This site is 100% ad supported. Please add an exception to adblock for this site.

514 Exam 1

Terms

undefined, object
copy deck
the pump action of the heart
contractility
the electrical system in the heart
conduction
even though the heart loses function because of this condition, the conduction system still works
heart failure
even though there's nothing wrong with the contractility of the heart, the patient needs a pacemaker because of loss of
conduction
changes in the intimal lining of blood vessels in the heart; total or partial obstruction of an artery in the heart or a branch of an artery (referred to in % blockage)
arteriosclerotic heart disease
(aka Coronary Artery Disease CAD)
with this disease there is a 30-40% increase in risk for CAD because blood vessels harden, kidneys are at risk
diabetes mellitus
take # of years x # of packs per day
calculate "pack years" for smoking

ex: 2ppd x 30 years = 60 pack years
30 minutes of exercise to increase heart rate to 80% of capability, 3x a week
amount of exercise necessary to lower heart disease risk
smoking
obesity
HTN
lifestyle
stress
cholesterol
modifiable risk factors for cardiovascular disease
age
gender
family history
race/ethnicity
diabetes mellitus (*except how you control it)
post-menopausal women
nonmodifiable risk factors for cardiovascular disease
"squeezing" pain the chest or nearby area due to lack of O2 to cardiac cells
caused by atherosclerosis
angina pectoris
*doesn't necessarily mean someone is having a heart attack
angina pain occurs every so often
relieve by nitroglycerin or rest
stays the same over time
stable angina
worsening angina pain, important to look for changes
unstable angina
angina pain increasing in frequency, severity, and/or duration
at night - blood pools in heart and chest, shortness of breath
nitroglycerin/rest may not relieve pain
acute coronary syndrome
cause:arterial spasms, not blockage
occurs early am
occurs at rest
common during REM sleep

90% seen in women
rare to infarct
Prinzmetal's (variant) angina
how long does it take for a cardiac cell to die from lack of O2?
4-6 minutes
1.Location - where at(chest, jaw, left arm, back, shoulders, epigastric)
2.Radiation - does it move?
3.Onset - how does it start?
4.Severity - how bad does it hurt?
5.Sensation - how does it feel? (sharp, knifelike, heavy, "sitti
Nursing assessment of angina pain
dyspnea, orthopnea (sit up to breathe), shortness of breath, dizzy, palpitations, lightheaded, GI (vagus nerve), perspiration, diaphoresis, pallor, anxiety, increase in weight (sign of heart failure)
Other symptoms with angina
cardiac catherterization
stress test (changes in ST segment)
EKG
Echocardiogram
TEE (like Echo, with scope in esophagus)
diagnostic tests for cardiac function
-If NPO
-are meds to be held
-can pt. have caffeine
-allergy to iodine or shellfish

post procedure:
assess airway, vital signs, cardiac fct, pulses in extremities, cap refill
push fluids after dye injections
The nursing responsibilities with cardiac testing
this is the medication of choice for treatment of angina; if it's potent it stings or burns when put in mouth; med is sensitive to heat, cold, light

*taken sublingually every 5 minutes; if pain is still there after 3 tablets, go to the emergen
Nitroglycerin
for treatment of angina, po, sometimes IV drip (NEVER push), topically with patches or ointment, spray
Side Effect: headache
Isodril, Isosorbide
morphine sulfate - 2 to 6 mg until pain relieved (IV push)
Beta Blockers-decrease work of heart
Ca Channel Blockers-vasodilators
Antiplatelets-aspirin
other medications for angina
what is an antidote to coumadin
vitamin K
PTT
Partial Thromboplastin Time

norm: 25-35 seconds
If you are on coumadin, what will your PTT likely be?
60-90
What is an antidote to Heparin?
protamine sulfate
what food can interfere with coumadin?
green leafy vegetables (vitamin K)
-maintain oxygenation (w supplement)
-monitor chest pain
-instruct any needed lifestyle changes
-monitor vital signs, pulse oximetry (need a doctor's order, but can get that later)
-monitor electrolytes - K, Na
-teach medications
nursing interventions for angina
What are the outcomes which are the goal of the medical and nursing treatemnt of Angina?
1.prevent progression of the disease
2.prevent MI
lack of oxygen to cardiac cells beyond the occlusion in a coronary artery due to blockage or spasm in the artery
myocardial infarction (MI)
main causes of death with MI
-50% die before reaching the hospital
-arrhythmias, dysrythmia - irregular
the longer the ischemia the greater cell death
a test that looks for this protein in the bloodstream during an MI; takes 20 minutes and is very accurate; will eliminate unnecessary admission to the hospital if someone is not infarcting
-normal level is 0 to 1.5 U
(with MI it is in the 100s)
Troponin 1
PTCA
percutaneous transcoronary angioplasty
-arrhythmias - due to lack of O2 & cell death
-CHF - from scarring on heart
-pulmonary edema
-shock - cardiogenic shock
anxiety and fear
complications post MI
Monitor:
-pain level
-monitor cardiac rhythm, heart sounds
-intake and output
-anxiety level
-electrolytes, ABGs, oxygenation
& educate the family
nursing interventions post MI
-analgesics
-nitroglycerin
-thrombolic therapy (TPA, Streptokinase)
-PTCA or stents, or arthrectomy
-surgery - CABG, Laser, pacemaker, AICD impant(defibrillator)
medical treatment for MI
what is lopressor?
beta blocker
tension of blood against arterial walls
blood pressure
cardiac output - the push of blood out of the heart to the blood vessels
systolic blood pressure
peripheral resistance to the flow of blood when heart is in rest and refilling
diastolic blood pressure
-SNS activity (fight or flight)
-circulating epinephrine/norepinephrine
-Renin-Angiotensin-Aldosterone
-Peptides from atrial and smooth muscle cells
-hormones - ADH, vasopressin, pregnancy
-arterio, atherosclerosis
physiological mechanisms of blood pressure regulation
BP is consistently elevated above 140/90 mmHg
New guidelines - over 120 systolic

same risk factors as for CAD
hypertension
stress
obesity
use of salt *
low Ca, K, Mg *
sedentary lifestyle
glucose intolerance *
excessive alcohol use *
modifiable risk factors for HTN
family history
age
ethnicity
gender
nonmodifiable risk factors for HTN
often asymptomatic
no diagnostic tests other than BP cuff
headache in back of head, neck, nocturia, confusion, nausea, vomiting
examination of retina
manifestations of HTN
-teach modifiable risk factors
-screen in the community
-usual to have NO symptoms
-exercise
-stop smoking
-lose weight
-restrict alcohol, caffeine
nursing care for HTN
BP is so high, pt at risk for stroke
systolic:240, diastolic:130
pregnancy, drug abuse - main causes
constant BP monitoring, gradually decrease BP
use of IV push meds or drip meds, call titrating meds
monitor renal function-BUN,
hypertensive crisis
education
monitor patient for compliance
teach importance of taking meds, following diet, exercise, stress reduction
side effect of meds - impotence or lack of energy and sex drive, depression; makes people feel bad so they stop taking med
nursing responsibilities for hypertension
a metabolic disorder; hyperglycemia because of either a lack of insulin or cellular resistance to insulin
diabetes mellitus
high blood glucose
above 120
-high blood glucose
-high levels of glucose in urine
-frequent urination (polyuria)
-frequent thirst (polydipsia)
signs and symptoms of hyperglycemia
what is the impact of diabetes on health?
-6th leading cause of death due to CV damage resulting in ASHD, CAD, CVA
-leading cause of end-stage renal failure
-blindness
-amputation
incidence and prevalence of diabetes
15.7 million (10.3 diagnosed, 5.4 undiagnosed)
increase in Type 2 in native american, hispanic
11% of people 65-74 have DM
beta cells of pancreas don't produce insulin; autoimmune disease where beta cells get destroyed
-genetic
-viral infection trigger
-chemical toxin trigger
Diabetes Type 1
high blood glucose despite availability of insulin; body is getting insulin but not enough to lower glucose levels; resistance to insulin caused by obesity, inactivity, illness, agen, medications
Type 2 Diabetes
family history
obesity (especially upper body)
inactivity
race/ethnic group - AA, AI, Hispanic
gestational DM
polycystic ovary syndrome
woman who delivered baby with birth weight over 9 lbs.
risk factors for diabetes type 2
hyperglycemia
polyuria
polydipsia
blurred vision
fatigue
parasthesia
skin infections
symptoms
-symptoms
-casual plasma glucose greater than 200 mg/dl
-fasting plasma glucose >126 mg/dl (norm=110)
-2 hr. plasma glucose >200 mg/dl
-glycosylated hemoglobin(A1C)-determines average blood sugar over past 2-3 months; >7-9% i
diagnosing DM2
results from breakdown of fat, overproduction of ketones by the liver, loss of bicarbonate; occurs in undiagnosed Type 1 or in Type 2 if treatment is not effective or body is under stress causing increase energy needs by the body
diabetic ketoacidosis (DKA)
"fruity" breath
nausea and vomiting
dry mouth
symptoms of diabetic ketoacidosis
this test:
-reflects blood sugard for past 120 days
-5% of all Hb is glycated (normal)
-range from normal to high as 25% if DM in badly out of control
-should be measured at least 2x a year
glycated hemoglobin (A1C)
why do you do fluid replacement slowly, when treating diabetic ketoacidosis?
because putting patient into hypoglycemia too quickly can result in fatal cerebral edema
-fluid replacement (9% normal saline): when blood sugar is down to 250 mg/dl some dextrose is added to IV
-regular insulin IV or SC
-K replacement (in IV) 3.5-5 is normal (alteration in K could cause heart attack)
-monitor blood glucose fr
treatment for diabetic ketoacidosis
a serious, life-threatening medical emergency, has a higher mortality rate than DKA.
-precipitating factors: infection, therapeutic agents, therpeutic procedures, chronic illness
-pathophysiology: brain cell shrinkage
hyperosmolar hyperglycemic state
-altered level of consciousness (lethargy to coma)
-neurological deficits (hyperthermia, motor or sensory impairments, seizures)
-dehydration (extreme thirst, dry skin & mucous membranes)
symptoms of hyperosmolar hyperglycemic state
-lower blood sugar levels
-replace fluids & electrolyte
-treat underlying conditions
treatment of hyperosmolar hyperglycemic state
formation of glucose from lipids in adipose & liver tissue
gluconeogenesis

*initiated when BS < 70 mg/dl
renal threshold for glucose 180 mg/dl above which glucose will be excreted in urine.
glucosuria
if you had a patient with:
BS>250mg/dl
plasma pH<7.3
bicarbonate<15 mEq/L
serum ketones
urine ketones
abnormal Na, Cl, K

what is the condition
Diabetic Ketoacidosis
if you had a patient with:
BS >600 mg/dl
plasma osmolarity >340 MOsm/L
altered consciousness
high Na in serum
severe dehydration

what is the condition?
Hyperosmolar Hyperglycemic State (HHS)

*precipitated by illness, infection, therapeutic agents.
what are complications of diabetes?
1.BS alterations (hyper or hypo)
2.macrocirculation problems-atherosclerosis
3.microcirculation problems-basement membrane of small blood vessels (eyes, kidneys)
what is the goal of diabetes treatment?
1.manage BS (<60-120 range most of the time) using meds, diet, exercise
2.lower risk factors for condition
3.routine screening for complications
4.implementing early Tx
5.Insulin
1.rapid acting
onset 0.25h, peak-1-1.5h,duration 3-4h
2.short acting
onset 0.5-1h, peak 2-3h, duration 4-6h
3.intermediate acting
onset 2h, peak 6-8h, duration 12-16h
4.long acting
onset 2h, peak 16-20h, duration 24+h <
insulin preparations
listpro is an example of what kind of insulin preparation?
rapid acting
ultralente is an example of what type of insulin preparation?
long acting
1.monitor glucose 4x a day
2.test urine for ketones if BS>240
3.continue insulin or oral hypoglycemic
4.sip 8-12 oz. of fluid hourly
5.substitute easily digested food/liquid with carb. equivalents if unable to take solid food
diabetes sick day management
low blood sugar or "insulin reaction"
hypoglycemia
shaky
dizzy
clumsy, jerky
sweating
hunger
headache
mood changes
confusion
seizure
symptoms of hypoglycemic (insulin reaction)

*sometimes there are no symptoms in people who had DM for years from neuropathy
-0.5 c.juice (followed by a normal meal)
-hard candy
-glucose tablets
-IV of dextrose
-glucagon
Tx for hypoglycemia - Sugar

*educated family members
indicators of tight diabetes control
BS 90-130 mg/dl
post parandial BS (after eating) <180
A1C <7%
decrease sys BP
increased HR
weak pulse
flat jugular vein
no edema
poor skin turgor
low urine output
high urine SpG
weight loss
normal respirations
Fluid Imbalance: Deficit
increased BP
increased HR
strong or bounding pulse
distended jugular vein
dependent edema
taut skin turgor
urine output may be low or normal
low urine Sp G
weight gain
resp: moist crackles, wheezes
Fluid Imbalance: Excess
Dx:
Deficit Fluid Volume
Decreased Cardiac Output
diagnoses with fluid deficit
what are the commonly administered IV fluids for fluid deficit?
dextrose in water solutions (D5W)
saline solutions
combined
multiple electrolyte solutions (ringers)
Excess Fluid Volume
Impaired Gas Exchange
Activity Intolerance
dizgnoses for Fluid Volume excess
3 categories of diuretics
loop
thiazide and thiazide-like
potassium-sparing
what are diuretics used for
Diuretics are used to enhance renal function and to treat vascular fluid overload and edema.
what are common side effects of diuretics?
Common side effects: orthostatic hypotension, dehydration, electrolyte imbalance, and possible hyperglycemia.
Risk for impaired fluid volume
Fatigue
Risk for injury
Risk for impaired oral mucous membrane
dx with sodium imbalance
hyponatremia and hypernatremia may lead to
seizures
what to do for possibility of seizures with hyponatremia and hypernatremia
start and IV
raise bed rails and pad bed
Decreased Cardiac Output
Activity Intolerance
Risk for Ineffective Health Maintenance
Dx with potassium imbalance
Major symptom: leg cramps
(calcium too)

give K enema, IV (never IV push - cause heart attack), oral
potassium imbalance: hypokalemia
NEVER administer undiluted potassium into the vein
NEVER administer undiluted potassium into the vein
Risk for injury
Decreased cardiac output
Disturbed thought processes
Risk for ineffective breathing pattern
Dx with Ca imbalance
increased neuromuscular excitability, muscle twitching, spasms, and possible tetany
hypocalcemia
decreased neuromuscular excitability, muscle weakness, and fatigue, cramps
*can also lead to kidney stones
hypercalcemia
evaluated primarily by measuring arterial blood gases
acid base balance
Decreased pH
Decreased HCO3
Decreased Paco2
Metabolic acidosis
Increased pH
Increased HCO3
Increased Paco2
Metabolic alkalosis
Decreased pH
Increased Paco2
Increased HCO3
Respiratory acidosis
Increased pH
Decreased Paco2
Decreased HCO3
Respiratory alkalosis
Decreased cardiac output
Risk for excess fluid volume
Risk for injury
Dx Client with Metabolic Acidosis
Anorexia
Nausea and vomiting
Abdominal pain
Weakness
Fatique
General malaise
Decreased levels of consciousness
Dysrhythmias
Bradycardia
Warm, flushed skin
Hyperventilation
Manifestations of Metabolic Acidosis
Risk for impaired gas exchange
Deficient fluid volume
More confusion, decreased level of consciousness
Dx Client with Metabolic Alkalosis
Confusion
Decreased levels of consciousness
Hyperreflexia
Tetany
Dysrhythmias
Hypotension
Seizures
Respiratory failure
Manifestations of Metabolic Alkalosis
Impaired Gas Exchange
Ineffective airway clearance
Dx Client with Respiratory Acidosis
Headache
Warm, flushed skin
Blurred vision
Irritability, altered mental status
Decreasing levels of consciousness
Cardiac arrest
Manifestations of Acute Respiratory Acidosis
Weakness
Dull headache
Sleep disturbances with daytime sleepiness
Impaired memory
Personality changes
Manifestations of Chronic Respiratory Acidosis
Ineffective breathing pattern
Risk for injury
Dx Client with Respiratory Alkalosis
Dizziness
Numbness/tingling around mouth, of hands and feet
Palpitations
Dyspnea
Chest tightness
Anxiety/panic
Tremors
Tetany
Seizures, loss of consciousness
Manifestations of Respiratory Alkalosis
Because of this, there is no such thing as “only diarrhea” or “simple diarrhea” in a child younger than 1 year.
Because kids can get into metabolic acidosis when they have diarrhea
In children, Vomiting can lead to
metabolic alkalosis
In children, Diarrhea can lead to
metabolic acidosis
signs of dehydration
dry skin, depressed fontanelles, depressed eye globes, no tearing, increased hematocrit (resulting from less subcutaneous fluid)
With Surgery: Depending on the degree of dehydration and/or type of electrolyte imbalance, cardiac dysrhythmia or heart failure may occur.
Liver and renal failure may also result Administer IV fluids as ordered. Monitor I&O. Monitor client for evidence of electrolyte imbalance
thirst
warm, dry skin with poor turgor
soft eyeballs - sunken w/blackish ribs
dry mucous membranes
weakness
malaise
rapid, weak pulse
hypotension
Dehydration in Diabetes
children need increased fluid to keep airway secretions moist after this event
an asthma attack
Why do CF kids need to be supervised during outside play
to guard against overexertion or heat exposure; they lose excessive sodium and chloride through perspiration
metabolic disturbances, such as diabetes, dehydration, severe hemorrhage, or drug ingestion also must be considered as possible causes of
Coma in children
If a patient is on TPN, which can be a problem?
dehydration
Pain: Heartburn
Imbalanced nutrition: Less than body requirements
Ineffective Health Maintenance
Dx Client with GERD
Heartburn
Regurgitation
Pain after eating
Dysphagia - difficulty swallowing
Chest pain
Belching
**Eat small, frequent meals to help alleviate some of these manifestations
Manifestations of GERD
a neuromuscular disturbance in which the cardiac sphincter is lax, allowing for easy regurgitation of gastric contents into the esophagus.
It is treated by feeding a thickened formula and keeping the infant upright after feedings.
GERD (achalasia) in infants
a condition in which the intestinal mucosa ineffectively absorbs nutrients including carbohydrates, proteins, fats, water, electrolytes, minerals, and vitamins resulting in their excretion in stool. Multiple different bowel disorders can lead to malabsor
malabsorption
Imbalanced nutrition: less than body requirements
Diarrhea
Knowledge deficit
Dx client with Malabsorption syndrome
Pathogens usually enter the urinary tract by ascending from the mucous membranes of the perineal area into the lower urinary tract
Bacteria that have colonized the urethra, vagina, or perineal tissues are the usual source of infection
UTI
inflammation of the urethra
Urethritis
inflammation of the prostate gland
ostatitis
inflammation of the urinary bladder
cystitis
inflammation of the kidney and renal pelvis
Pyelonephritis
More severe symptoms - very sick: fever, vomiting, hematuria - be hospitalized, need antibiotics
pyelonephritis
Short, straight urethra
Proximity of urinary meatus to vagina and anus
Sexual intercourse
Use of diaphragm and spermicidal compounds for birth control - hold bacteria
Pregnancy
risk factors for UTI in female
Uncircumcised
Prostatic hypertrophy
Rectal intercourse
risk factors for UTI in male
Aging
Urinary tract obstruction
Neurogenic bladder dysfunction - paralysis
Vesicoureteral reflux - urine backs up into kidneys
Genetic factors
Catheterization (if a lot of residue in bladder, and if pt couldn’t pee)
risk factors for UT (female & male)
the most common infection but also the leading cause of bacteremia and sepsis in older adults.
UTI
Factors that contribute to UTI include: poor hygiene, incomplete bladder emptying, inadequate fluid intake, and long-term indwelling catheters. In addition, chronic conditions and medications
factors that contributed to UTI
Pain
Impaired urinary elimination
Ineffective Health Maintenance
Dx for client with UTI
pain, burning, feel like you have to pee all the time, fever, vomiting, fatigue
symtpoms of UTI
Dysuria (painful/difficult urination)
Frequency
Urgency
Nocturia (voiding two or more times a night)
Pyuria (foul odor/cloudy)
Hematuria (bloody)
Suprapubic discomfort, back pain
Manifestations of Cystitis
Urinary
Urinary frequency
Dysuria
Pyuria
Hematuria
Flank pain
Costovertebral tenderness
Manifestations of Acute Pyelonephritis
Systemic
Vomiting
Diarrhea
Acute fever
Shaking chills
Malaise
Dx Manifestations of Acute Pyelonephritis
Intravenous Pyelography (IVP): evaluates the structure and excretory function of the kidneys, ureters, and bladder
**assess for allergies to seafood or iodine (for the dyes)
Voiding Cystourethrography: can detect structural or functional abnorm
Dx tests for UTI
Vesicoureteral reflux is the backflow of urine into ureters; It occurs because the valve that guards the entrance to the ureters is defective.
children with UTI

*this may require surgery to correct
Adequate hydration
Urinate at least every 4 hours
Avoid bubble bath
Females should wipe from front to back
Wear cotton underwear
Females should wash vulva area at least daily
Sanitary pads should be changed at least every 4
prevention of UTI
Compliance w/med - how do you know if pt is complaint?
count pills
What do you do if NPO for BP med
call physician
PTT - Partial Thromboplastin Time
25-35 seconds is normal
sodium
135-145 mEq/L is normal
potassium
3.5 - 5.1 mEq/L is normal
chloride
95-105 mEq/L is normal
Calcium
4.5 - 5.5 mEq/L is normal
Magnesium
1.5 - 2.5 mEq/L is normal
Fasting Blood Sugar
70-110 mg/dl is normal
White Blood Cells
5000 - 10000 per mcL is normal
Neutrophils
1935 - 7942 abosulte count is normal
Red Blood Cells
4.5 - 5.3 million is normal
Hemoglobin
13.0 - 18.0 g/100mL (men)
12 - 16 g/100mL (women)
BUN Blood urea nitrogen
5 - 25 mg/dl
serum creatinine
0.5 - 1.5 mg/dl
Hematocrit
37-49% (men)
36-46% (women)
Platelet
150,000 - 400,000 /mcL (or mm3)
ECG - P wave
depolarization of atriua (diastole)
ECG QRS complex
depolarization of ventricles (systole)
ECG QT interval
time from ventricular depolarization until ventricles begin to repolarize

Deck Info

166

permalink