Hypertension Flashcards
defintion
SBP>140mmHg
DBP>90mmHg
primary hypertension
unkown cause
secondary hypertension
phenochromocytome - tumour on adrenal gland
renal artery stenosis
Blood pressure
the pressure exerted on teh arterial walls during systole and diastole
rate presure product - HRxSV
measuring arterial BP
place cuff on arm
will not be able to hear anthing
increase cuff pressure to 160
slowly release pressure, note when you can start hearing tapping sound
continue decreasing pressure until tapping sound cant no longer be heard
effect on the population
all cause death - 9.4mil/year
no 1 physiloigical cause of global mortaility
prevalance
874 million adults worldwide are hypertensive
pre-hypertension
120-140mmHg
prevent hypertension occuring
as you get about 120, the risk increases quickly as a sliding scale
risk of a heart attack depending on BP
if you are hypertensive you are 7.4x more likely to have a MI
risk factors - unmodifiable
family history
age
sex
ethnicity
risk factors - modifiable
PA diet weight smoking sleep alcohol stress
repsonse to high BP
increase in VR, increase stretch on right atria through baroreceptors
bainbridge reflex - increase VR = increase HR
increase ANP release by atria
increase BNP
act on kidenys
increase Na+ excretion - increase water excretion
increase GFR
act on hypothalumus to decrease thrist
increase vasodilation via increase smooth muscle cGMP
decrease sympathetic tone
responce to low BP
decrease VR - no firing of baroreceptors
decrease ANP & BNP
afferent and efferent arteroile in JGA detect decrease
release renin
- convert angiotensinogen to angiotension I
- angiotension I to angiotension II via ACE
- increase vasoconstriction
- increases sypathetic activity
- decrease Na+ excretion via aldosterone from adrenal gland
- increase ADH (pituartry gland) - increase collecting duct absorption
increase thirst
= increase water absorption + increased BP
pharamalogical interventions
reduce BP
- ACE inhibitors
beta blockers - slow HR
diurectics
BP equation
QxTR=BP
what is heart rate variability
measure the difference between sympathetic and parasympathetic
you want high HR variability
nervous system response to increase BP
increases PNS, decrease SNS
SA node to reduce HR
relax ateriole smooth muscle to casue vasodilation, reducing TPR
ventrcular myocardium to decrease force of contraction to decrease Q
vascular resistance and aterial stiffnes with BP
arteries expand during systole
relax during diastole
when arteries bceom stiff, no longer able to move - makes heart work harder as no longer natural pushing of blood
creates turbulant flow - increases fatty streaks
how does central aortic stiffness lead to reduced end diastolic volume
increased LV afterload mycocardal hypertrophy impaired relaxation diastolic dysfunction reduced EDV
how does central aortic stiffness lead to damaged arteries
arteriole endothelial dysfunction
increased SBP
microvascular damage
Why is hypertension a strong risk factor for mortality/morbidity?
Heart
Heart – Diastolic dysfunction – MI and aneurysm – Ventricular hypertrophy – Heart failure – Atrial fibrillation – Ventricular fibrillation – Increased risk of ischaemia
Why is hypertension a strong risk factor for mortality/morbidity?
other organs
brain
kidney
eyes
effect of PA
reduce SBP by 5-7mmHg
reduced CVD risk by 20-30%
matches effect of pharamlogical interventions
why does PA reduce BP
- “Resetting” of the baroreceptors (change in BRS)
- Cardiac remodelling
- Fall in TPR
effect of PA on vascular health
- Increased endothelial function
- Decreased arterial stiffness
- Increase in arterial diameter
- Increase in vascular growth (angiogenesis)
- Improved perfusion (myocardial)
PA consideration for hypertensive patients
- Those with stage II hypertension (160/100 mmHg) should add moderate aerobic exercise only after initiating drug therapy
- Termination criteria for any exercise = 250/115 mmHg
- Some antihypertensives may impair thermoregulation, so be cautious of signs of heat intolerance
- Consider co-morbidities (e.g. retinopathy/vision)
