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Flashcards in 7.3 Blood Pressure Deck (30)
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1
Q

What is the difference between primary and secondary HTN? mmHG?

A

primary hypertension: most common, unknown etiology
secondary hypertension: result of pathology in another organ

more than 140/90

2
Q

What does HTN do to arteries? Which are most susceptible?

A

endothelial damage due to shearing forces on vessel walls
retinal arteries hypertensive retinopathy, blindness
renal arteries  renal failure
cerebral arteries  hemorrhagic stroke
increases atherosclerosis

3
Q

How does HTN lead to left ventricular hypertrophy?

A

hypertension increases afterload, resistance against the left ventricle
left ventricular hypertrophy without increase in vascular supply –> susceptible to ischemia, infarction
left ventricle chamber has reduced volume, reduces stroke volume and cardiac output
may also encroach on right ventricle chamber size

4
Q

How does HTN lead to renal disease?

A

increases atherosclerosis of kidney afferent and efferent arterioles of nephrons
damages fragile glomerular capillaries, filtration rate decreases, permeability increases
increased waste in blood, serum creatinine and blood urea nitrogen (BUN) increase
loss of serum proteins in urine (proteinuria)
Can lead to renal failure, end stage renal disease

5
Q

What is pulse pressure? Formula?

A

The “throb” of pulse

= systolic-diastolic

6
Q

What is MAP? How derived?

A

Average between systolic and diastolic
calculated: [MAP = diastolic + 1/3 (systolic – diastolic)]

theory: [MAP = CO X PVR]

7
Q

What 3 factors generally impact BP?

A

Blood Flow
Resistance
Blood Volume

8
Q

Systemically, what impacts blood flow?

A

local blood flow to an organ/region
bulk flow through capillaries
systemic blood flow through the entire body

9
Q

How is local blood flow auto regulated?

A

metabolic controls: low oxygen and high waste accumulates, causes vasodilation
increased metabolic products: H+, lactic acid, K+, adenosine, prostaglandins
releases Nitric Oxide (NO) –> vasodilation
myogenic controls
stretch due to increased pressure
smooth muscle contracts –> vasoconstriction
angiogenesis (long-term)
growth of new blood vessels to increase supply to the area

10
Q

What is capillary blood flow? What determines it?

A

movement of fluid between capillaries and tissue interstitial space
This is determined by the pressure, fluid and components that change from the arteriole to venule end of the capillary bed
Arteriole end: Fluid needs to leave the capillaries to bathe the tissues
Venous end: Fluid needs to return back to the capillaries to remove waste and retain blood flow.
Lymphatics: excess fluid and debris will be cleaned and returned to circulation through lymphatics.

11
Q

How does hydrostatic pressure contribute to capillary bulk flow?

A

fluid, blood pressure:

arteriole –> venule blood pressure (35 –> 17 mmHg)

12
Q

How does osmotic pressure contribute to capillary blood flow?

A

solute pressure (water follows solutes)
high concentration of plasma proteins and blood cells left in capillary (26mmHg)
low level of proteins in the interstitial fluid (0.1 to 5 mmHg)
=measure of the amount of solutes; water follows solutes

13
Q

What is the definition of net filtration pressure?

A

sum of hydrostatic and osmotic pressures between the capillaries and ICF

14
Q

What is the formula for net filtration pressure?

A

NFP = (OUT) – (IN)
or:
[NFP = (HPc + OPicf) – (HPicf + Opc)]

15
Q

What causes peripheral edema? When supine?

A

Venous congestion, increased venous pressure causes a build up of pressure in the capillary beds, this leads to edema (swelling) in the lower body
standing swelling in lower extremities, ankles
lying down  swelling in the sacral region, risk of bed sores

** If venous congestion is more than the lymphatic system can remove = edema

16
Q

What is the formula for calculating systemic blood flow?

A

Systemic blood flow IS cardiac output

CO= SVxHR

17
Q

What are the 3 factors that impact blood vessel resistance?

A

blood viscosity
blood vessel length
blood vessel diameter**

18
Q

How does blood viscosity impact BP? Some examples?

A

the “thickness” or stickiness of blood
increases with increased cells or formed elements in the blood
ex: increased hematocrit, dehydration, increased EPO (blood doping), genetic disorders
increased viscosity, increased resistance

19
Q

How does blood vessel length impact BP?

A

changes when blood vessels grow, during development, during increased tissue growth (tumors, adipose tissue)
increased length, increased resistance

20
Q

How does blood vessel diameter affect BP?

A

small tube high friction, high resistance
large tube  low friction, low resistance
LARGE changes, by a factor of 4 for each change in radius
Resistance= (nL/r^4)

21
Q

What is the major driver of resistance in the CV system?

A

ARTERIOLES!

They have the smooth muscle to change size

22
Q

What is the SNS impact of smooth muscle?

A

Systemic vasoconstriction= BP up, increased venous return

23
Q

What hormones increase BP? Lower?

A

epinephrine/norepinephrine released by renal medulla – enhances SNS (vasoconstriction)
ANP (atrial natriuretic peptide) – blocks SNS (vasodilation)

24
Q

What are the 3 ways the SNS can up BP?

A

1- Increase peripheral vascular resistance = VASOCONSTRICT
2- Increase HR
3- Increase stroke volume (thru contractility)

25
Q

How do chemoreceptors impact BP?

A

chemical receptors that respond to increased CO2, H+, O2
located: carotid artery, aorta, brain
sense –> CO2, or H+ build-up

26
Q

How do baroreptors impact BP?

Where are they located?

A

pressure sensors that respond to stretch of arteries
located: carotid artery, aortic arch, large neck and thoracic arteries
sense –> increased stretch, increased BP

27
Q

How are HR and BP integrated?

A
Cardiovascular Center in Medulla Oblongata
cardioacceleratory center (heart)
cardioinhibitory center (heart)
vasomotor center (blood vessels)
28
Q

How does the ANS effect HR?

A
heart
pacemaker cells (heart rate)
cardiac muscle cells (stroke volume)
blood vessels
arterioles (vasoconstriction/vasodilation, resistance)
veins (venous return, stroke volume)
adrenal medulla
increased epinephrine, norepinephrine (heart rate, stroke volume, vasoconstriction)

Increase venous return –> Increase stroke volume: heart muscle stretches so more contraction (by frank-starling) a compensatory increase

29
Q

How do the kidneys regulate BP?

A

via blood volume changes
increased blood volume = increased blood pressure
Kidneys filter the blood and can decide how much to retain Na+ and H2O in the blood
increased filtration rate decreased blood volume (more lost in urine)

30
Q

What kidney hormones do what to BP?

A

angiotensin II –> vasoconstriction
ANP –> Na+ loss, decrease blood volume
aldosterone –> Na+ retention, increased blood volume
ADH –> increased H2O retention, increased blood volume