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CAM201 Clinical Skills > Pulmonary HTN and pulmonary embolism > Flashcards

Pulmonary HTN and pulmonary embolism Flashcards

1
Q

Definition of pulmonary HTN

A

An increase in mean pulmonary arterial pressure (PAP) >25mmHg

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2
Q

General classification of pulmonary HTN

A

Pulmonary arterial hypertension (PAH)

  • Idiopathic PAH
  • HEritable
  • Drugs and toxins induces
  • Associated with APAH
  • Persistent pulmonary HTN of the newborn

Pulmonary HTN due to left heart disease

Pulmonary HTN due to lung diseases and/or hypoxaemia

  • Chronic obsructive pulmonary disease
  • Interstitial lung disease
  • Other pulmonary disease with mixed restrictive and obstructive pattern
  • Sleep-disorder breathing
  • Alveolar hypoventilation disorders
  • Chronci exposure to high altitude
  • Developmental abnormalities

Chronic thromboembolic pulmonary HTN

_PH with unclear and/or multifactoral mechanisms _

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3
Q

PCWP

A

Wedge pressure

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4
Q

Drugs and toxins that cause PAH

A

Definitely

  • Aminorex
  • Fenfluramine
  • Detenfluramine
  • Toxic rapeseed oil
  • Benfluorex

Likely

  • Amphertamines
  • Methamphetamines
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5
Q

Pulmonary hypertension (PH) characteristics and clinicla groups

A

Mean PAP >25mmHg

All clinical groups.

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6
Q

Pre-capillary PH charcteristics

A
  • Mean PAP >25mmHg
  • PWP <15mmHg
  • CO normal or reduced
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7
Q

Pre-capillary PH clinical group(s)

A
  1. Pulmonary arterial HTN
  2. PH due to lung diseases
  3. Chronic thromboembolic PH
  4. PH with unclear and/or multifactoral mechanisms
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8
Q

Postcapillary PH characteirtsics

A

(caused by left heart disease)

  • Mean PAP >25mmHg
  • PWP >15mmHg
  • CO normal or reduced
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9
Q

Post-capillary PH clinical groups

A

PH due to left heart disease

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10
Q

Passive PH

A

TPG <12mmHg

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11
Q

Reactive PH

A

May be additional cardiac remodeling

TPG >12mmHg

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12
Q

Vasoresponders

A

Patients who respond to calcium channel agonists - pressure in pulmonary circulation drops to a certain level, and CO remains the same.

Only about 10% respond to calcium channel antagonists.

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13
Q

Agents for testing vasoreactivity

A
  • IV epaprostenol
  • iNO
  • Adenosine IV
  • Iloprost inh
  • Sildenafil
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14
Q

World burden PH

A

Schistosomiasis: infectious organism that lays its eggs in the pulmonary circulation and obliterates it, causing destruction of the vascular bed, and thus high resistance.

High altitude: >2500m, chronically exposed to hypoxia, leads to vasoconstriction adn elevated pulmonary pressures - develop RHF.

Chronic inhereted: sickle cell disease, thalassaemia

HIV: 1% develop PH

Cardia diseases: high LAP and high elevation in pulmonary pressure.

  • Rheumatic valvular disease
  • Congenital heart disease
  • Endomyocardial fibrosis
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15
Q

Pathogenesis of PH

A

Vasoconstriction

  • Often triggered by hypoxia

Endothelial dysfunction: not normal signaling between endothelium and smooth muscle.

  • High flow or pressure (shunts)
  • Direct toxins (such as weight loss drugs)
  • Intimal proliferation (due to genetic predisposition)

Smooth muscle

  • Hyperplasia
  • Hypertrophy
  • Increased matrix deposition and fibroblast proliferation - walls become very stiff and non-compliant.

Thrombosis in situ

  • Due to obliteration of the vascular bed
  • Hence treatment with anticoagulants

Insult leads to vascular injury resulting in:

  • Decreased NO and prostacyclin, which are vasodilators
  • Upregulation of endothelin - potent vasoconstrictor
  • Upregulation of thromboxane - potent vasoconstriction and platelet adherence
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16
Q

Plexiform lesion

A

Pathopneumonic lesion in PH.

Uncontrolled cell proliferation, vascular outgrowth and failure of apoptosis - can be seen histologically.

17
Q

Signs and symptoms of PH

A

These are signs and symptoms of inadequate cardiac output:

  • Disease onset: no early symptoms of PH
  • First symptoms: progressive dyspnea on exertion, fatigue, palpitations, chest pain, dizziness, syncope, coughing.
  • End stage symptoms: symptoms and signs of RHF, edema, ascites.
18
Q

Physical examination fidings in PH

A
  • Loud pulmonic valve closure (P2)
  • Graham-Steele murmur
    • Pulmonic regurgitation
  • Right sided fourth heart sound
    • High pitched, pre-systolic sound
    • Resistance in RV filling due to reduced compliance (hypertrophy)
  • RV heave
  • Jugular venous distention
  • Hepatomegaly
  • Peripheral edema, ascites.
19
Q

Why is diagnosis of PH made late in the disease?

A

Due to:

  • Under-recognition
  • Non-specific symptoms
  • Confusion with other conditions
  • iPAH is a diagnosis of exclusion
20
Q

Who should be screened?

A

Individuals in high risk populations

  • Family history of iPAH
  • CT disease
  • Pulmonary embolism
  • Congenital heart disease
21
Q

Idiopathic PAH epidemiology

A
  • Young
  • F:M 1.8:1
  • 6-10% familial
    • 2q33 BMPR2 gene
  • Incidence 1-2/million
  • Prevalence 15-20/million
  • iPAH and associated PAH equally distributed
  • Prevalence 40/million
  • Under-diagnosis and under-reported
22
Q

Echocardiography in PH

A
  • Mild PH 36-50mmHg (eRVSP) or TR 2.8-3.4 m/s
  • RV size and function
  • LV diastolic and systolic function
  • Valve morphology and function
  • Shunts using ‘bubble’ study
  • ePVR
  • Pericardial effusion
23
Q

Pulmonary function testing (PFTs)

A

CAM201 Clinical Skills (14 decks)

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