6. SHOCK & HEMODYNAMIC PROTOCOLS

6.1 RUSH — Rapid Ultrasound for Shock and Hypotension

Sequence: lungs → heart → IVC → abdomen [1].

POCUS patterns

Reduced LV plus elevated IVC plus B-lines: cardiogenic shock. Causes include MI, myocarditis, cardiomyopathy, post-surgical dysfunction [1].

Hyperdynamic LV plus low or collapsible IVC plus no B-lines: hypovolaemic shock. Causes include haemorrhage, dehydration, early sepsis [1].

RV dilation plus underfilled LV plus elevated IVC: obstructive shock. Causes include massive PE, tension pneumothorax, tamponade [1,3].

Pericardial effusion plus chamber collapse: tamponade. Causes include trauma, uraemia, malignancy, post-surgical collection [1,3].

Variable IVC plus variable LV plus infection context: distributive or mixed shock. Causes include sepsis, anaphylaxis, mixed physiology [1].

6.2 Cardiac arrest POCUS

POCUS in cardiac arrest should be used as a time-limited adjunct integrated into ALS workflow, with the goal of minimizing interruptions to chest compressions [2]. A brief, protocol-defined subcostal assessment may be used to determine cardiac motion versus standstill and to screen for reversible causes [2]. The pause should be as short as necessary and should not prolong no-flow time beyond what is required for standard rhythm/pulse checks [2]. If the operator cannot obtain a diagnostic view rapidly, the scan should be abandoned and CPR resumed [2]. A dedicated 20-second ultrasound pause is generally longer than necessary for a binary assessment of cardiac motion versus standstill and should not be presented as a standard.

Cardiac activity versus standstill

Focused POCUS can distinguish discernible cardiac motion from standstill and may help predict futility [2]. Interpretation is operator-dependent; definitions vary across studies; interobserver reliability is imperfect [2].

Reversible causes

  1. Tamponade.

  2. Massive PE with RV dilation.

  3. Tension pneumothorax [1,3].

RV dilation alone does not confirm massive PE; it may also reflect chronic pulmonary hypertension, RV infarction, or other aetiologies [2]. Tension pneumothorax is better supported by lung POCUS findings plus clinical context [1,3]. Tamponade requires more than effusion: chamber collapse, IVC plethora, respiratory inflow variation, or regional compression, especially in postoperative or traumatic settings [1,3].

Traumatic arrest

Standstill suggests very poor survival and may support termination of resuscitation in selected settings [2]. Interpret within broader clinical context: mechanism, age, comorbidities, hypothermia, exsanguination, and local ToR criteria [2].

Medical arrest

Standstill suggests low but not zero survival [2]. Do not use standstill as the sole basis to cease resuscitation [2].

Serial standstill

Serial standstill of 10 minutes or more suggests very poor outcomes, but the evidence base is limited, with variable protocols, populations, definitions, and operator experience [2].

6.3 Dyspnea/acute heart failure integrated protocol

Assess:

Lung: B-line score, pattern, consolidation, effusion (see S4.1).

VExUS: IVC, hepatic vein, portal vein, intrarenal vein; grade 0–3 (see S5.2) [4].

Cardiac: LV, RV, pericardium, diastolic function, TR (see S2.4,S3). If LVDD is suspected or confirmed, apply CHEOPS optimization (see S3.5.10).

Patterns

Cardiogenic congestion: High lung ultrasound score, ideally diffuse B-line or extravascular lung water pattern [5]. VExUS grade 2–3; VExUS 2 is possible congestion, not confirmed severe congestion [4]. Objective evidence of elevated left-sided filling pressures: elevated E/e′ (see S3.5), LA enlargement, increased TRV, pulmonary oedema, invasive data if available [4]. Reduced LVEF is helpful but not required; HFpEF and acute diastolic dysfunction are common [4]. High lung score alone does not prove cardiogenic oedema [5]. Early isolated left-sided failure may produce B-lines before systemic venous congestion [4].

Non-hydrostatic pulmonary syndrome: High lung score [5]. VExUS grade 0–1 reduces but does not exclude congestion [4]. No objective evidence of elevated left-sided filling pressures [4]. Patchy B-lines, consolidation, atelectasis, ARDS, pneumonia, pulmonary haemorrhage, or alveolar-capillary permeability injury [5]. Treat the primary process. Avoid aggressive diuresis only when there is no evidence of central venous congestion or hypervolaemia; conservative fluid strategy in ARDS may still be appropriate [4]. Mixed hydrostatic plus permeability physiology is common, especially in sepsis with septic cardiomyopathy [4].

Systemic venous congestion without pulmonary oedema: VExUS grade 2–3 [4]. Low lung score reduces but does not exclude pulmonary oedema [5]. RV dilation or dysfunction (see S2.4) [4]. Elevated CVP, plethoric IVC (see S5.1), TR, hepatic vein diastolic attenuation or reversal, intrarenal venous diastolic loss or reversal [4]. Evaluate RV afterload: PE, pulmonary hypertension, RV infarction, severe lung disease, tamponade, MV-related RV afterload [4]. Avoid empiric liberal fluids when the RV is overdistended, with septal shift and LV filling impairment via ventricular interdependence [4]. Do not reflexively withhold all volume: if RV preload is genuinely low, a small tested fluid challenge or PLR with serial reassessment may be appropriate (see S5.6) [4]. Dynamic indices such as PPV/SVV are less reliable in RV failure (see S5.3).

Elevated MSFP: VExUS grade 2–3 [4]. Preserved biventricular systolic function, ideally including diastolic assessment [4]. No pulmonary oedema [5]. Suggests elevated effective venous return, increased CVP, altered venous capacitance, or elevated MSFP [4]. MSFP is inferred, not directly measured by VExUS [4]. Integrate CVP/RAP, RV size, hepatic and renal venous Doppler, intra-abdominal pressure, ventilation settings, and clinical volume status before diuresis [4]. VExUS is not a simple volume score [4].

LVDD optimization: If LVDD contributes to dyspnoea or acute heart failure: Use CHEOPS: chest ultrasound, haemodynamics, ventilation optimization, stabilization (see S3.5.10). Control heart rate and rhythm. Optimize afterload. Avoid unnecessary fluids. Decongest when safe. Titrate PEEP with biventricular reassessment. Reassess after diuresis, vasopressor changes, ventilator changes, and arrhythmia treatment.

6.4 PE-risk combined vascular POCUS

DVT (see S8.1) plus plethoric IVC (see S5.1) plus RV dilation (see S2.4): high suspicion for PE [1,3]. DVT alone: DVT confirmed; PE not excluded [1,3]. RV dilation plus plethoric IVC plus no DVT: PE still possible; distal or absent DVT [1,3]. Collapsible IVC plus no RV dilation plus no DVT: PE less likely; pretest probability still matters [1,3]. Clear lungs plus tachycardia plus hypoxaemia plus plethoric IVC: consider PE, pneumothorax, sepsis [1,3].

6.5 Acute aortic syndrome and aortic occlusion protocol

Acute aortic syndrome

Clinical context: chest, back, or abdominal pain; hypotension; pulse asymmetry; neurological deficit; severe lactic acidosis; pericardial effusion; new aortic regurgitation [7].

POCUS sequence: Parasternal long-axis: aortic root, aortic valve, pericardial effusion, aortic regurgitation [6]. Suprasternal notch: aortic arch and proximal descending aorta [6]. Superior intercostal/small-scale views: ascending and descending thoracic aorta as needed [6]. Subxiphoid/abdominal views: thoracoabdominal aorta and abdominal aorta [6].

Search for: Intimal flap [6,7]. Intramural haematoma, commonly wall thickening greater than 5 mm [6,7]. Penetrating atherosclerotic ulcer [6,7]. Thoracic aortic dilatation [6,7]. Pericardial effusion or tamponade [6,7]. Aortic regurgitation [6,7].

Action: If direct or indirect signs are present, proceed urgently to CTA or MRA and vascular/cardiac surgery consultation [7]. If imaging is nondiagnostic but suspicion remains high, proceed to definitive imaging without delay [7]. A negative POCUS does not exclude dissection [7].

Acute abdominal aortic occlusion

Clinical context: sudden lower-extremity weakness or numbness, absent femoral pulses, cold limbs, severe pain, metabolic acidosis, elevated lactate [8].

POCUS: Longitudinal midline abdominal aorta from xiphoid to bifurcation and distally when possible [8]. Colour and pulsed-wave Doppler [8]. Assess for intraluminal thrombus, absent or diminished distal flow, and normal or abnormal aortic calibre [8]. A normal aortic diameter does not exclude occlusion [8].

Action: If occlusion is identified or strongly suspected, expedite vascular surgery consultation and CTA if the patient condition allows [8].

6.6 Pitfalls

  1. Do not interrupt resuscitation unnecessarily; cardiac arrest scanning should be brief and protocol-driven.

  2. Standstill is not, in isolation, a basis to terminate resuscitation; integrate local ToR criteria and clinical context.

  3. Serial standstill ≥10 minutes suggests very poor outcome, but the evidence base is limited and heterogeneous; do not rely on it as a fixed cutoff.

  4. RV dilation alone does not confirm massive PE during arrest (see S2.4, S8.1).

  5. Aortic-specific pitfalls — see S8.4, S8.5.

  6. DVT/arterial-specific pitfalls — see S8.1.

  7. IVC/venous-specific pitfalls — see S5.7.

  8. Lung-specific pitfalls — see S4.6.

References

  1. Choi W, Cho YS, Ha YR, et al. Role of point-of-care ultrasound in critical care and emergency medicine: update and future perspective. Clin Exp Emerg Med. 2023;10(4):363-381. doi:10.15441/ceem.23.101.

  2. Soar J, Deakin CD, Nolan JP, et al. Adult advanced life support guidelines: key points. Resuscitation Council (UK); 2021.

  3. Jarman RD, McDermott C, Colclough A, et al. EFSUMB clinical practice guidelines for point-of-care ultrasound: part one (common heart and pulmonary applications). Ultraschall Med. 2023;44:e1-e24. doi:10.1055/a-1882-5615.

  4. Huard K, Deschamps J, Couture EJ, et al. Venous congestion in critical care: combining VExUS, lung ultrasound, and echocardiography. Ann Intensive Car. 2026;16:100127. doi:10.1016/j.aicoj.2026.100127.

  5. Mojoli F, Bouhemad B, Mongodi S, et al. Lung ultrasound for critically ill patients. Am J Respir Crit Care Med. 2019;199(6):701-714.

  6. Nishigami K. Use of aortic point-of-care ultrasound in conventional and emergent echocardiography. J Med Ultrason (2001). 2022;49(4):655-661.

  7. Nazerian P, Mueller C, Vanni S, et al. Integration of transthoracic focused cardiac ultrasound in the diagnostic algorithm for suspected acute aortic syndromes. Eur Heart J. 2019;40:1952-1960.

  8. Bloom B, Gibbons R, Brandis D, et al. Point-of-care ultrasound diagnosis of acute abdominal aortic occlusion. Clin Pract Cases Emerg Med. 2020;4(1):79-82. doi:10.5811/cpcem.2019.11.44311.