? Is it shockable?
pulseless VT - yes
64
What is this rhythm? Is it shockable?
VF - yes
65
What are the reversible causes which should be investigated when someone is having a cardiac arrest? (4 Hs and 4 Ts)
66
What are the two main types of cardiovascular sensory receptors involved in BP regulation?
baroreceptors - detect pressure/stretch chemoreceptors - detect chemical changes like o2, co2 and pH
67
Where are the baroreceptors located?
in the carotid sinus - at the bifurcation of the common carotid artery and the aortic arch
68
What type of receptors are baroreceptors and what do they sense?
they are mechanoreceptors that sense stretch of the vessel wall, reflecting changes in blood pressure (MAP)
69
What happens to baroreceptor firing when blood pressure falls?
firing rate decreases, which signals the medulla oblongata to increase sympathetic activity and decrease parasympathetic tone - raising HR, contractility and vasoconstriction
70
What neurotransmitter is released during increased sympathetic activity and what receptor does it act on?
norepinephrine - acts on b1 receptors in the heart = increased HR and contractility and acts on a1 receptors in blood vessels (vasoconstriction)
71
Where are the chemoreceptors located?
in the carotid bodies (near the carotid sinus) and aortic sinus (near the aortic arch)
72
List 2 conditions which have a systolic murmur. List 2 conditions which have a diastolic murmur. Mention their character and where they are best heard.
systolic: - mitral regurgitation: blowing, pansystolic, APEX - aortic stenosis: harsh, crescendo-decrescendo, 2nd ICS right diastolic: - aortic regurgitation: high-pitched decrescendo, L sternal border - mitral stenosis: low-pitched, rumbling, APEX
73
A 74-year-old man presents with chest pain, shortness of breath on exertion, and occasional fainting spells. On examination, you feel a slow-rising pulse and hear a harsh systolic murmur radiating to the neck. What is the most likely diagnosis?
aortic stenosis
74
A 68-year-old man complains of fatigue, palpitations, and breathlessness when lying flat. He has a displaced apex beat, and you hear a pansystolic murmur at the apex radiating to the axilla. What is the likely diagnosis?
mitral regurgitation
75
A 60-year-old man presents with palpitations, fatigue, and a thumping heartbeat he can feel in his chest and neck. He has a collapsing pulse and a high-pitched early diastolic murmur at the left sternal edge, best heard leaning forward. What is the likely diagnosis?
aortic regurgitation
76
A 45-year-old woman reports breathlessness, occasional blood-streaked sputum, and palpitations. She has a malar flush and a low-pitched, rumbling mid-diastolic murmur at the apex, preceded by an opening snap. What is the likely diagnosis?
mitral stenosis
77
What causes mitral regurgitation? List 4 symptoms and 4 signs.
backflow of blood from LV to LA during systole -> volume overload in LA and LV = dilation and pulmonary congestion symptoms: - dyspnoea - fatigue - palpitation - orthopnoea signs: - displaced, diffuse apex beat (volume overload) - pansystolic, blowing murmur at apex -> radiates to axilla - soft S1, S3 gallop may be present - signs of LHF
78
What causes aortic stenosis? List 4 symptoms and 4 signs.
79
What causes aortic regurgitation? List 4 symptoms and 4 signs.
80
What causes mitral stenosis? List 4 symptoms and 4 signs.
81
What pathophysiological mechanisms occur in distributive shock?
widespread vasodilation with normal blood volume