Shock Classification: 4 Types, Hemodynamics & Treatment

Q: How do I differentiate tension pneumothorax from cardiac tamponade at the bedside?

Both cause JVD + hypotension + tachycardia (obstructive shock). Tension PTX: absent/decreased breath sounds unilaterally, hyperresonance to percussion, tracheal deviation away from affected side (late sign). Tamponade: breath sounds normal bilaterally, muffled heart sounds, pulsus paradoxus >10 mmHg (SBP drops >10 on inspiration), confirmed by bedside echo showing pericardial effusion with diastolic RV collapse. Do not wait for CXR if clinical tension PTX — needle decompression immediately.

The 60-second version

Four shock types: hypovolemic (low CO/PCWP, high SVR), distributive (high CO, low SVR), cardiogenic (low CO, high PCWP/SVR), obstructive (low CO, high SVR, variable PCWP)
Septic shock: norepinephrine first-line vasopressor; blood cultures before antibiotics but antibiotics within 1h
Cardiogenic shock: avoid fluids; use dobutamine for inotropy; emergent PCI for STEMI with cardiogenic shock
Obstructive causes are immediately reversible: needle decompression for tension PTX, pericardiocentesis for tamponade, thrombolytics for massive PE
Anaphylaxis: IM epinephrine to vastus lateralis is first-line — not antihistamines, not IV diphenhydramine

Hemodynamic Classification and Profiles

The key hemodynamic parameters are cardiac output (CO), systemic vascular resistance (SVR), and pulmonary capillary wedge pressure (PCWP, a proxy for left heart filling pressure). **Hypovolemic shock** (hemorrhage, dehydration, burns, pancreatitis): low CO, high SVR (compensatory vasoconstriction), low PCWP (low preload). **Distributive shock** (sepsis, anaphylaxis, neurogenic, adrenal crisis): high CO (early), low SVR (massive vasodilation is the primary defect), normal/low PCWP. The warm, vasodilated early septic shock is classic: warm extremities, bounding pulses, wide pulse pressure before compensation. Late septic shock: CO falls due to myocardial depression. **Cardiogenic shock** (MI, acute decompensated HF, myocarditis): low CO (pump failure), high SVR (compensatory), high PCWP (fluid backs up behind failing ventricle) — the wet and cold patient. **Obstructive shock** (tension pneumothorax, cardiac tamponade, massive PE, aortic coarctation): low CO (mechanical obstruction prevents filling/ejection), high SVR, high or low PCWP (varies by cause). JVD present in tamponade and tension PTX but absent in hypovolemic.

Specific Clinical Presentations and Diagnosis

**Hypovolemic**: exam shows tachycardia, hypotension, flat JVD, dry mucous membranes, poor skin turgor, oliguria; trauma patients — look for bleeding source; Class I–IV hemorrhagic shock based on blood loss (Class I: <750 mL, HR <100; Class IV: >2000 mL, HR >140, negligible UO, confused). **Distributive (septic)**: fever/hypothermia, high WBC or bandemia, warm flushed skin, wide pulse pressure (SBP−DBP >40), high lactate (>2 mmol/L = septic shock criterion per Sepsis-3); source control is paramount. **Anaphylactic shock**: urticaria, angioedema, bronchospasm after allergen exposure — epinephrine IM first-line. **Neurogenic shock** (spinal cord injury T6 and above): bradycardia + hypotension (disruption of sympathetic chain) — triad of hypotension, bradycardia, warm extremities. **Cardiogenic**: JVD, S3 gallop, bilateral crackles, cool clammy extremities, pulmonary edema on CXR; STEMI + cardiogenic shock → emergent PCI. **Obstructive**: Tension PTX (absent breath sounds, tracheal deviation — needle decompression immediately before CXR); Tamponade (Beck's triad: hypotension + JVD + muffled heart sounds; pulsus paradoxus >10 mmHg; pericardiocentesis); Massive PE (acute cor pulmonale, right heart strain on ECG — S1Q3T3, echo shows RV dilation).

Management Principles by Shock Type

**Hypovolemic**: volume resuscitation (1:1:1 PRBCs:FFP:platelets for massive hemorrhage, 'balanced resuscitation'; crystalloid as bridge); identify and control bleeding source; transfusion threshold Hgb <7 (or <8 in cardiac disease); vasopressors as bridge only. **Septic shock**: Sepsis Hour Bundles — blood cultures × 2 then antibiotics within 1h, 30 mL/kg IV crystalloid bolus, vasopressors if MAP <65 after fluids, lactate remeasurement; norepinephrine = first-line vasopressor (increases SVR and MAP with minimal tachycardia); add vasopressin or epinephrine for refractory shock; hydrocortisone 200 mg/day for steroid-refractory septic shock. **Anaphylaxis**: IM epinephrine (0.3–0.5 mg, 1:1000) to vastus lateralis — first and most important intervention; antihistamines and steroids secondary. **Cardiogenic**: norepinephrine or dopamine for severe hypotension; avoid aggressive fluids (worsen pulmonary edema); dobutamine (inotrope) if low CO without severe hypotension; IABP or Impella mechanical support for refractory; emergent PCI for STEMI. **Obstructive**: tension PTX → immediate needle decompression (2nd ICS MCL) then chest tube; tamponade → pericardiocentesis; massive PE → anticoagulation ± thrombolytics (tPA) if hemodynamically unstable.

Test yourself

Quick check — 3 questions

1. A 28-year-old man is brought in after a motorcycle accident with blunt chest trauma. He is hypotensive (BP 78/50), tachycardic (HR 128), with absent breath sounds on the left, hyperresonance to percussion on the left, and tracheal deviation to the right. What is the immediate next step?

2. A 70-year-old man with anterior STEMI develops acute hypotension (BP 80/60) and respiratory distress 2 hours after arrival. Exam shows JVD, bilateral crackles, and cold clammy extremities. CXR shows pulmonary edema. What is the hemodynamic profile and most critical intervention?

3. A 22-year-old woman with no prior history develops sudden hypotension, urticaria, and stridor after eating at a restaurant. She is in anaphylactic shock. What is the correct first-line treatment and route of administration?

Frequently asked questions

How do I differentiate tension pneumothorax from cardiac tamponade at the bedside?

Both cause JVD + hypotension + tachycardia (obstructive shock). Tension PTX: absent/decreased breath sounds unilaterally, hyperresonance to percussion, tracheal deviation away from affected side (late sign). Tamponade: breath sounds normal bilaterally, muffled heart sounds, pulsus paradoxus >10 mmHg (SBP drops >10 on inspiration), confirmed by bedside echo showing pericardial effusion with diastolic RV collapse. Do not wait for CXR if clinical tension PTX — needle decompression immediately.

Why is norepinephrine preferred over dopamine as first-line vasopressor in septic shock?

Norepinephrine primarily increases SVR via α1 agonism with modest β1 effect, reliably raising MAP with less tachycardia than dopamine. Dopamine has a dose-dependent mechanism (low dose: DA receptors → renal vasodilation [minimal clinical benefit]; medium dose: β1 → increased inotropy/HR; high dose: α1 → vasoconstriction) and causes more arrhythmias (especially atrial fibrillation). The SOAP II trial showed dopamine was associated with more arrhythmias and possible harm in cardiogenic shock patients. Norepinephrine is the 2016 Surviving Sepsis Campaign first-line recommendation.

Practice makes permanent

Lock this into long-term memory

Progress Note's adaptive engine spaces your reviews automatically — so this stays with you through boards and onto the wards.

Start practicing free

Share Post LinkedIn Reddit

Continue the curriculum

Sepsis Criteria: Sepsis-3 Explained

Acute Coronary Syndrome: STEMI, NSTEMI, and Unstable Angina

Acute Kidney Injury: Prerenal, Intrinsic, and Postrenal