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CRH II > Hypotension/Hypertension > Flashcards

Hypotension/Hypertension Flashcards

1
Q

describe arterial blood pressure

A

normal systolic pressure: 120

normal diastolic: 80

normal MAP: 90

MAP = DBP + 1/3 (SBP-DBP)

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2
Q

what are determinants of blood pressure?

A

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!!

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3
Q

describe nervous regulation of the circulation and rapid control of arterial pressure

A
  1. 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)
  2. parasympathetic:
    -minimal effects on blood pressure
    -stimulation of vagus nerve: bradycardia
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4
Q

describe the kidneys and RASS and contributes to blood pressure

A
  1. kidneys: pressure diuresis
    -blood volume increases causing kidneys excrete more water
    -blood volume decreases causing kidneys to excrete less water (ADH/vasopressin mediated)
  2. 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
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5
Q

describe control of blood pressure (3)

A
  1. 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

  1. 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

  1. long term mechaniams
    -kidneys control blood volume
    -aldosterone
    -RAAS
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6
Q

describe how to measure blood pressure

A
  1. direct: arterial catheterization = gold standard but rarely done
  2. indirect:
    -doppler: measures systolic bp
    -oscillometric
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7
Q

describe systemic arterial hypertension

A
  1. sustained pathological increase in systemic arterial BP
    -systolic BP >160mmHg
    -MAP >130 mmHg
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8
Q

describe hypotension

A
  1. decreased arterial blood pressure
  2. systolic BP <90mmHg
  3. MAP <80
    -impaired tissue perfusion at MAP <60mmHg
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9
Q

describe diagnosis of hypertension

A
  1. systolic BP >160mmHg
    -results should be confirmed by repeated measurements on multiple occasions
  2. exception: evidence of target organ damage
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10
Q

describe causes of hypertension (3)

A
  1. situational: artificial elevation in BP created by stress of hospital, handling, and the act of obtaining BP
  2. secondary: high BP in the context of a known predisposing disease
    -CKD
    -AKI
    -DM
    -hyperadrenocorticism
    -hyperthyroidism
    -pheochromocytoma (adrenal tumor)
    -hyperaldosteronism
  3. idiopathic: systemic hypertension without a discernible underlying cause
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11
Q

describe target organ damage consequences of hypertension (4)

A
  1. kidneys:
    -CKD progression
    -increase in CK, SDMA, BUN
    -proteinuria
  2. eye:
    -acute blindness
    -retinal detachment
    -retinal hemorrhage
  3. brain:
    -encephalopathy
    -stroke
  4. 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

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12
Q

describe a hypertensive emergency

A
  1. marked hypertension (SBP > 180mmHg) in combination with evidence of TOD (mostly ocular/neuro)
  2. 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
  3. treatment usually in a 24 hour care facility: dangerous drugs, constant monitoring
  4. 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
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13
Q

describe IV antihypertensive medications

A
  1. more potent so more effective, but also more dangerous!!
    -definitely requires a 24 hour care facility
  2. easier to titrate to effect, most given as CRIs (turn up or down to increase or decrease effect)
  3. 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

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14
Q

describe oral antihypertensive medications

A
  1. not as effective but also not as dangerous (less likely to cause hypotension)
  2. options:
    -calcium channel blocker (amlodipine): preferred oral medication for emergency

-long term management, esp in CKD:
–ACE inhibitors: enalapril, benazepril
–angiotensin receptor blockers: telmisartan

  1. others:
    -alpha 1 blockers: prazosin, phenoxybenzamine
    –specifically used for pheochromocytoma
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15
Q

describe causes of hypotension

A
  1. reduction in preload
  2. reduction in cardiac function
  3. reduction in systemic vascular resistance
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16
Q

describe consequences of hypotension

A
  1. 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

  1. organs most sensitive to reperfusion:
    -kidneys: AKI
    -brain: altered mentation
    -heart: arrhythmias
17
Q

describe reduction in preload

A
  1. decreased venous return causes decreased preload which causes decrease cardiac output and hypotension
  2. 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)

18
Q

describe treatment of decreased preload

A
  1. hypovolemia:
    -IV fluid bolus: 10-20 ml/kg of balances isotonic fluid
    -hemorrhage may require transfusions
  2. obstruction of blood flow
    -start wth IV fluid bolus to increase preload
    -remove obstruction
    –GDV: decompress
    –pericardial effusion: pericardiocentesis
19
Q

describe reduction in cardiac function

A
  1. decreased inotropy causes decreased pumping which decreases cardiac output and causes hypotension
  2. primary heart disease: DCM
  3. secondary:
    -severe acidosis or alkalosis
    -toxin/drug exposure
    -SIRS/sepsis
20
Q

describe how to treat reduction in cardiac funcrion

A

positive inotropes: increase contractility

  1. dobutamine: effect is increased contractility
    -given IV as CRY
    -adverse effects: increased myocardial O2 demand, can cause arrhythmias, may cause mild vasodilation, cats: can cause seizures
21
Q

describe reduction in systemic vascular resistance

A
  1. inappropriate vasodilation resulting in maldistribution of blood flow, resulting in maldistributive or vasodilatory shock
  2. 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

22
Q

describe treatment of reduction of SVR

A
  1. norepinephrine: alpha receptor agonist, leads to vasoconstriction
    -first choice in sepsis!!
  2. dopamine: endogenous precursor to norepi
    -B agonist to increase inotropy
    -alpha agonist to cause vasoconstriction
    -moderate vasoconstriction and mild increase in cardiac output
  3. epinephrine:
    -potent B1, B2, A1, and A2 agonist
    -positive intotrope and chronotrope, vasoconstrictor, and bronchodilator
    -drug of choice in anaphyliaxis
    -used in CPR
  4. vasopressin/ADH
    -V1 receptor agonist = strong vasoconstriction
    -second line vasoconstrictor (expensive)
    -can also be used in CPR

CRH II (48 decks)

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