fluid overload

increase in circulating volume

concentration of solutes/solvents is equal

diuresis (peeing!)

supresses it--pee alot!

285-295 mOsm/kg

easy calculation for osmolality

what by definition is the hematocrit?

and normals

% RBCs and total blood volume

normals

men 41-50

women 36-45

in the opposite direction,

>55 dehydration because the % rbc is higher with the decreased amt of fluid in the vascular compartment

< 35 fluid overload; blood is actually diluted

sodium

and normal blood levels

major component of extracellular fluid

regulated by the kidneys

levels 135-145

below 135, from fluid overload

it is diluted! fluid follows water...

Blood urea nitrogen-measures end product of protein metabolism which forms annonia and is combined to form urea for excretion,

regulated by kidneys, liver, diet(protein intake), hydration status, drugs

normal levels 10-20 mg/dl adult

dehydration "dry"-anything that loses fluid

blood loss, sweat, vomiting, diarrhea, wound drainage, ng drainage, third spacing, caffeine, alcohol, inadequate intake,

excess fluid int he body leaves the vascular space and gets   into the tissues causing swelling, esp. in dependent areas like the extremities, sacrum, periorbital areas, feet, ankles, calf

* the vascular compartment could be dry if flid is leaking out of the vascular space which could cause signs and syptoms of dehydration. this occurs alot after surgery or someone receives alot of IV fluid (major traumatic event)

dizziness from low BP

confusion fro low BP (not enough O2 to the brain) and changes in sodium levels

weakness

feces is hard (fluid moves from the bowels)

decrease urine output

objective data for fluid vol. deficit

skin tenting

mucous membranes dry

flattened veins,

neurologic-confused,

hypotensive inc. HR, dec BP

serum NA, osmolality, HCT, and BUN all increased

urine specific gravity increased

300 L/day

800 cc from food

dec. c.o.

dec urine output

dry mucus membranes

orthostatic hypertension-risk of injury/fall

cognitive imparement

restoration of hydration status

encourage oral intake(if npo give iv's

monitor i/o

monitor wt

monitor osmolality, electrolytes, esp sodium, Bun, HCT

for fluid losses from burns, diarrhea, vomiting, bleeding, severe intracellular dehydration

pushes fluid back into the cell,

fluid, no electrolytes electrolyte solution can become dilluted

5% dextrose in water (D5W)

or 45% normal saline (0.45NS)

adding water and electrolytes

D5.45 NACL

D5 and 1/2 (D5.33 NS) D5.9NS

adding both water and electrolytes

extra solutes will pull fluid from the intracellular space back into the extracellular space

good for postoperative swelling (pulls fluid back into blood vessels) and takes extra fluid out of the interstitial space, (decreases edema)

good for people in mild to mod. fluid overload

hypervolemia

can be from:

fluid vol. excess

related to :

• fluid volume shift to extracellular or intracellular space (either in the vascular space or between cells or in cells)
• increased intake
• decrease output
• diseases; kidney failure, chf, pituitary probs.

Edema

pulm congestion (crackles in lungs)

inc. bp

JVD**

neuro changes, confusion due to brain swelling

decrease osmoloality, dec. HCT, dec. Na, dec. BUN

pt is "wet", fluid overload

measure vitals, I/O qshift, diuretics-lasix, furosemide, (watch potassium)

lungs-crackles

watch o2 sat

Na, BUN, HCT, creatine, osmolality

keep hob elevated

press. stockings, pneumatic cuffs for venous return

monitor wt daily

weight-measure daily

1 KG of body wt.

return to normal fluid balance

vitals wnl

balance i and o

normal na, BUN, HCT, osmolality

clear lungs,

o2 normal

processed, packaged, brine

discuss third spacing

and its complications

fluid shifts into the interstitial spaces

abdominal "ascites", pericardial, pleural and joint spaces

complications:  fluid vol. deficit in the intravascular space with fluid vol. excess in the tissues, esp. bad for the lungs!

**pts have fluid overload in the interstitial spaces, but are dehydrated in the vascular spaces causing s/s of dehydration! 

fluid shift---- imbalance in homeostasis

surgery

heart failure-pump doesn't work well so fluid has nowhere to go except to the tissues, esp. the lungs)

kidney failure-water can't get out b/c kidneys just aren't working

normal sodium

hyponatremia

causes?

pathophysiology

sodium less than 135

increased loss : diuretics, vomiting, diarrhea, excessive sweat

inadequate intake

pathophysiology: cells swell! due to the fluid shift

neurologic-headache, confusion, etc.

cardiovascular-decreased BP, tachycardia, thready pulse

pulm:crackles

gi;n/v

dry skin and mucous membranes

lead to seizure and death

less Na, more water, water follows Na, if low, can't move anywhere!

medical and nsg management of hyponatremia

restore Na levels

reduce Na loss, prevent diarrhea and vomiting

restore Na balance

hypernatremia

etiology and risks?

pathophysiology?

etiology:  excessive fluid loss or excessive sodium intake

patho:  fluid shift causing cellular dehydration

increased myocardial depolarization-arrythmias

early- polyuria, anorexia, weakness, restlessness

late-confusion, seizures, coma, tremors, muscle twitching, rigid paralysis

replace fluid loss-dehydration

sodium restriction

cantelope

citris juices

bananas

tomatoes

green leafy veggies

hypokalemia

etiology and risks?

pathophysiology?

etiology-inadequate intake of potassium

excessive output of potassium

patho-  increased excitability of nerves and muscles

clinical manifestations of

hypokalemia

cardio-ECG changes- "t-wave changes, dysrhythmias, arrest, etc.

gi-anorexia, abd. distension

musculoskeletal-weakness, flabbiness, leg cramps

neuro-confusion, convulsions, coma

never push!

K-tabs, crushable, or in an IV solution 10 in solution in bag

hyperkalemia

etiology and risk factors

pathophysiology

etiology- retension of K-kidneys, ckd

excessive intake of potassium

release from cells following trauma****

pathophysiology--- altered excitability of nerves/muscles

cardiopulm- hypotension, cardiac and resp arrest due to muscle paralysis-when super high

gi-intestinal colic, diarrhea

muscular- parasthesias, muscle irritability

kayexalate-give oral or ng or enema (if can't swallow)

it is  a cation exchange resin-pulls K and fluid out of intravascualar space

can't come out the kidneys...they are unable

restore potassium balance- administer fluids and encourage diuresis

utilize cation exchange resin

etiology-inadequate intake of calcium or vit D

parathyroid disease or removal

patho-increased neuro excitability

moves from bones to blood

neuromuscular -numbness and tingling of hands, toes, and lips, facial twitching, tetany, seizures

cardiovascular-hypotension, dysrhythmias, weak pulse

skeletal-spont. fx.

move pt with caution-bone fx

hypercalcemia

etiology/risks?

patho?

1- metastatic malignancy..bone, brain, lung, breast, prostate-goes into bloodstream

2-thiazide diuretic therapy-potassium sparing diuretic so keeps Ca also, ,

3. hyperparathyroidism

patho-decreased neuro excitability

urinary-polyurea-related to osmotic diuresis-kidneys try to get rid of Calcium

GI- anorexia, constipation, nausea, abd. distension

neuromuscular-fatigue, depression, muscle weakness

restore balance with loop diuretics and IV hydration

avoid Ca containing products for awhile

safety precautions- seizure potential therefor watch pt for potential falls

hypophospatemia

etiology/risk?

patho?

manifestations?

inverse of calcium

from excessive loss or lack of intake

manifests as decreased cardiac and resp. function, weakness, confusion, etc.

this is rare!

hyperphospatemia

risk/etiology

manifestations

see in chronic renal pts-do dialysis to get rid of

see from excessive intake or inability to excrete

see often in chronic renal pts.

early symptoms:  tachycardia, palplitations

late; tetany, hyperreflexia

major leading cause of blindness?

most frequent cause of non-traumatic amputation?

related to less intake and absorbtion

see Myocardial irritability, convulsions, etc.

replacement fixes problem

see muscle weakness, areflexia, resp. paralysis, sedation

outcome management

iv hydration and diuretics

low glucose levels stimulate what?

High glucose levels stimulate what?

low-  stimulate hte release of stored glucose

high-stimulates Beta cells to release more insulin

both of these happen in the pancreas

nervous, shakey, dizzy, confused, headache, hunger, cold clammy skin, fast heartbeat, irritability

need to give something to increase the glycemic index

metaboic syndrome

chronic-systemic disease

insulin deficiency

decrease in the ability of the body to utilize insulin

disorder of the pancreas

glucose is not transported into the cells so blood glucose rises

1)  decreased glucose utilization

2)increased fat mobilization

3)  Increased protein utilization

nerve, intestine and kidney cells don't need insulin to transport glucose into the cells

skeletal cardiac and fat cells do

ingested glucose can't be transported into cells, so plasma glucose rises

• muscles are crying for glucose so fat stores are broken down
• ketones are formed and produce H2 ions 

          1)acid/base balance is disturbed-metabolic acidosis 2)ketones excreted by kidneys and lungs, so found in urine(fruity breath)

• lipid breakdown increases lipid levels(leads to atherosclerosis)

cardial= polyuria, polydipsia, polyphagia(pee, thirst, hungry)

wt. loss

blurred vision-late sign

pruritis-itchy

vaginitis-yeast

weakness, fatigue, dizziness

slow wound healing

act as an immunosuppressive

increase sugar

increase wt.

2 fasting glucoses>126

2 post prandial glucose>180

2 random glucose >200

plus symptoms

fasting for diabetes is how many hours

post prandial

fasting-12 hrs

post prandial-1-2 hrs after eating

fasting glucose of 110 or higher

post prandial of 140 or higher

HGA1c is what?

normal?

blood test for glucose over previous 3 months

normal 4.5-6

glycosylated Albumin?

Ketonuria?

Proteinuria?

glycosoylated Albumin-indicates glucose levels over previous 7-10 days

Ketonuria-product of fat breakdown

Proteinuria-indicates early renal damage and neuropathy

(protein in the urine)

risks- genetic, sedentary lifestyle, fat, lack of exercise, increase sugar

symptoms-no symptoms

below 6!

glucose>126

A1C above 6

longer "n"

nph-well under control

take amt at dinner

70% NPH-lasts longer

30% regular-this will get you through breakfast, then longer acting is ther ther

CSII-continuous subcutaneous insulin infusion

for Type 1

basal rate with bowluses before meals

catheter and needles are replaced q 2-3 days

improves HbA1c, reduced risk of hypoglycemia

uses fast acting insulin so there is less variability of glucose levels

helps control glucose spikes after meals/snacks

improved retinopathy

required education about pump has empowered patients to take control

the sooner started the better

early CSII use-longer honeymoon phase, and preserves beta cell function

requires individualized dosing algorithms

still requires frequent glucose testing

1. eat breakfast within 1 hr . of insulin dose, unless rapid

2. eat carbs 3 hrs later

3.  eat lunch 4-5 hrs after am insulin

4. eat supper at reg time

5.  eat bedtime snack consistently

6. dietician should provide initial instructions

not well controlled

"wacky"

• measures how fast a food is likely to raise blood sugar
• glucose is given 100GI, and other foods are identified in relation to glucose
• higher numbers mean quicker rise in blood sugar

causes-insulin overdose, omitting meals, vomiting, alcohol intake

symptoms-early-shaking, irritability, tachycardia, hunger, pale, paresthesias

laet-headache, blurred vision, slurred speach, confusion, lethargy, coma, seizure, death

depends more on symptoms than on actual blood glucose levels

start with carbs

oj, soda, milk

glucagon(subq or IM)

IV dextrose 50%

too little insulin available for hte needs of the body

hyperglycemia-med. emergency

fat breaks down-increased rr/depth

fruity breath

dehydration then occurs-kidneys try to excrete the ketones, osmotic diuresis with Na, Cl, and bicarb

acidosis causes vomiting

more water loss through high RR

electrolytes-Na and K lost in urine, Hydrogen moves into the intracellular space, K moves to the extracellular space, further potential for vomiting

Hallmark signs-ketosis, acidosis, dehydration, electrolyte imbalance

causes of death-dehydration-hypovolemic shock, acute tubualr necrosis, uremia

abdominal pain

weakness

anorexia

dehydration

fruity breath

kussmaul respirations

tachycardia

hypotension

rehydrate-0.9 NS, poss. NG tube

restore K balance-initial hyperkalemia(movement extracellular)

after hydration-sever hypokalemia

cardiac probs likely

careful replacement of "k" if there is adequate urine output(don't want to stress kidneys)

correct ph-sodium bicarb

often high Phosphate(inverse with Ca)

monitor calcium levels

give insulin- iv insulin(regular only), too dehydrated for subQ dosing, regular insulin drip (100 U in 100 ml 0.9NS) blood sugar q30 min.

stop IV insulin when BS reaches about 250 and stablizes

hyperglycemic, hyperosmolar, Nonketotic syndrome

(HHNS)

really bad-DKA- or hyperglycemia

most often seen with type 2 diabetics

extreme hyperglycemia 600 to 2000

profound dehydration

mild ketonuria

no acidosis

causes; glococorticoids, diuretics, surgical or majorillness stress, UTI, burns, acute infection, MI, CVA, GI bleed

severe hyperglycemia(600-2000)

no or slight hetosis

profound dehydration-circulatory collapse

hyperosmolality-high concentrated plasma and high BUN

excessive thirst

altered LOC

rehydration-initially 0.9 NS then 0.45NS

replace electrolytes as in DKA

insulin drip-watch drop in insulin as hydration occurs

dextrose IV when BS=250

since most are older pts. very careful tx= cardiac, renal, liver diseases

macrovascular complications of diabetes

microvascular

macrovascular-CVA, CAD,Infection, PVD, HTN

micro-Retinopathy, Nephropathy, Neuropathy over time

neuropathic pain is also seen!

heart disease-Hypertension, hyperlipidemia, MI

risk of stroke

potential for blindness

end stage renal disease

nervous system damage

amputation of the lower extremities

periodontal disease

6th leading cause of death due to disease

neuropathy

minor trauma

ulceration

poor healing

gangrene

anterior pituitary disorder

overproduction of GH, benign tumor

dx-MRI-

tx-removal of gland/tumor

but then pt will need hormone replacement

rare

panhypopituitrism verses selective

usually due to tumors or autoimmune

tx-tumor removal f/b hormone replacement

rare-see in lung ca

Increase amt of ADH is released

decrease in Na-hyponatrimia

fluid retention

conce. urine

seizure precautions

inc. risk of falls

thirsty

post. pituitary disorder

caused by decreased ADH

blood sugar is normal

water intoxication

Polyuria

Poydipsia

see in head injury/tumor CNS is affected

can be seen with Graves disease

or see in hyper or hypo thyroidism

autoimmune

too much thyroid

dx with hormone levels-TSH, T3, T$

(potential for thyrotoxicosis-thyroid storm

medical emoergency

high bp, arrythmias, heart failure, high rr, hot skin, sweaty, )

tx-synthroid(replacement)

tired

brittle hair

dry skin

lethargic

hyperparathyroidism

primary

secondary

rare

primary- parathyroid surgery or benign tumor

secondary-chronic kidney failure, CKD, ARF

increase CA, dec. Phosphate, monitor for tetiney

see in radical neck surgery

replace with calcium(CaGlucate)

disorder of the Adrenal Cortex-over production

dx. with plasma cortisol levels

tx-surgical removal adrenalectomy, radiation

moon face, increase in amt of hair

increase dose of steroids over a period of time

underproduction of the adrenal cortex

tx with hormone replacement

autoimmune-rare

dx with crisis usually!

crisis is sudden and puts stress on the body, see with sudden steroid withdrawl, or after removal of adrenal glands

adrenal medulla  tumor

chatacholamine release

diagnose with 24 hour urine

1.  primary HTN(essential/idiopathic)

no single, identifiable cause, multifactorial

2.  secondary HTN

there is an identifiable cause

renal artery stenosis-any kidney disease

adrenal tumor(inc. in symp. stim, inc. in chatacholamines)

pheochrycmocytoma

pituitary syndrome(stim. adrenals and then cat. response)

pregnancy

drug use..Cocaine

also

isolated systolic HTN/pesudohypertension-older adults

BP cuff too tight around rigid arteries

"white "coat Htn

what happens to men when give them BP meds?

women?

men-ED

women decrease libedo

discuss primary HTN morbidity and mortality

90% have primary HTN

middle aged or older adults

"Silent Killer"

highest incidence in African-Americans wehn compared to whites, hispanics

organ damage: heart, brain(stroke), retinas(micorvasc. damage), kidneys, vascular damage

HTN with stage 1/2/3/4 kidney disease

long term complications

as age develop artherosclerosis

long term complications

cirrhosis, coarctation or congenital narrowing of aorta, endocrine disorders, medications, inhibitors taken with tyramine-containing foods, estorgen replacement drugs, oral contraceptives, NSAIDS, neuroligic disorders, preg. induced HTN, renal disease 

lead to a HTN crisis

BP so high that you have a risk for a stroke

high BP-headache

catacholamine release

mental status change

initially tachycardic, then decrease in HR

alittle SOB

diaphoresis, "flushed"

anxiety, on edge

modifiable verses non-modifiable risk factors for HTN

modifiable-diet, stress, smoking, sedentary lifestyle, wt, BMI, diabetes, alcohol use

non-age, gender, race, family history

sympathetic nervous system-INC and DEC HR/CO

baroreceptors-cause hypotension/hypertension/fluid replacement

vascular endothelium-narrows over time

renal system-renin-angiotension-aldosterone system-this is huge!

endocrine system- thyroid and others

CO is big part of BP regulation!

the renin-angiotensin-Aldosterone system

when is it good?

bad?

good-if you're in an accident

but if have chronic kidney disease-not so good!

often asymptomatic

headache?

organ damage-heart, kidney, retinas, brain, vasc. system,

nocturia-n/v, confusion, visual disturbances,

retinal examination-hemmorrhage, exudates, papillemdema-opthomologist

stroke, heart attack, renal failure

complications of HTN

hypertensive heart disease(CAD)

left ventricular hypertrophy

cerebrovascular disease

peripheral vascular disease

nephrosclerosis

retinal damage

lifestyle modifications for HTN

diet-DASH

Weight reduction

sodium reduction

alcohol

smoking-tar and nicotine

exercise

stress reduction

check BP, may be too low to give.

lower BP by preventing conversion of angiotension I to II in the lungs,

Prevents vasoconstriction and water retension

useful for asthmatics, heart failure, peripheral vascular disease pts,

can cause dry cough, rash, angioedema, hyperkalemia, or renal failure

less effective in African-Americans, contraindicated in pregnancy

nursing considerations with heart disease and the elderly

venous system is less elastic

ausculatory gap

sensitivity to BP changes

people on antihypertensives give meal then BP decreases, bc bloodsupply to GI changes with digestion, then don't give BP meds with meals!

rapid, significant elevations in systolic and or diastolic BP

(systolic>220, diastolic >140)

90% mortality rate within one year if left untreated

more common with younger clients, African American Men, pregnancy, collagen or renal disease

must be treated rapidly to prevent brain injury, renal injury, and cardiac injury

most common cause is untreated HTN!

cerebral edema

acute renal failure

slowly reduce bp by no more than 25% within 2 hrs toward 160/100 in 2-6 hrs

avoid rapid BP drops

MUST BE ON CARDIAC MONITOR and give Nipride esp in ICU/ER, IV or continuous drip

ph 1-infancy to 3rd decade-clinically silent

ph 2-3rd or 4th decade-may be clinically silent, STABLE ANGINA

ph 3- 4th decade and on:  enough occlusion to cause angina, PLaque Ruptures

ph 4- 4th decade on:   greater degree of occlusion, MI, coronary syndromes

ph 5, 4th decade on Calcification

thrombus then embolism

definition of CAD

and etiology/pathophysiology

impaired blood flow to the pump becase arteries that supply myocardium are partially occluded due to athesclerosis

fatty streak

fibrous plaque

complicated lesion

consider collateral circulation in the coronary arteries

LDL, want this number low

has greater effect on plaque

HDL- good cholesterol, carries cholesterol back to the liver

>40

LDL-gad, carries cholesterol to non-hepatic tissues

<160 if less than two other risk factors

< 130 if 2 or more risk factors

triglycerides

<150

CAD chief complaints

and

related symptoms

cardiac-chest pain, palpitations, tachycardia

respiratory-dyspnea, exertional dyspnea, orthopnea, paroxysmal noct. dyspnea

related:  fatigue, syncope, wt. gain, irritability

BMI normal

overwt

obese

normal:  19-25

overwt.  : 25-30

obese:   >30

squeezing of the chest

def.-pain in the chest or nearby area due to lack of oxygen to cardiac cells

caused by atherosclerosis-fatty plaque

not nec. does angina mean someone is having a heart attack

blood supply< blood demand

myocoardial ischemia

arterosclerosis

vs.

atherosclerosis

artherosclerosis-

Arteriosclerosis -hardening of the arteries

atherosclerosis-plaque

To clarify, a patient with arteriosclerosis (hardened arteries) may not have atherosclerosis (plaque), but a patient with atherosclerosis does have arteriosclerosis. Patients often have both conditions, which can cause a decrease in the blood flow to the heart muscle

chronic stable-pattern comes and goes-Nitro- occurs with physical exertion or emotion

silent ischemia

nocturnal

unstable-increasing in frequency, quality, severity, and/or duration, nitro or rest may not relieve the pain

prinzmetals-caused by arterial spasm not blockage, usually occurs in the am, occurs at rest without precipitating factor,

especially common during REM sleep

pqrst

Precipitating-what events/activities precipitated pain

quality of pain-feel like-dull, sharp, squeezing

radiation of pain-back, neck, jaw

severity- 1-10 scale

timing-when did it begin, changes in pain since start, had this pain before?

decrease severity of symptoms

prevents episodes of angina

prevent worsening of disease process

prevent death from sudden cardiac arrest

encourage lifestyle changes

treatment regime for angina

med of choice-Nitro

action-dilates coronary arteries, promotes blood flow

other drugs PO-Iosordil

IV drip only

topically patch or ointment, watch patches-one dose doesn't equal another, remove patches at night

spray

other meds morphine (2-6 mg IV for pain)

Beta blockers-decrease work of heart and oxygen consumption by decreasing HR and blockingrenin (metoprolol_olols)

ca channel blockers-vasodilators, opens coronary arteries

antiplatelet-ASA and plavix to decrease stickiness of platelets

liplid lowering drug (long term)

bedrest for femoral approaches for 6 hrs.

assess insertion site for hematoma

monitor pulses distal to insertion site

radial or femoral approach

lack of oxygent to cardiac cells beyond the occlusion in a coronary artery due to blockage or spasm in the artery

causes cell death=tissue death=organ death

described based on location of heart damage

arrythmias-irregularities in conduction system, too fast or too slow

50% of pts who have an MI die before ever reaching the hospital

the longer the ischemia, the greater the cell damage or death

chest pain ont relieved by rest

have them describe, not all pain follows the same pattern

changes in vital signs

physical assessment

nausea and vomiting

the anterior wall of the heart, encompasses the left ventricle

early morning

cold

dysrhythmias

heart failure

cardiogenic shock

papillary muscle dysfunction

ventricualr aneurysm

pericarditis

dressler syndrome

Tropin T-blood draw

it is a protein released into the bloodstream during an MI

lab test takes 20 mins and is very accurate, elevates within 3 hrs.

remains in blood 14-21 days

will eliminate need for admission if false alarm

normal level <0.2

specific to cardiac muscle,

if this level is normal= pt. is not having a heart attack

isoenzymes

Treponin and CK-MB

CkMB-isoenzyme of creatine kinase, increases in 3-6 hrs elimination is in 3-4 days

analgesics, ASA, Nitro, thrombolytis (must be started within 6 hrs TPA, Streptokinase)

anticoagulants, diuretics when there is fluid overload,

PTCA with stents or arthrectomy, Surgery CABG, laser surgery, pacemaker, AICD

anticoagulant-keeps clot from forming

thrombolytic-breaks up the clot

MONA

morphine

oxygen

nitrates

ASA

dissolve the clot

absolute contraindicated-hemorragic stroke, intracranial tumor, active internal bleeding

relative contraindicated-recent trauma, current use of anticoagulants, recent surgery, pregnancy

daily wts, monitor i/o assess for JVD, edema, peripheral pulses, anasarca, hepatomegaly, breathsounds

goal: normal fluid balance, I=O, stable wt, clear breath sounds, no edema

give high fiber diet

remember-they have had Morphine and are bedridden

give adequate water

stool softener-colace

bedside commode

avoid valsalva maneuver

no straining

goal- normal bowel function

back, flank pain

bleeding at iv sites

neuro status

NO im shots

goal- monitor and prevent bleeding

to prevent heat attack what things can you take

exercise

folic acid 400 mg

omega 3

ASA

Niacin

enzyme Q10