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CRS2 > Hypertension and Pulmonary Hypertension > Flashcards

Hypertension and Pulmonary Hypertension Flashcards

1
Q

What is the equation for blood pressure?

A

BP= CO x PVR

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2
Q

What are the guidelines for when an increased BP is too high?

A

Systolic > 160mmHg warrants further investigation

Diastolic > 100mmHg warrants further investigation

Age (possible 1-3mmHg/year after 8 years)

Breed (sighthounds have 10-20mmHg higher BP)

Obesity (small increase)

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3
Q

What is the pathophysiology of hypertension?

A

Initiating causes:

  • chronic fluid accumulation
  • persistently increased heart rate
  • chronic vasoconstriction

Perpetuating causes:

  • small artery changes –> vessel no longer reacts appropriately to vasoconstriction and vasodilation, hyaline arteriosclerosis, vascular smooth muscle hypertrophy
  • renal disease
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4
Q

Describe the relationship between renal disease and hypertension

A

Renal disease ↔ hypertension

BP cannot remain persistently elevated without abnormal sodium handling (chronic renal failure/insufficiency)

Kidney disease of any type results in areas of ischaemia that leads to activation of the RAAS

Kidney disease leads to dilation of the afferent arteriole and constriction of the efferent arteriole resulting in dramatic rises in glomerular pressures which leads to renal damage and proteinuria

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5
Q

What is the aetiology of hypertension?

A

Artefact- stress induced/ white coat hypertension

Primary= idiopathic

Secondary:

  • renal disease
  • hyperadrenocorticism (increased salt & water retention, overproduction of renin)
  • hyperthyroidism (increases sensitivity of myocardium to catecholamines)
  • diabetes mellitus (volume expansion due to hyperglycaemia, overproduction of renin)
  • phaechromocytoma
  • hyperaldosteronism
  • drug therapy (steroids, NSAID, cyclosporin A, phenylpropanolamine)
  • diet
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6
Q

What are the clinical signs of hypertension?

A

None initially

Only present with end organ damage (>180mmHg or if 30mmHg rise within 48 hours):

  • ocular (acute blindness, intraocular haemorrhage)
  • CNS (disorientation, ataxia, stupor, seizures, strokes)
  • renal (PU/PD, proteinuria)
  • cardiac (left ventricular hypertrophy if chronic–> murmur, arrhythmias, CHF)
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7
Q

What methods are available to measure BP directly?

A

Invasive (arterial catheter required)

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8
Q

What methods are available to measure BP indirectly?

A

Compressive cuff (non-invasive)

Doppler

Oscillometric

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9
Q

What are the advantages and disadvantages of Doppler to measure BP?

A

Advantages- faster

Disadvantages- requires more training, more user variability, noise, only systolic BP

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10
Q

What are the advantages and disadvantages of oscillometric measurement of BP?

A

Advantages- automatic (therefore straightforward), gives diastolic, systolic and mean

Disadvantages- time consuming

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11
Q

When should hypertension be treated?

A
  • Risk end-organ damage (EOD)
  • Underlying disease identified –> treat underlying disease
  • Clinical signs

BP:
160-179mmHg - moderate risk- treat if repeatable findings of evidence of EOD
>180mmHg - severe risk of EOD- aggressively treat

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12
Q

What are the treatment options for hypertension?

A

Diuretics frequently used in humans but only in emergency setting in veterinary patients

Beta blockers rarely used apart from in hyperthyroid cats (poor results as a single agent in other conditions)

ACEI:

  • more efective in pathologies that lead to elevated renin levels (renal failure, Cushings, diabetes)
  • first choice in patients with proteinuria
  • frequently insufficient as a single agent but should always be considered

Ca channel blockers:

  • first line treatment
  • first choice in cats, commonly added to ACEI in dogs
  • rapid onset

Combination of above

Angiotensin II receptor blocker:

  • new
  • Telmisartan
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13
Q

Why do patients with left sided heart failure develop secondary pulmonary hypertension?

A

When left side fails, it impacts the right side

Patient with left sided congestive failure – pressure in pulmonary veins goes up – right side of heart now ejecting blood into system that is under higher pressure than normal

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14
Q

What is pulmonary hypertension?

A

Defined as:

  • Systolic pulmonary artery pressure (PA) >35mmHg
  • Diastolic PA pressure >10mmHg
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15
Q

Name causes of pulmonary hypertension

A
  • Alveolar hypoxia with pulmonary vasoconstriction/ remodelling- Severe respiratory disease (e.g. IPF, neoplasia, etc.)
  • Pulmonary vascular obstructive disease (pulmonary thromboembolism, heart worm disease)
  • Pulmonary overcirculation (large congenital left to right shunts)
  • High pulmonary venous pressure (left sided heart failure of various causes)
  • Idiopathic
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16
Q

What is the pathophysiology of pulmonary hypertension?

A
  • Increased pulmonary vascular resistance (PVR) causes increase in PA pressure
  • Vasoconstriction due to hypoxia increases PVR and pulmonary hypertension (PH) can occur or worsen if already present
  • Severe PH will induce angioproliferative changes that will permanently reduce vascular compliance and lumen size
  • When enough of these vessels are damaged and their ability to dilate is lost there is an increase in PVR and hence an increase in PA pressure
  • Pulmonary arterial vasoconstriction is a normal response to alveolar hypoxia although the magnitude varies among species
  • Principle behind this mechanism preferentially perfuse well ventilated areas
  • In normal animals this mechanism only induces mild PH and therefore it does not appear clinically significant, but in diseased animals this mechanism can be very important in disease progression
17
Q

What are the clinical signs of pulmonary hypertension?

A

• Variable and can be very subtle
• NB signs of primary disease- esp. respiratory
• See in breeds predisposed to airway disease/ valvular disease- WHWT, CKCS
• Tend to see PH in middle aged to older dogs, no sex predilection
• Suspect PH when you see the following without an obvious cause
- persistent respiratory difficulty
- fatigue
- exercise intolerance

Most common signs:

  • Exercise intolerance
  • Cough
  • Respiratory difficulty
  • Syncope
18
Q

What can be found on clinical exam of an animal with pulmonary hypertension?

A
  • Right sided murmur (tricuspid insufficiency)
  • With severe PH can have split S2 (pulmonic valve closes later than aortic valve)
  • Signs of primary disease
19
Q

What can be seen on thoracic radiographs of animals with pulmonary hypertension?

A
  • Cardiomegaly (esp. right sided)
  • Enlarged pulmonary arteries
  • Right sided heart failure signs (hepatomegaly, large caudal vena cava, pleural effusion)
  • Pulmonary parenchymal infiltrates
20
Q

What can be seen on echocardiography of animals with pulmonary hypertension?

A

• Changes are proportional to severity of PH
• RV hypertrophy (>1/2 thickness of LV wall) and dilation
• Pulmonary artery dilation
• RA enlargement
Flattened IVS

21
Q

What are the treatment options for pulmonary hypertension?

A

There is no cure

  • treat underlying disease
  • Sildenafil (Viagara)
  • Pimobendan
  • Oxygen therapy
  • Endothelin antagonists (Bosentan)

CRS2 (64 decks)

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