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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

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
What are the levels of resistance to flow in terms of RV work and how does this differ relative to the systemic circulation?
* 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
Features of exercise induced pulmonary hemorrhage in horses
o Hemorrhage from pulmonary capillaries into alveolar space o Predominant in caudodorsal lung fields
27
Exercise induced pulmonary hemorrhage in horses histo
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
Exercise induced pulmonary hemorrhage in horses is a consequence of
o ↑CO o Lack of sufficient pulmonary vasodilation o ↑ blood viscosity with exercise
29
Exercise induced pulmonary hemorrhage in horses pathophys
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
What is cattle brisket dz
* 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
Etiology of brisket dz
* 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
Lung response to hypoxia: acute
pulmonary arteriole constriction
33
Lung response to hypoxia: chronic
(3wks):  Vascular hypertrophy  Medial hypertrophy  Adventitial proliferation o Loss of peripheral PAs → ↑ PVR → PH
34
Causes brisket dz
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
Lesions brisket dz: general
* 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
Lesions brisket dz: liver
early nutmeg appearance to severe lobular and vascular fibrosis o Depend on chronicity of passive congestion
37
Lesions brisket dz: lungs
o Variable degree of atelectasis o Interstitial emphysema o Edema o Pneumonia o Pulmonary arterial thrombosis frequent
38
Lesions brisket dz: heart
RVH and dilation o Cardiac apex displaced to L o RA flaccid and enlarged
39
Lesions brisket dz: histo
o Hypertrophy of medial in small arteries o PA rupture (aneurysm) can result in acute death
40
Lesions brisket dz: IHC
* Immunohistochemistry/electron microscopy studies o Swelling + cytoplasmic vacuolization of pulmonary IV macrophages + endothelial cells o Vacuolation of myocardial interstitial cells
41
Tx brisket dz
* Move to lower alititude o Hyperbaric chambers at high elevations * Minimal restraint/stress/excitement * Supportive care: diuretics, thoracocentesis * Treat concurrent dz
42
How can genetic selection help brisket dz
* 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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