patho 16- alterations in blood pressure

blood pressure

measure of pressure exerted by the left ventricle as the blood goes to the aorta, measures blood flow and tissue perfusion

systolic

highest value, normal= less than 120, pressure as the left ventricle contracts

diastolic

lowest value, normal= less than 80, pressure as left ventricle relaxes

pulse pressure

(pp) difference between diastolic and systolic, compares the blood volume and how distended the arteries are, do not want this to widen or narrow

widening pulse pressure

can be seen with ICP

narrowing pulse pressure

not enough volume in left ventricle can be caused by heart failure, shock or fluid loss

calculation of pulse pressure

SBP- DBP= PP,

main factors in blood pressure regulation

blood volume, peripheral resistance, cardiac output, nervous system control, endocrine control

normal blood volume and affect on bp

5 Liters, increases to blood volume increase cardiac output which can increase blood pressure

main controls of blood volume

aldosterone and ADH

peripheral resistance

shows changes in radius of arteries and blood viscosity, diameter decreases with vasoconstriction= increased friction= increased blood pressure (opposite: vasodilation= diameter widens= less friction= lower blood pressure

what controls blood vessel diameter and blood viscosity

autonomic nervous system and RAAS, can compensate for changes in cardiac output

cardiac output calculations

stroke volume times heart rate= volume of blood ejected with each heartbeat (around 70ml)

regulation of cardiac output

autonomic nervous system, increasing hr or stroke volume can increase cardiac output, compensates for changes in resistance

nervous system control of blood pressure

vasomotor center, baroreceptors, chemoreceptors

vasomotor center

detects changes in blood pressure, resistance and cardiac output, sends nerve impulse to arteriole smooth muscle through ANS, gets messages from baroreceptors and chemoreceptors

baroreceptors

pressure sensitive receptors in arteries, detect changes of stretching and shrinking of vessel

chemoreceptors

in carotid arteries and aorta, detect oxygen, co2 and ph levels, send ANS response to regulate ventilation, also signals vasomotor center

chemoreceptors detection of low oxygen causes the vasomotor center to do what

cause vasoconstriction

endocrine control of blood pressure

epinephrine and norepinephrine, ADH, R-A-A System

epinephrine and norepinephrine in blood pressure regulation

increases blood pressure, heart rate and stroke volume, short term response, fast response

ADH regulation of blood pressure

conserves water in response to decreased blood volume, decreased blood pressure or increased osmolarity, fast response and short term, from posterior pituitary

RAAS

triggered by decreased renal perfusion, increases overall release of NE from sympathetic nerves to raise bp, activates thirst mechanism

RAAS function

maintains stable circulating volume and pressure ,

long term blood pressure regulation

RAAS

causes of decreased renal perfusion

low blood pressure, volume or sodium levels

process of RAAS

-liver is always producing angiotensinogen and sending it into circulation

-when triggered kidney releases renin, renin enters blood and convert angiotensinogen to angiotensin 1

-lungs convert angiotensin 1 to angiotensin 2

effects of angiotensin 2

controls blood pressure and blood volume, potent vasoconstrictor, signals adrenal cortex to release aldosterone and stimulates posterior pituitary to release ADH

hypertension

disease of arteries, causes endothelial injury with can innate atherosclerosis

leading risk factor for cardiovascular disease

hypertension

types of HTN

can be essential, secondary, or malignant

essential hypertension

unknown origin of hypertension, patients will be on anti hypertensives for life

secondary hypertension

due to another disorder (renal cause is common among diabetics) or exogenous substances (cocaine, brith control pills, excess aldosterone, glucocorticosteriods)

malignant hypertension

accelerated fatal hypertension, sudden elevation of blood pressure, diastolic values exceeding 120

hypertension risk factors

non modifiable- race, gender, family history, age: modifiable- weight, dietary habits (high sodium or fat, alcohol), activity levels, smoking

diagnosis of hypertension

elevated diastolic blood pressure 2 consecutive times at separate visits

stages of hypertension

only used upon diagnosis, not done by nurses, pre-hypertensive, stage 1 and stage 2

pre-hypertension stage

systolic 120-129, encouraging lifestyle changes can often reduce blood pressure to normal range

stage 1 and 2 hypertension

1= systolic 130-139 and diastolic 80-89, stage 2= systolic over 140 and diastolic over 90

common complications of hypertension

stroke, retinal blindness, MI, heart failure, changes in GFR, peripheral arteries are affected

brain compilations due to hypertension

increase stroke risk, increases dementia, can lead to atherosclerosis of cerebral vessels, weakens vessels in brain to increase risk of hemorrhage

retinal damage causing blindness is accelerated by

hypertension and hyperglycemia

cardiac complications of hypertension

atherosclerosis in vessels causes decreased blood flow or infarct, hypertrophy can occur due to increased pressure, ventricular hypertrophy causes less room for blood inside ventricle and can lead to heart failure

renal complication of hypertension

decrease glomerular filtration rate, increased BUN and creatinine

orthostatic hypotension

abnormal drop is blood pressure when standing, generally over 20 points systolic or 10 points diastolic, assess by taking bp- laying, sitting and standing

s/sx or orthostatic hypotension

dizziness, syncope, frequent falls

causes of orthostatic hypotension

reduced circulating volume- dehydration, medication, advanced age, prolonged bed rest causing loss of vascular tone

treatment for orthostatic hypotension

treat cause if known, fluids, watch for fall risk, teach pt to dangle on side of bed before standing up, can have elastic ted hose (to increase blood return to heart)

lipoproteins

carriers of lipid molecules in the blood, not water soluble, all 3 types of lipoproteins contain cholesterol but differentiated by the amount

high density lipoprotein

want these, goal 40-60. mg/dl, contain mostly protein, excess amounts will be eliminated

low density lipoproteins

low levels associated with better cardiovascular outcomes, goal is less than 100mg/dl, over 160 is considered high, contain mostly cholesterol, excess gets deposited in blood vessels and lead to atherosclerotic plaque

very low density lipoproteins

mostly triglycerides, being used for energy is good but all remaining VLDL will be converted to LDL and cause atherosclerosis

triglycerides

stored fat cells used for energy

cholesterol

needed to make cell membranes and hormones, usually the liver makes enough to cover need, liver synthesizes cholesterol by metabolizing lipids

lipid metabolism

2 pathways- exogenous and endogenous, both get end products of bile and cholesterol

exogenous lipid metabolism

regulates dietary intake and bile acid loss in stool, intake of fats plays a role

endogenous pathway of lipid metabolism

occurs in liver to synthesize cholesterol and metabolize lipids, triglycerides can be used as energy or stored in adipose tissue (can cause hypercholesterolemia)

hypercholesterolemia

excessive cholesterol in the blood, primary is due to genetics and secondary is mainly based on obesity and lifestyle

primary hypercholesterolemia

causes extremely high lipid levels in healthy adults, later diagnosis in life like 30s-40s

secondary hypercholesterolemia

due to obesity, diabetes can accelerate effects of high lipids, smoking can damage endothelial cells and accelerate atherosclerosis, exercise can help to manage symptoms

unsaturated fats

considered 'good' fats, liquid at room temperature, contain essential fatty acid (ex. corn, olive, peanut oil)

saturated fats

'problem fats', solid at room temperature, mainly come from animals, not necessary for our health, harder to digest, more cholesterol (ex. fat on meat, lard, butter)

atherosclerosis

hardening and narrowing of arteries limiting blood flow, caused by fatty plaque deposits in inner lining of arteries, less responsive to dilation or constriction

ischemia

narrowing of arteries causing decreased blood flow, can lead to infarct, pain with activity due to lack of oxygen

infarct

total obstruction of blood flow, can lead to necrosis, intense pain

development of atherosclerosis

injury to endothelial cells of vessels, inflammation ignited by injury, plaque formation (platelets accumulate at injury site and narrows vessel)

inflammation process of atherosclerosis formation

monocytes go to injury site, convert to macrophages and engulf lipoproteins, macrophages and smooth muscles cells get distended with LDLs= foam cells, foam cells can damage cell walls

things that can damage endothelial cells

smokin, hypertension, hyperglycemia

plaque lesion types

fatty streak, stable plaque and unstable plaque

fatty streak

yellow colored streaks or spots on arteries, everyone has them, static by age 20

stable plaque

liquid stable core of lipids, thick fibrous cap, similar to a 'scab' of platelets

unstable plaque

vulnerable lesion, prone to rupturing, if ruptures can cause thrombus and block blood flow

cause of unstable plaque rupturing

turbulent blood flow

atherosclerosis risk factors

advancing age, genetic lipoprotein disorders, men (overall), women after menopause, hyperlipidemia, obesity, smoking. hyperglycemia with poor control

tests for atherosclerosis

lipid panel- done if cholesterol screening comes back elevated, CRP ( c reactive protein)- marker for systemic inflammation

complications of atherosclerosis

hypertension, PAD, CAD, MI

PAD

peripheral artery disease, if plaque deposits in peripheral arteries, pain in affected area with activity, sudden pain can signal infarct

CAD/MI from atherosclerosis

when plaque builds up in coronary arteries that supply blood to the heart, CAD is leading death in USA due to MI

Cushing's triad

from increased ICP, decreased respiratory rate, widening pulse pressure, decrease hr and pulse