Pulmonary hypertension - Revision history

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2026-03-22T09:24:20Z

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	===WHO Classification<ref>Ryan, J. et al. (2012) The WHO classification of pulmonary hypertension: A case-based imaging compendium. Pulmonary Circulation, 2(1).</ref>===		===WHO Classification<ref>Ryan, J. et al. (2012) The WHO classification of pulmonary hypertension: A case-based imaging compendium. Pulmonary Circulation, 2(1).</ref>===
	*~~'''~~Group 1~~'''~~: Pulmonary ''arterial'' hypertension		*Group 1: Pulmonary ''arterial'' hypertension
	**Idiopathic		**Idiopathic
	**Associated with:		**Associated with:
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	***Portal hypertension		***Portal hypertension
	***[[Congenital heart disease]]		***[[Congenital heart disease]]
	*~~'''~~Group 2~~'''~~: PH due to left heart disease		*Group 2: PH due to left heart disease
	**Associated with:		**Associated with:
	***Coronary artery disease		***Coronary artery disease
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	***[[Valvular disease]]		***[[Valvular disease]]
	***Advanced age		***Advanced age
	*~~'''~~Group 3~~'''~~: PH due to lung diseases		*Group 3: PH due to lung diseases
	**Associated with:		**Associated with:
	***[[COPD]]		***[[COPD]]
	***[[Interstitial lung disease]]		***[[Interstitial lung disease]]
	***Any other lung disease causing [[hypoxemia]]		***Any other lung disease causing [[hypoxemia]]
	*~~'''~~Group 4~~'''~~: PH due to chronic [[thromboembolism\|thromboembolic disease]]		*Group 4: PH due to chronic [[thromboembolism\|thromboembolic disease]]
	*~~'''~~Group 5~~'''~~: PH of unclear multifactorial mechanisms		*Group 5: PH of unclear multifactorial mechanisms
	**Associated with:		**Associated with:
	***[[Sarcoidosis]]		***[[Sarcoidosis]]
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	[[File:PulArtHyperandEmphysemaMark.png\|thumb\|CT chest with contrast showing prulmonary artery hypertension (red arrow) and evidence of emphysema (blue arrow).]]		[[File:PulArtHyperandEmphysemaMark.png\|thumb\|CT chest with contrast showing prulmonary artery hypertension (red arrow) and evidence of emphysema (blue arrow).]]
	''Some, all or none of the following findings may be present.''		''Some, all or none of the following findings may be present.''
	*~~'''~~[[BNP]]:~~'''~~ Elevated<ref name="Wilcox"></ref>		*[[BNP]]: Elevated<ref name="Wilcox"></ref>
	*~~'''~~[[ECG]] findings~~'''~~ (similar to acute pulmonary embolism):		*[[ECG]] findings (similar to acute pulmonary embolism):
	**Right axis deviation		**Right axis deviation
	**Evidence of right heart strain on bedside ultrasound or CT		**Evidence of right heart strain on bedside ultrasound or CT
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	*Tricuspid valve regurgitation		*Tricuspid valve regurgitation
	*Estimate systolic pulmonary artery pressure (SPAP) with echo<ref>Critical USG. Echocardiographic assessment of pulmonary artery pressure. 2012. http://www.criticalusg.pl/en/echo/tte/tutorials/echocardiographic-assessment-of-pulmonary-artery-pressures</ref>		*Estimate systolic pulmonary artery pressure (SPAP) with echo<ref>Critical USG. Echocardiographic assessment of pulmonary artery pressure. 2012. http://www.criticalusg.pl/en/echo/tte/tutorials/echocardiographic-assessment-of-pulmonary-artery-pressures</ref>
	**SPAP = ~~'''~~Max TR gradient~~'''~~ + ~~'''~~Mean RAP~~'''~~		**SPAP = Max TR gradient + Mean RAP
	**Cannot use this method with vent-dependent patients, pulmonic stenosis		**Cannot use this method with vent-dependent patients, pulmonic stenosis
	**Max TR gradient as measured by tricuspid regurgitation (TR) jet, which >90% of adults have		**Max TR gradient as measured by tricuspid regurgitation (TR) jet, which >90% of adults have
	**Use parallel CW Doppler line across TR jet in apical view		**Use parallel CW Doppler line across TR jet in apical view
	**Obtain dense TR profile below the line with well-defined envelope and measure peak = ~~'''~~Max TR gradient~~'''~~		**Obtain dense TR profile below the line with well-defined envelope and measure peak = Max TR gradient
	**Estimate right atrial pressure (RAP) with IVC diameter from subcostal view		**Estimate right atrial pressure (RAP) with IVC diameter from subcostal view
	{\|class="wikitable"		{\|class="wikitable"
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	===Optimize Circulation===		===Optimize Circulation===
	#~~'''~~Optimize (usually reduce) RV preload~~'''~~:		#Optimize (usually reduce) RV preload:
	#*Usually euvolemic or hypervolemic, rarely need IV fluids so [[diuretics]] can benefit and treat the RV failure<ref>Ternacle, J et al. Diruetics in Normotensive Patients with Acute Pulmonary Embolism and Right Ventricular Dilation. Circulation Journal. Vol 77(10) 2013. 2612-618.</ref>		#*Usually euvolemic or hypervolemic, rarely need IV fluids so [[diuretics]] can benefit and treat the RV failure<ref>Ternacle, J et al. Diruetics in Normotensive Patients with Acute Pulmonary Embolism and Right Ventricular Dilation. Circulation Journal. Vol 77(10) 2013. 2612-618.</ref>
	#**[[Furosemide]] 20-40mg IV		#**[[Furosemide]] 20-40mg IV
	#**Furosemide drip at 5-20mg/hr		#**Furosemide drip at 5-20mg/hr
	#*If suspect [[sepsis]] or [[hypovolemia]], small (250-500cc) NS challenge to assess fluid responsiveness. If not responsive to IVF challenge, start [[vasopressin]] or [[norepinephrine]](MAP > 65 mmHg).		#*If suspect [[sepsis]] or [[hypovolemia]], small (250-500cc) NS challenge to assess fluid responsiveness. If not responsive to IVF challenge, start [[vasopressin]] or [[norepinephrine]](MAP > 65 mmHg).
	#~~'''~~Increase cardiac output~~'''~~:		#Increase cardiac output:
	#*Once MAP >65 mmHg, start low dose [[dobutamine]] (5-10mcg/kg/min)		#*Once MAP >65 mmHg, start low dose [[dobutamine]] (5-10mcg/kg/min)
	#*Improves inotropic support and theoretically decreases pulmonary vascular resistance		#*Improves inotropic support and theoretically decreases pulmonary vascular resistance
	#~~'''~~Reduce RV afterload~~'''~~:		#Reduce RV afterload:
	#*Avoid [[hypoxia]], maintain O2 sat >90% (increases pulmonary vasoconstriction)		#*Avoid [[hypoxia]], maintain O2 sat >90% (increases pulmonary vasoconstriction)
	#*Avoid [[hypercapnia]] (increases pulmonary vascular resistance)		#*Avoid [[hypercapnia]] (increases pulmonary vascular resistance)
	#*Avoid [[acidosis]]		#*Avoid [[acidosis]]
	#~~'''~~Treat [[arrhythmias]]:~~'''~~		#Treat [[arrhythmias]]:
	#*[[SVT]] most common although may also become bradycardic (aflutter and afib occur equally)		#*[[SVT]] most common although may also become bradycardic (aflutter and afib occur equally)
	#*Treatment of aflutter is often more successful than afib		#*Treatment of aflutter is often more successful than afib
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	===Optimize Oxygenation===		===Optimize Oxygenation===
	*~~'''~~noninvasive oxygenation:~~'''~~ attempt nonrebreather mask or high flow nasal cannula to maximize oxygenation. Use NIPPV with caution as positive pressure decreases preload and increases right sided pressures.		*noninvasive oxygenation: attempt nonrebreather mask or high flow nasal cannula to maximize oxygenation. Use NIPPV with caution as positive pressure decreases preload and increases right sided pressures.
	*'''Intubate as a last resort:''' RSI meds cause hypotension worsening RV ischemia. hypercapnea and hypoxia worsen pulmonary artery vasoconstriction. positive pressure ventilation decreases preload and increases right sided pressures.		*'''Intubate as a last resort:''' RSI meds cause hypotension worsening RV ischemia. hypercapnea and hypoxia worsen pulmonary artery vasoconstriction. positive pressure ventilation decreases preload and increases right sided pressures.
	*'''Intubated patients''' should be optimized to increased O2 delivery and minimize hypercapnia, maintain low tidal volumes and low PEEP as tolerated		*'''Intubated patients''' should be optimized to increased O2 delivery and minimize hypercapnia, maintain low tidal volumes and low PEEP as tolerated
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	==Chronic Therapies==		==Chronic Therapies==
	===Prostacyclins===		===Prostacyclins===
	~~'''~~Mechanisms of action~~'''~~: vasodilatation, inhibit platelet aggregation		Mechanisms of action: vasodilatation, inhibit platelet aggregation
	*[[Epoprostenol]], Iloprost, Treprostinil, Beraprost		*[[Epoprostenol]], Iloprost, Treprostinil, Beraprost
	**Complications include acute decompensation if stopped abruptly, diarrhea, edema, headache		**Complications include acute decompensation if stopped abruptly, diarrhea, edema, headache
	===Phosphodiesterase Type 5 (PDE5) Inhibitors===		===Phosphodiesterase Type 5 (PDE5) Inhibitors===
	~~'''~~Mechanism of Action~~'''~~: vasodilation, increases RV contractility		Mechanism of Action: vasodilation, increases RV contractility
	*[[Sildenafil]]		*[[Sildenafil]]
	*Complications include hypotension with administration of nitrates, flushing, epistaxis, headache		*Complications include hypotension with administration of nitrates, flushing, epistaxis, headache
	===Endothelin receptor antagonists===		===Endothelin receptor antagonists===
	~~'''~~Mechanism of Action~~'''~~: vasodilation via vascular modulation		Mechanism of Action: vasodilation via vascular modulation
	*[[Bosentan]], Ambrisentan		*[[Bosentan]], Ambrisentan
	**Complications include liver failure, supratherapeutic INR,		**Complications include liver failure, supratherapeutic INR,

Ostermayer at 00:42, 16 January 2026

2026-01-16T00:42:13Z

← Older revision		Revision as of 00:42, 16 January 2026
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	{{~~Adult top}} [[~~pulmonary hypertension (peds)~~]].''~~		{{AdultPage\|pulmonary hypertension (peds)}}
	==Background==		==Background==
	[[File:Illu pulmonary circuit.jpg\|thumb\|Pulmonary circuit anatomy.]]		[[File:Illu pulmonary circuit.jpg\|thumb\|Pulmonary circuit anatomy.]]

Rossdonaldson1: /* Background */

2024-04-10T17:09:33Z

Background

← Older revision		Revision as of 17:09, 10 April 2024
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	[[File:Illu pulmonary circuit.jpg\|thumb\|Pulmonary circuit anatomy.]]		[[File:Illu pulmonary circuit.jpg\|thumb\|Pulmonary circuit anatomy.]]
	[[File:Pulmonary hypertensive arteriopathy (4348170715).jpg\|thumb\|Micrograph showing arteries in pulmonary hypertensive with marked thickening of the walls.]]		[[File:Pulmonary hypertensive arteriopathy (4348170715).jpg\|thumb\|Micrograph showing arteries in pulmonary hypertensive with marked thickening of the walls.]]
			[[File:Molecular Pathology.png\|thumb\|Three major signaling pathways involved in the pathogenesis of pulmonary arterial hypertension.]]
	*Mean PA pressure >25 mmHg as assessed by right heart catheterization		*Mean PA pressure >25 mmHg as assessed by right heart catheterization
	**Since right ventricle is dependent on preload, RV contractility and afterload, severe pulmonary arterial hypertension causes pathological changes to right ventricle		**Since right ventricle is dependent on preload, RV contractility and afterload, severe pulmonary arterial hypertension causes pathological changes to right ventricle

Rossdonaldson1: /* Evaluation */

2024-04-10T17:07:26Z

Evaluation

← Older revision		Revision as of 17:07, 10 April 2024
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	==Evaluation==		==Evaluation==
			[[File:PulArtHyperandEmphysemaMark.png\|thumb\|CT chest with contrast showing prulmonary artery hypertension (red arrow) and evidence of emphysema (blue arrow).]]
	''Some, all or none of the following findings may be present.''		''Some, all or none of the following findings may be present.''
	*'''[[BNP]]:''' Elevated<ref name="Wilcox"></ref>		*'''[[BNP]]:''' Elevated<ref name="Wilcox"></ref>

Rossdonaldson1: /* Background */

2024-04-10T16:55:13Z

Background

← Older revision		Revision as of 16:55, 10 April 2024
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	==Background==		==Background==
	[[File:Illu pulmonary circuit.jpg\|thumb\|Pulmonary circuit anatomy.]]		[[File:Illu pulmonary circuit.jpg\|thumb\|Pulmonary circuit anatomy.]]
	[[~~By Yale Rosen from USA -~~ Pulmonary hypertensive ~~arteriopathyUploaded by CFCF, CC BY-SA 2.0, https://commons.wikimedia.org/w/index~~.~~php?curid=31128156~~\|thumb\|Micrograph showing arteries in pulmonary hypertensive with marked thickening of the walls.]]		[[File:Pulmonary hypertensive arteriopathy (4348170715).jpg\|thumb\|Micrograph showing arteries in pulmonary hypertensive with marked thickening of the walls.]]
	*Mean PA pressure >25 mmHg as assessed by right heart catheterization		*Mean PA pressure >25 mmHg as assessed by right heart catheterization
	**Since right ventricle is dependent on preload, RV contractility and afterload, severe pulmonary arterial hypertension causes pathological changes to right ventricle		**Since right ventricle is dependent on preload, RV contractility and afterload, severe pulmonary arterial hypertension causes pathological changes to right ventricle

Rossdonaldson1: /* Background */

2024-04-10T16:53:42Z

Background

← Older revision		Revision as of 16:53, 10 April 2024
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	==Background==		==Background==
	[[File:Illu pulmonary circuit.jpg\|thumb\|Pulmonary circuit anatomy.]]		[[File:Illu pulmonary circuit.jpg\|thumb\|Pulmonary circuit anatomy.]]
			[[By Yale Rosen from USA - Pulmonary hypertensive arteriopathyUploaded by CFCF, CC BY-SA 2.0, https://commons.wikimedia.org/w/index.php?curid=31128156\|thumb\|Micrograph showing arteries in pulmonary hypertensive with marked thickening of the walls.]]
	*Mean PA pressure >25 mmHg as assessed by right heart catheterization		*Mean PA pressure >25 mmHg as assessed by right heart catheterization
	**Since right ventricle is dependent on preload, RV contractility and afterload, severe pulmonary arterial hypertension causes pathological changes to right ventricle		**Since right ventricle is dependent on preload, RV contractility and afterload, severe pulmonary arterial hypertension causes pathological changes to right ventricle

Rossdonaldson1: /* Background */

2024-04-10T16:51:44Z

Background

← Older revision		Revision as of 16:51, 10 April 2024
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	{{Adult top}} [[pulmonary hypertension (peds)]].''		{{Adult top}} [[pulmonary hypertension (peds)]].''
	==Background==		==Background==
			[[File:Illu pulmonary circuit.jpg\|thumb\|Pulmonary circuit anatomy.]]
	*Mean PA pressure >25 mmHg as assessed by right heart catheterization		*Mean PA pressure >25 mmHg as assessed by right heart catheterization
	**Since right ventricle is dependent on preload, RV contractility and afterload, severe pulmonary arterial hypertension causes pathological changes to right ventricle		**Since right ventricle is dependent on preload, RV contractility and afterload, severe pulmonary arterial hypertension causes pathological changes to right ventricle

Rossdonaldson1: /* Acute Management */

2024-04-10T15:24:29Z

Acute Management

← Older revision		Revision as of 15:24, 10 April 2024
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	''First intervention should always be to check any medication pumps. Resume medication immediately. If malfunctioning or empty, most pumps/patients have card with hot-line to call if their pulmonologist is not available''		''First intervention should always be to check any medication pumps. Resume medication immediately. If malfunctioning or empty, most pumps/patients have card with hot-line to call if their pulmonologist is not available''
	#Assess for triggers for decompensation (Treat infection. Consider pulmonary embolism. Evaluate for arrhythmia)		#Assess for triggers for decompensation (Treat infection. Consider pulmonary embolism. Evaluate for arrhythmia)
	#Assess volume status. IVC ultrasound less helpful as will be dilated at baseline. Generally want to avoid fluids. PH patients do not tolerate rapid changes in hemodynamics.		#Assess volume status. [[IVC ultrasound]] less helpful as will be dilated at baseline. Generally want to avoid fluids. PH patients do not tolerate rapid changes in hemodynamics.
	#Consider early ~~ionotropes nad~~ pressors		#Consider early [[inotropes]] and [[pressors]]
	#For tachydysarrhythmia, avoid AV nodal blocking agents like beta blockers or calcium channel blockers. Decrease in inotropy can be fatal. Do NOT rate control. Consider cardioversion and rhythm control		#For tachydysarrhythmia, avoid AV nodal blocking agents like [[beta blockers]] or [[calcium channel blockers]]. Decrease in inotropy can be fatal. Do NOT rate control. Consider cardioversion and rhythm control
	#Avoid intubation/NIPPV if at all possible. ~~PPV~~ can diminish preload which can lead to rapid decompensation and death		#Avoid [[intubation]]/[[NIPPV]] if at all possible. Positive pressure ventilation can diminish preload which can lead to rapid decompensation and [[death]]
	#Further details below		#Further details below

Zbuchwald: /* General Principles of Management for Hypotensive Patient with Pulmonary Hypertension */

2024-03-29T21:50:39Z

General Principles of Management for Hypotensive Patient with Pulmonary Hypertension

← Older revision		Revision as of 21:50, 29 March 2024
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	#Consider early ionotropes nad pressors		#Consider early ionotropes nad pressors
	#For tachydysarrhythmia, avoid AV nodal blocking agents like beta blockers or calcium channel blockers. Decrease in inotropy can be fatal. Do NOT rate control. Consider cardioversion and rhythm control		#For tachydysarrhythmia, avoid AV nodal blocking agents like beta blockers or calcium channel blockers. Decrease in inotropy can be fatal. Do NOT rate control. Consider cardioversion and rhythm control
	#Avoid intubation if at all possible. PPV can diminish preload which can lead to rapid decompensation and death		#Avoid intubation/NIPPV if at all possible. PPV can diminish preload which can lead to rapid decompensation and death
	#Further details below		#Further details below

Rossdonaldson1 at 16:05, 1 July 2020

2020-07-01T16:05:23Z

← Older revision		Revision as of 16:05, 1 July 2020
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	{{Adult top}} [[~~pulmonayr~~ hypertension (peds)]].''		{{Adult top}} [[pulmonary hypertension (peds)]].''
	==Background==		==Background==
	*Mean PA pressure >25 mmHg as assessed by right heart catheterization		*Mean PA pressure >25 mmHg as assessed by right heart catheterization