L34: Systemic Hypertension (Swift) Flashcards
CO =
CO = HR x SV
What metabolites cause local vasodilation/BP regulation in systemic vasculature?
CO2
ADP
Organic acids
Systemic BP regulation by autonomic nervous system
Increased BP –> increased vagal stimulation –> increased parasympathetic tone –> decreased HR
Decreased BP –> increased sympathetic tone –> increased adrenal stimulation –> increased aldosterone secretion
Renin-angiotensin-aldosterone system
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)
Systemic hypertension =
Persistently increased blood pressure
Associated diseases that cause secondary systemic HT
- renal dz (common)
- hyperthyroidism
- primary hyperadrenocorticism
- hyperaldosteronism
- pheochromocytoma
- polycythemia
- drugs
Organ damage to kidneys with systemic HT
- proteinuria
- glomerulosclerosis
*kidney failure can either cause or be a consequence of high blood pressure
Organ damage to eyes with systemic HT
- vascular tortuosity
- retinal hemorrhage
- retinal detachment
Organ damage to brain with systemic HT
Stroke (hemorrhagic, ischemic)
Seizures
Organ damage to HEART with systemic HT**
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
damage to vascular system with systemic HT
Hemorrhage (epistaxis)
-uncommon
CS of systemic HT
- acute blindness (most common)
- neuro signs (seizure, mentation change)
- or no CS!
Measurement of systemic HT
Direct: SAP, DAP, MAP (most invasive)
Indirect: doppler, oscillometric
Advantages/disadv. of Dopplers
-more accurate in small animals
Cuff size
Width should be about 40% of the diameter of the leg
When to measure BP
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
Systolic and diastolic BP should be less than:
SAP
Management options of systemic HT
- 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
ACE inhibitors for tx of systemic HT
- 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
Ca channel blockers for tx of systemic HT
- 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
Angiotensin receptor blockers for tx of SHT
- Losartan
- used with ACE inhibitors
- can increase GFR and cause renal failure potentially
- long term effects unknown
Adrenergic blockers for tx of SHT
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
Hydralazine
Vasodilator
- used in fat patients that we want to reduce their BP
- lowers BP, but may cause reflex tachycardia
Nitroprusside
NO donor –> vasodilation
-can cause cyanide toxicity after few days use
Diuretics not effective for tx of SHT
:)
Emergency tx of HT
IV: nitroprusside, esmolol or labetalol
Oral: hydralazine or amlodipine
Monitor BP; goal =
BP =
BP = CO x PVR
3 types of systemic HT
Primary
Secondary
White coat
Most common underlying cause of systemic HT
Renal disease (usually chronic)
Iatrogenic causes of SHT
Corticosteroids (hyperadrenocorticism)
Phenylpropanolamine (vasoconstriction)
Cyclosporin A
Erythropoietin (increases blood viscosity)
NSAIDs
Electrolyte solutions (expand blood volume)
Adrenergic agonists
*most of these cause vasoconstriction
