Physiology and management of shock

Question 1

What is shock?

Answer 1

Condition of inadequate perfusion to sustain normal organ function

Question 2

What are the 5 main classes of shock?

Answer 2

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

Question 3

What can cause hypovolemic shock?

Answer 3

Blood loss
Interstitial fluid loss
Pure water deficit (rare)

Question 4

How does the baroreceptor reflex compensate for hypovolemic shock?

Answer 4

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

Question 5

How will sympathetic output compensate for hypovolemic shock?

Answer 5

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

Question 6

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

Answer 6

Reduced capillary hydrostatic pressure

Inward net filtration

Question 7

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

Answer 7

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

Question 8

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

Answer 8

Heart rate
Stroke volume (inotropy)
Both

Question 9

What does the frank starling relationship state?

Answer 9

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

Question 10

What effect will inotropy have on the frank starling curve?

Answer 10

Increased contility; curve shift upwards

Question 11

Why will a failing heart result in pulmonary congestion?

Answer 11

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

Question 12

What are some tips surrounding fluid prescribing?

Answer 12

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

Question 13

What can cause cardiogenic failure?

Answer 13

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

Question 14

What are the clinical signs of cardiogenic shock?

Answer 14

Poor forward flow; hypotension/ shock, fatigue, syncope

Backpressure; pulmonary oedema, elevated JVP, hepatic congestion

Question 15

What physiological mechanisms will increase inotropy?

Answer 15

Sympathetic nervous system

Question 16

How can we pharmacologically increase inotropy?

Answer 16

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

Question 17

Should you give fluids in cardiogenic shock?

Answer 17

No; will likely result in pulmonary congestion

Fluids will shift the frank starling curve to the right

Question 18

How is cardiogenic shock managed?

Answer 18

Inotropic agents

Inotropes will shift the frank starling curve upwards

Question 19

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

Answer 19

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

Question 20

What phase of the cardiac cycle will obstructive shock affect?

Answer 20

Filling rather than ejection

Question 21

How is obstructive shock treated?

Answer 21

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

Question 22

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

Answer 22

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

Question 23

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

Answer 23

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

Question 24

What is the physiology of distributive shock?

Answer 24

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

Question 25

What are the 3 main subtypes of distributive shock?

Answer 25

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

Question 26

What is the benefit of testing lactate levels in sepsis?

Answer 26

Detect hypoperfusion before hypotension occurs

Question 27

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

Answer 27

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

Question 28

What is the mainstay of treatment for anaphylactic shock?

Answer 28

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

Question 29

What test is performed to confirm the diagnosis of anaphylaxis?

Answer 29

Serum mast cell tryptase

Question 30

What are the clinical features of neurogenic shock?

Answer 30

Hypotension due to loss of sympathetic tone | Inappropriate bradycardia due to unopposed vagal tone

Question 31

What should you NOT do in someone with neurogenic shock?

Answer 31

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

Question 32

What is the mainstay of treatment for neurogenic shock?

Answer 32

Dopamine/ NA | Vasopressors/ inotropes

Question 33

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

Answer 33

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

Question 34

Why is recoil so important in CPR?

Answer 34

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

Question 35

Describe high quality CPR

Answer 35

``` 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 ```

Question 36

What are the ECG findings for hyperkalaemia?

Answer 36

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

Question 37

What is the treatment for hyperkalaemia?

Answer 37

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

Question 38

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

Answer 38

T wave; can put them into VF

Question 39

What waveform capnography is aimed for in resuscitation?

Answer 39

ETCO2 3.0 kPa during CPR associated with good prognosis

Question 40

What is end tidal CO2?

Answer 40

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

Question 41

What can be done to reduce transthoracic impedance?

Answer 41

``` Energy selected Electrode size Distance between electrodes Size of chest Hirsute chest shaven Good electrode contact ```

Question 42

What is transthoracic impedance?

Answer 42

Body's resistance to current flow

Question 43

What is normal human impedance?

Answer 43

Varies from 25-180 ohms

Question 44

What is the unit of measurement of transthoracic impedance?

Answer 44

Ohms

Question 45

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

Answer 45

``` Body mass Age Disease Skin resistance Tissue type and amount ```

Question 46

What are the shockable cardiac arrest rhythms?

Answer 46

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

Question 47

What is the other name for polymorphic VT?

Answer 47

Torsade De Pointes

Question 48

What drugs are recommended in shockable cardiac arrest?

Answer 48

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

Question 49

What are the non-shockable cardiac arrest rhythms?

Answer 49

Asystole; absent QRS activity, P waves may persist | PEA; clinical features of cardiac arrest, ecg assoc with output

Question 50

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

Answer 50

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

Question 51

What are the clinical signs of tension pneumothorax?

Answer 51

Decreased breath sounds Hyper-resonant percussion Tracheal deviation

Question 52

What are the ways to secure an airway in CPR?

Answer 52

Supraglottic; LMA, i-gel Tracheal tube Intubation

Question 53

What does the PR interval represent?

Answer 53

Delay of AV node to allow filling of ventricles

Question 54

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

Answer 54

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

Question 55

What features of bradycardia increase the risk of asystole?

Answer 55

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

Question 56

What is the treatment for regular broad QRS complexes?

Answer 56

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

Question 57

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

Answer 57

AF with BBB | Pre-excitable AF

Question 58

What is the treatment for regular narrow QRS complex tachycardia?

Answer 58

Vagal maneuvers | Adenosine 6mg rapid IV bolus

Question 59

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

Answer 59

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

Question 60

What scoring systems are used in AF?

Answer 60

CHa2DS2VASc score for thromboembolic risk | HAS-BLED score for bleeding risk

Question 61

What is the rate controlling drugs used in AF?

Answer 61

Beta blocker | Use CCB in patients whom beta blockage is CI

Question 62

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

Answer 62

Heart failure

Question 63

What drugs are used for rhythm control in AF?

Answer 63

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

Question 64

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

Answer 64

Adenosine, diltiazem, verapamil, digoxin | Block AV node and can cause a relative increase in pre-excitation