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Small Animal Medicine Exam 3 (Spring 2016) > L33: Pulmonary Hypertension (Swift) > Flashcards

L33: Pulmonary Hypertension (Swift) Flashcards

1
Q

PAP forumla

A

PAP = (PBF x PVR) + PCWP

PCWP = P in the left atrium

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2
Q

Main differences between systemic and pulmonary circulation**

A

Pulmonary system has:

  • lower resistance
  • lower pressure
  • higher capacitance
  • increased CO2 leads to vasoDILATION
  • decreased O2 leads to vasoCONSTRICTION
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3
Q

Natural vasoconstrictors in the lungs (4)

A

Endothelin-1
Angiotensin II (increased in CHF)
Thromboxane
Serotonin

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4
Q

Natural vasodilators in the lungs (3)

A

Nitric oxide (NO) - a therapy for pulm. HT
Prostacyclin (PGI2)
Oxygen (causes vasodilation in the lungs)

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5
Q

How is vasodilatin/vasoconstriction regulated at the local level in the lungs?

A

Nitric oxide, PGI2, and ET-1 are sourced from the endothelial cells lining blood vessels in the lungs. Whichever is in excess (ET-1 vs. NO and PGI2) determines whether there is vasoconstriction or dilation

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6
Q

Pulmonary endothelial dysfunction occurs when:

A
  • increased ET-1 or decreased NO and pGI2 –> vasoconstriction
  • a high blood pressure damages endothelium and causes even more vasoconstriction and higher BP
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7
Q

Why does pulmonary HT cause vascular remodeling?

A
  • ET-1 and AT-11 are chronically increased –> intimal and smooth muscle hypertrophy
  • is eventually irreversible
  • vasoconstriction dominates
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8
Q

Poiseuille’s Law

A
  • radius will increase or decrease flow by a factor of 4

- if radius decreases, have to increase pressure to maintain flow –> hypertension

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9
Q

Microvascular thrombosis can be either a cause or effect of PHT

A

:)

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10
Q

PHT can result from increased:

A

Pulmonary vascular resistance (PVR)
Pulmonary blood flow (PBF)
Pulmonary capillary wedge pressure (PCWP) (increased LA pressure)

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11
Q

Causes of increased PVR

A

1) primary PHT (rare)
2) HWD (most common): causes arteritis, embolism –> edema and congestive heart failure
3) Chronic pulmonary disease (asthma, chronic bronchitis, hypoxic vasoconstriction)
4) PTE
5) high altitude (global hypoxia)
6) hypoventilation (from anesthesia, obesity, nueromuscular dz)

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12
Q

Causes of increased PBF

A
  • congenital shunts (most common)

- increased CO (from anemia, hyperthyroidism)

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13
Q

Eisenmenger’s physiology

A

A large volume L to R shunt can increase PBF so much that it causes permanent vascular change and severe PHT, ultimately causing a shunt REVERSAL as pressure in pulmonary tree exceeds pressure in the heart
-results in pulmonary vascular resistance

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14
Q

Causes of increased PCWP (post-capillary hypertension)**

A
  • increased LA and pulmonary venous pressure (L-sided CHF)
  • diastolic PAP within 5 mm of PCWP

Mitral valve disease or DCM –> L-sided CHF –> Increased LA pressure or pulmonary venous pressure –> increased PCWP –> increased vascular resistance

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15
Q

Consequences of PHT

A
  • decreased CO
  • hypoxemia
  • cor pulmonale (R side of heart hypertrophies due to pressure overload –> myocardial failure –> RV dilation –> RHF)
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16
Q

CS of PHT

A
  • RHF (ascites, wt. loss, poor appetite)
  • cyanosis
  • syncope
  • cough, dyspnea
17
Q

Differentials for ascites

A
  • dec. oncotic pressure
  • inc. hydrostatic pressure
  • dec. lymphatic drainage
  • septic exudate
  • neoplastic effusion
  • chyle
18
Q

Ddx for dyspnea/cyanosis

A

Cardiac dz: CHF, HWD

Resp. Dz: infection, inflammation, neoplasia, pleural effusion

19
Q

Signs of PHT on ECG

A

Deep S waves

Right axis deviation

20
Q

Diagnostic evaluation of PHT patient

A 
CBC (look for infection, allergic/parasitic)
Chem (albumin)
UA: proteinuria
Fluid analysis
Heartworm test
SpO2/PaO2 to evaluate V/Q mismatch
Thoracic rads
21
Q

Things to look for on thoracic rads of PHT patient

A
  • pleural fluid/pulmonary edema
  • cardiac or vascular enlargement: L or R side?
  • tortuous blunted pulm. aa
  • airway or parenchymal dz (distribution helps determine CHF vs. bronchopneumonia)
22
Q

Dx of PHT

A

Measure PAP:

  • direct method (gold standard) involves cardiac catheterization and anesthesia
  • indirect method: perform echo and estimate based on RV hypertrophy, MPA dilation, and pulmonic/tricuspid regurgitation
23
Q

PI/TR**

A

Pulmonic/tricuspid regurgitation

  • tricuspid regurge is an indication of SYSTOLIC pressure
  • pulmonic regurge is an indication of DIASTOLIC pressure

PI/TR is an estimate of PAP

24
Q

Normal pulmonary artery pressure (PAP)

A
25
Q

Diseases assoc. with pulmonary artery hypertension

A 
Idiopathic and familial PH
HWD
Congenital shunts
Collagen vascular dz
Eisenmenger's syndrome
26
Q

Diseases assoc. with PH with L-sided heart disease

A 
Myxomatous mitral valve disease
Myocardial disease (ie. DCM)
27
Q

Diseases assoc. with PH associated with lung disease/hypoxemia

A

COPD
Interstitial lung disease
High altitude
Alveolar ventilation disorders

28
Q

Diseases assoc. with PH caused by thromboembolic disease

A

Thrombotic obstruction of PAs

Non-thrombotic obstruction (ie. Parasites, neoplasia)

29
Q

Misc. diseases causing PHT

A

Compression of pulmonary vessels
Lymphadenopathy
Granulomatous disease

30
Q

PHT causes a pressure overload of the RV in cor pulmonale

A

:)

31
Q

Changes in pressures assoc. with L-sided CHF

A
  • PAP may be increased due to high PCWP with normal PVR
  • increased LA and pulmonary venous pressure with severe mitral regurge, cardiomyopathies, or mitral stenosis
  • chronically increased PCWP may lead to increases in PVR and disproportionate increases in PAP
32
Q

When will pressure in pulmonary arterial tree not equal pressure in the RV?

A

When there is pulmonic stenosis

33
Q

Normal pressure gradient

A

(Pressure gradient b/w RA and RV)

25 mmHg

34
Q

PG + pressure in RA = ** (normally)

A

PAP or Pressure in RV

35
Q

Tx of PHT

A
  • tx underlying cause if possible, except or R to L shunts

- tx hypoxia and R-CHF with oxygen, diuretics, and ACE-inhibitors

36
Q

Methods of decreasing PVR (txs)

A
  • oxygen (acute tx only)
  • NO (acute tx only)
  • Ca channel blockers (can have systemic side effects)
  • ACE inhibitors (little effect on PAP)
  • synthetic prostacyclin (extremely expensive)
  • ET-1 receptor antagonists (Bosentan)
  • phosphodiesterase inhibitors
  • anti-thrombotics (only use if think PTE is cause of PHT)

*few actually succeed!

37
Q

Phosphodiesterase inhibitors

A

Sildenafil: causes modest decrease in PAP and may improve CS
-beware in L-CHF: may increase LV preload and precipitate pulmonary edema

Tadalafil (Viagra): longer-acting

Pimobendan
-a positive inotrope that causes systemic and pulmonary vasodilation

38
Q

Tx of choice for alveolar hypoxia

A

Oxygen

39
Q

Side effect of high dose Ca channel blockers

A

Systemic hypotension

Small Animal Medicine Exam 3 (Spring 2016) (9 decks)

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