Shock

Definition

• Physiologic state characterised by a systemic impairment in oxygen delivery as a result of reduced tissue perfusion, almost universally mediated by low blood pressure ($D{O}_2<\dot{V}{O}_2$)

Pathophysiology

$$\underset{\text{Perfusion Pressure}}{\text{MAP}-\text{CVP}}=\text{CO}\times \text{SVR}$$

• MAP = mean arterial pressure
• CVP = central venous pressure (pressure in the vena cava)
• CO = cardiac output
  • $\text{CO}=\text{HR}\times \text{SV}$
  • Stroke volume is dependent upon preload, contractility and afterload
• SVR = systemic vascular resistance
• Low perfusion pressure must therefore be due to:
  • Low preload ⇒
    • hypovolaemic (e.g. trauma, GI haemorrhage, severe diarrhoea)
    • obstructive ∵ of obstruction to venous return to the LV (e.g. massive PE, pericardial tamponade, tension pneumothorax)
    • tachycardic arrythmogenic shock because of short diastolic filling time
  • Low contractility ⇒ cardiogenic (e.g. Acute MI, severe heart failure exacerbation, viral myocarditis)
  • Low heart rate ⇒
    • Bradycardic arrhythmogenic shock
  • Low systemic vascular resistance ⇒ distributive (e.g. sepsis, anaphylaxis, spinal cord trauma)
  • Other types:
    • Toxin-mediated shock (e.g. cyanide and carbon monoxide)

Classification

• Cardiogenic shock
  • Depressed contractility: ACS, myocarditis, myocardial contusion, cardiomyopathy, drug overdose (e.g. CCB or beta-blocker)
  • Acute valvular dysfunction: Papillary muscle or chordae tendinae rupture, infective endocarditis, severe aortic stenosis or mitral stenosis
  • Arrhythmia: Tachycardia (e.g. VT, AF, SVT), bradycardia (e.g. heart block)
• Hypovolaemic shock
  • Haemorrhagic
    • Traumatic: external or internal (e.g. haemothorax, haemoperitoneum, retroperitoneal haemorrhage)
    • Non-traumatic: external (e.g. haemoptysis, haematemesis, PV bleeding) or internal (e.g. haemothorax, ruptured AAA, bleeding diathesis)
  • Non-haemorrhagic
    • External (e.g. GI losses from diarrhoea and vomiting, burns, hyperthermia, high-output fistulae)
    • Internal (e.g. bowel obstruction, pancreatitis)
• Obstructive shock
  • Intrinsic to cardiovascular system
    • Pulmonary embolism
    • Air embolism
    • Myxoma
    • Amniotic fluid embolism
  • Extrinsic to cardiovascular system
    • Tension pneumothorax
    • Cardiac tamponade
    • Abdominal compartment syndrome
    • Dynamic hyperinflation: Excessive ventilation with severe bronchospasm (Asthma Exacerbation, COPD)
• Distributive shock
  • Anaphylaxis
  • Sepsis
  • Neurogenic: Loss of sympathetic tone from high spinal cord trauma or epidural anaesthesia
  • Drug related: Vasodilator antihypertensive agents, nitrates, strong analgesics
  • Acute adrenal insufficiency: Addison’s disease, discontinuing long-term steroids
• The mnemonic CHOD can be used to remember the above, however a better framework may be PROVED?:
  • Cardiogenic (Pump)
  • Rhythm abnormalities
  • Obstructive
  • Hypovolaemia (Volume)
    • In the trauma patient consider: SCALPeR: scalp/street, chest, abdomen, long bones, pelvis and retroperitoneum
      • Steet refers to external blood loss at the scnes and other pre-hospital haemorrhage
  • Endocrine (these often cause a mixed classification, but its inclusion ensures things like Adrenal Crisis, hypo/hyperthyroidism, Diabetic ketoacidosis, severe acidosis/alkalosis are not missed)
  • Distributive
  • ?: is it real (check the BP measurement, is the arterial line really in an artery and is the transducer at the correct height)

Clinical Features

• Haemodynamics
  • Hypotension (MAP < 65 mmHg or significant drop from baseline)
  • Elevated shock index (HR/SBP) >0.8
  • Urine output < 0.5 mL/kg/hour
  • Dark urine
  • ↑ troponin
• Skin perfusion
  • Cool hands and knees are an early sign of vasoconstriction with reduced cardiac output
  • Mottling
    • Suggests active endogenous vasoconstriction, implying that the patient would benefit from ionotropy not vasopressors
  • Capillary refill time (>5 seconds)
• Neurological
  • Altered mental status (agitation → delirium → solmnolence), generally more of a sign of septic shock
• Respiratory
  • ↑ respiratory rate
  • ↓ oxygen saturation
• Hepatological
  • ↑ bilirubin, AST, ALT
• Nephrology
  • ↓ Urine output
  • ↑ Creatine
• Haematological
  • ↑/↓ platelets
  • ↑ INR which can lead to DIC
  • ↑ lactate and ↓ $\mathrm{HCO}{}_3{}^{-}$

Approach to Undifferentiated Shock

Primary Survey

• Call early for a senior doctor to help
• Assess airway patency
  • Exclude airway obstruction and asphyxia
• Start monitoring (pulse oximetry, ECG, BP)
• Assess breathing:
  • Oxygenation (saturation probe)
  • Ventilation (end tidal CO2, chest auscultation)
  • Exclude tension pneumothorax and massive haemothorax
• Assess circulation
  • Peripheral and central temperature/capillary refill
  • Vital signs (heart rate, blood pressure)
  • Equipment check
    • Exclude artifactual shock and equipment failure as the cause of shock, e.g. IABP malfunction, ECMO circuit problems, vasopressor infusion drug error.
  • Head-to-toe exposure
    • Exclude externally obvious haemorrhage
    • Exclude anaphylaxis/angioedema
  • 12-lead ECG
  • Point of care TTE: rapid assessment with cardiac echo and RUSH exam
    • Exclude cardiac tamponade
    • Exclude massive PE

Overview of RUSH Exam

• Heart: LV function, RV dilation, pericardial effusion/tamponade
• IVC: size and collapsibility (volume responsiveness)
• Lungs: B-lines (pulmonary oedema), pneumothorax (absence of sliding)
• Abdomen: free fluid (haemoperitoneum, ruptured AAA)
• Aorta: AAA
• Lower limbs: DVT (if PE suspected)

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• Establish venous access
• Collect a series of generic laboratory investigations, most importantly an ABG
• Mobile Chest X-ray
• Assess neurology (i.e. spinal injury)
  • Exclude neurogenic (“spinal”) shock

Empirical Resuscitation

• Ventilate the intubated patient with low-moderate PEEP (0.1cmH2O/kg)
• Commence fluid bolus: 10 ml/kg
  • Generally 30 mL/kg within the first 3 hours for sepsis
  • Give as a fluid challenge: 250-500mL over 10-15 minutes
    • Assess MAP response and dnyamic predictors (PP variations, PLR)
  • Balanced crystalloid (hartmann’s or plasmalyte) generally preferred to normal saline unless:
    • Hypochloraemic alkalosis (e.g. vomiting, NGT losses)
    • Hyperkalaemia
    • Traumatic brain injury
    • Meningitis
  • Albumin
    • Albumin 4% reasonable alternative to crystalloid in large-volume resuscitation in septic shock
    • Albumin 20% used in hepatic failure/spontaneous bacterial peritonitis, hepatorenal syndrome
• Commence/escalate vasopressor infusion (see below)
  • The optimal initial vasopressor is unknown as is the optimal MAP
    • In septic shock, it appears the initial pressor of choice is noradrenaline
• Antibiotics after peripheral cultures are obtained if sepsis is possible
• Steroids in patients with suspected adrenal crisis
  • When in doubt about adrenal insufficiency, a reasonable approach is to give 6 mg dexamethasone and check a cortisol level simultaneously¹

Secondary Survey

• Focused history:
  • Immediate events preceding the collapse
  • Drug administration history
  • Recent interventions
  • Relevant background history
  • Collateral from recently attending staff/family
  • Important history points:
    • ? chest pain/diaphoresis
    • Fevers, rigors, immunosuppression
    • Allergen exposure
    • Trauma/blood loss
    • Known cardiac disease, new dyspnoea
    • Chest procedure
    • Malignancy (PE)
    • Exogenous steroid use or adrenal disease
• Focused examination and investigations
  • ECG
  • CXR
  • ABG with special attention to lactate
  • Head to toe examination
    • Fluid status (JVP, skin, mucous membranes, heart sounds, lung sounds, CRT, HR, SBP, urine output, IVC and collapsability)
    • Sources of sepsis
    • Toxidromes
    • Abdominal examination, looking for AAA, retroperitoneal haematoma and pancreatitis
  • Bedside abdominal and chest ultrasound, looking for collections
  • Formal (skilled) TTE, looking for valvular dysfunction, LVOT obstruction, regional wall motion abnormalities and septal defects
• Labs
  • FBC
  • UEC
  • LFT
  • Inflammatory markers (CRP and procalcitonin)
  • Blood cultures x 2
  • Troponin and BNP
  • Coagulation studies and D-dimer
  • Cortisol level
  • TSH and free T4 level

• More than one type of shock may co-exist in the same patient for example:
  • Sepsis + hypovolaemia
  • Sepsis + sepsis induced cardiomyopathy

Approach to Refractory Shock

• Diagnostic tests:
  • Cardiac imaging:
    • Repeat POCUS
    • Formal echocardiography
    • Review CT imaging if available
    • Evaluate for unsual forms of shock (e.g. LVOT obstruction)
  • Laboratory investigations:
    • ABG/VBG and EUCs
    • Glucose level
    • CMP
    • TSH and FT4
    • CRP, procalcitonin and blood cultures
• Treatment options:
  • Optimise MAP target
    • Central arterial line (femoral or axillary) as opposed to radial artery
    • Reducing MAP target
  • Review medications and stop hypotension inducing medications
    • Haemodynamically stable analgosedation (e.g. ketamine infusion)
    • Discontinue alpha-blockers being used for BPH
  • Optimise pre-load
    • Reduce PEEP
    • Evaluate for auto-PEEP
    • Re-evaluate fluid status and consider volume administration if appropriate
  • Metabolic optimisation
    • Temperature management
    • Intravenous calcium in patients with low ionised calcium
    • pH optimisation:
      • Bicarbonate
      • Ventilator management
      • Dialysis
    • IV thiamine for beriberi
    • Steroids may enhance vascular responsiveness to vasopressors
    • Thyroid hormone replacement for decompensated hypothyroidism
      • Probably treat with T3 to achieve more rapid improvement
  • Vasopressor optimisation
    • High dose noradrenaline
    • Can consider second vasopressor (e.g. terlipressin)
    • If mottling present: pivot from vasopressors to inotropes
    • Consider right heart catheterisation for refractory or diagnostically unclear shock
  • RV optimisation
    • Correct all reversible causes of elevated PVR: hypoxia (target SaO₂ >92%), hypercapnia, acidosis, over-distension on the ventilator
    • Pulmonary vasodilators: inhaled nitric oxide, nebulised iloprost (prostacyclin analogue)
    • Milrinone is the preferred inotrope when there is combined LV + RV failure — it reduces PVR while supporting both ventricles
    • Prone positioning reduces PVR in ARDS with cor pulmonale
  • Heart rate optimisation
    • Atropine
    • Isoprenaline
    • Pacing
  • Mechanical circulatory support
    • Invasive aortic balloon pump
    • Impella
    • VA-ECMO

Trauma Related Shock

Vasopressors and Ionotropes

• Start noradrenaline early — don’t wait for large volumes of fluid; fluid overload is harmful
• Peripheral vasopressor use (short-term, large proximal vein) is acceptable to avoid delaying treatment while CVC inserted
• Corticosteroids for vasopressor-refractory septic shock: hydrocortisone 200 mg/day IV (APROCCHSS, ADRENAL trials)
• Titrate to MAP 65 (not higher in most cases — SEPSISPAM trial: no benefit at MAP 80–85)

Noradrenaline

0.01-3 mcg/kg/min IV infusion (central line preferred)

• First line vasopressor in distributive and most forms of shock

• Predominantly ${\alpha }_1$ agonist with some ${\beta }_1$ ⇒ ↑ SVR and mild ↑ HR/CO

• Can be run peripherally short-term (forearm or antecubital) at low doses while CVC inserted

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Metaraminol

Bolus: 0.5-2 mg IV PRN | Infusion: 15-30 mg in 500 mL at 15-60 mL/hr

• Predominantly ${\alpha }_1$ agonist; also causes indirect noradrenaline release

• Used widely in peri-operative setting and as bridge vasopressor pre-noradrenaline

• Can be given peripherally; suitable in ward or theatre setting

• Tachyphylaxis with prolonged use

• Reflex bradycardia can occur - treat with atropine

• Less titratable than noradrenaline infusion

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Adrenaline

Anaphylaxis: 0.3-0.5 mg IM (thigh) | Shock infusion: 0.01-1 mcg/kg/min IV

• Anaphylaxis: IM adrenaline (Epipen 0.3 mg or ampoule 1:1000) is the drug of first choice

• Septic shock: Second agent alongside noradrenaline when additional inotropic support needed; associated with increased lactate that does not reflect true worsening

• Cardiogenic shock: Adrenaline has more arrhythmogenic risk than other inotropes

• Cardiac arrest: 1 mg IV every alternate loop

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Terlipressin

Bolus: 0.85–2.5 mg IV bolus q4–6h | Infusion: 1.3–5 mg/24h

• $V_1$ receptor agonist (smooth muscle vasoconstriction)
• Hepatorenal syndrome type 1: terlipressin + albumin is first line
• Variceal bleeding: 2mg IV bolus then 1 mg q4-6h for up to 5 days
• Used in refractory septic shock as noradrenaline-sparing agent (off-label in Australia)
• Risk: digital/skin ischaemia, bradycardia, mesenteric ischaemia — monitor carefully
• Avoid in ischaemic heart disease, peripheral vascular disease

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Dobutamine

2–20 mcg/kg/min IV infusion

• ${\beta }_1$ and ${\beta }_2$ agonist - positive inotropy, chronotropy; reduces SVR (vasodilatory)
• Used in cardiogenic shock with adequate MAP (often combined with noradrenaline)
• Risk of tachycardia and arrhythmia; may worsen hypotension in true hypovolaemia

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Milrinone

0.125–0.75 mcg/kg/min IV (load: 25–50 mcg/kg over 10 min, often omitted)

• Used in cardiogenic shock, especially post-cardiac surgery or when β-receptor downregulation limits dobutamine effect
• Useful in pulmonary hypertension (reduces PVR)
• Longer half-life — effects accumulate, harder to titrate; prolonged hypotension if overdosed
• Renally cleared — dose-reduce in AKI

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Phenylephrine

Bolus 50–200 mcg IV | Infusion 10–300 mcg/min

• Pure α₁ agonist — vasoconstriction without inotropic effect

• Useful in tachycardia-associated shock where noradrenaline’s β₁ effect is undesirable (e.g., HOCM, AF with fast ventricular rate)

• Reflex bradycardia — use cautiously in bradycardic patients

• Can worsen cardiogenic shock by increasing afterload without supporting cardiac output

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Situation	First agent	Add / escalate to	Avoid
Undifferentiated shock	Noradrenaline	Fluid trial first; escalate based on 6-step framework	—
Septic shock (vasodilatory)	Noradrenaline	Terlipressin (refractory); hydrocortisone; adrenaline if inotrope also needed	Excess fluid, dopamine
Cardiogenic shock (LV)	Noradrenaline (MAP support)	Dobutamine or milrinone (inotropy); IABP/Impella/VA-ECMO escalation	Dopamine, excessive adrenaline
RV failure	Noradrenaline	Milrinone (reduces PVR + inotrope); adrenaline; inhaled iloprost/NO	Vasodilators, aggressive fluid loading in RV dilation
Anaphylaxis	Adrenaline 0.5 mg IM	Adrenaline IV infusion; fluids; glucagon if on β-blockers	Any delay to adrenaline
Peri-operative / spinal hypotension	Metaraminol 0.5–2 mg IV bolus	Noradrenaline infusion once CVC placed; phenylephrine if bradycardic	—
Bradycardic shock	Atropine → isoprenaline infusion	Temporary transvenous pacing	Phenylephrine, metaraminol (worsen bradycardia)
LVOTO / HOCM	Phenylephrine + fluid bolus	Esmolol infusion (rate control)	Inotropes, vasodilators, tachycardia-promoting agents
Adrenal crisis	Hydrocortisone 100 mg IV + saline	Noradrenaline if MAP not restored	Delaying hydrocortisone for investigations
![[Pasted image 20260228203914.png	448]]

Fluid Responsiveness

• Fluid responsiveness is 10-15% increase in cardiac output in response to a fluid chalenge or pre-load augmentation manoeuvre
• Not the same as needing fluid:
  • Is the patient fluid responsive? (Will CO rise with fluid?)
  • Does the patient need fluid? (Is tissue perfusion inadequate and likely to improve with more preload?)
• Generally dynamic predictors are better than static predictors (e.g. CVP, PCWP, RAP/LVEDP)

Challenges

Passive leg raise

• Method
  • Start with the patient semi-recumbent at 45°
  • Raise legs to 45° while simultaneously lowering the torso to flat (or raise legs from flat if already supine)
  • This transfers ~300 mL of venous blood from the lower limbs into the central circulation — an autologous, reversible fluid challenge
  • Assess CO or a surrogate at baseline and at 60–90 seconds after position change (effect is transient)
  • Return patient to original position — the effect is fully reversible
• Positive: ≥10% increase in cardiac output (or arterial pulse pressure as a surrogate)
• Limitations
  • Cannot be performed if: raised intracranial pressure, unstable pelvic/femoral fractures, intra-abdominal hypertension (may not transfer adequate volume)
  • Requires real-time CO measurement — qualitative BP change alone is insufficient
  • Must measure CO response within 60–90 seconds (effect wanes)

Pulse pressure variation

• Positive: PPV > 13% predicts fluid responsiveness
• Limitations: requires all criteria to be met:
  • Fully controlled mechanical ventilation (no spontaneous breathing efforts — even small triggered breaths invalidate the result)
  • Regular cardiac rhythm (arrhythmias — particularly AF — invalidate the result)
  • Tidal volume ≥8 mL/kg ideal body weight (low Vt ventilation, as in lung-protective strategies, reduces cyclic variation even in responsive patients → false negatives)
  • No severe RV failure (RV failure independently causes high PPV regardless of volume status)
  • Chest closed (open chest post-cardiotomy invalidates)

Mini Fluid Challenge

• Technique: Give 100 mL of crystalloid over 1 minute and assess CO response (via arterial PP or POCUS VTI)
• Positive: ≥6% increase in PP or VTI → likely fluid responsive

Measures

• Best: POCUS VTI (left ventricular outflow tract velocity-time integral) — multiply by LVOT area for CO; serial VTI alone is sufficient for trending
• Acceptable: arterial pulse pressure change (less precise but reasonable)
• Pulse oximetry pleth waveform: some evidence but unreliable in vasoconstriction
• Avoid: relying on BP alone — MAP change is an insensitive surrogate for CO change

IVC collapsibility/distensibility

• Bedside POCUS assessment of the IVC
• In spontaneously breathing patients using the collapsibility index
  • Measured in the subxiphoid view
  • Collapsibility > 50% suggests fluid responsiveness
  • Collapsibility <15-20% suggests volume overload/non-responsiveness

$$\text{IVC collapsibility}=\frac{{\text{IVC}}_{\text{max}}-{\text{IVC}}_{\text{min}}}{{\text{IVC}}_{\text{max}}}\times 100\%$$

• In mechanically ventilating patients use the distensibility index
  • Distensibility >18% predicts fluid responsiveness

$$\text{IVC collapsibility}=\frac{{\text{IVC}}_{\text{max}}-{\text{IVC}}_{\text{min}}}{{\text{IVC}}_{\text{min}}}\times 100\%$$

Steroids

• Corticosteroids should not be used routinely for patients with septic shock
  • the weight of evidence does not support a benefit in terms of patient-orientated outcomes
  • ACTH stimulation tests are not useful in this patients
  • hydrocortisone 200 mg IV daily is an option for septic shock patients who are refractory to vasopressors (e.g. adults requiring IV noradrenaline at 20-30 micrograms/h) and no other cause found; despite an absence of convincing supportive evidence of benefit
• Corticosteroids should be used in patients who have shock and a specific indication for corticosteroid therapy
  • e.g. anaphylaxis, known steroid dependence (e.g. for chronic immunosuppression), known hypoadrenalism, other steroid-responsive conditions like asthma or rheumatoid arthritis

Fluid Replacement in Dehydrated Patients

Fluid replacement in dehydrated patients

1. Resuscitate intravascular volume until perfusion is normalised as above with 20 mL/kg boluses of crystalloid (normal saline preferred)
2. Calculate fluid losses (generally at least 10% of body weight if patient is dehydrated and hypotensive, i.e. 70kg patient is depleted of 7L of fluid)
3. Subtract from this defecit the amount of fluid already given for resuscitation (e.g. if 2L given during resuscitation, a 70kg patient still requires 5L of fluid)
4. Replace this amount over the next 24 hours together with maintenance fluid and ongoing losses

• Use 4:2:1 rule, or add 60mL to their weight for hourly fluid requirement ⇒ 110mL/hr ≈ 2.5L/day
• Total fluid to be replaced is 7.5 L

5. Replace half in first 8 hours and remainder in next 16 hours

• 3.75L over 8 hours ≈ 450 mL/h
• 3.75L over 16 hours ≈ 230 mL/h

6. Monitor adequacy of replacement by perfusion and vital signs, urine output and electrolyte changes

Appendix

Drug	Alpha-1	Beta-1	Beta-2	Dopamine	Effect on SVR	Effect on HR	Effect on CO	Effect on BP
Phenylephrine	+++	0	0	0	↑↑	↓ / ↔	↓	↑↑
Metaraminol	+++	+ (indirect)	0	0	↑↑	↔ / ↑	↔ / ↑	↑↑
Vasopressin (V1 agonist)	0	0	0	0	↑↑	↔	↓	↑
Noradrenaline	+++	++	0	0	↑↑	↑	↔ / ↑	↑↑
Adrenaline (Low dose)	+	+++	++	0	↓	↑	↑	↔ / ↑
Adrenaline (High dose)	++	+++	++	0	↔ / ↑	↑	↑	↑↑
Dopamine (Low dose)*	0	+	0	++	↔	↑	↑	↑
Dopamine (Moderate dose)*	+	++	0	++	↑	↑	↑	↑↑
Dopamine (High dose)*	++	++	0	++	↑↑	↑	↔ / ↑	↑↑
Dobutamine	0 / +	+++	++	0	↓	↑	↑↑	↓ / ↔ / ↑
Isoprenaline	0	+++	+++	0	↓	↑↑	↑↑	↓ / ↔
Milrinone (PDE inhibitor)	0	0	0	0	↓	↔ / ↑	↑↑	↓ / ↔ / ↑

Sources

• Youtube Videos
  • Strong Medicine
    • Shock Playlist | Strong Medicine - Yotuube
    • An Approach to Shock - YouTube
    • Sepsis and Septic Shock - YouTube
• LITFL:
  • Shock • LITFL • CCC Differential Diagnosis
  • Shock Hot Case • LITFL • CCC Hot Case
  • Corticosteroid Therapy for Shock • LITFL • CCC shock
  • Venous Return and Shock • LITFL • CCC Cardiology
• Deranged Physiology
  • Definition and classification of shock
  • Approach to the undifferentiated shock patient
• UpToDate: Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock
• Undifferentiated Shock — ICU One Pager
• Vasopressors — ICU One Pager
• Fluid Responsiveness - could this hemodynamically unstable patient respond to IV fluids? — ICU One Pager

Footnotes

1. Dexamethasone does not interfere with the cortisol level allowing one to perform an ACTH stimulation test later if indicated ↩