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Critical care - Management of shock Flashcards

1
Q

What is shock

A

State of cellular and tissue hypoxia

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2
Q

Causes of shock (Hint: Oxygen d___, c____, u____

A

reduced oxygen delivery

increased oxygen consumption

inadequate oxygen utilization

or a combination of these processes

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3
Q

What does cellular hypoxia result in?

A

Cell membrane ion pump dysfunction, intracellular edema, leakage of intracellular
contents > extracellular space, inadequate regulation of intracellular pH

Results ultimately in acidosis, endothelial dysfunction, stimulation of inflammatory and anti-inflammatory cascades

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4
Q

Is shock reversible?

A

Shock is initially reversible, but must be recognized and treated immediately to prevent progression to irreversible organ dysfunction

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5
Q

What is “undifferentiated shock”?

A

situation where the shock is recognised but the cause is unclear

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6
Q

Stages of shock

A
  1. Initial
  2. Compensatory
  3. Progressive
  4. Refractory
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7
Q

4 stages of shock - initial

A
  • Body switches from aerobic to anaerobic metabolism
  • Elevated lactic acid level
  • Subtle changes in clinical signs (tachycardia, modest change in SBP)
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8
Q

4 stages of shock - compensatory

A

Sympathetic nervous system stimulated –> increase catecholamine (adrenaline, noadrenaline) release –> cardiac contractility

Neurohormonal response: vasoconstriction and blood shunted to vital organs

Aldosterone released + urine output (<30ml/hr)

Increased heart rate

Increased glucose levels

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9
Q

4 stages of shock - progressive

A
  • Electrolyte imbalance
  • Metabolic acidosis
  • Respiratory acidosis
  • Peripheral oedema
  • Irregular tachyarrhythmias
  • Hypotension
  • Pallor
  • Cool and clammy skin
  • Altered level of consciousness

start inotropes/vasopressors in the progressive stage

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10
Q

4 stages of shock - refractory

A

Irreversible cellular and organ damage

Impending death

Anuria and acute renal failure develops

Acidemia further depresses CO

Hypotension becomes severe, often RESISTANT TO IONOTROPES

Multi organ failure(MOF) and death follows

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11
Q

Types of shock

A
  1. Cardiogenic shock
  2. Hypovolemic shock
  3. Distributive shock
  4. Obstructive shock
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12
Q

Types of shock - Cardiogenic shock

A

Due to myocardium dysfunction:
- Myocardial pump failure following MI

Due to cardiac conduction system dysfunction:
- Brady/tachy arrythmia, VF, VT, heart block

Due to valvular dysfunction:
- Acute insufficiency
- Decompensated stenosis

In summary: due to impaired cardiac output

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13
Q

Types of shock - Hypovolemic shock

A

Due to loss of blood:
- Hemorrhagic, non-traumatic (PPH)
- Traumatic hemorrhage

Due to loss of body fluids:
e.g. excessive vomiting/diarrhoea

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14
Q

Types of shock - Distributive shock

A

No loss of fluid or blood. Infection releases cytokines which cause vasodilatation and leaking of capillaries where plasma goes into interstitial space –> volume in blood vessels decrease –> hypotension

Characterized by severe peripheral vasodilation, as Sympathetic system is not
able to maintain the tone of blood vessels

  • Septic shock
  • Anaphylactic shock
  • Neurogenic shock (bradycardia is unique to neuro shock!!)
  • Endocrine shock
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15
Q

Types of shock - Obstructive shock

A

Something is obstructing the cardiac output –> heart cannot pump effectively –> shock

  • Pulmonary embolism
  • Cardiac tamponade
  • Hemothorax
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16
Q

2 methods of compensatory mechanisms

A
  1. Sympathetic nervous system
  2. Activation of the RAAS (Renin angiotensin aldosterone system)

Note: both aims to maintain BP & tissue perfusion

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17
Q

Compensatory mechanism - Sympathetic nervous system

A
  1. Maximization of cardiac output (thru baroreceptor
    activation)
    - Increase in HR + Increase in contractility (SV)
    - Increased sympathetic tone causes vasoconstriction –> increases venous return –> increase preload = Increase in CO
  2. Maintain adequate circulating volume
    - Increased sympathetic tone –> arteriolar vasoconstriction –> redistribution of blood flow to vital organs
  3. Stimulation of adrenal gland
    - Secretion of adrenaline, noradrenaline and
    cortisol
    - Aids in augmenting arteriolar and venous tone –> vasoconstriction
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18
Q

Compensatory mechanism - Activation of RAAS

A
  1. Renal protective actions
    - Detect hypoperfusion, aldosterone stimulates secretion of angiotensin II
    - Angiotensin II preferentially constricts the efferent
    arteriole to maintain GFR and prevent pre-renal AKI
  2. Maintaining adequate circulating volume
    - Aldosterone stimulates cells in the collecting
    tubules of the kidney to increase sodium reabsorption –> improves cardiac output
    - Angiotensin II causes vasoconstriction by acting on vascular endothelial cells
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19
Q

Compensated vs uncompensated shock observations - Neuro

A

Compensated:
- Alert, oriented
- +/- Irritability

Uncompensated:
- Altered mental status
- Obtunded (less than a stupor, more than lethargy)

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20
Q

Compensated vs uncompensated shock observations - Cardio

A

Compensated:
- Tachycardia

Uncompensated:
- Tachycardia, Hypotension (MAP <60)

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21
Q

Compensated vs uncompensated shock observations - Respi

A

Compensated:
- Tachypnea
- Increased work of
breathing(WOB)

Uncompensated:
- Tachypnea
- Decreased spO2
- ARDS

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22
Q

Compensated vs uncompensated shock observations - Renal/GU

A

Compensated:
- Decreased urine output (<0.5ml/kg/h)

Uncompensated:
- Prerenal azotemia
- Metabolic acidosis
- Anuria (no urine)

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23
Q

Compensated vs uncompensated shock observations - GI

A

Compensated:
- Nausea
- Anorexia

Uncompensated:
- Absence/Hypoactive bowel sounds
- Ischemic bowel

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24
Q

Compensated vs uncompensated shock observations - Endocrine

A

Compensated:
- Hyperglycemia

Uncompensated:
- Hypoglycemia

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25
Q

Compensated vs uncompensated shock observations - Integumentary

A

Compensated:
- Warm extremities w/ normal cap refill

Uncompensated:
- Cold extremities w/ slow cap refill

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26
Q

Compensated vs uncompensated shock observations - Labs

A

Compensated:
- Decreased venous PO2

Uncompensated:
- Elevated lactate

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27
Q

What is the diagnostic criteria for SIRS (systemic inflammatory response syndrome)

A

Presence of ≥ two of the following criteria:
- 36C < Temp > 38C
- RR > 20/min OR PaCO2 < 32mmHg
- HR > 90 bpm
- 4000/mm3 < WBC > 12000/mm3 or > 10% bands
- Bands > 10%

28
Q

How to diagnose shock?

A
  1. Labs (to determine degree of end organ perfusion)
    - lactate > 2mmol
    - renal panel: AKI as evidenced by creatinine
    - liver function tests (transaminitis suggests ischemic hepatitis)
    - troponin: raised with MI
    - ABG/VGB
  2. Point of care ultrasound (POCUS) studies: test of choice for undifferentiated shock patient
    - focused assessment with sonography for trauma (FAST) + echocardiography
    - Rapid ultrasound in shock (RUSH)
29
Q

General management of shock - Airway + Breathing

A
  • Provide supplemental O2 to avoid complications of hypoxemia

Consider advanced airway manoeuvres if
- Patient requires airway protection
- Severe HD compromise
- Hypercapnic respiratory failure
- Hypoxemic respiratory failure

30
Q

General management of shock - Circulation

A

Establish vascular access + blood samples for testing
(2 large-bore proximal peripheral IV)

Begin immediate hemodynamic monitoring: telemetry, pulse, ox, BP
+/- invasive monitoring: arterial line

Provide immediate hemodynamic support
- Fluid resus
- Fluid challenge/passive leg raise test if fluid responsiveness is in doubt
- Determine need for vasopressors, inotropes, blood transfusions

Insert urine catheter for monitoring of renal perfusion

31
Q

IV fluid resuscitation commonly used solutions

A
  1. Sodium Chloride injection, USP
  2. Lactated Ringer’s injection (Hartmann’s solution)
  3. Plasma-Lyte A
  4. 0.45% Sodium Chloride injection, USP with added sodium bicarbonate
32
Q

IV fluid resuscitation - Sodium chloride injection USP

A

Has a high concentration of chloride

Can induce hyperchloremia/ hyperchloremic metabolic acidosis!

Consider ringer’s/hartmann’s solution

33
Q

IV fluid resuscitation - Ringer’s/Hartmann’s solution

A

can induce increased neutrophilic count due to high lactate content

34
Q

Use of vasopressors/inotropes for resuscitation

A

Only be given after adequate amount of hydration after IV fluids

Considerations:
1) Adequate volume resuscitation?
2) Selection and titration
3) Route of administration
4) Adjustment for tachyphylaxis and hemodynamic effects

Drug of choice: usually norepinephrine (increases venous return, vascular resistance and CO more than epinephrine)

35
Q

Vasopressors for resuscitation - Norepinephrine (noradrenaline)

A
  • Initial vasopressor of choice in septic, cardiogenic, and hypovolemic shock
36
Q

Vasopressors for resuscitation - Epinephrine (adrenaline)

A
  • Initial vasopressor of choice in anaphylactic shock
  • Typically an add-on agent to norepinephrine in septic shock when an additional agent is required to raise MAP to target
  • Alternative first-line agent if norepinephrine is contraindicated
  • Increases heart rate; may induce tachyarrhythmias and ischemia.
37
Q

Vasopressors for resuscitation - Dopamine

A

Not very commonly used nowadays

  • An alternative to norepinephrine in septic shock in highly selected patients (eg. with absolute of relative bradycardia and a low risk of tachyarrhythmias).

More adverse effects (eg, tachycardia, arrhythmias) at high doses and LESS EFFECTIVE THAN NOREPINEPHRINE for reversing hypotension in septic shock.

Lower doses should not be used for renal protective effect and can cause hypotension during weaning.

38
Q

General management of shock - Disability & Exposure

A

POCUS
CXR
ECG
ABG w/ serum lactate, glucose
FBC, RP, LFT, Coags, Trop, septic workup

Critical therapy
- Corticosteroids for adrenal crisis
- Adrenaline/antihistamines for anaphylaxis
- Needle thoracostomy for tension pneumothorax

Clinical goals:
Neuro: Alert, GCS 15
Labs: Normolactatemia ≤ 2mEq/L, base deficit ≤ 2,
normoglycemia, electrolytes replete

39
Q

What is the Surviving Sepsis Campaign Bundle?

A

Includes specific steps that need to be initiated within 1 hour of sepsis recognition, also known as the 1-Hour Sepsis Bundle

40
Q

Surviving Sepsis Campaign Bundle - Step 1

A
  1. Measure Lactate Level

Why: Elevated lactate (>2 mmol/L) indicates tissue hypoperfusion and anaerobic metabolism.

If the initial lactate level is >2 mmol/L, remeasure within 2-4 hours to assess improvement or worsening.

41
Q

Surviving Sepsis Campaign Bundle - Step 2

A
  1. Obtain Blood Cultures Before Administering Antibiotics

Why: Blood cultures help identify the causative organism and guide antibiotic therapy.

Cultures should be collected before antibiotics, but antibiotics should not be delayed if obtaining cultures takes too long.

42
Q

Surviving Sepsis Campaign Bundle - Step 3

A
  1. Administer Broad-Spectrum Antibiotics

Why: Early antibiotic therapy significantly reduces mortality.

Start empiric broad-spectrum antibiotics within the first hour to cover likely pathogens, adjusting based on culture results.

e.g. Eg. IV piperacillin-tazobactam (broader gram –ve coverage and Pseudomonas) & IV vancomycin (Methicillin Resistant Staph
Aureus)

Monitor: C-reactive protein, Pro-calcitonin, white blood cell, blood/urine/ETT culture

43
Q

Surviving Sepsis Campaign Bundle - Step 4

A
  1. Begin Rapid Administration of IV Fluids

How: Administer 30 mL/kg of crystalloid fluids (e.g., normal saline 1000ml over 30 mins or Ringer’s lactate) for patients with:
Hypotension (MAP <65 mmHg).
Lactate ≥4 mmol/L (indicating severe tissue hypoperfusion).

Consider colloids after fluid resuscitation with crystalloid (~4 to 6L) has failed to achieve goal or clinically significant edema from it

Monitor:
- MAP >65mm Hg
- urine output >0.5ml/kg/hr
- Central Venous Pressure 8 – 12 mmHg

44
Q

Surviving Sepsis Campaign Bundle - Step 5

A
  1. Apply Vasopressors If Hypotension Persists After Fluid Resuscitation

Why: To maintain a target mean arterial pressure (MAP) ≥65 mmHg. Improve end organ perfusion by increasing blood pressure or cardiac output

1st choice: IV NOREPINEPHRINE (little change in heart rate and less increase in stroke volume)

2nd choice: IV epinephrine or vasopressin or dopamine

45
Q

Management of septic Shock

A

Supplemental O2 to reach target ≥ 92%

Mech Vent - Long pulse pressure ventilation

Search closely for symptoms and signs of infectious source

Administer rapid IV boluses of isotonic crystalloid to reach target MAP ≥ 65mmHg and urine output ≥ 0.5mL/kg/h

Consider inotropic support if inadequate response to IV fluids OR constrained by fluid overload

Initiate empiric, broad-spectrum IV antibiotics within 1 hour of presentation w/ maximal dosing

Achieve source control where possible

Anemic – transfuse RBC to target Hb > 7 g/dL

If adrenal insufficiency or refractory shock suspected – stress dose glucocorticoid

Provide analgesia and sedation

46
Q

Management of neurogenic shock

A

ABCD w/ c-spine stabilization – establish definitive airway early rather than late

Thorough neurologic examination

Check for bladder distension – insert IDC ASAP

Administer glucocorticoids within 8 hours of isolated non penetrating traumatic spinal cord injury (TSCI)

Treat hypotension w/ fluids or bloods as appropriate, escalating to inotropes when needed – aim MAP of at least 85 – 90
mmHg

Treat bradycardia w/ atropine or external pacing

Treat pain, provide DVT/stress ulcer/pressure sore prophylaxis

Modulate temperature for patients

47
Q

What is anaphylactic shock and what causes it?

A

A form of distributive shock characterized by massive vasodilation, increased vascular permeability, and airway compromise. Resulting in severe hypotension, tissue hypoperfusion, and organ dysfunction.

Can be non-immunologic:
- due to activation of mast cells and histamine

Response in Anaphylactic shock is primarily due to cytokines.

48
Q

Management of anaphylactic shock

A

ABCD +/- supplemental O2 where needed

Immediate intubation if evidence of impending airway obstruction from angioedema

IM Adrenaline 0.3 – 0.5mg – repeated every 5-15mins as needed

Volume resuscitation w/ IV fluids

H1 + H2 antihistamine

Glucocorticoid

+/- bronchodilators for bronchospasm not responding to adrenaline

Remove from allergen - stingers

Continuous monitoring

For Refractory Anaphylaxis:
Start adrenaline infusion beginning @ 0.1 mcg/kg/min +/- second vasopressor when needed

49
Q

Types of cardiogenic shock - “Dry/wet and cold”

A

Cold: Hypoperfusion causes cool, clammy extremities.

Dry: No signs of fluid overload (non-congested).

Wet: Signs of fluid overload, like pulmonary edema or peripheral edema (congested).

50
Q

Management of cardiogenic shock

A

Treat the underlying cause: antiarrhythmic drugs, revascularization, surgery

Supportive care: HOB raised, stop/modify meds that may worsen symptoms (e.g. anti HTN)

Dry and Cold (noncongested):
- Fluid bolus only if hypotensive
- Reassess for response + clinical signs of volume overload
- If shock persists, start VASOPRESSOR (norA)
- Administer INOTROPES* IF HYPOPERFUSION PERSISTS DESPITE FLUIDS + VASOPRESSOR (dobutamine/dopamine/milrinone)

Wet and Cold(congested):
- Administer INOTROPIC therapy, add on VASOPRESSOR if needed to maintain perfusion. (do not give fluids)
- Once SBP > 90mmHg, start diuretics/nitrates to treat AHF
- Can consider NIV for respi support

51
Q

Management of hypovolemic shock

A

Priority: Immediate haemodynamic support thru aggressive fluid resuscitation

Haemorrhagic:
- Arrest bleeds externally, send to definitive treatment for internal bleeds
- TRANSFUSE ASAP – USE UNCROSSMATCHED O -VE IF EMERGENCY
- Massive Transfusion Protocol (MTP) in 1:1:1 ratio
- Be mindful of lethal diamond(combination of severe bleeding, brain injury, abdominal injury, and chest trauma ):
- Warm blood, warm patient
- Correct coagulopathy, hypocalcemia
- Tranexamic Acid(TXA) for severe traumatic injury

Non-haemorrhagic:
- Treat underlying etiology
- GI losses: antiemetics, antidiarrheal
- Third spacing: e.g. treat for pancreatitis/bowel obstruction
- Increased insensible fluid losses: e.g. treat for burns, antipyretic therapy for fever
- renal losses: e.g. cessation of diuretics,
treatment of diabetes insipidus
- Supportive care: e.g. to treat concomitant
electrolyte derangements
- Continue replacement of ongoing loss as needed

52
Q

Common causes of obstructive shock

A

Obstruction of heart/great vessels -> inability of heart to circulate blood -> ↓ CO -> compensatory ↑ SVR

Pulmonary embolism or severe Pulmonary artery Hypertension(PAH):

  • Obstruction of vasculature -> ↓ PCWP (wedge pressure) -> ↑ RV pressure -> Right heart failure
  • ↑ RV pressure -> ↑ pressure on LV by the RV -> ↓ LV diastolic filling -> ↓ CO
  • Right heart failure -> ↓ LV preload -> ↓ CO

Tension pneumothorax
* ↑ intrathoracic pressure -> ↓venous return -> ↓ preload -> ↓ PCWP
* ↑ intrathoracic pressure -> ↓ LV diastolic filling -> ↓ CO

Cardiac tamponade
* ↑ pericardial pressure -> ↑ RV pressure -> ↓ RV diastolic filling -> right heart failure -> ↓ LV preload ->↓ CO
* ↑ pericardial pressure -> ↑ LV pressure -> ↓ LV diastolic filling -> ↓ CO
* ↑ LV pressure -> ↑ PCWP -> ↑ RV pressure

53
Q

Management of obstructive shock

A

Provide immediate hemodynamic support:
Fluid resuscitation for patients who are preload-dependent and/or fluid responsive
Consider vasopressors/inotropic support

Treat underlying cause:
Pericardiocentesis for cardiac tamponade
Thrombolytic therapy in PE or embolectomy in PE
Needle thoracostomy followed by chest tube placement for tension pneumothorax
+/- surgical intervention if needed

54
Q

A 55-year-old male patient is brought to the emergency department after experiencing severe vomiting and diarrhea for the past 48 hours. On examination, he appears anxious and restless. His blood pressure is 90/60 mmHg, heart rate is 120 bpm, respiratory rate is 22 breaths per minute, and his skin feels cool and clammy. Despite his low blood pressure, the patient has no signs of cyanosis, and his capillary refill time is slightly prolonged. Blood tests reveal mild hypokalemia and a slight increase in lactate levels.

Based on the clinical presentation, which of the following physiological responses is most likely occurring during this compensatory stage of shock?
A. Vasodilation of peripheral blood vessels to improve tissue perfusion
B. Decreased heart rate to maintain blood pressure
C. Increased cardiac contractility due to activation of the sympathetic nervous system
D. Decreased respiratory rate to conserve energy

A

C

Sympathetic stimulation → vasoconstriction (not vasodilation - A is wrong)

Peripheral vasoconstriction, not vasodilation, occurs to maintain blood flow to vital organs (Skin cool and clammy, prolonged capillary refill → Indicate peripheral vasoconstriction)

Heart rate increases (tachycardia) to maintain cardiac output.

BP drops not because of compensation, it’s an effect of shock HR increases to increase CO

55
Q

A 68-year-old female patient was admitted to the ICU with septic shock secondary to a urinary tract infection. Despite aggressive treatment, including intravenous fluids, vasopressors, and broad-spectrum antibiotics, her condition continues to deteriorate. On examination, her blood pressure is 60/40 mmHg, heart rate is 140 bpm, and respiratory rate is 35 breaths per minute. Her skin is cold, mottled, and cyanotic.

Arterial blood gas analysis shows severe metabolic acidosis, and her lactate levels are significantly elevated.

The patient is unresponsive to fluid resuscitation, and her urine output has drastically decreased.

Which of the following best explains the pathophysiological state observed in this patient during the refractory stage of shock?

A. Compensatory mechanisms are actively maintaining perfusion to vital organs, but tissue oxygenation is still compromised.
B. Peripheral vasoconstriction has been overridden, leading to widespread vasodilation and improved tissue perfusion.
C. Irreversible cellular damage has occurred due to prolonged hypoperfusion, and even aggressive treatment is unlikely to restore organ function.
D. The body’s metabolic demands have decreased, resulting in reduced cardiac output and improved systemic resistance.

A

C.

Cellular edema, cells swell up and burst

Despite aggressive treatment, fail to restore organ functions –> most likely multi-organ failure

56
Q

A 60-year-old female patient was admitted to the hospital with a history of severe gastrointestinal bleeding. Initially, she was alert but complained of feeling lightheaded. Her blood pressure was 90/60 mmHg, heart rate was 120 bpm, and her respiratory rate was 24 breaths per minute. After receiving intravenous fluids, her blood pressure stabilized temporarily. However, a few hours later, her condition began to deteriorate again. On re-examination, her blood pressure dropped to 70/50 mmg, heart rate was 140 bpm, and respiratory rate was 30 breaths per minute. She was now lethargic, and her skin felt cold and clammy. Blood tests showed worsening metabolic acidosis and increased lactate levels. Her urine output had decreased significantly over the past few hours.

Which of the following findings is most characteristic of the progressive stage of shock in this patient?
A. Hypotension that responds immediately to fluid resuscitation
B. Widespread tissue ischemia leading to metabolic acidosis and increasing lactate levels
C. Normal urine output despite hypotension
D. Mild tachycardia with stable blood pressure

A

Ans: B. In the progressive stage of shock, the body’s compensatory mechanisms begin to fail, leading to worsening hypotension, hypoperfusion, and widespread tissue ischemia. This results in the accumulation of lactic acid, causing metabolic acidosis

A: not clear (is the response due to fluid resus or compensation?)
C: Normal urine output despite hypotension can be possible in compensatory state too
D: does not suggest any signs of deterioration

57
Q

Despite further aggressive treatment with fluids, vasopressors, and blood transfusions, her condition continued to worsen. After 6 hours, her blood pressure was critically low at 50/30 mmHg, heart rate was 160 bpm, and she was unresponsive. Her skin was mottled and cyanotic, with no detectable urine output. Blood tests revealed severe metabolic acidosis and extremely elevated lactate levels.

Which of the following findings most strongly indicates that the patient has progressed to the refractory stage of shock?

A. Persistently low blood pressure despite aggressive treatment, accompanied by multi-organ failure
B. Tachycardia and hypotension that partially respond to fluid resuscitation
C. Mild metabolic acidosis with an improvement in lactate levels
D. Cool and clammy skin with tachycardia as compensatory mechanisms

A

Ans: A. The refractory (irreversible) stage of shock is characterized by persistent hypotension and multi-organ failure that DO NOT IMPROVE WITH AGGRESSIVE INTERVENTIONS, such as fluids and vasopressors. The body’s compensatory mechanisms are exhausted, leading to widespread cellular damage that is irreversible

No urine output: indicates AKI
Critically low BP

58
Q

A 65-year-old male patient presents to the emergency department with fever, chills, and confusion. He has a history of diabetes mellitus and hypertension. On examination, he is febrile (39.5°C), with a blood pressure of 85/55 mmHg, heart rate of 120 bpm, and respiratory rate of 26 breaths per minute. His skin is warm and flushed, and he has dry mucous membranes. Blood tests show elevated white blood cell count, high lactate levels, and positive blood cultures for Escherichia coli. Despite fluid resuscitation, his blood pressure remains low, and vasopressors are started.

Which of the following best explains the underlying pathophysiology of the shock observed in this patient?

A. Increased systemic vascular resistance due to peripheral vasoconstriction
B. Decreased cardiac output due to reduced preload
C. Widespread vasodilation and capillary leak leading to relative hypovolemia
D. Increased systemic vascular resistance with reduced cardiac contractility

A

Febrile –> underlying infection –> distributive shock –> no loss of blood or plasma, fluid comes out of blood vessels and go somewhere else (cytokines causes rapid vasodilation and leakage of fluid out of blood vessels) –> relative hypovolemia

In septic shock, the primary mechanism is widespread vasodilation caused by the release of inflammatory mediators, along with increased capillary permeability that leads to fluid leakage from the intravascular to the interstitial space. This results in relative hypovolemia, which is not seen in other types of shock like cardiogenic or hypovolemic shock.

59
Q

A 32-year-old female with a known allergy to peanuts accidentally ingests food containing peanut traces. Within minutes, she develops difficulty breathing, widespread hives, and swelling of her lips and tongue. She is brought to the emergency department, where her blood pressure is found to be 70/40 mmHg, heart rate is 130 bpm, and she is in acute respiratory distress. Despite immediate administration of epinephrine, intravenous fluids, and antihistamines, her condition remains critical.

What is the most likely cause of the hypotension observed in this patient during an episode of anaphylactic shock?

A. Decreased cardiac output due to myocardial depression
B. Increased capillary permeability leading to third-spacing of fluids
C. Massive vasoconstriction resulting in reduced perfusion to peripheral tissues
D. Decreased respiratory rate leading to carbon dioxide retention

A

Ans: B

Anaphylactic shock is a type of distributive shock, no volume is lost.

In anaphylactic shock, the release of histamines and other mediators causes massive vasodilation and increased capillary permeability, leading to fluid shifting out of the bloodstream into the tissues. This “third-spacing” is responsible for the drop in blood pressure.

60
Q

A 45-year-old male patient is brought to the emergency department after a motorbike accident. He was found to have a T4 spinal cord injury. On arrival, his blood pressure is 75/50 mmHg, heart rate is 50 bpm, and he is alert but complains of weakness in his lower limbs. He has warm, dry skin, and no signs of external bleeding or trauma elsewhere.

Which of the following best differentiates neurogenic shock from other types of distributive shock?

A. Bradycardia due to unopposed parasympathetic activity
B. Tachycardia with warm, flushed skin
C. Decreased systemic vascular resistance due to anaphylactic mediators
D. Elevated cardiac output with increased systemic vascular resistance

A

Ans: A. Neurogenic shock is characterized by a loss of sympathetic tone due to spinal cord injury, leading to bradycardia, unlike other forms of shock, where tachycardia is common. This happens because the sympathetic nerves are damaged, resulting in unopposed parasympathetic activity.

In neurogenic shock, you find BRADYCARDIA, all other types of shock will be tachycardia!

61
Q

A 58-year-old male with a history of hypertension and coronary artery disease presents to the emergency department with acute onset of chest pain, shortness of breath, and profuse sweating. His symptoms began 2 hours ago. On examination, he is found to be pale, diaphoretic, and anxious. Vital signs reveal a blood pressure of 80/60 mmHg, heart rate of 110 bpm, respiratory rate of 28 breaths per minute, and oxygen saturation of 88% on room air. Lung auscultation reveals crackles at the bases, and his jugular veins are distended. An ECG shows ST-elevation in the anterior leads, and troponin levels are elevated. Despite initial treatment with oxygen, nitrates, and aspirin, his blood pressure continues to drop, and he becomes increasingly lethargic.

Which of the following pathophysiological mechanisms best explains the development of cardiogenic shock in this patient?

A. Increased systemic vascular resistance with adequate cardiac output to maintain perfusion
B. Decreased cardiac contractility leading to reduced cardiac output and systemic hypoperfusion
C. Massive vasodilation leading to a relative hypovolemia
D. Acute loss of circulating blood volume due to hemorrhage

A

B

62
Q

A 45-year-old female presents to the emergency department with sudden onset of severe chest pain and shortness of breath. She reports that the symptoms started 30 minutes ago while she was at rest. She has a history of recent leg surgery for a fracture and has been on bed rest for the past two weeks. On examination, her blood pressure is 70/45 mmg, heart rate is 130 bpm, and respiratory rate is 30 breaths per minute. She appears anxious, and her neck veins are distended. Lung auscultation reveals clear breath sounds bilaterally. An ECG shows sinus tachycardia with a right axis deviation, and a bedside echocardiogram demonstrates a dilated right ventricle.

What is the most likely underlying cause of this patient’s obstructive shock, and what is the pathophysiological mechanism?

A. Massive pulmonary embolism causing increased right ventricular afterload and decreased left ventricular filling
B. Cardiac tamponade leading to compression of the heart chambers and impaired cardiac output
C. Tension pneumothorax causing mediastinal shift and compression of the great vessels
D. Acute myocardial infarction causing severe left ventricular dysfunction and reduced cardiac output

A

Ans: A.

The patient’s history of recent surgery and prolonged bed rest raises the suspicion of a massive pulmonary embolism (PE), which is a common cause of obstructive shock. The sudden onset of chest pain, shortness of breath, and distended neck veins suggests increased pressure in the right heart. A massive PE leads to increased right ventricular afterload, which impedes the flow of blood from the right side to the left side of the heart, reducing left ventricular filling and cardiac output

63
Q

A 30-year-old female is brought to the emergency department after accidentally consuming food that triggered her severe peanut allergy. She developed rapid-onset difficulty breathing, widespread hives, and swelling of her lips and tongue. Her blood pressure is 70/40 mmHg, heart rate is 120 bpm, and she is in acute respiratory distress. She has been diagnosed with anaphylactic shock.

In the context of managing anaphylactic shock, which vasopressor is the most appropriate to administer first, and why is it preferred over others commonly used in different types of shock?

A. Epinephrine, because it causes both vasoconstriction and bronchodilation, addressing multiple pathophysiological mechanisms
B. Norepinephrine, because it is the most potent vasoconstrictor and will rapidly increase blood pressure
C. Dopamine, because it improves heart rate and cardiac output without significant risk of arrhythmias
D. Vasopressin, because it acts on V1 receptors to increase systemic vascular resistance without affecting heart rate

A

A.
For other types of shock, give norepinephrine. For ANAPHYLACTIC shock, give epinephrine.

Epinephrine is the vasopressor of choice for anaphylactic shock, because it addresses multiple mechanisms critical to reversing the condition. It causes vasoconstriction (which helps to increase blood pressure), bronchodilation (which relieves respiratory distress), and stabilizes mast cells to prevent further release of inflammatory mediators. These combined effects make it ideal for treating the multi-system effects of anaphylaxis.

64
Q

A 68-year-old male is admitted to the intensive care unit with septic shock secondary to pneumonia. He has a history of chronic obstructive pulmonary disease (COPD) and diabetes. On examination, he is febrile, hypotensive with a blood pressure of 85/50 mmHg, and tachycardic with a heart rate of 130 bpm. Laboratory tests reveal elevated prothrombin time (PT), activated partial thromboplastin time (aPTT), low platelet count, and elevated fibrin degradation products (e.g., D-dimer).

Which type of shock is most likely to predispose this patient to Disseminated Intravascular Coagulation (DIC), and what is the underlying mechanism?

A. Hypovolemic shock due to acute blood loss leading to reduced perfusion and tissue ischemia
B. Cardiogenic shock due to impaired cardiac output resulting in organ dysfunction
C. Obstructive shock due to impaired blood flow from conditions like tension pneumothorax
D. Distributive shock due to systemic infection and the release of pro-inflammatory cytokines

A

Ans: D

Distributive shock, particularly septic shock, is the type that predisposes patients to DIC (Answer D). The systemic infection results in the release of pro-inflammatory cytokines, leading to widespread endothelial activation, coagulation cascade activation, and the formation of microthrombi. This process consumes platelets and clotting factors, resulting in a coagulopathy known as DIC.

65
Q

What is SOFA used for?

A

Sequential organ failure assessment

Assess the degree of organ dysfunction in ICU patients.

Monitor the progression of organ failure over time.

Serve as part of the Sepsis-3 definition to identify sepsis in patients with suspected infection.

66
Q

Components of the SOFA score

A

evaluates six organ systems, assigning a score from 0 (normal function) to 4 (severe dysfunction) for each. The total score ranges from 0 to 24

  1. Respiratory
    - Low PaO₂/FiO₂ ratios indicate respiratory failure
  2. Coagulation
    - Lower platelet counts indicate coagulopathy, which may reflect disseminated intravascular coagulation (DIC) or bone marrow suppression
  3. Liver
    - Higher bilirubin levels indicate hepatic dysfunction.
  4. Cardiovascular
    - Assess if increasing vasopressors needed to maintain MAP>65?
  5. CNS
    - Assess GCS
  6. Renal
    - Assess creatinine and urine output
67
Q
A

PPNP 3 (19 decks)

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