Cardiovascular Alterations

laminar flow

• plasma flows next to endothelial cells

• components flow through center of blood vessel rapidly and without friction

turbulent flow

• disrupted mixed flow

• crosswise

• requires more pressure

systole

ventricular contraction

diastole

ventricular relaxation and filling

resistance

opposition to flow caused by friction

peripheral vascular resistance

sum of resistance in all vessels

afterload

pressure required to move blood out of ventricle

preload

volume of blood in ventricles after diastole

load imposed on heart before contraction

supraventricular arrhythmia

irregular heart rate

atrial issue

ventricular arrhythia

• AC node juncitonal issue

• conduction system of ventricles

• life threatening

chronic venous insufficiency

venous hypertension in lower extremities

venous hypertension

• sustained increase in venous bp of lower extremities

cause of venous hypertension

incompetent veins

valves do not pump back to the heart

DVT and impaired pumps

age

symptoms of chronia venous insufficiency

• edema (pressure leads to fluid leaking into interstitial space)

• hyperpigmentation (rbc death and iron deposit)

• necrosis of subcutaneous fat (skin atrophy due to failed nutrition)

• stasis dermatitis from loss of fat

• skin breaks open (venous ulcer) over ankle

hemosiderin

a golden-brown, iron-storage protein complex that forms when red blood cells break down and release their iron

triad of virchow

• risk for developing spontaneous thrombi

• injury

• venous flow

• hypercoagulability

injury to vessel endothelium occurs from

• plaques from cholesterol

• turbulent flow

• toxins such as bacteria, smoke, radiation,

abnormalities of blood flow

• turbulence triggers platelets

• stasis causes platelt pooling

primary hypercoaguability of blood

• hereditary defects in proteins that involve clotting

• factor 5

• throbin gene mutation

secondary hypercoagulability of blood

• aquired

• lupus

• polycythemia vera\sickle cell

• dehydration

• post-partum high factors

• oral contraceptives

• hormone replacements

• neoplastic syndromes

• long airline travel

deep venous thrombosis

thrombosis (clot formation) of a vein with inflammatory response within a vessel wall

symptoms of deep venous thrombosis

• pain swelling, tenderness from inflammation

complications from deep venous thrombosis

• risk for pulmonary embolism if piece breaks off

• reccurent episodes

• leads to venous insufficiency bc of stretching

prevention of deep venous thrombosis

• early ambulation post surgery or post birth

• bed excersises

• stockings

• sequential compression devices on calf

blood pressure equation

COxPVR

cardiovascular center

neural mechanism for control of blood pressure in reticular formation of medulla and lower 3 of pons

short term regulators

help for temporary imbalance in bp (dehydration, rising, acute hemmorhage)

intrinsic reflexes for bp

• short term neural

• baro receptors for pressure in carotid and aortic, they stretch

• chemoreceptors via oxygen or hydrogen

baroreceptors

pressure receptors in carotid and aoritic

respond to stretch

parasympathetic short term response

• ANS

• vagal nerve slows HR

Sympathetic stimulation for short term

• increase heart rate

• constrict blood vessels

short term humoral mechanism

hormones

RAAS

• short term humoral

• angiotensin 2 is a vasoconstrictor

• end with aldosterone

• kidneys make sodium

• water follows

Vasopressin

• short term humoral

• releases from pituitary gland due to low bp, bv, or high osmolarity

• vasoconstrictive

• instructs kidneys to conserve water

Epinephrine and norepinephrine

• arenal gland

• sympathetic

• increase hr

• contractility

• vascular tone

• short term humoral

what organs regulate long ter BP

• kidneys by regulaing extracellular fluit

equilibrium point

how the kidney knows to regulate bp (normal pressure)

kidneys response to increase in volume

• increase water secretion diuresis

• increase sodium excretion natiuresis

diuresis

water sectrion

natiuresis

salt secretion

naturetic peptides

• peptide hormones from heart

• ANP in right atrium

• secretes sodium

• BNP in ventricle

• sodium in urine

ANH

from kidney when bp is low

BNP

from kidney when BP is high

hypertension diagnosis

• diagnosed after 5mins rest and 30mins stimulant free

• measure many times

• patient is not crossing legs

normal bp

• less than 120

• less than 80

elevated bp

• 120-129

• less than 80

stage 1 hypertension

• 130-139 OR

• 80-89

hypertension stage 2

• 140 OR

• 90

hypertensive crisis

• higher than 180

• and or

• 120

primary hypertension

no specific cause

genetic

environment

hormonal

causes of primary hypertension

• dysfunction of SNS, RAAS, natriuretic

• inflammation

• obesity

• insulin resistance

how does SNS raise BP

• increase HR

• increase vasoconstriction

how does insulin resistance lead to high bp

hyperinsulinemia leads to narrowing

how does RAAS dysfunction cause high BP

• more soum

• more h20

• more resistance

how does obesity cause high bP

• changes adipocytes

• increased SNS

• increased RAAS

• induces inflammation

• leptin

how do natiuretic peptides raise bp

• increase bv

primary htn

• essential hypertension

• non modifiable and modifiable

why is menopause htn risk

• lose protective abilities of estrogen

gene that makes african americans sensisitve to salt

• 1g salt

• raised 5mmHg

how does sleep cause htn bp

• nocturnal dipping is needed

insurance instability

rates of undiagnosed bp

neighborhood

high poverty and high crime has high bp

jackson heart study

• low risk of HTN with high SES

immigration

adaptation to american lifestyle

secondary htn

• renal

• adrenocortical

• pheochromocytoma

• coarctation

• drugs

• caused by another disease

renal htn

• renal disease

• renovascular disease

• lower renal flow (atherosclerosis) and activation of RAAS

adrenocortical

-secondary

hyperaldosteronism (sodium maintain)

cushing disease

pheochromocytoma

tumor of adrenal medulla stimulates epi and norepi

coarctation aorta

peds

increase systolic

systolic elevation stresses - leading to -

• left ventricular hypertrophy

• CHF

• arrhythmias

• sudden death

elevated pulse pressures lead to - which causes

• stretched and damaged arteries

• aneurysms

• atherosclerosis

• CAD and PAD

• thrombus formation

nephrosclerosis

progressive damage to vessels (turbulent flow and cnstiction)

leads less blood flow to nephrons

htn increases what kidney disease

diabetic nephropathy

stroke from htn

• dilation of small nonelastic vessels in brain cause a hemmorhage

• ischemic stroke due to atheroscletoric formation

dementia from htn

• narrowing and sclerosis leads to hypoperfusion and white matter is demyelinated

retinopathy

small blood vessels in eyes

symptoms of a htn crisis

• brain (stroke_

• headache

• restlessness

• visual disturbances

• cannot regulate flow into capillary beds

• ischemia

• hemorrhage

prevalance in elderly

increases with age vessel stiffening increases resistance

less receptive baroreceptors

need to have smaller doses of meds

orthostatic hypotension

• drop in bp upon standing

causes of orthostatic hypotension

• reduced BV

• drugs (hypertensive meds)

• aging dim ability to inc hr (less pumps)

• bed rest (reduction of plasma)

• ANS (parkinsons)

symptoms of orthostatic hypotension

• dizziness

• blurriness

• syncope

aneurysm

abnormal dilation (local) of a blood vessel

most common aneurysm

aortic

risk factors for aneurysm

• athersclerosis MOST COMMON

• hypertension

• traumatic injuries

• infections

• congenital

how aneurysm comes from atherosclerosis

• plaque formation inside vessel

• erode vessel wall

• contributes to inflammation

how does htn cause aneurysm

• increases stress on wall

berry aneurysm

small dilations at a bifurcation

fusiform

circumferential

all the way around

balloon

saccular

partial circumferential

dissecting

localized tear in vessel and blood enters the vessel wall to create blood filled cavity

how do aneurysms grow

• increased tension until it ruptures

2 kinds of aortic aneurysm

• thoracic

• abdominal

thoracic aortic aneurysms symptoms and cause

• atherosclerosis main cause

• usually asymptomatic

• symptoms come from encroaching size

• substernal chest pain (mimics a heart attack) radiates to neck and back

• dyspnea from tracheal pressure (stridor)

• dysphasia from esophageal pressure (hoarsness as well)

• distension of neck veins (superior vena cava)

aortic aneurysms can occur where

• from the ascending arch down into the abdomen

surgery for aneurysm

5cm+

abdominal aneurysms cause and symptoms

• 50+

• atherosclerosis

• hypertension

• smoking

• usually asymptomatic

• first sign is a pulsating mass

• lumbar nerve compression (pain that radiates to legs)

• mid abdominal/lower back pain

• blood stasis

aortic dissection

• intima is torn and blood flows into the media

• life threatening condition

risk factors for aortic dissection

• hypertension

• men 40-60

• anything that weakens the elastic and smootg muscle (media) plaques, conn tiss disease, chronic inflammation

• traumatic injuries (car accidents with chest on wheel)

symptoms of aortic dissection

• pain (blood flow is a tearing type pain)

• high pain leaves bp high (perpetuates the condition in a vicious cycle)

aortic dissection treatment

• antihypertensive meds

• procedure