Hyper/Hypotension Flashcards
what are the determinants of stroke volume
- preload (venous return)
- afterload
- contractility
what are the determinants of cardiac output
- heart rate
- stroke volume
what are the determinants of systemic vascular resistance
- systemic neurohormonal factors
- local auto regulation
- local tissue/vascular factors
what are the determinants of MAP
- cardiac output
- systemic vascular resistance
what is blood pressure
the force applied per unit area of vessel wall
affected by blood volume, compliance, and resistance
arterial vs venous pressure
arteries: high pressure
veins: low pressure
allows blood to move from high to low pressure
what is the major determinant of blood flow/maintaining tissue perfusion
blood pressure
(ohm’s law: deltaP = Q x R)
what are short term BP regulatory mechanisms
baroreceptor reflex
ANS
myogenic control
local autoregulation
what are long term BP regulatory mechanisms
RAAS
natriuretic peptides
what happens if hypotension goes untreated
low BP –> poor tissue perfusion –> dec O2 delivery to vital organs –> shock –> organ failure –> death
what happens if hypertension goes untreated
high BP –> high blood flow –> end organ damage –> heart failure –> arrhythmias and death
does heart disease cause systemic hypertension
NO - but systemic hypertension can cause heart disease
what are the end organs affected by hypertension
brain
heart
kidneys
eyes
evaluate function of these organs if patient is hypertensive
ways to measure blood pressure
- direct measure
- standard oscillometry
- doppler ultrasound
direct BP measurement
arterial line is placed, machine calculates MAP
GOLD STANDARD but not clinically applicable
standard oscillometry
BP cuff temporarily inflates to occlude arteries, then measures oscillations of the arterial wall as the cuff dilates and blood flows back in
MAP is measured, SBP and DBP are calculated
doppler ultrasound
ultrasonic crystals emit ultrasonic waves and detect frequency shift between emitted and returning frequency to emit an audible signal
what are the perfusion parameters during hypotensive shock
mentation: QAR, obtunded, stupor
MM: pale or injected, CRT >2 or <1 sec
HR: tachycardia, bradyarrhythmia, tachyarrhythmia, bradycardia (cats)
temp: cool extremities
pulses: poor/absent or bounding
types of hypotensive shock
- hypovolemic
- cardiogenic
- vasodilatory
hypovolemic shock
decreased blood volume leading to hypotensive shock (hemorrhage, GI/kidney loss, GDV)
dec venous return –> dec preload –> dec SV, CO, MAP
what causes tachycardia during hypovolemic shock
baroreceptor reflex - senses the drop in MAP and causes an increase in HR, contractility, and vasoconstriction
cardiogenic shock
decreased cardiac function leading to hypotensive shock
primary or secondary cardiac disease
vasodilatory shock
decreased vascular resistance leading to hypotensive shock
(sepsis, anaphylaxis, systemic inflammation w/o infection)
causes injected MM and CRT <1 sec
how do you treat hypotension
PRIMARILY NEED TO TREAT UNDERLYING DISEASE
can treat symptom of hypotension by:
1. increasing preload
2. increasing SVR
how to increase preload
administer shock dose of fluids to increase SV
NOT indicated for heart disease
how to increase SVR
IV fluid therapy + vasopressors
vasopressors: NE, epi, dopamine, ADH
systemic hypertension
failure of the body’s normal physiologic adaptations to normalize BP
leads to inc CO, SVR, or both –> inc. MAP
situational hypertension
increases in blood pressure caused by anxiety or stress
if BP is abnormal –> take a second reading to confirm
if stressor is removed then BP will return normal
chronic hypertension
can be primary (idiopathic) or secondary to underlying disease
is primary or secondary chronic hypertension most common
secondary hypertension
baroreceptor reset
baroreceptors become less sensitive to high BP with chronic hypertension
causes the set point of activation to become higher –> baseline BP becomes higher
primary chronic hypertension
idiopathic; no clinically apparent systemic disease is identified; suggests that one or both of the neurohormonal and renal systems for regulating BP are abnormal
secondary chronic hypertension
- inc SNS (chronic stress, hyperthyroid, hyperadrenocorticism)
- inc catecholamine (adrenal tumor)
- inc volume (renal disease, hyperadrenocorticism, diabetes mellitus, hyperaldosteronism)
- inc SVR (RAAS activation in renal disease, impaired production of vasodilators)
effects of hypertension
increased afterload –> pressure overload –> concentric hypertrophy of ventricles –> decreased diastolic function
maladaptive response to systemic hypertension
ventricular hypertrophy and vascular remodeling contribute to further damage and tissue hypoxia, infarction, and organ dysfunction
treatment of hypertension
PRIMARILY NEED TO TREAT THE UNDERLYING DISEASE
treat the symptom of hypertension by:
1. blocking SNS (a1/a2, B blockers)
2. inhibiting RAAS (ACE inhibitors, ARBs)
3. peripheral vasodilation (amlodipine)
