Obstructive Shock (Adult)

Overview

Obstructive shock is a form of circulatory failure caused by mechanical obstruction to blood flow into or out of the heart, resulting in critically reduced cardiac output despite normal or increased intravascular volume.[1] Unlike cardiogenic shock (intrinsic pump failure) or hypovolemic shock (volume depletion), obstructive shock results from extracardiac factors physically impeding cardiac filling or ejection.

Clinical Pearl: Obstructive shock is a medical emergency requiring immediate identification and reversal of the underlying cause. Standard resuscitation measures (fluids, vasopressors) are temporizing only - definitive treatment requires relieving the obstruction.[2]

The three classic causes of obstructive shock:

Additional causes:

• Severe aortic stenosis (fixed outflow obstruction)
• Hypertrophic obstructive cardiomyopathy (dynamic outflow obstruction)
• Constrictive pericarditis (impaired filling)
• Atrial myxoma (inflow obstruction)
• Superior vena cava syndrome (impaired venous return)

Exam Detail: MRCP/FRACP and FRCEM commonly test differentiation between causes of obstructive shock using clinical signs and POCUS findings. Key exam topics include Beck's triad, pulsus paradoxus, and indications for emergency pericardiocentesis vs thrombolysis.

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Epidemiology

Incidence by Cause

Obstructive Shock in Cardiac Arrest

Prevalence in PEA arrest:[6]

• Massive PE: 2-10% of all cardiac arrests
• Cardiac tamponade: 1-3% of cardiac arrests
• Tension pneumothorax: 1-5% of trauma cardiac arrests

Survival with prompt intervention:

• Massive PE with thrombolysis: 30-50% survival
• Cardiac tamponade with drainage: 60-80% survival
• Tension pneumothorax with decompression: 70-90% survival

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Aetiology and Pathophysiology

Mechanisms of Obstructive Shock

Common pathway:[1,2]

1. Physical obstruction to blood flow
2. Reduced ventricular preload OR increased afterload
3. Decreased stroke volume and cardiac output
4. Hypotension and tissue hypoperfusion
5. Compensatory tachycardia and vasoconstriction
6. Cardiovascular collapse if obstruction not relieved

Massive Pulmonary Embolism

Definition: PE causing hemodynamic instability (SBP > 90 mmHg or vasopressor requirement)[3]

Pathophysiology:[7]

• Acute obstruction of pulmonary arterial circulation (greater than 50% occlusion typically required)
• Sudden increase in RV afterload
• RV dilation and dysfunction (acute cor pulmonale)
• Interventricular septum shifts leftward (D-shaped LV)
• Reduced LV preload and cardiac output
• Hypoxemia from V/Q mismatch and shunt
• Release of vasoconstrictors (serotonin, thromboxane) worsens pulmonary hypertension

Hemodynamic profile:

• Elevated right atrial pressure
• Elevated pulmonary artery pressure
• Low cardiac output
• Normal or low PCWP

Clinical Pearl: In massive PE, the RV acutely dilates but cannot generate pressures greater than 40-50 mmHg because it is a thin-walled chamber. If pulmonary artery systolic pressure exceeds this, suspect chronic thromboembolic disease with RV hypertrophy.[7]

Cardiac Tamponade

Definition: Life-threatening compression of the heart by pericardial fluid accumulation preventing adequate filling[4]

Pathophysiology:[8]

• Pericardial effusion accumulates (acute or chronic)
• Intrapericardial pressure rises
• When intrapericardial pressure exceeds right heart filling pressures:
  • Right atrial collapse in systole
  • Right ventricular collapse in diastole
  • Impaired venous return
  • Reduced stroke volume
• Equalization of diastolic pressures (RA = RV = PA diastolic = PCWP)
• Compensatory tachycardia maintains cardiac output temporarily
• Progression to PEA arrest

Rate of accumulation matters:

• Rapid accumulation (trauma, rupture): 100-200 mL causes tamponade
• Slow accumulation (malignancy, uremia): 1-2 L may accumulate before tamponade
• Pericardium can stretch to accommodate slowly accumulating fluid

Tension Pneumothorax

Definition: Progressive air accumulation in pleural space with one-way valve effect, causing mediastinal shift and cardiovascular collapse[5]

Pathophysiology:[9]

• Air enters pleural space (trauma, iatrogenic, spontaneous rupture)
• One-way valve prevents air escape
• Progressive positive intrapleural pressure
• Lung collapse on affected side
• Mediastinal shift to contralateral side
• Compression/kinking of great veins (SVC, IVC)
• Reduced venous return to right heart
• Decreased cardiac output
• Cardiovascular collapse

Key distinction from simple pneumothorax:

• Simple pneumothorax: no mediastinal shift, hemodynamically stable
• Tension pneumothorax: mediastinal shift, hemodynamic compromise

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Clinical Presentation

General Features of Obstructive Shock

Common signs across all causes:

• Hypotension (SBP > 90 mmHg)
• Tachycardia
• Tachypnoea
• Elevated JVP (distended neck veins)
• Cool, clammy peripheries
• Altered mental status
• Oliguria

Clinical Pearl: The combination of hypotension + elevated JVP should immediately raise suspicion for obstructive shock. This differentiates it from hypovolemic shock (flat neck veins) and distributive shock (warm peripheries initially).[2]

Differentiation by Cause

Massive Pulmonary Embolism

Symptoms:

• Sudden onset dyspnoea (80-90%)
• Chest pain (50-60%) - pleuritic or substernal
• Syncope or presyncope (30-40%)
• Haemoptysis (20-30%)
• Anxiety, sense of impending doom

Signs:

• Hypotension, tachycardia
• Tachypnoea, hypoxemia
• Elevated JVP
• RV heave (if RV dilated)
• Loud P2 (pulmonary hypertension)
• Right-sided S3 or S4
• Signs of DVT (unilateral leg swelling) in 30-50%

ECG findings:[10]

• Sinus tachycardia (most common, 40%)
• Right heart strain: S1Q3T3 pattern (classic but present in only 10-20%)
• Right axis deviation
• Right bundle branch block (new)
• T-wave inversions in V1-V4 (RV strain pattern)
• Atrial fibrillation (new onset)

Cardiac Tamponade

Beck's Triad:[4]

1. Hypotension
2. Elevated JVP (distended neck veins)
3. Muffled/distant heart sounds

Sensitivity: Only 10-40% of patients have all three signs

Pulsus paradoxus:[11]

• Exaggerated (greater than 10 mmHg) fall in systolic BP during inspiration
• Measured by deflating BP cuff slowly during respiration
• SBP at which first Korotkoff sounds heard only during expiration
• SBP at which Korotkoff sounds heard throughout respiratory cycle
• Difference greater than 10 mmHg = pulsus paradoxus

Other signs:

• Kussmaul's sign (JVP rises with inspiration - less common than in constrictive pericarditis)
• Tachycardia
• Cool peripheries
• Narrow pulse pressure
• Pericardial rub (if pericarditis present)

ECG findings:

• Low voltage QRS (> 5 mm in limb leads)
• Electrical alternans (alternating QRS amplitude - highly specific)
• Sinus tachycardia

Tension Pneumothorax

Classic presentation:[5,9]

• Sudden dyspnoea
• Chest pain (pleuritic)
• Hypotension
• Tachycardia

Signs:

• Absent breath sounds on affected side
• Hyperresonance to percussion on affected side
• Tracheal deviation away from affected side (late sign)
• Distended neck veins
• Reduced chest wall expansion on affected side
• Subcutaneous emphysema (may be present)
• Cyanosis

Clinical Pearl: Tension pneumothorax is a clinical diagnosis - do NOT wait for imaging in a hemodynamically unstable patient. If clinical suspicion is high, perform immediate needle decompression.[9]

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Investigations

Point-of-Care Ultrasound (POCUS)

POCUS is the most valuable rapid diagnostic tool in suspected obstructive shock:[12]

Cardiac views:

McConnell's sign: RV free wall akinesis with preserved apical contractility (specific for PE)

Lung ultrasound for pneumothorax:[13]

• Absent lung sliding (highly sensitive for pneumothorax)
• Absent B-lines (comet-tail artifacts)
• Lung point (transition between lung sliding and no sliding - confirms PTX, highly specific)
• Barcode sign on M-mode (vs "seashore sign" in normal lung)

Additional Investigations

For massive PE:

• CT pulmonary angiography (if stable enough to transport)
• D-dimer (if low/moderate pre-test probability)
• Troponin (RV strain marker, prognostic)
• BNP/NT-proBNP (RV dysfunction marker)
• ABG (hypoxemia, hypocapnia, increased A-a gradient)

For cardiac tamponade:

• Echocardiography (formal TTE if time permits)
• Chest X-ray (enlarged cardiac silhouette - "water bottle" heart)
• ECG (low voltage, electrical alternans)

For tension pneumothorax:

• Do NOT delay treatment for imaging in unstable patients
• CXR (if stable): absent lung markings, mediastinal shift, tracheal deviation
• CT chest: confirms diagnosis, identifies underlying cause

Laboratory Investigations

All causes:

• FBC (anaemia, thrombocytopenia)
• Coagulation (pre-procedure, DIC screening)
• Renal function, electrolytes
• Lactate (tissue hypoperfusion marker)
• Troponin (elevated in PE with RV strain, tamponade)
• ABG (hypoxemia, acid-base status)

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Management

General Principles

Immediate priorities:[2]

1. Recognize obstructive shock (hypotension + elevated JVP)
2. Identify the cause (POCUS, clinical assessment)
3. Treat the specific cause (definitive management)
4. Supportive care (oxygen, IV access, monitoring)

Important caveats:

• Fluids may be harmful - excessive fluids can worsen RV overload in PE and increase intrapericardial pressure in tamponade
• Vasopressors are temporizing - maintain perfusion while preparing definitive treatment
• Speed is critical - mortality increases rapidly without cause-specific treatment

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Massive Pulmonary Embolism

Risk stratification:[3,14]

Immediate management of massive PE:[3]

1. Anticoagulation:

• Unfractionated heparin 80 units/kg bolus, then 18 units/kg/hr infusion
• Target APTT 60-80 seconds (1.5-2.5× control)
• LMWH acceptable if not planning thrombolysis

2. Systemic thrombolysis (if hemodynamically unstable):

• Alteplase (tPA): 100 mg IV over 2 hours, OR 0.6 mg/kg over 15 minutes (max 50 mg) for cardiac arrest
• Contraindications (relative in life-threatening PE):
  • Recent surgery (> 3 weeks)
  • Recent stroke (> 3 months)
  • Active bleeding
  • Intracranial pathology

3. Vasopressors:

• Norepinephrine to maintain MAP ≥65 mmHg
• Avoid excessive fluids (worsens RV overload)
• Judicious fluid challenge (250-500 mL) only if clearly hypovolemic

4. Consider advanced therapies:

• Catheter-directed thrombolysis (lower bleeding risk, local expertise required)
• Mechanical thrombectomy (surgical or catheter-based)
• Surgical embolectomy (if thrombolysis contraindicated or failed)
• ECMO (bridge to definitive therapy in refractory shock)

Clinical Pearl: In cardiac arrest due to PE, thrombolysis should be given and CPR continued for 60-90 minutes after administration, as lysis takes time. Do not terminate resuscitation prematurely.[15]

ESC 2019 Recommendations for high-risk PE:[3]

• Systemic thrombolysis is first-line for hemodynamically unstable PE (Class I)
• Surgical embolectomy or catheter-directed therapy for failed thrombolysis or contraindications (Class I)
• VA-ECMO as bridge to recovery or intervention (Class IIa)

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Cardiac Tamponade

Immediate management:[4,8]

1. Emergency pericardiocentesis:

• Indication: Hemodynamic compromise due to tamponade
• Approach: Subxiphoid (most common) or apical
• Guidance: Ultrasound/echo-guided preferred (reduces complications)
• Needle: 18G spinal needle or catheter-over-needle
• Aspiration: Even 20-50 mL can dramatically improve hemodynamics
• Drain placement: Leave drain for ongoing drainage if recurrence expected

Pericardiocentesis technique (subxiphoid approach):

1. Position patient at 30-45° (brings heart closer to chest wall)
2. Identify entry point: Left of xiphoid process, 1-2 cm inferior
3. Advance needle at 30-45° toward left shoulder
4. Aspirate continuously while advancing
5. Attach to 3-way stopcock and syringe
6. Drain fluid, send for analysis (cytology, culture, biochemistry)
7. Consider leaving pigtail catheter for ongoing drainage

2. Supportive measures (while preparing for drainage):

• IV fluids: Small boluses (250-500 mL) may transiently improve preload
• Avoid excessive fluid (can worsen tamponade)
• Vasopressors: Norepinephrine to maintain perfusion
• Avoid intubation if possible (positive pressure ventilation worsens hemodynamics)
• If intubation required: Use ketamine, minimize PEEP

3. Definitive management:

• Surgical pericardial window: For recurrent effusions, traumatic hemopericardium
• Pericardiectomy: For constrictive pericarditis, recurrent tamponade
• Treat underlying cause: Malignancy, infection, uremia, etc.

Exam Detail: Classic exam question: "Why avoid positive pressure ventilation in tamponade?" Answer: PPV increases intrathoracic pressure, further reduces venous return, and worsens tamponade physiology. Spontaneous breathing maintains negative intrathoracic pressure that supports venous return.[8]

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Tension Pneumothorax

Immediate management:[5,9]

1. Emergency decompression (do NOT wait for imaging):

Needle thoracostomy:

• Site: 2nd intercostal space, midclavicular line (traditional) OR 4th/5th intercostal space, anterior axillary line (preferred - less failure rate)
• Needle: 14G or larger cannula, minimum 5 cm length (8 cm in obese)
• Technique: Insert perpendicular to chest wall, just above rib (avoid neurovascular bundle)
• Confirmation: Rush of air, clinical improvement

Finger thoracostomy:

• Preferred in trauma and arrest settings
• Site: 4th/5th intercostal space, mid-axillary line (safe triangle)
• Technique: Skin incision, blunt dissection through intercostal muscles, finger into pleural space
• Allows immediate decompression and chest tube insertion

2. Chest tube (definitive treatment):

• Insert immediately after needle decompression
• 28-32 Fr tube for trauma, 24-28 Fr for spontaneous PTX
• Connect to underwater seal or flutter valve

3. Treat underlying cause:

• Trauma: Assess for ongoing air leak, associated injuries
• Iatrogenic: Review procedure, prevent recurrence
• Spontaneous: Consider pleurodesis for recurrent cases

Clinical Pearl: Needle thoracostomy fails in up to 30-50% of cases due to insufficient needle length, particularly in obese patients or when performed at the 2nd ICS. The 5th ICS anterior axillary line has higher success rates.[16]

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Obstructive Shock in Cardiac Arrest

Recognition:[6]

• PEA with organized ECG rhythm but no pulse
• Clinical context suggesting PE, tamponade, or tension PTX
• POCUS during rhythm check (RV dilation, pericardial effusion, absent lung sliding)

Management during CPR:

Resuscitative thoracotomy:[17]

• Consider for traumatic cardiac arrest with suspected tamponade or massive hemorrhage
• Anterolateral thoracotomy in 5th intercostal space
• Allows direct cardiac massage, pericardiotomy, aortic cross-clamping
• Best outcomes: penetrating cardiac injury with witnessed arrest and signs of life

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Complications

Complications of Obstructive Shock

Procedure-Related Complications

Pericardiocentesis:

• Myocardial puncture (1-5%)
• Coronary artery laceration (> 1%)
• Pneumothorax (2-5%)
• Arrhythmias (1-5%)
• Infection (> 1%)

Needle thoracostomy:

• Failure to decompress (30-50%)
• Lung laceration
• Intercostal vessel injury
• Infection

Thrombolysis:

• Major bleeding (5-10%)
• Intracranial hemorrhage (1-3%)
• Minor bleeding (10-20%)

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Prognosis

Outcomes by Cause

Prognostic Factors

Massive PE:[3]

• Cardiac arrest at presentation: 50-70% mortality
• Hypotension without arrest: 25-40% mortality
• Need for mechanical ventilation: poor prognosis
• RV dysfunction persisting greater than 24 hours: worse outcomes

Cardiac tamponade:[4]

• Etiology matters: Traumatic and malignant have worse prognosis
• Time to drainage: Delays increase mortality
• Underlying disease: Determines long-term outcome

Tension pneumothorax:[5]

• Time to decompression critical
• Associated injuries (trauma) determine overall outcome
• Iatrogenic: Generally good prognosis with prompt treatment

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Prevention

Primary Prevention

Pulmonary embolism prevention:

• VTE prophylaxis in hospitalized/immobile patients
• Early mobilization post-surgery
• Anticoagulation for AF and prosthetic valves
• Graduated compression stockings for high-risk patients

Tension pneumothorax prevention:

• Careful technique during central line insertion, thoracentesis
• Lung-protective ventilation in mechanically ventilated patients
• Monitoring patients with known lung disease

Cardiac tamponade:

• Careful anticoagulation monitoring
• Pericarditis treatment to prevent effusion development
• Surveillance in high-risk conditions (malignancy, renal failure)

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Key Guidelines

1. ESC 2019: Diagnosis and Management of Acute Pulmonary Embolism[3]
2. ESC 2015: Diagnosis and Management of Pericardial Diseases[18]
3. ATLS 10th Edition: Chest Trauma and Tension Pneumothorax[19]
4. ERC 2021: Cardiac Arrest in Special Circumstances[15]

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Exam Scenarios

SBA Question 1

Scenario: A 55-year-old man with known metastatic lung cancer presents with progressive dyspnoea over 2 weeks. His BP is 80/50 mmHg, HR 120 bpm, JVP is markedly elevated, and heart sounds are difficult to hear. ECG shows low voltage QRS complexes and electrical alternans. What is the most likely diagnosis?

A) Massive pulmonary embolism
B) Cardiac tamponade
C) Tension pneumothorax
D) Acute myocardial infarction
E) Septic shock

Answer

Answer: B) Cardiac tamponade

This patient has classic features of cardiac tamponade:

• Beck's triad: Hypotension, elevated JVP, muffled heart sounds
• ECG findings: Low voltage QRS, electrical alternans
• Risk factor: Malignancy (common cause of pericardial effusion)
• Subacute presentation: 2-week history allows gradual effusion accumulation

Electrical alternans (alternating QRS amplitude) is highly specific for large pericardial effusion with tamponade physiology.[4]

SBA Question 2

Scenario: A 28-year-old woman on combined oral contraceptive pills presents with sudden collapse. She is hypotensive (BP 75/40 mmHg) with distended neck veins. Bedside echocardiography shows a dilated RV with septal flattening and no pericardial effusion. What is the most appropriate immediate management?

A) IV fluid bolus 30 mL/kg
B) Emergency pericardiocentesis
C) Needle thoracostomy
D) Systemic thrombolysis with alteplase
E) Dobutamine infusion

Answer

Answer: D) Systemic thrombolysis with alteplase

This patient has clinical and echocardiographic features of massive pulmonary embolism:

• Risk factor: Oral contraceptive use
• Hypotension with elevated JVP
• Echo: RV dilation with septal flattening (D-sign), no pericardial effusion

For high-risk (massive) PE with hemodynamic instability, systemic thrombolysis is first-line treatment (ESC Class I recommendation).[3]

Excessive IV fluids may worsen RV overload. Pericardiocentesis is not indicated (no effusion). Needle thoracostomy is for tension pneumothorax. Dobutamine may help RV function but does not address the obstruction.

SBA Question 3

Scenario: During central venous catheter insertion in the right internal jugular vein, a mechanically ventilated ICU patient suddenly becomes hypotensive (BP 70/40 mmHg) with oxygen saturation dropping to 85%. Breath sounds are absent on the right side with hyperresonance. What is the most appropriate immediate action?

A) Order urgent chest X-ray
B) Perform CT pulmonary angiogram
C) Perform needle decompression of right chest
D) Administer IV fluid bolus
E) Increase PEEP to improve oxygenation

Answer

Answer: C) Perform needle decompression of right chest

This is classic presentation of iatrogenic tension pneumothorax complicating central line insertion:

• Sudden hypotension and desaturation
• Absent breath sounds on ipsilateral side
• Hyperresonance to percussion

Tension pneumothorax is a clinical diagnosis - imaging should NOT delay treatment in a hemodynamically unstable patient. Immediate needle or finger thoracostomy is life-saving.[9]

Increasing PEEP would worsen the situation by further increasing intrathoracic pressure.

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Viva Scenario

Examiner: "A 45-year-old man is brought to resus after a witnessed collapse at home. He is unresponsive with a weak pulse. His BP is 70/40 mmHg, HR 130 bpm, and his neck veins are markedly distended. You have access to bedside ultrasound. Talk me through your approach."

Candidate approach:

Initial assessment: "This patient is in shock with elevated JVP, which suggests obstructive shock as the most likely category. I need to rapidly differentiate between the three main causes:

• Massive pulmonary embolism
• Cardiac tamponade
• Tension pneumothorax

While preparing for POCUS, I would simultaneously:

• Ensure IV access and attach monitoring
• Give high-flow oxygen
• Brief history from family: any recent immobility, DVT, trauma, malignancy, or chest symptoms"

Examiner: "He has a history of lung cancer diagnosed 3 months ago. How does this change your thinking?"

Candidate: "Lung cancer significantly increases my suspicion for both PE (hypercoagulable state) and cardiac tamponade (malignant pericardial effusion). I would prioritize:

POCUS assessment:

1. Cardiac views: Looking for:

   • Pericardial effusion with RA/RV collapse → tamponade
   • RV dilation with D-shaped LV → massive PE

2. Lung ultrasound: Looking for:

   • Absent lung sliding with lung point → pneumothorax

3. IVC assessment:

   • Plethoric, non-collapsing IVC → elevated right heart pressures (both PE and tamponade)"

Examiner: "Your cardiac ultrasound shows a moderate pericardial effusion with right ventricular diastolic collapse. What do you do?"

Candidate: "This confirms cardiac tamponade. I would:

Immediate actions:

1. Call for cardiology/cardiothoracic surgery backup
2. Prepare for emergency pericardiocentesis
3. Give a small fluid bolus (250-500 mL) to temporarily improve preload
4. Have norepinephrine ready to maintain perfusion during the procedure
5. Avoid intubation if possible - positive pressure ventilation will worsen tamponade

Pericardiocentesis:

• Ultrasound-guided, subxiphoid approach
• 18G needle with syringe, advance toward left shoulder under real-time echo guidance
• Even 20-50 mL drainage can produce dramatic hemodynamic improvement
• Leave a pigtail catheter for ongoing drainage given malignant etiology

Post-procedure:

• Confirm improvement with repeat echo
• Send fluid for cytology, culture, biochemistry
• Oncology review for management of malignant effusion
• May need pericardial window for definitive management"

Examiner: "What if the echo had shown a dilated RV with septal flattening instead of pericardial effusion?"

Candidate: "That would indicate massive PE rather than tamponade. Given hemodynamic instability, I would:

1. Systemic thrombolysis with alteplase 100 mg over 2 hours (or 50 mg bolus if near-arrest)
2. Start heparin anticoagulation
3. Norepinephrine to maintain MAP ≥65 mmHg
4. Avoid excessive fluids which can worsen RV overload
5. Consider ECMO if deteriorating despite thrombolysis
6. Contact interventional cardiology for potential catheter-directed therapy if thrombolysis fails or is contraindicated"

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Patient Explanation (Layperson Level)

"You are experiencing a type of shock called 'obstructive shock.' This happens when something is physically blocking blood from flowing through your heart properly.

There are three main causes:

1. Pulmonary embolism (blood clot in the lungs): A blood clot has traveled to your lungs and is blocking blood flow. We may need to give you a strong clot-dissolving medication or perform a procedure to remove the clot.

2. Cardiac tamponade (fluid around the heart): Fluid has built up in the sac around your heart and is squeezing it, preventing it from filling properly. We need to drain this fluid using a needle inserted through your chest wall - this usually provides immediate relief.

3. Tension pneumothorax (trapped air in the chest): Air has leaked into the space around your lung and is building up pressure, pushing on your heart and preventing blood from returning to it. We need to release this trapped air immediately using a needle or small tube.

All of these conditions are medical emergencies, but they are treatable if we act quickly. The treatment depends on identifying exactly which problem you have, which is why we're doing ultrasound scans and other tests right now.

Once we treat the underlying blockage, your blood pressure should improve and your organs will get the blood flow they need again."

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References

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2. Standl T, Annecke T, Cascorbi I, et al. The Nomenclature, Definition and Distinction of Types of Shock. Dtsch Arztebl Int. 2018;115(45):757-768. doi:10.3238/arztebl.2018.0757

3. Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism. Eur Heart J. 2020;41(4):543-603. doi:10.1093/eurheartj/ehz405

4. Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. Eur Heart J. 2015;36(42):2921-2964. doi:10.1093/eurheartj/ehv318

5. Roberts DJ, Leigh-Smith S, Faris PD, et al. Clinical Presentation of Patients With Tension Pneumothorax: A Systematic Review. Ann Surg. 2015;261(6):1068-1078. doi:10.1097/SLA.0000000000001073

6. Bergum D, Nordseth T, Mjølstad OC, et al. Causes of in-hospital cardiac arrest - Incidences and rate of recognition. Resuscitation. 2015;87:63-68. doi:10.1016/j.resuscitation.2014.11.007

7. Matthews JC, McLaughlin V. Acute right ventricular failure in the setting of acute pulmonary embolism or chronic pulmonary hypertension: a detailed review of the pathophysiology, diagnosis, and management. Curr Cardiol Rev. 2008;4(1):49-59. doi:10.2174/157340308783565384

8. Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003;349(7):684-690. doi:10.1056/NEJMra022643

9. Leigh-Smith S, Harris T. Tension pneumothorax--time for a re-think? Emerg Med J. 2005;22(1):8-16. doi:10.1136/emj.2003.010421

10. Ferrari E, Imbert A, Chevalier T, et al. The ECG in pulmonary embolism. Predictive value of negative T waves in precordial leads--80 case reports. Chest. 1997;111(3):537-543. doi:10.1378/chest.111.3.537

11. Curtiss EI, Reddy PS, Uretsky BF, Cecchetti AA. Pulsus paradoxus: definition and relation to the severity of cardiac tamponade. Am Heart J. 1988;115(2):391-398. doi:10.1016/0002-8703(88)90487-5

12. Labovitz AJ, Noble VE, Bierig M, et al. Focused cardiac ultrasound in the emergent setting: a consensus statement of the American Society of Echocardiography. J Am Soc Echocardiogr. 2010;23(12):1225-1230. doi:10.1016/j.echo.2010.10.005

13. Volpicelli G, Elbarbary M, Blaivas M, et al. International evidence-based recommendations for point-of-care lung ultrasound. Intensive Care Med. 2012;38(4):577-591. doi:10.1007/s00134-012-2513-4

14. Jaff MR, McMurtry MS, Archer SL, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension. Circulation. 2011;123(16):1788-1830. doi:10.1161/CIR.0b013e318214914f

15. Lott C, Truhlář A, Alfonzo A, et al. European Resuscitation Council Guidelines 2021: Cardiac arrest in special circumstances. Resuscitation. 2021;161:152-219. doi:10.1016/j.resuscitation.2021.02.011

16. Inaba K, Ives C, McClure K, et al. Radiologic evaluation of alternative sites for needle decompression of tension pneumothorax. Arch Surg. 2012;147(9):813-818. doi:10.1001/archsurg.2012.751

17. Burlew CC, Moore EE, Moore FA, et al. Western Trauma Association critical decisions in trauma: resuscitative thoracotomy. J Trauma Acute Care Surg. 2012;73(6):1359-1363. doi:10.1097/TA.0b013e318270d2df

18. Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases. Eur Heart J. 2015;36(42):2921-2964. doi:10.1093/eurheartj/ehv318

19. American College of Surgeons Committee on Trauma. ATLS: Advanced Trauma Life Support Student Course Manual. 10th ed. American College of Surgeons; 2018.

20. Konstantinides SV, Torbicki A, Agnelli G, et al. 2014 ESC guidelines on the diagnosis and management of acute pulmonary embolism. Eur Heart J. 2014;35(43):3033-3069. doi:10.1093/eurheartj/ehu283

21. Roy PM, Colombet I, Durieux P, et al. Systematic review and meta-analysis of strategies for the diagnosis of suspected pulmonary embolism. BMJ. 2005;331(7511):259. doi:10.1136/bmj.331.7511.259

22. Kearon C, Akl EA, Ornelas J, et al. Antithrombotic Therapy for VTE Disease: CHEST Guideline and Expert Panel Report. Chest. 2016;149(2):315-352. doi:10.1016/j.chest.2015.11.026

23. Levine MJ, Lorell BH, Diver DJ, Come PC. Implications of echocardiographically assisted diagnosis of pericardial tamponade in contemporary medical patients: detection before hemodynamic embarrassment. J Am Coll Cardiol. 1991;17(1):59-65. doi:10.1016/0735-1097(91)90704-c

24. Tsang TS, Enriquez-Sarano M, Freeman WK, et al. Consecutive 1127 therapeutic echocardiographically guided pericardiocenteses: clinical profile, practice patterns, and outcomes spanning 21 years. Mayo Clin Proc. 2002;77(5):429-436. doi:10.4065/77.5.429