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CLASP - Sudden Death > Physiology and management of shock > Flashcards

Physiology and management of shock Flashcards

1
Q

What is shock?

A

Condition of inadequate perfusion to sustain normal organ function

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2
Q

What are the 5 main classes of shock?

A

Hypovolaemic; loss of circulating volume resulting in reduced preload and cardiac output
Cardiogenic; myocardial dysfunction causing reduction in systolic function and cardiac output
Obstructive; physical obstruction to the filling of the heart; reduced preload and cardiac output
Distributive; significant reduction in SVR beyond the compensatory limits of increased cardiac output
Cytotoxic; uncoupling of tissue oxygen delivery and mitochondrial oxygen uptake

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3
Q

What can cause hypovolemic shock?

A

Blood loss
Interstitial fluid loss
Pure water deficit (rare)

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4
Q

How does the baroreceptor reflex compensate for hypovolemic shock?

A

Sense stretch in cartoid sinus (CN 9) and aortic arch (CN 10)
Decreased stretch results in decreased afferent input to medullary CV centers via CN 9
Inhibit parasympathetic outflow resulting in increased sympathetic output

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5
Q

How will sympathetic output compensate for hypovolemic shock?

A

Sympathetic chronotropy and inotropy
Release of vasoconstrictors; adrenaline, angiotensin, NA, vasopressin
Redirects fluid from peripheral and sensory organs
Resulting lactic acidosis drives chemoreceptors to enhance the response
Circulating vasodilators will increase in the decompensatory stages

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6
Q

How will capillary absorption of interstitial fluid compensate for hypovolemic shock?

A

Reduced capillary hydrostatic pressure

Inward net filtration

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7
Q

How will the hypothalamo-pituitary-adrenal response compensate for hypovolaemic shock?

A

Intrarenal baroreceptors mediate renin release from JGA
Resulting angiotensin 2 enhances vasoconstriction and ADH secretion
Enhances renal reabsorption of sodium and water

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8
Q

Very simplistically, what are the 3 ways to increase cardiac output?

A

Heart rate
Stroke volume (inotropy)
Both

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9
Q

What does the frank starling relationship state?

A

The greater the end diastolic volume (preload), the greater the ventricular ejection in systole and therefore the greater the SV

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10
Q

What effect will inotropy have on the frank starling curve?

A

Increased contility; curve shift upwards

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11
Q

Why will a failing heart result in pulmonary congestion?

A

Decreased contractility of heart
EDV will increase to maintain SV
Backwards pressure resulting in pulmonary congestion

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12
Q

What are some tips surrounding fluid prescribing?

A

Remember its a drug
Consider the individual patient
Consider fluid AND electrolyte requirements
Consider difference between resuscitation and maintenance fluids

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13
Q

What can cause cardiogenic failure?

A 
Acute MI 
Valve dysfunction; acute mitral prolapse 
Myocarditis 
Cardiomyopathy
Myocardial contusion
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14
Q

What are the clinical signs of cardiogenic shock?

A

Poor forward flow; hypotension/ shock, fatigue, syncope

Backpressure; pulmonary oedema, elevated JVP, hepatic congestion

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15
Q

What physiological mechanisms will increase inotropy?

A

Sympathetic nervous system

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16
Q

How can we pharmacologically increase inotropy?

A

Beta and dopaminergic stimulation
Dobutamine, adrenaline
Dopamine, dopexamine
Milrinone/ levosimendan

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17
Q

Should you give fluids in cardiogenic shock?

A

No; will likely result in pulmonary congestion

Fluids will shift the frank starling curve to the right

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18
Q

How is cardiogenic shock managed?

A

Inotropic agents

Inotropes will shift the frank starling curve upwards

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19
Q

What is the function of an intra-aortic balloon pump?

A

Counter pulsation
Inflation during ventricular diastole (augmented diastole) to increase coronary artery filling
Deflation during ventricular systole to reduce afterload and reduce oxygen demand of the heart

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20
Q

What phase of the cardiac cycle will obstructive shock affect?

A

Filling rather than ejection

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21
Q

How is obstructive shock treated?

A

PE; anticoags +/- thrombolysis
Tamponade; pericardial drainage
Tension pneumothorax; decompression and chest drainage

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22
Q

What are the ultrasound appearances of a massive PE resulting in obstructive shock?

A

Dilated, hypokinetic RV
Bowing of interventricular septum
Hyperkinetic RV at apex (McConnells sign)

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23
Q

What are the ultrasound appearances of a cardiac tamponade resulting in obstructive shock?

A

Fluid accumulation in pericardial sac
Compressess each chamber
Impaired cardiac filling and contraction

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24
Q

What is the physiology of distributive shock?

A

Vasodilatory
Initially, high cardiac output but insufficient to maintain forward perfusion due to massive dilation of vessels
Then, due to reduced venous return, cardiac output will fall

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25
Q

What are the 3 main subtypes of distributive shock?

A

Septic; bacterial endotoxin mediated capillary dysfunction
Anaphylactic; mast cell release of histaminergic vasodilators
Neurogenic; loss of sympathetic outflow following spinal injury

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26
Q

What is the benefit of testing lactate levels in sepsis?

A

Detect hypoperfusion before hypotension occurs

27
Q

In terms of treatment of sepsis, what has changed from sepsis 6?

A

Early use of vasopressors to improve perfusion and minimize excessive fluid volumes (30ml/kg)
As a general rule, when you’re putting up the 3rd bag of fluids, call for help for administration of vasopressors

28
Q

What is the mainstay of treatment for anaphylactic shock?

A

Adrenaline; acts as both a vasoconstrictor and a mast cell stabiliser
500 micrograms IM

29
Q

What test is performed to confirm the diagnosis of anaphylaxis?

A

Serum mast cell tryptase

30
Q

What are the clinical features of neurogenic shock?

A

Hypotension due to loss of sympathetic tone

Inappropriate bradycardia due to unopposed vagal tone

31
Q

What should you NOT do in someone with neurogenic shock?

A

Exacerbate vagal tone, there will be no compensatory sympathetic measures
This includes suction down ET tube or a PR exam

32
Q

What is the mainstay of treatment for neurogenic shock?

A

Dopamine/ NA

Vasopressors/ inotropes

33
Q

What are the 8/9 reversible causes of cardiac arrest?

A 
4 (5) Hs: 
Hypovolaemia
Hypoxia
Hypothermia
Hypo/ hyperkalaemia
Hypoglycaemia 
4 Ts: 
Tension pneumo
Tamponade (cardiac) 
Thrombosis (MI or PE)
Toxins
34
Q

Why is recoil so important in CPR?

A

Cyclical changes in intrathoracic pressure alternately push blood out and suck blood into the chest during recoil

35
Q

Describe high quality CPR

A 
30:2 
Center of chest
5-6 cm depth with recoil
2 per second 
Continuous when airway secures 
Switch CPR provider every 2 min to avoid fatigue
36
Q

What are the ECG findings for hyperkalaemia?

A 
Peaked T waves 
Flattened P wave 
Prolonged PR 
Depressed ST segment
Prolonged QRS 
Sine-wave pattern (peri-arrest)
37
Q

What is the treatment for hyperkalaemia?

A

10mls 10% calcium gluconate
Insulin; actrapid 10 units with 50ml 50% dextrose
Salbutamol nebs

38
Q

In terms of manual defibrillation, what section of the cardiac cycle should you NOT shock at?

A

T wave; can put them into VF

39
Q

What waveform capnography is aimed for in resuscitation?

A

ETCO2 3.0 kPa during CPR associated with good prognosis

40
Q

What is end tidal CO2?

A

End tidal CO2 (EtCO2) is the maximum expired carbon dioxide concentration during a respiratory cycle.

41
Q

What can be done to reduce transthoracic impedance?

A 
Energy selected
Electrode size
Distance between electrodes
Size of chest
Hirsute chest shaven
Good electrode contact
42
Q

What is transthoracic impedance?

A

Body’s resistance to current flow

43
Q

What is normal human impedance?

A

Varies from 25-180 ohms

44
Q

What is the unit of measurement of transthoracic impedance?

A

Ohms

45
Q

What is the cause of human to human variation in transthoracic impedance?

A 
Body mass
Age
Disease
Skin resistance
Tissue type and amount
46
Q

What are the shockable cardiac arrest rhythms?

A

VF; bizarre irregular waveform, no recognizable QRS, random frequency and amplitude
pVT; broad complex rhythm, rapid rate, constant QRS morphology

47
Q

What is the other name for polymorphic VT?

A

Torsade De Pointes

48
Q

What drugs are recommended in shockable cardiac arrest?

A

After 3rd shock;
Adrenaline 1mg IV
Amiodarone 300mg IV

49
Q

What are the non-shockable cardiac arrest rhythms?

A

Asystole; absent QRS activity, P waves may persist

PEA; clinical features of cardiac arrest, ecg assoc with output

50
Q

What drugs are recommended in non-shockable cardiac arrest rhythms?

A

Adrenaline 1mg IV at start then every 3-5 mins

51
Q

What are the clinical signs of tension pneumothorax?

A

Decreased breath sounds
Hyper-resonant percussion
Tracheal deviation

52
Q

What are the ways to secure an airway in CPR?

A

Supraglottic; LMA, i-gel
Tracheal tube
Intubation

53
Q

What does the PR interval represent?

A

Delay of AV node to allow filling of ventricles

54
Q

What is the treatment for symptomatic bradycardia (shock, syncope, MI, heart failure)?

A

Atropine 500 mcg IV, can be repeated up to a max of 3mg

Transcutaneous pacing

55
Q

What features of bradycardia increase the risk of asystole?

A

Recent asystole
Mobitz type 2 AV block
Complete heart block with broad QRS
VEntricular pause >3s

56
Q

What is the treatment for regular broad QRS complexes?

A

VT; amiodarone 300mg IV over 20 -60mins then 900mg over 24 hours

57
Q

What are the causes for irregular broad QRS complexes - hemodynamically stable?

A

AF with BBB

Pre-excitable AF

58
Q

What is the treatment for regular narrow QRS complex tachycardia?

A

Vagal maneuvers

Adenosine 6mg rapid IV bolus

59
Q

If a patient has been in AF for more than 48 hours, what is the treatment?

A

Should NOT be treated by cardioversion (electrical or chemical) until they have been fully anticoagulated for at least 3 weeks
If cardioversion required urgently, give LMWH or IV heparin followed by a continuous infusion to maintain APPT at 1.5-2x reference control value

60
Q

What scoring systems are used in AF?

A

CHa2DS2VASc score for thromboembolic risk

HAS-BLED score for bleeding risk

61
Q

What is the rate controlling drugs used in AF?

A

Beta blocker

Use CCB in patients whom beta blockage is CI

62
Q

In what patients is digoxin or amiodarone considered for rate control in AF?

A

Heart failure

63
Q

What drugs are used for rhythm control in AF?

A

Chemical cardioversion; flecainide (do not use in established heart failure, known left ventricular impairment or IHD or prolonged QTc)
Amiodarone can be used (unless QTc prolonged) but less likely to achieve prompt cardioversion

64
Q

What drugs should be avoided in patients with WPW and AF?

A

Adenosine, diltiazem, verapamil, digoxin

Block AV node and can cause a relative increase in pre-excitation

CLASP - Sudden Death (6 decks)

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