Arterial hypotension

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Based on the textbook content retrieved, here is a comprehensive overview of arterial hypotension:

Arterial Hypotension

Definition

Arterial hypotension is clinically significant when:

Systolic BP < 90 mmHg, or
Mean arterial pressure (MAP) < 60–65 mmHg

At these thresholds, autoregulatory mechanisms are overwhelmed and selective vasoconstriction can no longer preserve adequate blood flow to vital organs.

MAP = Diastolic BP + [Pulse pressure / 3]

A single episode of undifferentiated hypotension with a marked BP < 80 mmHg carries an in-hospital mortality of ~18%.

Pathophysiology

Hypotension arises from one or more of the following haemodynamic derangements:

Mechanism	Category of Shock	Examples
Reduced cardiac preload (↓ circulating volume)	Hypovolemic	Haemorrhage, dehydration, vascular leakage
Pump failure (↓ cardiac output)	Cardiogenic	Acute MI, arrhythmia, myocarditis, valvular dysfunction
Loss of vasomotor tone (↓ SVR)	Distributive	Sepsis, anaphylaxis, neurogenic shock
Mechanical obstruction	Obstructive	Pulmonary embolism, cardiac tamponade, tension pneumothorax

Mixed forms are common — e.g., septic shock combines distributive, cardiogenic, and hypovolemic elements simultaneously.

Clinical Presentation

Early / compensated phase:

Tachycardia (sympathetic response)
Mild blood pressure elevation initially (increased contractility)
Peripheral vasoconstriction → cool skin, sluggish capillary refill
Tachypnoea (compensatory respiratory alkalosis)
In distributive shock: paradoxically warm, flushed peripheries

Overt shock:

Hypotension (SBP < 90 mmHg or MAP < 60 mmHg)
Altered mental status (confusion, disorientation, coma)
Oliguria (urine output < 5–15 mL/hr in advanced states)
Cold, clammy, mottled/cyanotic skin
Loss of peripheral pulses
Hyperlactataemic metabolic acidosis (anaerobic metabolism)
Hypothermia (even in septic shock)
Eventual bradycardia (from myocardial ischaemia in advanced cases)

Shock Index = HR / SBP. Normal: 0.5–0.7. A persistent index > 1.0 indicates impaired left ventricular function and is associated with increased mortality.

Orthostatic Hypotension

A distinct presentation where BP falls on assuming an upright posture. Causes include:

Volume depletion / venous pooling
Drugs: diuretics, antihypertensives, nitrates, calcium channel blockers, MAOIs, phenothiazines, opiates, L-dopa, alcohol, TCAs
Autonomic failure: Shy-Drager (multiple system atrophy), diabetes, amyloidosis, Guillain-Barré, AIDS, chronic alcoholism, POTS

Management

1. Fluid Resuscitation

Haemorrhagic shock: isotonic crystalloid (10–20 mL/kg) as initial step; if >2 units PRBCs needed, use balanced 1:1:1 ratio of PRBCs : FFP : platelets
Septic shock: 30 mL/kg IV crystalloid bolus; transfuse PRBCs at Hb < 7 g/dL
Cardiogenic shock: fluids must be used cautiously — risk of pulmonary oedema

2. Vasopressors

Indicated when fluid resuscitation alone is insufficient to restore MAP ≥ 65 mmHg:

Agent	Indication	Dose
Norepinephrine	First-line for distributive (septic), cardiogenic, neurogenic shock	0.05 mcg/kg/min, titrate every 3–5 min
Vasopressin	Adjunct to norepinephrine in septic shock	0.03–0.04 units/min (fixed rate)
Phenylephrine	Pure vasoconstriction; useful if tachyarrhythmia limits NE	Titrated to MAP
Dobutamine	Inotropic support in cardiogenic or septic shock (combined with NE)	5 mcg/kg/min

In septic/vasodilatory shock, permissive hypotension to MAP 60–65 mmHg does not appear superior to standard targets. — Goldman-Cecil Medicine

In haemorrhagic shock, vasopressors are ancillary only — their use is associated with increased mortality; focus must remain on haemorrhage control and blood product resuscitation. — Rosen's Emergency Medicine

3. Treat the Underlying Cause

Haemorrhage: haemostasis (direct pressure, REBOA, surgery)
Sepsis: antimicrobials within 1 hour, source control
Cardiogenic: revascularisation (PCI/thrombolysis), IABP for refractory cases
Obstructive: drainage (pericardiocentesis, chest needle/tube), thrombolysis for massive PE

Special Contexts

Neurogenic shock (spinal cord injury): NE is a reasonable first choice; phenylephrine if purely vasodilatory or tachyarrhythmia develops
Epidural/spinal anaesthesia: uterine blood flow is preserved unless arterial hypotension occurs — prevention is critical in obstetric patients
Raised ICP: arterial hypotension → autoregulatory cerebral vasodilation → ↑ CBV → ↑ ICP → ↓ CPP (vicious cycle; hypotension must be avoided)
CRRT vs. intermittent HD: CRRT enables effective solute removal even in the presence of arterial hypotension — Goldman-Cecil Medicine, Barash Clinical Anesthesia

Sources: Goldman-Cecil Medicine, 26e | Rosen's Emergency Medicine, 10e | Bradley & Daroff's Neurology in Clinical Practice, 8e | Miller's Anesthesia, 10e | Fuster & Hurst's The Heart, 15e

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Here are thorough, structured notes on Arterial Hypotension drawn from the textbooks in the library — primarily Goldman-Cecil Medicine, Rosen's Emergency Medicine, and Miller's Anesthesia.

Arterial Hypotension — Textbook Notes

1. Definition

Arterial hypotension is clinically defined as:

Systolic BP < 90 mmHg, or
Mean Arterial Pressure (MAP) < 60 mmHg

MAP = Diastolic BP + (Pulse Pressure ÷ 3)

These cut-points reflect population norms and are somewhat arbitrary — borderline values must always be interpreted in the context of the full clinical picture. A patient with chronic hypertension may be hypoperfused at a "normal" BP.

When BP is normal but hypoperfusion is suspected, a serum lactate should be checked immediately:

Lactate > 2 mmol/L → consistent with hypoperfusion/shock
Lactate > 4 mmol/L → specific cut-point to establish shock
Even mild elevations within normal range (< 2 mmol/L) can indicate increased risk of death

2. Pathophysiology

Arterial hypotension results from failure of one or more components of the circulatory system. The final common pathway is inadequate oxygen delivery to tissues.

Haemodynamic Mechanisms

Mechanism	Category	Haemodynamic Profile
↓ Circulating volume → ↓ venous return → ↓ preload → ↓ CO	Hypovolemic	↓ CO, ↑ SVR (compensated)
Primary pump failure → ↓ CO	Cardiogenic	↓ CO, ↑ SVR, ↑ filling pressures
Loss of peripheral vasomotor tone → ↓ SVR	Distributive	↑ or normal CO, ↓ SVR
Mechanical blockage → ↓ CO	Obstructive	↓ CO, ↑ SVR

Compensatory responses (activated by baroreceptors/chemoreceptors when CO falls):

Sympathetic activation → tachycardia + increased inotropy
Peripheral vasoconstriction → redistribution of blood flow to heart and brain
Increased venous tone → ↑ venous return and preload
These mechanisms temporarily sustain oxygen delivery — but when volume loss is too great, compensation fails and overt hypotension occurs

Cellular & Metabolic Consequences

Tissue hypoperfusion → switch to anaerobic metabolism → lactic acidosis
Splanchnic and hepatic blood flow severely reduced → ileus, hepatic ischaemia
Continued hypoperfusion → multisystem organ failure

3. Classification of Shock (Causes of Arterial Hypotension)

A. Hypovolemic Shock

Caused by loss of circulating volume:

Haemorrhagic: trauma, GI bleeding, ruptured aortic aneurysm, surgical bleeding
Non-haemorrhagic: severe dehydration, vomiting/diarrhoea, burns (skin losses), ascites (liver failure, ovarian cancer), vascular leakage (e.g., dengue fever toxin-mediated endothelial damage)
In the post-operative setting: inadequate intraoperative fluid replacement, third-space translocation, neuraxial (spinal/epidural) blockade causing venous capacitance pooling

Clinical signs (volume-dependent): tachycardia is often the only sign with ≤10% blood volume loss; at ~40% loss, lactic acidosis, severe hypotension, and reduced CO are all evident.

Haemorrhagic Shock Classification (American College of Surgeons):

Class	Blood Loss	% Volume	BP	HR	Urine Output	Mental Status
I	< 750 mL	< 15%	Normal	< 100	> 30 mL/hr	Slightly anxious
II	750–1500 mL	15–30%	Normal	> 100	20–30 mL/hr	Mildly anxious
III	1500–2000 mL	30–40%	↓	> 120	5–15 mL/hr	Anxious, confused
IV	> 2000 mL	> 40%	↓	> 140	Negligible	Confused, lethargic

B. Distributive Shock

Caused by loss of vasomotor tone (↓ SVR):

Septic shock — most common cause overall; accounts for > 50% of all shock cases
Anaphylaxis — hypotension + cutaneous (urticaria, angioedema) + respiratory (bronchospasm) features; epinephrine is the drug of choice
Neurogenic shock — follows major spinal cord injury; loss of sympathetic tone → bradycardia + hypotension (unlike other shock types)
Iatrogenic sympathectomy — high spinal/epidural block (to T4) → loss of vascular tone + cardiac accelerator fibre block → risk of arrest even in young healthy patients

C. Cardiogenic Shock

Pump failure causes:

Acute myocardial infarction (most common)
Acute valvular dysfunction
Arrhythmias
Myocarditis
Ventricular wall rupture

Left ventricular failure → pulmonary oedema → arterial hypoxaemia → further worsening of oxygen delivery (vicious cycle). Compensatory peripheral vasoconstriction → increased afterload → further worsens pump function.

D. Obstructive Shock

Mechanical obstruction of circulation:

Massive pulmonary embolism (saddle embolus)
Cardiac tamponade (pericardial compression)
Tension pneumothorax
Status asthmaticus

E. Mixed Shock

Common in sepsis — simultaneously combines distributive (loss of vasomotor tone), cardiogenic (myocardial depression), and hypovolemic (dehydration + vascular leak) components.

4. Clinical Features

Early / Pre-shock (Compensated)

Tachycardia (dominant early sign)
Temporary mild BP rise (increased inotropy)
Cool, pale peripheries with sluggish capillary refill (peripheral vasoconstriction)
Tachypnoea (compensatory respiratory alkalosis against incipient metabolic acidosis)
Exception: in early distributive shock — warm, flushed skin due to impaired vasomotor control

Overt Shock

Hypotension (SBP < 90 or MAP < 60 mmHg)
Altered mental status — confusion, disorientation, agitation → coma
Oliguria — urine output < 5–15 mL/hr (advanced)
Skin — cold, clammy, mottled, cyanotic; loss of peripheral pulses
Hypothermia — even in septic shock
Lactic acidosis — anaerobic metabolism; drives increased respiratory effort
Paroxysmal bradycardia — in advanced shock from worsening myocardial ischaemia

Useful Bedside Indices

Shock Index = HR ÷ SBP; normal 0.5–0.7; persistent > 1.0 indicates impaired left ventricular function
Pulse pressure (SBP − DBP): narrows early in hypovolemic/cardiogenic shock; may widen in distributive shock

5. Diagnosis

Clinical Assessment

History: trauma → hypovolemic; chest pain → cardiogenic; fever/infection → septic; spinal injury → neurogenic
Examine: jugular venous distension (cardiogenic, obstructive), flat neck veins (hypovolemia), skin temperature/perfusion, peripheral pulses

Investigations

Serum lactate — earliest and most sensitive marker of hypoperfusion; obtained as soon as possible
ABG — base deficit, correlation of PaO₂/PaCO₂ with oximetry/capnography
CBC, electrolytes, renal and liver function, urinalysis
ECG — rule out ACS as cause of cardiogenic shock
Bedside ultrasound (RUSH protocol — Rapid Ultrasound in Shock):
- Cardiac chambers: size, filling, contractility → suggests cardiogenic shock
- Pericardial effusion → suggests obstructive (tamponade)
- IVC collapsibility → suggests hypovolemia
- Hemoperitoneum → suggests haemorrhagic shock
- Pneumothorax / haemothorax screening
Chest X-ray — cardiomegaly + pulmonary oedema (cardiogenic); oligaemic lung fields (massive PE, status asthmaticus)

6. Management

General Principles

IV access is a priority — large-bore peripheral (×2) for rapid resuscitation; central line preferred for vasopressor administration
Goal: restore MAP ≥ 65 mmHg, clear lactate, restore urine output and mental status
Treat the underlying cause simultaneously

A. Fluid Resuscitation

Shock Type	Fluid Strategy
Hypovolemic/Distributive (sepsis)	20–30 mL/kg crystalloid bolus; initial challenge of 500 mL over 20–30 min
Haemorrhagic (trauma)	Start with 1–2 L crystalloid; massive haemorrhage → 1:1:1 ratio of PRBCs : FFP : platelets
Cardiogenic	Cautious — 125–250 mL bolus only; risk of pulmonary oedema
Obstructive	Not primarily fluid — relieve obstruction first

Crystalloids are preferred over colloids (less expensive; no evidence colloids improve outcomes)
Balanced crystalloids (PlasmaLyte, Lactated Ringer) have lower chloride than normal saline — potential advantage uncertain
Hetastarches are contraindicated — associated with worse outcomes
PRBC transfusion threshold: Hb < 7 g/dL in most shock types; < 8 g/dL in acute MI/cardiogenic shock

B. Vasopressors

Used when fluid resuscitation alone is insufficient to restore target MAP:

Agent	Mechanism	Indication	Dose
Norepinephrine	α₁ (vasoconstriction) + β₁ (inotropy)	First-line for distributive, cardiogenic, neurogenic shock	0.05 mcg/kg/min; titrate every 3–5 min to MAP ≥ 65
Vasopressin	V1 receptor (vasoconstriction)	Add-on to NE in refractory septic shock; alternative in nonseptic distributive shock	0.03–0.04 units/min (fixed)
Phenylephrine	Pure α₁ (vasoconstriction)	Neurogenic shock with pure vasodilation; or tachyarrhythmia limiting NE use	Titrated to MAP
Epinephrine	α + β (vasoconstriction + inotropy)	Drug of choice for anaphylaxis; associated with ↑ mortality in cardiogenic shock — avoid	Variable
Dopamine	Dose-dependent: DA, β, α	Theoretical renal vasodilation at low dose — no proven renal protection; more side effects than NE	1–20 mcg/kg/min
Dobutamine	β₁ inotrope	Add-on in cardiogenic or septic shock with low CO	5–15 mcg/kg/min
Milrinone	PDE-3 inhibitor (inotrope + vasodilator)	Cardiogenic shock — reduces afterload without increasing myocardial O₂ demand	Infusion

In haemorrhagic shock, vasopressors are ancillary only — their use is associated with increased mortality; haemorrhage control and blood products remain the priority.

In vasodilatory shock (sepsis), permissive hypotension to MAP 60–65 mmHg is not superior to standard targets.

C. Respiratory Support

Supplemental oxygen for all patients with suspected shock
Intubation is indicated for: significant respiratory distress, severe hypotension, or severe acidosis — do not attempt noninvasive ventilation in shock (less effective, no airway protection)
Benefits of mechanical ventilation in shock:
- Protects airway; reduces aspiration risk
- Decreases work of breathing → reduces oxygen demand
- Improves gas exchange → increases oxygen delivery
- In cardiogenic shock: reduces cardiac afterload via positive intrathoracic pressure
Caution: initiating mechanical ventilation can worsen hypotension (positive intrathoracic pressure ↓ venous return) — have vasopressors ready

D. Specific Cause Treatment

Shock Type	Specific Intervention
Haemorrhagic	Direct pressure, REBOA, surgical haemostasis
Septic	Antimicrobials within 1 hour + source control + 30 mL/kg crystalloid
Cardiogenic (ACS)	Urgent PCI/thrombolysis; intraaortic balloon pump (IABP) for refractory cases
Tamponade	Pericardiocentesis
Tension pneumothorax	Needle thoracostomy → chest tube
Massive PE	Thrombolysis or embolectomy
Anaphylaxis	Remove trigger; epinephrine (drug of choice); steroids; H1+H2 blockers; fluids
Neurogenic	NE first-line; phenylephrine if pure vasodilation or tachyarrhythmia

7. Special Situations

Orthostatic (Postural) Hypotension

BP falls on assuming upright posture due to inadequate autonomic compensation
Causes: volume depletion, venous pooling, autonomic neuropathy (diabetes, amyloidosis, Guillain-Barré, AIDS, alcoholism), drugs (diuretics, antihypertensives, nitrates, calcium channel blockers, sildenafil, MAOIs, phenothiazines, opiates, L-dopa, TCAs, alcohol)
Primary autonomic failure: Shy-Drager syndrome (multiple system atrophy), Riley-Day syndrome

Raised ICP

Arterial hypotension → cerebral autoregulatory vasodilation → ↑ CBV → ↑ ICP → ↓ CPP → vicious cycle; hypotension must be prevented/corrected urgently

Neuraxial (Spinal/Epidural) Anaesthesia

High spinal block to T4 blocks both vascular tone AND cardiac accelerator fibres → bradycardia + hypotension → can lead to cardiac arrest even in young, healthy patients
Treat with phenylephrine or ephedrine

Renal Replacement Therapy

CRRT (continuous renal replacement therapy) enables effective solute removal even in the presence of arterial hypotension — an advantage over intermittent haemodialysis

Obstetrics

Spinal/epidural anaesthesia does not reduce uterine blood flow unless arterial hypotension develops — prevention is critical

Sources: Goldman-Cecil Medicine, 26e (Chapter 92) | Rosen's Emergency Medicine, 10e (Chapter 3) | Miller's Anesthesia, 10e (Chapter 76) | Bradley & Daroff's Neurology in Clinical Practice, 8e | Barash Clinical Anesthesia, 9e

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