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Small Animal Final Year > Hypertension > Flashcards

Hypertension Flashcards

1
Q

What can cause persistently elevated systemic BP? (3)

A

–Fear or excitement

–Typically requires more than just one abnormal reading

–Drugs (Fluid therapy, steroids, cyclosporin A, phenylpropanolamine)

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2
Q

Define the hypertension values (2) and what can change these? (3)

A

–Systolic > 160 mmHg warrants further investigation

–Diastolic > 100 mmHg warrants further investigation

–Age (possible 1 – 3 mmHg/year after 8 yrs)

–Breed (sighthounds have 10 – 20 mmHg Higher BP)

–Obesity (small increase)

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3
Q

What does diagnosis of persistently elevated systemic blood pressure be on? (2)

A
  • Underlying condition
  • End organ damage producing clinical signs. Retinal hemorrhage is often seen.
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4
Q

What is the BP equation?

A

BP = CO x PVR

BP = (SV x HR) x PVR

  • BP: Blood pressure
  • CO: Cardiac output
  • PVR: Peripheral vascular resistance
  • SV: Stroke volume
  • HR: Heart rate
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5
Q

What are the inititating cause of hypertension (3)

A

–Chronic fluid accumulation

–Persistently increased heart rate

•E.g. Hyperthyroid cat

–Chronic vasoconstriction

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6
Q

What are the perpetuating causes of hypertension? (4)

A

–Small arteries changes:

  • Extravasation of plasma into the vessel wall (hyaline arteriosclerosis)
  • Vascular smooth muscle hypertrophy
  • Permanent changes in vascular meaning that the vessel no longer reacts to VC and VD – hard to control the BP

–Renal disease

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7
Q

What is the pathophysiology of renal disease and hypertension?

A

–Chronic damage to kidney and failure of Na handling

–BP can not remain persistently elevated without abnormal sodium handling (chronic renal failure/insufficiency)

–Kidney disease of any type result in areas of ischaemia that lead to activation of the RAAS

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

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8
Q

What is the aetioogy of hypertension?

A
  • Artefact
  • Stress induced
  • White-coat hypertension
  • Primary (idiopathic)
  • No underlying disease detected
  • Most common in Humans (95%)

–Diet and life style related

  • Rare in veterinary patients
  • Secondary
  • Underlying disease detected
  • Most common in veterinary patients (> 80%)
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9
Q

Name primary causes of hypertesnsion (8)

A

–Renal disease

•30-40% of dogs with CRF have hypertension

–Disturbance in neuroendocrine factors and body fluid balance

–Hyperadrenocorticism (dog)

–Increases renal retention of salt and water

–Overproduction of renin: vasoconstriction

–Hyperthyroidism (cat)

–Increases sensitivity of myocardium to cathecolamines

–Diabetes mellitus (dog and cat)

–Volume expansion due to hyperglycaemia

–Overproduction of renin:vasoconstriction

–Phaechromocytoma (rare)

–Hyperaldosteronism (rare)

–Drug therapy

–steroids, NSAID, cyclosporin A, phenylpropanolamine

–Diet

–Not as significant as in Humans

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10
Q

What are the clinical signs of HT?

A
  • None at the initial phases
  • Patients perception (Humans: headaches, general unease)
  • “Aging” - depression
  • Only present with end organ damage
  • > 180 mmHg or if 30 mmHg rise within 48 hours
  • Ocular (hypertensive retinopathy)
  • Acute blindness, retinal detachment
  • Intraocular haemorrhage
  • Acute onset and blindness – normally minimum of 200mmHg
  • CNS (hypertensive encephalopathy)
  • Disorientation, ataxia, stupor
  • Seizures, Strokes
  • Renal (proteinuria)
  • Pu/Pd
  • Cardiac (left ventricular hypertrophy)
  • Murmur, Arrhythmias
  • CHF
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11
Q

How can we measure systemic hypertension (2)

A

•Direct

–Invasive (requires arterial catheter)

–Intra operatively

–ICU inpatients

•Indirect

–Non invasive (compressive cuff)

–Commonly used on clinics

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12
Q

What are the 2 methods of indirect systemic HT measurement?

A

–Doppler

•Manual

–Requires more training

–More user variability

–Noise

–Until flow returns

  • Faster
  • Only systolic BP

–Oscillometric (High definition oscillometric)

•Automatic

–Straightforward

  • Time consuming
  • Systolic, diastolic and mean
  • Let cff slow and when blood flow starts it detect this (systolic). When it stops detecting a change – diastolic
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13
Q

How do we approach the measurement of BP? (4)

A

–Quiet and comfortable area (with owner but preferably without)

–Patient allowed to acclimate to the room and people for 5 to 10 minutes, before starting the examination.

–Sedation should be avoided and gentle restrain in a comfortable position

–Same operative each time? (person)

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14
Q

What cuff size do we use?

A

Cuff width size should measure 40% of the cuff site circumference

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15
Q

What happens if the cuff is too big?

A

Under estimate

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16
Q

What happens if the cuff is too small?

A

Over estimate

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17
Q

Where do you place a cuff in a cat and dog?

A

Cuff placed on a limb (cats) or tail (dogs)

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18
Q

Where is the cuff when you take a measurement?

A

Level of the heart

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19
Q

What measurement do we record? (9)

What do we do with the first reading?

A

–Results

•Sys/Diast Mean

–Method

–Area (limb or tail)

–Cuff size used

–Patients’ position

–Stress level

–Amount of restraint

–Therapeutic protocol

–Person performing

•First measurement should be discarded and an average of 3 to 7 (?10) consecutive measurements should be obtained.

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20
Q

When do we treat the HT? (3)

A
  • Risk end organ damage (EOD)
  • Underlying disease identified

–Always treat the underlying disease e.g. cushings or diabetes. Then assess BP again

–Low to moderate risk of end organ damage (systolic > 160 mmHg)

•No underlying disease identified

–Clinical signs

•Low to moderate risk of end organ damage (systolic > 160 mmHg)

–No clinical signs

•Moderate to high risk of end organ damage (systolic > 180 mmHg

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21
Q

How could we treat HT? (7)

A
  • Life style
  • Diet (salt restriction)

–First line in Humans

–Not used in veterinary

•Diuretics (volume depletion)

–Frequently used in humans

–Only in emergency setting in veterinary patients

  • β-blockers RARE to use to control hypertension (or at all)
  • ACEI
  • Ca channel blockers
  • Combination of the above
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22
Q

What B blockers can we use for HT? (2) Which do we not use in asthma?

What do they do?

When is it treatment of choice?

A

–Atenolol (β1 selective)

–Propanolol (non selective) (NOT to asthmatic)

–Reduce heart rate and contractility

–Treatment of choice in hyperthyroid cats- atenolol

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23
Q

How do ACE inhibitors work?

Give an example (3)

Where is it first choice?

A

–Blocking the RAAS

  • Benazepril, Enalapril, Imidapril
  • First choice in dogs and patients with proteinuria
24
Q
  1. How do ca channel blockers work?
  2. Give an example?
  3. Where is it a first choice?
  4. When is it commonyl added?
A
  1. Inhibit calcium influx to the cell
  2. Amlodipine
  3. First choice in cats (proven efficacy)
  4. Commonly added to ACE-I in dogs
25
Q

•Angiotensin II receptor blocker:

  1. Give an example
  2. Why is it good in CKD cats?
A
  1. Telmisartan
  2. Reduction of proteinuria associated with chronic kidney disease (CKD) in cats
26
Q

What are the goals of HT treatment?(8)

A
  • Reduce blood pressure
  • < 150/95 mmHg
  • > 120 mmHg
  • Reduce EOD risk
  • Decrease proteinuria
  • Alleviate clinical signs
  • Prevent further deterioration of organ function
  • Depends on the underlying disease
  • Minimise hospitalisation
  • Owner compliance
27
Q

What must we monitor for with Angiotensin II receptor blocker?

A

hypotension-

28
Q

Pulomonary circulation:

  1. Pressure?
  2. Resistance?
  3. Capacitance system?
A
  1. Low
  2. Low
  3. High
29
Q

What do low pulmonary circularion pressure minimise teh workload of?

A

RV

30
Q

What are Increases in pulmonary blood flow are usually accommodated with minimal increase in pulmonary artery pressure due to? (3)

A

–Highly distensible thin walls of the pulmonary vasculature

–Recruitment of underperfused vessels

–Large pulmonary capillary surface area.

31
Q

Systole pressure:

  1. RA?
  2. RV?
  3. LA?
  4. LV?
A
  1. 5
  2. 25
  3. 10
  4. 120
32
Q

Diastole pressure:

  1. RA?
  2. RV?
  3. LA
  4. LV?
A
  1. 0-3
  2. -1
  3. 0-5
  4. -1
33
Q

Define Pulmonary Hypertension in terms of systole and diastole?

A

–Systolic pulmonary artery pressure (PA) >35mmHg

–Diastolic PA pressure >10mmHg

34
Q

What are the causes of pulomary hypertension?? (5)

A

1.Alveolar hypoxia with pulmonary vasoconstriction / remodelling (lung disease)

–Severe respiratory disease e.g IPF, neoplasia etc

2.Pulmonary vascular obstructive disease

–Pulmonary thromboembolism

–Heart worm disease

3.Pulmonary overcirculation

–Large congenital shunts – shoving too much blood through pulmonary vasculature – changes in nature and becomes more like systemic arterials

4.High pulmonary venous pressure

–Left sided heart failure of various causes

5.Idiopathic

–Raise PABP – unknown why

35
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. Permanently damage the vessels – unable to reverse HT
  • When enough of these vessels are damaged and their ability to dilate is lost there is an increase in PVR and hence increase 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 is does not appear clinically significant, however in disease animals this mechanism can be very important in disease progression
36
Q

What is the pathophysiology of shunts?

A
  • Large volumes of blood shunting through the lungs due to congenital heart disease can lead to pulmonary arterial remodelling
  • Increased blood flow can raise perfusion pressure and damage pulmonary vessels
37
Q

What is the Pathophysiology of chronic pulmonary venous hypertension?

A
  • Can induce structural changes in pulmonary capillaries and increase the muscularity of resistance arterioles
  • Pulmonary oedema associated with high venous pressures contribute to increased pulmonary vascular resistance by causing reduced lung compliance and increased resistance to airflow
  • Hypoxia induced PA vasoconstriction
38
Q

What is the pathophysiology of pulomary HT is there are Permanent changes in pulmonary arterioles which cannot be reversed?

A
  • PH causes RV hypertrophy and dilation
  • RV diastolic pressure will eventually increase leading to an increase in venous pressures leading to right sided heart failure
  • Cor pulmonale = right sided changes induced by PH caused by pulmonary vascular/parenchymal disease
  • Cardiac output reduces as RV function declines leading to exertional dyspnoea, fatigue and syncope
  • Under perfuse LHS – causing collapse
39
Q

Breeds predisposed pulomary HT?

What age?

Sex?

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
40
Q

•Suspect PH when you see what without an obvious cause? (3)

A

–Persistent respiratory difficulty

–Fatigue

–Exercise intolerance

41
Q

What are the clinical feature most common signs of pulonary HT? (6)

A

–Exercise intolerance

–Cough

–Respiratory difficulty

–Syncope

–BUT remember those cases with left sided congestive heart failure

–Clinical signs of PTE can be very variable and include: dyspnoea, tachycardia, lethargy, altered mentation, vomiting, diarrhoea

•Sudden resp difficulty and nothing much on xray – always consider!!!!!!!

42
Q

What are the physical findings of pulmonary HT?(4)

A
  • Right sided murmur (damaged and dilated). Tricuspid insufficient
  • With severe PH can have split S2
  • Signs of primary disease?

–Chronic lung disease – crackles, cyanosis

–Murmur associated with left sided disease if LCHF is the cause

  • Right sided murmur > L side!
  • Right sided heart failure – ascites
43
Q

How can you daignose pulmonary HT? (6)

A
  • Historical and clinical findings – high index of suspicion
  • Thoracic radiographs
  • Echocardiography
  • Electrocardiography
  • Invasive cardiac catheterisation
  • CT scan
44
Q

What on thoracic radiographs suggest PHT? (6)

A

–Cardiomegaly – especially right sided enlargement

–Enlarged pulmonary arteries*

–R apical murmur > L apical murmur

–Right sided heart failure signs – hepatomegaly, large caudal vena cava, pleural effusion

–Pulmonary parenchymal infiltrates – reflecting primary lung disease on radiographs

–Sudden right sided congested HF

45
Q

What is wrong?

A

Big fat arteries

Big RS?

46
Q

What is the issue?

A

Big right side – reverse D

47
Q

What is wrong here?

A

Pulmonary Hypertension
Not much on an increase in LS
Huge RS – sternal contact. Pushing the trachea
Difficulty breathing and collapse
Secondary to IPF

48
Q

What can be seen on echocardiography of PHT? (5)

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
49
Q

What is wrong here? RPLA

A

See a huge amount of right side. Normal – only occupy top of image and hidden away. R same as L – v suspicious

50
Q

What can be seen on this RPLA?

A

Pulmonary HT – measure the speed of tricuspids regurgitation
Pressure gradient across the normal -20mmHG = 1M/sec. More than 2M/sec – pulmonary hypertension

51
Q

What does this show?

A

Tricuspid regurgitation

52
Q

What can be seen on this Echo – left parasternal long axis view?

A

R side here bigger than L

53
Q

What does this Echo – Left parasternal long axis view with colour Doppler show?

A

Regurgitation across mitral and tricuspid

54
Q

What view is this?

A

RPSA

55
Q

What is the treament for pulmonary HT? (7)

A
  • There is no cure
  • Few treatment options
  • Treat underlying disease
  • Sildenafil (Viagra)

–Effective in some cases BUT there is usually limited capacity for pulmonary vasodilation and NB concurrent systemic vasodilation and hypotension!

  • Pimobendan
  • Oxygen therapy
  • Enothelin antagonists - Bosentan
56
Q

What is pimobendan and how does it work?

A
  • Inodilator
  • Calcium-sensitizing drug
  • Positive inotrope
  • PDE III inhibitor
  • Vasodilation
  • Antithrombotic activity
  • ‘Feel good’ factor ? mechanism
57
Q

Complete this table

A

Small Animal Final Year (317 decks)

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