Hypotension and Shock
Hypotension and Shock - Renal-focused approach to hypotension, shock, vasopressors and shock-associated AKI.
Practical orientation: Shock management is kidney-protective when it restores perfusion without causing avoidable fluid overload.
Use first: clinical summary and algorithm.
Then: differential diagnosis, workup and management tables.
Escalate: use red flags and biopsy/urgent-care sections.
Clinical summary
Hypotension
Absolute SBP <90 or MAP <65, or relative drop from baseline; not synonymous with shock.
Shock
Tissue hypoxia due to inadequate oxygen delivery or utilization.
Kidney risk
Persistent renal hypoperfusion causes reduced GFR and may progress to ATN.
Initial management
Treat cause while resuscitating with fluids, vasopressors and inotropes based on hemodynamics.
Hypotension-induced AKI
Renal autoregulation uses prostaglandin-mediated afferent dilation and angiotensin II-mediated efferent constriction to preserve GFR. NSAIDs and RAAS inhibitors can impair these compensatory mechanisms. When perfusion pressure falls below the autoregulatory range, GFR falls and persistent hypoperfusion can lead to tubular injury.
Shock categories
| Type | Typical causes | Hemodynamic pattern |
|---|---|---|
| Hypovolemic | Blood loss, fluid loss. | Low preload and low cardiac output. |
| Distributive | Sepsis, anaphylaxis, pancreatitis, liver failure. | Low systemic vascular resistance; cardiac output may be high early. |
| Cardiogenic | Myocardial infarction, severe CHF, arrhythmia, valvular disease. | High filling pressures and low cardiac output. |
| Obstructive | Pulmonary embolism, tamponade, tension pneumothorax. | Impaired filling or outflow. |
Workup
| Domain | Tests |
|---|---|
| Perfusion | Lactate, mental status, urine output, capillary refill. |
| Organ injury | Renal/liver tests, CBC, coagulation profile, ABG. |
| Cardiac | ECG, troponin, BNP/NT-proBNP, bedside echo/TTE. |
| Infection | Cultures and source-directed imaging. |
| Imaging | CXR, bedside ultrasound, additional CT/US as needed. |
Vasopressors and inotropes
| Agent | Practical role |
|---|---|
| Norepinephrine | First-line vasopressor for most septic/distributive shock. |
| Vasopressin | Add-on to norepinephrine when MAP target not reached or catecholamine sparing desired. |
| Epinephrine | Alternative/add-on vasopressor; more beta effect. |
| Dopamine | Not preferred; more arrhythmias and low-dose dopamine does not prevent AKI. |
| Dobutamine/milrinone | Consider when cardiogenic component or low output persists despite vasopressors. Adjust milrinone in kidney dysfunction. |
Orthostatic hypotension
| Cause group | Examples |
|---|---|
| Volume depletion | Fluid loss, overdiuresis, overdialysis, adrenal insufficiency, anemia. |
| Autonomic dysfunction | Diabetes, amyloidosis, Parkinson disease, multiple system atrophy. |
| Drugs | Antihypertensives, alpha-1 blockers, trazodone, SSRIs, MAO inhibitors, TCAs, vasodilators. |
| Treatment | Volume repletion, remove causative drugs, slow posture changes, compression, fludrocortisone, midodrine or droxidopa when appropriate. |