Hypotension/Hypertension Flashcards
describe arterial blood pressure
normal systolic pressure: 120
normal diastolic: 80
normal MAP: 90
MAP = DBP + 1/3 (SBP-DBP)
what are determinants of blood pressure?
MAP = CO x SVR
CO = SV x HR
SV: preload, afterload, contractility
HR: sympathetic versus parasympathetic tone
SVR:
-local: prostaglandins, histamine, NO
-systemic: vasopressin, angiotensin II, sympathetic tone
kidneys regulate the amount of fluid in the system!!
describe nervous regulation of the circulation and rapid control of arterial pressure
- sympathetic nervous system:
-basal tone: can increase or decrease
-norepinephrine: most important neurotransmitter
–binds to alpha-1 receptors on vessels = vasoconstriction
–binds to beta-1 receptors on heart = tachycardia and inotropy (increase in heart rate and contractility) - parasympathetic:
-minimal effects on blood pressure
-stimulation of vagus nerve: bradycardia
describe the kidneys and RASS and contributes to blood pressure
- kidneys: pressure diuresis
-blood volume increases causing kidneys excrete more water
-blood volume decreases causing kidneys to excrete less water (ADH/vasopressin mediated) - kidneys produce renin when blood flow to kidney decreases
-angiotensin II: causes renal retention of salt and water and vasoconstriction
-stimulates aldosterone production: causes increase in sodium reabsorption by kidney tubules
describe control of blood pressure (3)
- arterial pressure control mechanisms that act within seconds or minutes
-SNS: baroreceptor mechanism, CNS ischemic mechanism, and chemoreceptor mechanism
-results in vasoconstriction and increased HR and contractility to provide greater pumping ability
-when pressure suddenly rises too high, the same control mechanisms operate in revere direction
- arterial pressure control mechanisms that act after many minutes
-RAAS vasoconstrictor mechanism
-stress relaxation of the vasculature: stretch = vessels accomodate stretch so can act as intermediate buffer
-shift of fluid through tissue capillary walls in and out of circulation to readjust blood volume as needed
- long term mechaniams
-kidneys control blood volume
-aldosterone
-RAAS
describe how to measure blood pressure
- direct: arterial catheterization = gold standard but rarely done
- indirect:
-doppler: measures systolic bp
-oscillometric
describe systemic arterial hypertension
- sustained pathological increase in systemic arterial BP
-systolic BP >160mmHg
-MAP >130 mmHg
describe hypotension
- decreased arterial blood pressure
- systolic BP <90mmHg
- MAP <80
-impaired tissue perfusion at MAP <60mmHg
describe diagnosis of hypertension
- systolic BP >160mmHg
-results should be confirmed by repeated measurements on multiple occasions - exception: evidence of target organ damage
describe causes of hypertension (3)
- situational: artificial elevation in BP created by stress of hospital, handling, and the act of obtaining BP
- secondary: high BP in the context of a known predisposing disease
-CKD
-AKI
-DM
-hyperadrenocorticism
-hyperthyroidism
-pheochromocytoma (adrenal tumor)
-hyperaldosteronism - idiopathic: systemic hypertension without a discernible underlying cause
describe target organ damage consequences of hypertension (4)
- kidneys:
-CKD progression
-increase in CK, SDMA, BUN
-proteinuria - eye:
-acute blindness
-retinal detachment
-retinal hemorrhage - brain:
-encephalopathy
-stroke - heart and blood vessels
-left ventricular hypertrophy
brain and eye can be very obvious clinically/more common presenting reasons, kidney and heart changes are less outwardly obvious
describe a hypertensive emergency
- marked hypertension (SBP > 180mmHg) in combination with evidence of TOD (mostly ocular/neuro)
- GOAL: decrease SBP by 10% over the first hour, then another 15% over the next several hours (25% total reduction), then normalization over the next couple weeks
-probs acclimated to the higher blood pressure, so not normalize completely at first or will act hypotensive - treatment usually in a 24 hour care facility: dangerous drugs, constant monitoring
- IV meds vs oral:
-if in GP, do some diagnostics and some oral meds before sending down the road
-oral less effective than IV but require less monitoring
describe IV antihypertensive medications
- more potent so more effective, but also more dangerous!!
-definitely requires a 24 hour care facility - easier to titrate to effect, most given as CRIs (turn up or down to increase or decrease effect)
- options:
-fenoldopam: dopamine 1 receptor agonist that causes renal arterial vasodilation, natriuresis, increased GFR, and diuresis
-nitroglycerine: metabolized to nitric oxide to cause vasodilation
-hydralazine: potent arterial vasodilator
describe oral antihypertensive medications
- not as effective but also not as dangerous (less likely to cause hypotension)
- options:
-calcium channel blocker (amlodipine): preferred oral medication for emergency
-long term management, esp in CKD:
–ACE inhibitors: enalapril, benazepril
–angiotensin receptor blockers: telmisartan
- others:
-alpha 1 blockers: prazosin, phenoxybenzamine
–specifically used for pheochromocytoma
describe causes of hypotension
- reduction in preload
- reduction in cardiac function
- reduction in systemic vascular resistance
describe consequences of hypotension
- decreased perfusion causes decreased oxygen delivery and SHOCK
-increase in sympathetic tone causes tachycardia and inotropy increase and vasoconstriction
-RAAS is stimulated, resulting in vasoconstriction
-aldosterone: decreased Na excretion and increased water reabsorption in kidneys
- organs most sensitive to reperfusion:
-kidneys: AKI
-brain: altered mentation
-heart: arrhythmias
describe reduction in preload
- decreased venous return causes decreased preload which causes decrease cardiac output and hypotension
- decreases in preload caused by:
-hypovolemia: hemorrhage, GI/kidney fluid loss (severe dehydration), cavitary effusions
-obstruction of blood flow; GDV (obstruct CdVC), pericardial effusion (obstruct RA so it cannot fill)
describe treatment of decreased preload
- hypovolemia:
-IV fluid bolus: 10-20 ml/kg of balances isotonic fluid
-hemorrhage may require transfusions - obstruction of blood flow
-start wth IV fluid bolus to increase preload
-remove obstruction
–GDV: decompress
–pericardial effusion: pericardiocentesis
describe reduction in cardiac function
- decreased inotropy causes decreased pumping which decreases cardiac output and causes hypotension
- primary heart disease: DCM
- secondary:
-severe acidosis or alkalosis
-toxin/drug exposure
-SIRS/sepsis
describe how to treat reduction in cardiac function
positive inotropes: increase contractility
- dobutamine: effect is increased contractility
-given IV as CRI
-adverse effects: increased myocardial O2 demand, can cause arrhythmias, may cause mild vasodilation, cats: can cause seizures
describe reduction in systemic vascular resistance
- inappropriate vasodilation resulting in maldistribution of blood flow, resulting in maldistributive or vasodilatory shock
- most common causes:
-sepsis: excessive NO production by cytokines and direct vasoactive properties of carious other inflammatory mediators
-anaphylaxis: IgE produced in response to allergen binds to mast cells and causes release of histamines, leukotrienes, and others to promote vasodilation and increased vascular permeability
describe treatment of reduction of SVR
- norepinephrine: alpha receptor agonist, leads to vasoconstriction
-first choice in sepsis!! - dopamine: endogenous precursor to norepi
-B agonist to increase inotropy
-alpha agonist to cause vasoconstriction
-moderate vasoconstriction and mild increase in cardiac output - epinephrine:
-potent B1, B2, A1, and A2 agonist
-positive intotrope and chronotrope, vasoconstrictor, and bronchodilator
-drug of choice in anaphyliaxis
-used in CPR - vasopressin/ADH
-V1 receptor agonist = strong vasoconstriction
-second line vasoconstrictor (expensive)
-can also be used in CPR
