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Applied physiology and pharmacology > Shock and critical illness > Flashcards

Shock and critical illness Flashcards

1
Q

Signs of shock

A

Rapid and weak pulse (tachycardia with reduced stroke volume)

Mean arterial pressure may be reduced or normal, but pulse pressure reduced

Breathing is rapid and shallow

Urine output is reduced

There may be reduced mental awareness or confusion

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2
Q

Hypovolemic shock

A

Inadequate filling

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3
Q

Hypovolemic shock causes?

A

Haemorrhage, diarrhoea, vomiting, third space losses (burns)

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4
Q

Cardiogenic shock

A

Inadequate cardiac output

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5
Q

Cardiogenic shock causes

A

Stroke volume: MI, myocarditis, Takotsubo (stress induced cardiomyopathy)

Bradycardia

Tachyarrhythmias

Acute valve rupture

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6
Q

Distributive shock

A

Excessive vasodilatation

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7
Q

Distributive shock causes

A

Septic

Anaphylactic

Neurogenic

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8
Q

Obstructive shock causes

A

Cardiac tamponade
PE
IVC obstruction

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9
Q

Changes to Guyton graph in hypovolemic shock

A

CVP volume line lower on the graph, therefore intersects the starling curve at a lower CO (reduced blood supply)

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10
Q

How does hypovolemic shock affect CO?

A

Reduced preload therefore reduced contractility via the Frank-Starling mechanism

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11
Q

Fall in pressure leads to what immediate response

A

Reduction in baroreceptor and cardiopulmonary receptor activity - removes inhibitory impulses to the NTS - increase in sympathetic outflow

Increase in circulating vasoactive hormones (adrenaline, noradrenaline).

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12
Q

Effect of increasing the sympathetic outflow in hypovolemic shock

A

Myocardial contractility permits greater SV at lower filling pressure and increased HR - CO raised.

Higher starling curve means intersects with hypovolemic line at same CO as non hypovolemic (with normal starling)

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13
Q

Kidney response to falling blood pressure

A

Kidneys act like a high pressure baroreceptor: fall in pressure -pressure natriuresis, release of renin for raised levels of angiotensin II.

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14
Q

What happens to ADH in shock

A

Increased release of ADH (if >10-15% fall in ECV)

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15
Q

Effect of RAAS

A

Vasoconstriction - increased tone to capacitance vessels and retention of salt and water.

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16
Q

If blood loss is less than 15%..

A

Compensated haemorrhage

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17
Q

As perfusion falls what happens to chemoreceptors?

A

Hypoperfusion and hypoxia - carotid bodies ‘stagnant hypoxia’ - activates the chemoreceptors.

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18
Q

What as well as ‘stagnant hypoxia’ activates the chemoreceptors?

A

Anaerobic conditions -pyruvate generated from glycolysis channels into lactic acid cycle (pyruvate is converted to lactate) - type-A lactic metabolic acidosis (pH <7.35)

19
Q

What is the response to the fall in pH and chemoreceptor activation?

A

Chemoreceptor activation contributes to the sympathetic activation (above) also targets the NTS - increase phrenic nerve firing and increase ventilation rate

20
Q

How does hyperventilation compensate for metabolic acidosis?

A

Through loss of volatile acid CO2 (respiratory loss)

21
Q

Vasculature in shock

A

Vasoconstricted (to raise afterload)

22
Q

What happens to body fluid after hours in hypovolemic shock?

A

Absorption of interstitial fluid into depleted circulation

23
Q

What allows fluid to move from the interstitium to the circulation?

A

Fall in venous pressure and sympathetic mediated rise in postcapillary resistance ratio lowers the capillary BP - (lower than interstitium) net absorption across the capillary wall

24
Q

How is the patient stabilised with hypovolemic shock?

A

Fluid resuscitation: Isotonic glucose, isotonic saline, blood

25
Q

Best fluid to give to patient? Why

A

Blood ideal as due to proteins, it will remain in the plasma

26
Q

How does cardiogenic shock affect the frank starling curve?

A

Frank-starling curve flattening, reduced flow/CO for the same CVP.

27
Q

How to ‘counteract’ cardiogenic shock?

A

Venoconstrict

Increase blood volume

28
Q

What does the body view cardiogenic shock as?

A

Hypovolemic shock, reduced blood supply/pressure to the baroreceptors and kidney

29
Q

Levels of … can diagnose HF

A

BNP

30
Q

Left sided heart failure cause

A

Ischaemic damage to the heart and severe hypertension and atherosclerosis increase afterload, reduces efficiency and cardiac output. Hypertrophy of LV reduces cardiac perfusion and cardiac filling.

31
Q

Right sided heart failure cause

A

High blood pressure in the pulmonary arteries increases the workload of the right ventricle. Over time, this causes the right ventricle to fail, this can be induced secondary to LVF.

Right ventricular weakness, back up in vena cava and extremities.

32
Q

Signs of RHF

A

Ascites and enlarged liver/spleen. Raised CVP, distended jugular veins. Dependent oedema plus reduced oncotic pressure resulting from fluid retention by the kidneys

33
Q

Signs of LHF

A

Left ventricle hypertrophy.

Pulmonary oedema and pleural effusion. Apex beat displaced to the left (left ventricular dilation)

34
Q

Sepsis 6

A

Sepsis 6: give oxygen, give IV fluids, antibiotics, take blood culture, serum lactate and urine output measurement

35
Q

Anaphylactic treatment

A

Adrenaline, O2, iv fluids, im/iv chlorphenirame, im/iv hydrocortisone

36
Q

Heart failure reduce fluid retention?

A

Loop diuretics

37
Q

Heart failure improve afterload?

A

ACE inhibitors, nitrates, ARB

38
Q

Heart failure improve contractility?

A

Inotropes, dobutamine, milrinone, levosimendan

39
Q

Mechanical haemodynamic support?

A

Intra-aortic balloon pump

40
Q

What is septic shock initially characterized by?

A

A fall in peripheral vascular resistance

41
Q

What does widespread poor perfusion of some tissues lead to?

A

Metabolic acidosis

42
Q

Septic shock has a high mortality often caused by

A

Renal failure

43
Q

As heart failure progresses to shock, treat with

A

Adrenoreceptor agonist

44
Q

Long term beta blocker treatment may cause?

A

Transient postural hypotension

Applied physiology and pharmacology (18 decks)

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