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Anaesthetics > Shock > Flashcards

Shock Flashcards

1
Q

Shock is when the circulatory system fails to deliver sufficient oxygen to tissues to meet basic tissue energy demands. State the 4 pathophysiological mechanisms that lead to shock along with the main mechanism leading to shock in each

A

Distributive shock (64%) - Reduced systemic vascular resistance and altered O2 extraction
Hypovolemic shock (16%) - Reduced cardiac output
Cardiogenic shock (16%) - Reduced cardiac output
Obstructive shock (2%) - Reduced cardiac output

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2
Q

What is the formula of cardiac output?’
What is the formula for MAP?

A

CO = SV (stroke volume) x HR
MAP = CO x SVR (systemic vascular resistance)

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3
Q

What are the 3 factors that control each SV and SVR, giving the one factor in each that treatment targets

A

SV: Governed by preload (stretching of myocardial cells), myocardial contractility, and afterload. Trick here there are 2: You can control the preload by increasing venous return as well as contractility via inotropes. These very same inotropes are what control vasoconstriction to increase SVR to preserve BP (but reduces perfusion)
SVR: Vessel length, blood viscocity, and vessel diameter. Controlled by vasopressors (noradrenaline)

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4
Q

What is stroke volume based on?

A

Stroke volume is based on the volume of blood pumped out by the LV in one contraction => dependent on Preload (Frank Starling). No questions on Frank starling so use this image

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5
Q

What is the most common type of distributive shock? Give 3 others
How is Cardiac output in this type of shock?
Briefly explain how each leads to shock

A

Most common = Septic Shock. Others include Anaphylactic, Neurogenic, and adrenal insufficiency
Cardiac output in Distributive shock is typically increased (unlike all other types) but is still insufficient to maintain perfusion (altered oxygen extraction)
Sepsis: -> Cytokine release from infection leading to inflammation => vasodilation and capillary leak => shock
Anaphylaxis: First exposure causes IGE formation. The second exposure leads to mast cells and basophils releasing histamine => inflammation => vasodilation and capillary leak
Neurogenic: Spinal cord injury => SNS damage => vasodilation and bradycardia
Adrenal insufficiency: reduced cortisol => reduced alpha-1 receptors on arterioles => no vasoconstriction => vasodilation

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6
Q

What is considered hyperlactatemia?

A

Hyperlactatemia = lactate >1.5mmHg

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7
Q

Explain the mechanism at which hypovolemic shock occurs

A

Hemorrhage or extreme fluid loss leads to extreme volume loss => reduced BP => SNS activated => increased HR, contractility, and vasoconstriction => vasoconstriction causing reduced perfusion to maintain BP => oxygen demand > oxygen delivery => anaerobic resp => lactic acidosis (>1.5mmol/L) and tissue ischemia

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8
Q

What is being referred to when they say “valvular insufficiency”?

A

Valvular insufficiency = valves not working properly => regurgitation for example

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9
Q

What are the causes for cardiogenic shock?

A

MI or valvular insufficiency

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10
Q

Explain the mechanism at which cardiogenic shock occurs

A

Myocardial ischemia, caused by either MI or valvular insufficiency => LV dysfunction => reduced myocardial contractility (reduced stroke volume) => reduced CO => Myocardial ischemia (vicious cycle)

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11
Q

What are the causes of Obstructive shock?
Explain the mechanism at which each cause leads to obstructive shock

A

Pulmonary Embolism: Obstruction to RV flow (due to embolism) => reduced LV preload => reduced SV => reduced CO
Cardiac Tamponade: Rigid pericardium => reduced LV filling => reduced CO
Tension pneumothorax: Obstruction of great vessels due to pressure => reduced venous return => reduced LV filling => reduced CO

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12
Q

Shock may appear differently in different people due to variation in causes of shock, physiological compensatory mechanisms (age), etc… How might a patient on a beta blocker present differently from someone who is not in the context of shock?

A

They will present the same way however the the patient on a beta blocker may not have tachycardia due to the medication.

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13
Q

What BP would we consider to be in shock?

A

SBP <90 or 40mmHg below baseline

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14
Q

What is considered reduced urine output in adults?

A

<0.5ml/kg/hr
Normal is 1ml/kg/hr

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15
Q

Give all the signs of shock

A

Hemodynamic: 3
Hypotension (SBP <90 or 40mmHg below baseline)
Tachycardia
Tachypnea

Clinical signs: 3
Skin: Cold/clammy skin/cyanosis/mottling (except initially in distributive/septic shock)
Kidney: Urine output <0.5ml/kg/hr (common as medulla has high energy demand => renal failure)
Brain: Altered mental status (anxiety, confusion, agitation)

Biochemical signs: 2
Metabolic acidosis
Hyperlactatemia (>1.5mmol/L)

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16
Q

Shock is one of the major causes of end-organ damage acutely. Many emergencies such as sepsis, diarrhea, and anaphylaxis may all lead to shock leading to this. How does the CNS system present end-organ dysfunction?

A

Encephalopathy

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17
Q

What is encephalopathy?

A

From ChatGPT:
Encephalopathy is a term used to describe a broad range of brain dysfunctions, often characterized by altered mental status, confusion, cognitive impairment, or changes in behavior caused by various underlying conditions such as infections, metabolic abnormalities, liver dysfunction, or toxic exposures. It reflects a global brain dysfunction that can manifest as a spectrum of neurological symptoms, ranging from mild confusion to severe impairment, impacting an individual’s cognitive and neurological function. Identification of the underlying cause is crucial in managing encephalopathy, as treatments focus on addressing the specific condition triggering the brain dysfunction

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18
Q

Shock is one of the major causes of end-organ damage acutely. Many emergencies such as sepsis, diarrhea, and anaphylaxis may all lead to shock leading to this. How does the cardiovascular system present end-organ dysfunction?

A

Tachy/brady arrhythmias, myocardial ischemia (cardiogenic shock), respiratory depression (silent chest)

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19
Q

Shock is one of the major causes of end-organ damage acutely. Many emergencies such as sepsis, diarrhea, and anaphylaxis may all lead to shock leading to this. How does the Respiratory system present end-organ dysfunction?

A

Hypoxia, ARDS, hypercapnia

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20
Q

Shock is one of the major causes of end-organ damage acutely. Many emergencies such as sepsis, diarrhea, and anaphylaxis may all lead to shock leading to this. How does the Renal system present end-organ dysfunction?

A

Pre-renal failure => acute tubular necrosis due to injury from reduced perfusion => reduced urine output (<0.5ml/kg/hr)
Take it like this, reduced perfusion in kidney due to medulla needing a lot of energy => earlier sign. This will cause necrosis in the tubules => acute tubular necrosis

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21
Q

Shock is one of the major causes of end-organ damage acutely. Many emergencies such as sepsis, diarrhea, and anaphylaxis may all lead to shock leading to this. How does the GI system present end-organ dysfunction?

A

Reduced motility => constipation
Pancreatitis
Stress ulceration (erosions that may occur via sepsis, shock or stress!)
Gut ischemia => increased intestinal permeability to bacteria and endotoxins
Acalculous cholecystitis

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22
Q

Shock is one of the major causes of end-organ damage acutely. Many emergencies such as sepsis, diarrhea, and anaphylaxis may all lead to shock leading to this. How does the Hepatic system present end-organ dysfunction?

A

Ischemic hepatitis
Intrahepatic cholestasis

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23
Q

Shock is one of the major causes of end-organ damage acutely. Many emergencies such as sepsis, diarrhea, and anaphylaxis may all lead to shock leading to this. How does the metabolic system present end-organ dysfunction?

A

Hyperglycemia (glycogenolysis, gluconeogenesis)
Hypertriglyceridemia
(hypoglycemia as well?)

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24
Q

Quick hx! Shock

A

Recent illness? Fever? (distributive)
Chest pain? SOB? (cardiogenic/obstructive)
Trauma (hypovolemic)
GI losses (hypovolemic)
Abdominal pain (hypovolemic/distributive)
Immunocompromised => steroids, transplant, chemo, HIV, splenectomy (septic/distributive)
Medications
Recent hospitilizations

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25
Q

What is the normal INR in people not on an anticoag? How much would be elevated?
On an anticoag?
What type of shock may directly raise this?

A

No anticoag <1.1 elevated would be >1.5
Anticoag => between 2 and 3
Septic shock specifically may raise this

26
Q

Investigations for shock. (think of causes and go)
When you get good, start thinking of possible results of these tests and what they will show you

A

Bedside:
ECG => arrythmias/ST segment changes => cardiogenic shock
Urinalysis (dipstick) => Nitrites/blood/protein/leukocytes => septic shock
Blood glucose => Altered glucose metabolism

Lab:
Serum lactate => hypovolemic? This just indicates systemic hypo perfusion but hyperlactatemia typically seen in hypovolemic shock first due to vasoconstriction
RFT/LFTs => for end-organ damage
Cardiac enzymes (troponin and BNP) to determine myocardial damage from myocardial ischemia in cardiogenic shock
FBC with differentials => reduced Hb in hemorrhage, increased WCC in sepsis, Thrombocytopenia (may be cause of bleeding)
Coag studies (INR/PT and aPTT times) => coagulopathy or also raised in septic shock
ABG
D-Dimer (PE)
Blood cultures/urine cultures/lavage
Other imaging e.g. CT angio can be used based on etiology

27
Q

You are asked to see a patient in ED who is in a very unstable condition and can deteriorate at any moment. As you begin taking a history you notice that it is likely further deterioration is imminent. What questions would you ask him?

A

AMPLE History when no time for full history
Allergies
Medications
Past medical history (pertinent)
Last meal
Events surrounding presentation

28
Q

What is the adult dose for IM adrenaline?

A

0.5mg

29
Q

When giving fluids, in how much time do you want a 500ml bolus to be infused?

A

<15 minutes ideally

30
Q

What are the signs of fluid overload?

A

Very important especially with pulmonary oedema and cardiogenic shock as well as patients with HF (who will have pulmonary oedema)

Peripheral oedema (hands and feet/ankle)
Hypertension
Cramping/headaches
Bilateral crepitations (+/- wheeze) with increased RR
reduced SpO2

31
Q

You are conducting an ABCDE assessment on a patient with anaphylactic shock. While examining them, you notice that their capillary refill time is 4 seconds. What is your intervention?

A

Hartmann’s solution same as saline => 500ml bolus and reassess

32
Q

You are conducting an ABCDE assessment on a 31 year old patient with shock. While examining them, you notice a stridor. What is your likely diagnosis and intervention?

A

Anaphylactic shock. Confirm with hives, urticaria, or tongue swelling. Ensure patent airway. If not go for head-tilt/jaw thrust or intubation (keep in mind RSI) and administer 0.5mg IM adrenaline

33
Q

You are conducting an ABCDE assessment on a 31 year old patient with anaphylactic shock. Initial resuscitation is complete and the patient is relatively stable. What is your next step?

A

Antihistamine Chlorphenamine IV 10mg
Steroid Hydrocortisone IV 200mg

34
Q

You are conducting an ABCDE assessment on a 31 year old patient with shock. They are on a non-rebreather mask with SPO2 at 93% but was at 98% 5 minutes ago. Once arriving to step D, you find that the patient flexes their arm to pain, responds to your voice yet only mumbles. What is your GCS score and your next step?

A

GCS: 3/4, 2/5, 3/6 =>8
Check airway if still secure, if not, GCS <9 => intubate
Switch to Bag mask ventilation also cuz of low GCS score

35
Q

You are conducting an ABCDE assessment on a 31 year old patient with shock. They have asymmetrical breathing with hyper resonance unilaterally on the left side and are tripoding. What is your most likely diagnosis? What type of shock?

A

left sided pneumothorax => obstructive shock

36
Q

You are conducting an ABCDE assessment on a 31 year old patient with shock. They have bilateral creps and wheeze. Give 2 likely diagnoses

A

Pulmonary oedema
Pneumonia

37
Q

You are conducting an ABCDE assessment on a 31 year old patient with shock. They only have a wheeze bilaterally heard throughout. Give the most likely diagnosis and a differential

A

Anaphylactic shock
Life-threatening asthma

38
Q

You are conducting an ABCDE assessment on a 31 year old patient with shock. They have bilateral creps and wheeze, no fever. You notice their RR is 44/min.
What is your diagnosis?
What are we concerned about?
What part of the management should we be very cautious with?

A

Pulmonary oedema
With a high RR (>40), it is a very strong predictor of an imminent cardiac arrest which is exacerbated significantly by the presence of pulmonary oedema
Fluid should be cautiously given in these cases as giving more fluid will worsen the pulmonary oedema making the cardiac arrest more likely

39
Q

You are conducting an ABCDE assessment on a 31 year old patient with shock. They have bilateral creps and wheeze, no fever. You notice their RR is 28/min. They have a capillary refill time of 4s. What is your next step
What co-morbidity is important to consider?

A

Pulmonary oedema but RR<28 so not very imminent threat of cardiac arrest but fluid overload may precipitate it regardless =>
Give IV saline but 250ml increments and assess for fluid overload (look at peripheries for swelling)
HF is an important comorbidity as it might make it harder. Clinical judgement and asking for senior help is paramount

40
Q

You are conducting an ABCDE assessment on a 31 year old patient with shock. You notice they have normal temperature peripheries despite their state. What is your most likely diagnosis?

A

Distributive shock specifically septic shock which is initially warm before becoming cold in late sepsis

41
Q

Define Occult

A

Hidden, not easily observed

42
Q

You are conducting an ABCDE assessment on a 31 year old patient with shock. They have a history of a RTA. You cannot find the source of the bleeding to localize and control it. What is your next step and name 5 areas you will check for occult bleeding.

A

If the patient is hemodynamically stable, CT
If the patient is not => FAST POCUS (point of case ultrasound) => operating theatre immediately
If bleeding is not directly found, look at these areas
1) Pelvis
2) Long bones
3) Pleural space
4) Peritoneal space
5) Retroperitoneum

43
Q

What is the goal of fluid resus in sepsis?

A

> 30ml/kg of fluid bolus (saline) in first hour

44
Q

How can you assess Pre-load optimization

A

This is done by inserting a central venous catheter into the internal jugular vein and passing it to the SVC to assess central venous pressure (1) or to the pulmonary artery bifurcation for pulmonary artery wedge pressure (2)

45
Q

What are indications to stop giving fluids? (as in switch to maintenance fluids in an emergency)

A

Evidence of fluid overload (peripheral oedema, hypertension etc…)
Patient resuscitated/Pre-load optimized

46
Q

You are conducting an ABCDE assessment on a 31 year old patient with shock. Central venous pressure is consistent with pre-load optimization and Cap refill time is still 3.5 and HR is still elevated with MAP of 49 despite giving adequate fluids. What is your next step? What is your target?

A

Target vitals + MAP >65mmHg
If fluid resus is not sufficient and pre-load has been optimized, we are left with vasopressors (noradrenalin, vasopressin)

47
Q

What is SvO2?

A

Mixed venous oxygen saturation

48
Q

What are the 4 phases of treatment (also goals of treatment) in Shock

A

1) Salvage: Obtain SBP >90 (normotension) AND perform life-saving measures (e.g. PCI)
2) Optimization: Provide adequate O2 AND optimize CO, SvO2 and Lactate
3) Stabilization: Organ support AND minimize complications
4) De-escalation: Wean from vasoactive agents (not just vasopressors) AND achieve -ve fluid balance (fluid out > fluid in) => back to normal

49
Q

What is the gold standard diagnosis of cardiogenic shock

A

Coronary angiography (catheter inserted in arm and contrast injected)

50
Q

The role of POCUS (point of care US) in hemorrhagic shock and trauma is evident. What is the role of POCUS in cardiogenic shock

A

It is most useful here as it can identify cardiogenic shock that will worsen with treatment (as in fluid overload leading to pulmonary oedema and cardiac arrest). This will differentiate it from the much more common septic/distributive shock which needs an increased amount of fluid resus (>30ml/kg in first hour)

51
Q

You are conducting an ABCDE assessment on a 60 year old patient with Cardiogenic shock. They have a known history of Mitral regurgitation. What revascularization therapy would you recommend? What are other indications for that intervention. Why is this the preferred therapy in these cases?

A

Usually PCI is the preferred method of revascularization therapy but in this case CABG (coronary artery bypass graft) is the better surgery because of ease of access to also repair the defect/valve problem.
Indications: Mitral regurgitation or septal rupture (not sure how this applies to other valves)

52
Q

What do you give during fibrinolytic therapy. Class and specific name

A

tissue plasminogen activator - Alteplase

53
Q

You are conducting an ABCDE assessment on a 60 year old patient with Cardiogenic shock. They had an MI 3 hours ago. You have allocated him to have PCI (percutaneous coronary intervention) after performing a coronary angiogram but 80 minutes later and it is still unavailable what is your next step.

A

The cutoff is 90 minutes. I would refer to senior help and if granted, I will administer fibrinolytic therapy (alteplase - tpa)

54
Q

You are conducting an ABCDE assessment on a 60 year old patient with Cardiogenic shock. A colleague suggests giving the patient a beta blocker. You refuse, why?

A

Betablockers are withheld in the acute setting due to chance of worsening cardiogenic shock by reduced HR.

55
Q

You are conducting an ABCDE assessment on a 60 year old patient with Cardiogenic shock. What is your full management plan?

A

Withhold Beta blocker
1)Dual Antiplatelet therapy + DOAC => Aspirin and clopidogrel/tecagrelor + Apixiban/Dabigitran
2) Revascularization therapy => Coronary angiography followed by PCI.
If unable to complete within 90 minutes, begin fibrinolysis therapy with Alteplase
3) Treat hypovolemia with caution (250ml boluses) and monitor regularly for fluid overload
If unable to resuscitate despite giving fluids and optimizing preload, give vasopressor (NA)
4) If all else fails, Mechanical circulatory support (IABP, VAD, ECMO)

56
Q

You are conducting an ABCDE assessment on a 60 year old patient with Cardiogenic shock. They deteriorate and you go through the management plan but nothing seems to work. They are in the operating theatre. The decision as to what to do next is not clear but the consultant thinks a transplant is whats best. What mechanical circulatory support would you opt to?

A

Ventricular assist device as this can be used as a bridge therapy as the future management plan is finalized

57
Q

Give a brief explanation to each of the 3 types of mechanical circulatory support

A

1) IABP: Catheter is inserted via femoral artery into the descending aorta. It is inflated to occlude 90% of the lumen during diastole to improve perfusion in the coronary arteries (remember that they are perfused based on the backflow of blood into the opening right after the aortic valve). It is deflated during systole to provide increased flow due to the vacuum force the deflation creates
2) Ventricular assist device: (like a walking dialysis machine) Carries blood out of the heart and is then pumped to either the aorta or pulmonary artery (like in the name it is assisting the ventricles in contracting). This acts as a bridge therapy AKA waiting for something such as transplantation or bridge to recovery…
3) ECMO (extracorporeal membrane oxygenation): Similar to CABG as it is a bypass. Blood is pumped outside the heart to an oxygenator which will ventilate the blood and then a pump will send the blood back into the tissues.

58
Q

There are 2 types of ECMO. What are they? What are they used for?

A

Venovenous can be used outside the theatre and is used to provide respiratory support
Venoarterial is used in the theatre and gives both respiratory support and hemodynamic support (oxygenation)

59
Q

During anaphylactic shock, you give 2 doses of IM adrenaline and it doesnt seem to work. What will you do next?

A

Call for help from an intensivist or anesthesiologist to administer IV adrenaline or continuous adrenaline IV

60
Q

Why do we use hartmann’s solution in anaphylactic shock

A

There can be massive fluid shift in anaphylactic shock. This solution is better at rebalancing the electrolytes especially potassium

61
Q

You are conducting an ABCDE assessment on a 12 year old with anaphylactic shock. They are now better 2 hours after coming in. What should be done until discharge?

A

Continue providing supportive care and continue to observe the patient for 4 hours following last administration of adrenaline.
They must be discharged with an individualized management plan, an adrenaline autoinjector and a followup with an allergist.

62
Q

You are conducting an ABCDE assessment on a 60 year old patient with Hypovolemic shock following an RTA. They are deteriorating very quickly and have lost 2L of blood so far. The team hasnt had time to cross-check blood. What will you do?

A

Give immediate transfusion of un-crossmatched blood until cross-matched blood becomes available

Anaesthetics (6 decks)

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