L34: Systemic Hypertension (Swift) Flashcards

1
Q

CO =

A

CO = HR x SV

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2
Q

What metabolites cause local vasodilation/BP regulation in systemic vasculature?

A

CO2
ADP
Organic acids

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3
Q

Systemic BP regulation by autonomic nervous system

A

Increased BP –> increased vagal stimulation –> increased parasympathetic tone –> decreased HR

Decreased BP –> increased sympathetic tone –> increased adrenal stimulation –> increased aldosterone secretion

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4
Q

Renin-angiotensin-aldosterone system

A

1) In response to decreased renal perfusion, renin released from kidney.
2) renin stimulates angiotensin (which is released from liver) to transform to angiotensin I
3) angiotensin I converted to angiotensin II by ACE (released from pulmonary and renal endothelium)
4) angiotensin II stimulates:
- increased sympathetic activity
- Na and H2O retention
- adrenals to secrete more aldosterone
- vasoconstriction, increased BP
- ADH secretion from pituitary glands (increases H2O absorption)

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5
Q

Systemic hypertension =

A

Persistently increased blood pressure

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6
Q

Associated diseases that cause secondary systemic HT

A
  • renal dz (common)
  • hyperthyroidism
  • primary hyperadrenocorticism
  • hyperaldosteronism
  • pheochromocytoma
  • polycythemia
  • drugs
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7
Q

Organ damage to kidneys with systemic HT

A
  • proteinuria
  • glomerulosclerosis

*kidney failure can either cause or be a consequence of high blood pressure

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8
Q

Organ damage to eyes with systemic HT

A
  • vascular tortuosity
  • retinal hemorrhage
  • retinal detachment
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9
Q

Organ damage to brain with systemic HT

A

Stroke (hemorrhagic, ischemic)

Seizures

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10
Q

Organ damage to HEART with systemic HT**

A

Myocardial hypertrophy
Gallop, murmur

  • LV hypertrophy seen with systemic HT, whereas RV hypertrophy most common with pulmonary HT
  • in cats with HCM, must rule out HT as a primary cause
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11
Q

damage to vascular system with systemic HT

A

Hemorrhage (epistaxis)

-uncommon

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12
Q

CS of systemic HT

A
  • acute blindness (most common)
  • neuro signs (seizure, mentation change)
  • or no CS!
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13
Q

Measurement of systemic HT

A

Direct: SAP, DAP, MAP (most invasive)
Indirect: doppler, oscillometric

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14
Q

Advantages/disadv. of Dopplers

A

-more accurate in small animals

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15
Q

Cuff size

A

Width should be about 40% of the diameter of the leg

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16
Q

When to measure BP

A

When there are signs of possible target organ damage:

  • retinal hemorrhage
  • acute blindness
  • proteinuria
  • azotemia
  • seizures
  • murmur, arrhythmia, gallop

Or when have known associated disease:
-renal dz, hyperadrenocorticism, DM, pheo, hyperthyroid, primary hyperaldosteronism

17
Q

Systolic and diastolic BP should be less than:

A

SAP

18
Q

Management options of systemic HT

A
  • salt restriction: not effective
  • ACE inhibitors (blocks AG I –> AG II)
  • Ca channel blockers
  • Angiotensin receptor blockers
  • Adrenergic blockers
  • Non-specific alpha and beta blockers
  • others: hydralazine, nitroprusside, diuretics
19
Q

ACE inhibitors for tx of systemic HT

A
  • block AG I –> AG II
  • cause vasodilation
  • Na and H2O excretion
  • reduce sympathetic tone, cardiac and vascular hypertrophy
  • may slow progression of renal disease by reducing glomerular pressure and proteinuria
  • decrease GFR, so may cause/worsen azotemia
  • overall mild effects and fairly ineffective
  • first line choice in dogs, and cats with proteinuria
20
Q

Ca channel blockers for tx of systemic HT

A
  • Amlodipine, diltiazem
  • decrease Ca influx into vascular smooth muscle cells to cause vasodilation
  • first line tx in NON-proteinuric cats
  • second line tx in dogs and proteinuric cats if combined with ACE inhibitor
21
Q

Angiotensin receptor blockers for tx of SHT

A
  • Losartan
  • used with ACE inhibitors
  • can increase GFR and cause renal failure potentially
  • long term effects unknown
22
Q

Adrenergic blockers for tx of SHT

A

Beta-blockers:

  • decrease HR and contractility to reduce CO
  • atenolol, propanolol
  • 1st line for cats with hyperthyroidism
  • may be used for pheo, but only AFTER an alpha-antagonist is given*

Alpha blockers:

  • cause peripheral vasodilation
  • phenoxybenzamine, prazosin
  • 1st line for pheos

*monitor for hypotension while using adrenergic blockers

23
Q

Hydralazine

A

Vasodilator

  • used in fat patients that we want to reduce their BP
  • lowers BP, but may cause reflex tachycardia
24
Q

Nitroprusside

A

NO donor –> vasodilation

-can cause cyanide toxicity after few days use

25
Q

Diuretics not effective for tx of SHT

A

:)

26
Q

Emergency tx of HT

A

IV: nitroprusside, esmolol or labetalol
Oral: hydralazine or amlodipine

Monitor BP; goal =

27
Q

BP =

A

BP = CO x PVR

28
Q

3 types of systemic HT

A

Primary
Secondary
White coat

29
Q

Most common underlying cause of systemic HT

A

Renal disease (usually chronic)

30
Q

Iatrogenic causes of SHT

A

Corticosteroids (hyperadrenocorticism)
Phenylpropanolamine (vasoconstriction)
Cyclosporin A
Erythropoietin (increases blood viscosity)
NSAIDs
Electrolyte solutions (expand blood volume)
Adrenergic agonists

*most of these cause vasoconstriction