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Pathophysiology II: Hypertension

Terms in this set (17)

Hypertension
Most common in primary care and if can control will decrease risk of cardiovascular disease
Primary (Essential) vs Secondary
Primary is idiopathic. Secondary means that the hypertension is due to something else
JNC 8
Pre-Hypertension = 120-139/80-99
Stage I = 140-159/90-99
Stage 2 = >160/>100

Need 2 readings of 140/90 on 2 separate occasions to diagnose. Want to keep everyone under 60 at 140/90. If older than 60 want to keep them at 150/90.
Properties of Arteries
Blood is flowing through with high velocity and slows down when it hits the capillaries. Arteries have more resistance because there's more smooth muscle.
Taking Blood Pressure
Basically when you're pumping up for the cuff, you're pumping it higher than the systolic pressure to cut off blood flow to create turbulent flow. The 1st sound i the systolic and then when it equalizes and the turbulent flow disappears thats the diastolic.
Pulse Pressure
Systolic - Diastolic
Mean Arterial Pressure (MAP)
CO x TPR. CO = SV x HR
What are some physiological causes that increase blood pressure?
Intravascular volume, autonomic nervous system, RAAS and vascular mechanism.
Intravascular Volume
An increase in volume will cause an increase in CO and increase blood pressure. Determined by Na. Kidneys can either excrete or reabsorb Na. Renal disease that can affect function. Things that can effect it = RAS, excessive NA intake, nephrotic syndrome, SIADH and CKD.
Autonomic Nervous System
Sympathetic discharge will increase BP and parasympathetic will decreases BP.

A1 = Vasoconstriction of vessels (increase PR) and increases Na reabsorption in kidneys (increases SV)

A2 = Negative feedback - will inhibit norepinephrine to decreases sympathetic discharge.

B1 = Will increases HR and contractility to increase CO

B2 = Vasodilation via relaxation of smooth muscle - decreases BP

If you're on a BB make sure to TAPER OFF Because abrupt discontinuation will lead to rebound hypertension because of up or down regulation of receptors.

Examples = pheochromocytoma, increased sympathetic outflow, carotid sinus baroreceptors
RAAS
ANG II (increases PR) and aldosterone (increases CO)

Triggered by decrease of Na filtration sensed by macula densa, decreased stretch in baroreceptor of afferent arteriole, sympathetic innervation of renin releasing cells.

Examples = Hyperaldosteronism, cushing's syndrome, anything that will decrease renal perfusion
Vascular Mechanism
Determined by compliance and diameter (increases PR). Often due to smooth muscle contraction or inability to relax (vascular tone).

Can be adjusted by vasoactive substances secreted by endothelium like Nitric Oxide.

Can also be due to ion channel involved in muscle contraction. Can have Na/Ca exchanger dysfunction where can't get Ca out so you can't relax.

Example = arteriosclerosis. Anything that increases PR, Na-H exchanger dysfunction, coarctation of Aorta
Pressure Natriuresis
Basically ANP and BNP which causes the increase secretion of Na with increased volumes. Those with hypertension usually have impaired natriuresis. Salt-resistant hypertension is when body needs increased pressure to trigger natriuresis. Salt-impaired hypertension is when natriuresis is impaired.
Secondary Hypertension
Means something else is the problem, need to treat underlying problem.

Want to do an EKG, UA/microalbumin, HCT, blood glucose, CMP, TSH, Ca, lipid profile (after 9-12 hour fast).

Causes = RAS, increases ICP, white coat, pheochromocytoma, drug/toxins, hyperthyroidism, preeclampsia, obesity
Hypertensive Urgency
180/110 without end organ damage
Hypertensive Emergency
180/110 with end organ damage
What should you always remember in chronic hypertension patient?
Autoregulatory range shifts higher so "normalizing" blood pressure might cause ischemia.
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