Review Note
Last Update: 02/17/2025 02:33 AM
Current Deck: ACG Part 2::Thoracic SSU
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Commit #284668
SS_TS 1.4 Discuss the pathophysiology of pulmonary hypertension and methods available to the anaesthetist to manipulate pulmonary vascular resistance and pulmonary artery pressures
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Commit #284668PH defined as PAP at rest >25mmHg
- Mild 25-40
- Mod 41-55
- Severe >55
Pathophysiology
- (i) Group 1 - pulmonary arterial hypertension (PAH)
- (ii) Group 2 - PH caused by left-sided heart disease (PH-LHD)
- (iii) Group 3 - PH caused by lung diseases, hypoxia, or both (PH-LD)
- (iv) Group 4 - PH caused by pulmonary artery obstructions (chronic thromboembolic pulmonary hypertension [CTEPH])
- (v) Group 5 - PH with unclear or multifactorial mechanisms
Can be classified by pre-capillary, post-capillary and combined.
Diagnosis
- Gold standard for diagnosis and classification = right heart catheter
- TTE can be used to estimate likelihood of PH
- TR velocity
- TAPSE/sPAP ratio
Methods to manipulate PVR and PAPs
Drugs reducing PVR
- Calcium channel blockers e.g. nifedipine, diltiazem
- MOA: competitive antagonism of VGCC (L type) à reduces calcium influx à reduces intracellular calcium ⋅
- Heart effects – reduces SAN automaticity, AVN conductivity and inotropy
- Vessel effects – arterial vasodilation
- Side effects
- CVS – may precipitate cardiac failure (from reduced CO), hypotension, reflex tachycardia
- Resp – worsening of hypoxic pulmonary vasoconstriction
- Prostacyclin (PGI2)
- IV epoprostenol – via CVL
- MOA: increases adenylate cyclase -> increases cAMP-> reduces calcium -> vasodilator and inhibits platelet aggregation
- Side effects – hypotension, tachycardia, facial flushing, headache
- Inhaled iloprost– selective for lung vasculature; requires 6-9x/day administrations
- Endothelin-1 receptor antagonist e.g. bosentan
- Endothelin-1 is a potent vasoconstrictor, which affects ETA receptors and GqPCR to cause vasoconstriction
- Side effects – hepatotoxicity (requires monthly LFTs), teratogen, oedema
- Phosphodiesterase-5 inhibitors e.g.sildenafil
- MOA – inhibits cGMP breakdown-> reduces calcium-> reduces arteriolar smooth muscle tone -> vasodilation
- Side effects – hypotension, flushing, headache, visual disturbance, erect penis
- Nitric oxide ⋅ Inorganic gas produced by L-arginine
- MOA – activates adenylate cyclase -> increased cGMP-> reduces calium, arteriolar smooth muscle -> vasodilation
- Side effects – worsening of HPV with increasing shunt, increases CBF, inhibits platelet aggregation, metHb
- Inhalational anaesthetic agents
- GTN
- MOA – prodrug metabolized to NO ->activates guanylate cyclase -> increased cGMP -> reduced intracellular calcium
- Effects – venous and arterial vasodilation
- Sodium nitroprusside
- MOA – produces NO -> venous and arterial vasodilation
Drugs increasing PVR
- N2O
- Adrenaline, noradrenaline, dopamine
- Other factors increasing PVR
- Hypoxia
- Hypercapnoea
- Acidosis
- Extremes of lung volume
- PGE2, PGF2a, thromboxane A2, histamine
(Gold Coast Notes)