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11. Acquired heart dz > PH > Flashcards

PH Flashcards

1
Q

Definition

A

↑ PA pressure
* Systolic >30mmHg
* Diastolic >19mmHg
* Mean >14mmHg

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2
Q

Mechanisms for pulmonary hypertension

A
  • ↑ PVR
    o ↑ resistance to pulmonary venous drainage
    o ↓ CSA of pulmonary vascular bed
     Loss of pulmonary vessels
     Luminal narrowing
     Pulmonary vasoconstriction
  • ↑pulmonary blood flow (RV CO)
    o Persistent exposure to ↑ blood flow → pulmonary artery pathology
    o Permanent ↑ PVR
  • ↑blood viscosity
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3
Q

Etiology/classification

A
  1. PAH
  2. PVH 2nd to L heart dz
  3. PH 2nd to pulmonary dz
  4. PH from PTE
  5. Misc
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4
Q

Precapillary PH causes

A

o Idiopathic
o Systemic to pulmonary shunt: VSD, ASD, PDA
o Collagen vascular dz
o Drugs/toxins
o Vasoactive substances: TXA2, histamine, serotonine, endothelin
o PTE
o Persistent PH of the newborn
o ↑ blood flow
o HW

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5
Q

Pathophys L to R shunt PH

A

 ↑ pulmonary blood flow
 Shear stress on pulmonary endothelial lining → PH
 Significant PH can result in sunt reversal → Eisenmenger physiology

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6
Q

Causes of PH from incr blood flow

A

anemia, thyrotoxicosis, exercise

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7
Q

Pathophys PH w/ HW

A

 Physical presence of HW and by products
 Potentially irreversible endothelial damage

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8
Q

Capillary PH causes

A

o Pulmonary diseases:
 Asthma, bronchitis, bronchomalacia
 Interstitial lung disease: pulmonary fibrosis
o PTE
o Lungworms
o Neoplasia
o Sleep disorder breathing
o Alveolar hypoventilation disorders
o Chronic exposure to high altitude

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9
Q

Post capillary PH causes

A

= pulmonary venous hypertension
o L sided heart disease and secondary LAE
 From ↑LAP
 CVD, MVS, CM
o Pulmonary venous obstruction
o Neoplasia
o Congenital abnormalities

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10
Q

Misc causes

A

o Compression of pulmonary vessels
o Lymphadenopathy
o Neoplasia
o Fibrosing mediastinitis
o Granulomatous dz
o Sarcoidosis, histiocytosis, lymphangiomatosis

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11
Q

Feline PH causes

A

few case reports associated with
* PTE, R to L shunting PDA, HW, chronic upper airway obstruction, Aelurostrongylus abstrutus

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12
Q

Pathologic features of PH

A
  • Grade 1: medial hypertrophy
  • Garde 2:
    o Medial hypertrophy
    o Cellular intimal proliferation
  • Grade 3: partially reversible
    o Intimal hyperplasia → lumen occlusion
    o Early arterial dilation
  • Grade 4: irreversible
    o Advanced arterial dilation
    o Plexiform lesions in muscular arteries and capillaries
  • Grade 5: angiomatoid formation (terminal) plexiform lesions
  • Grade 6: fibrinoid acute necrotizing arteritis
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13
Q

Features of pulmonary vascular bed

A

low pressure, low resistance, high capacitance
o PAP determined by: RV CO (blood flow), PVR, PVP

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14
Q

Pathophys of primary PH

A

imbalance btw vasoconstriction and dilation

  • RV systolic overload from PH
    o Diastolic overload from TR
    o ↓ RV systolic performance with exercise
  • LV diastolic UNDERload
    o Reduced compliance
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15
Q

Vasoconstriction agents

A

Alveolar hypoxia
ET1
Serotonin
TxA2
PDGF

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16
Q

Alveolar hypoxia on PVR

A

physiologic response shunting blood from hypoventilated areas → better ventilated areas of the lungs

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17
Q

ET1 PVR

A
  • Released from vascular endothelium in response to changes in
    o Blood flow
    o Vascular stretch
    o [Thrombin]
  • Causes: vasoconstriction, SM growth, ↑collagen synthesis, promotes vascular remodelling
  • ↑ [ET1] in Hu with PH, also reported in dogs
18
Q

Serotonin effect on PVR

A
  • Vasoconstrictor
  • Promote SM cell hypertrophy and hyperplasia
19
Q

TXA2 and PGI effect on PVR

A
  • Arachidonic metabolite of PA vascular cells
  • TXA2: vasoconstrictor
    o Predominates in patients w PH
  • Prostacyclin: vasodilator, inhibitor of platelet activation, antiproliferative properties
20
Q

Platelet derived GF effect on PVR

A
  • Induce PA SM cell proliferation and migration
21
Q

Vasodilator agents

A

NO

22
Q

NO effect on PVR

A
  • Potent vasodilator, inhibitor of platelet activation and SM cell proliferation
  • Synthetized from arginine and O2 by NOS enzyme in endothelium
    o Activate cGMP → vasodilation
    o cGMP inactivated by PDE5 isoenzyme
23
Q

Cardiac KT pressure study PH 2nd to HW

A
  • PA: ↑systolic, mean, diastolic P
  • PCWP: should be normal
  • RV: ↑ systolic P
24
Q

Cardiac KT pressure study PH 2nd to MVS

A
  • PA: ↑
    o Normal in early stage of dz
    o ↑ as a reflect of ↑LAP
    o Late stage can have marked ↑
  • PCWP: should be elevated from ↑LAP
    o ↑a and v wave
    o Prolonged Y descent
  • RV: elevated if PH present
25
Q

What are the levels of resistance to flow in terms of RV work and how does this differ relative to the systemic circulation?

A
  • RV have thin walls and high compliance
    o Can accommodate high volumes at physiologic pressures
    o Marked preload dependence and RV-LV interdependence
  • RV performance depend on afterload
    o Less tolerant to pressure overload
     Unable to face acute ↑PVR
     Inefficient against PH
    o Preload reserve helps to preserve RV function with PH (Frank Starling mechanism)
     Eccentric hypertrophy
    o RVH will occur to ↓ wall stress: Laplace law
     Concentric hypertrophy
26
Q

Features of exercise induced pulmonary hemorrhage in horses

A

o Hemorrhage from pulmonary capillaries into alveolar space
o Predominant in caudodorsal lung fields

27
Q

Exercise induced pulmonary hemorrhage in horses histo

A

o Edema
o Pulmonary capillary and alveolar hemorrhage
 RBC in alveoli and interstitial space
o Disruption of capillary and alveolar endothelium
 RBC, platelets and macrophages accumulation
o Venoocclusive remodelling of intralobar PVs → ↑ stiffness and ↓ vascular compliance
 Collagen deposition
 SM hypertrophy
 Intimal hyperplasia w/I PV

28
Q

Exercise induced pulmonary hemorrhage in horses is a consequence of

A

o ↑CO
o Lack of sufficient pulmonary vasodilation
o ↑ blood viscosity with exercise

29
Q

Exercise induced pulmonary hemorrhage in horses pathophys

A

o Ventilation inhomogeneity caused by small airway dz
 Poor collateral ventilation + small airway dz → underventilation of certain lung units
 Extreme fluctuation in alveolar pressure of underventilated areas
* Parenchymal tearing
* Alveolar capillary rupture
o Mechanical constraint of abdominal viscera on dorsocaudal lungfield
 Can lead to parenchymal tearing → alveolar capillary rupture
o Stress failure of pulmonary capillaries
 High transmural pressures
* High pulmonary capillary P and low alveolar P
* Tissue failure → hemorrhage
 PCP >70mmHg→ disrupt endothelial and alveolar epithelial tight jcts
* Hemorrhage in interstitium/alveoli

30
Q

What is cattle brisket dz

A
  • Bovine high mountain disease
    o Non contagious swelling of edematous fluid in
     Ventral parasternal muscles (brisket) region
     Ventral aspect of body → abdomen, submandibular region
    o Cattles raised at high altitude in West USA (Colorado, Wyoming, NM, Utah)
31
Q

Etiology of brisket dz

A
  • Hypoxic condition in high altitude
    o Pulmonary arterial hypertension
     Pulmonary vascular shunting is normal mechanism for ventilation-perfusion mismatch
  • Divert deO2 blood to better oxygenated regions of lungs = dorsal aspect
  • Strong response in cattle, horses, pigs
     Exaggerated shunting in response to hypoxia
    o Bovine lungs: small size compared to BW, lobulated
    o Severe ↓ pulmonary caoacity
  • Pulmonary hypertension → RVH and RVEH → R-CHF
32
Q

Lung response to hypoxia: acute

A

pulmonary arteriole constriction

33
Q

Lung response to hypoxia: chronic

A

(3wks):
 Vascular hypertrophy
 Medial hypertrophy
 Adventitial proliferation
o Loss of peripheral PAs → ↑ PVR → PH

34
Q

Causes brisket dz

A

o Inherited:
 Genetic predisposition
 Altered chemoR activity
 Myocardial metabolism
o Acute viral/bacterial pulmonary disease can exacerbate hypoxia
o Plants associated with ↑ incidence
 Locoweed shown to induce dz
* Oxytorpis and Astragalus spp with alkaloid swainsonine

35
Q

Lesions brisket dz: general

A
  • Generalized edema
    o Most severe in ventral subQ tissues, skeletal musculature, perirenal tissues, mesentery, GI tract walls
    o Ascites, hydrothorax, pericardial effusion
    o Transudate fluid: low cellularity and low protein fluid → R-CHF
36
Q

Lesions brisket dz: liver

A

early nutmeg appearance to severe lobular and vascular fibrosis
o Depend on chronicity of passive congestion

37
Q

Lesions brisket dz: lungs

A

o Variable degree of atelectasis
o Interstitial emphysema
o Edema
o Pneumonia
o Pulmonary arterial thrombosis frequent

38
Q

Lesions brisket dz: heart

A

RVH and dilation
o Cardiac apex displaced to L
o RA flaccid and enlarged

39
Q

Lesions brisket dz: histo

A

o Hypertrophy of medial in small arteries
o PA rupture (aneurysm) can result in acute death

40
Q

Lesions brisket dz: IHC

A
  • Immunohistochemistry/electron microscopy studies
    o Swelling + cytoplasmic vacuolization of pulmonary IV macrophages + endothelial cells
    o Vacuolation of myocardial interstitial cells
41
Q

Tx brisket dz

A
  • Move to lower alititude
    o Hyperbaric chambers at high elevations
  • Minimal restraint/stress/excitement
  • Supportive care: diuretics, thoracocentesis
  • Treat concurrent dz
42
Q

How can genetic selection help brisket dz

A
  • Genetic selection of individuals by PAP measurements → ↓ prevalence
    o At 5000-7000ft (1500-2000m): normal PAP = 34-41mmmHg
     PAP >48mmHg = at risk, potential genetic carrier
     Grey zone: 41-48mmHg → breed with caution
     Consider age of animal: if <1y/o → difficult to interpret
    o If altitude <5000ft → sometimes hypoxic conditions not sufficient to induce ↑PAP
     Not use for breeding selection
     Identify animals susceptible at higher altitudes
     Animals moved at higher altitude should remain 3wks before testing

11. Acquired heart dz (18 decks)

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