NUR326 Exam 3 Flashcards
What are the 3 functions of the GI system?
- Provide nutrients to the body with propulsive and mixing movements
- Secretion of digestive juices
- absorption of nutrients
What do gastric glands secrete?
HCl, IF, and gastrin
What are the layers of the stomach?
mucosa layer - inner layers made of g cells, chief, and epithelial cells, contains blood vessels
muscle layers - 2, help propel food from the stomach to the small intestine
serosa - outer layer, acts as a covering for inner layers
What do G cells do?
produce gastrin - a hormone that facilitates the production of HCl
What to parietal cells do?
produce HCl to break down food and produce IF to protect mucosa
What to chief cells do?
secrete pepsin
What do epithelial cells do?
secrete a bicarbonate rich solution to coat and protect the mucosa
What are plicae circilares?
Folds of the mucous membrane in the inner wall of the small intestine. They have millions of intestinal villi (which each contain microvilli)
This combination helps increase the surface area of the SI.
What are the crypts of Lieberkuhn?
intestinal glands that secrete about 2L of fluid every day into the lumen of the intestine
What are goblet cells?
secrete large amounts of mucus to protect the SI from damage of acidic gastric juices
What is the ileocecal sphincter?
area where food passes from the SI to the LI
Upper GI problems:
Which are caused by esophageal disorders and which are caused by inflammatory disorders of the stomach?
Esophageal Disorders - GERD and Hiatal Hernia
Inflammatory Stomach - Gastritis, Acute Gastroenteritis, PUD
What are the causes of dysphagia? (Mechanical vs Neuromuscular Dysfunction)
Mechanical - stenosis/stricture, diverticula, tumors
Neuromuscular - CVA, achalasia (LES can’t open properly)
GERD definition, etiology, CM, and complications
def - backflow of gastric acid from the stomach into the esophagus
etiology - anything that alters the closing strength of the LES or increases abdominal pressure (ex - fatty foods, spicy foods, obesity, pregnancy)
CM - heartburn*, dyspepsia, regurgitation, chest pain, dysphagia, and pulmonary symptoms
Complications - ulceration, scarring, strictures, Barret’s esophagus
Barret’s Esophagus
development of abnormal metaplastic tissue (premalignant), 3x increase in developing adenocarcinoma of the esophagus, only a 17% survival rate
Hiatal Hernia: definition and types
definition - defect of the diaphragm that allows the stomach to pass into the thorax
types -
sliding hernia - less severe, small, often does not need treatment
paraesophageal hernia - part of the stomach pushes through the diaphragm and stays there
Hiatal Hernia: patho, CM, RF, and treatment
patho - unknown, but could be due to age, an injury or another type of damage could weaken the diaphragm muscle, and putting too much pressure on those muscles could cause (straining, vomiting)
CM - asymptomatic*, belching, dysphagia, chest or epigastric pain
RF - age, obesity, and smoking
Treatment - avoid things that increase pressure, have small and frequent meals, avoid laying down after eating, weight control, and antacids
* Gerd and HH commonly coexist
Acute Gastritis: def, etiology
def - temporary inflammation of the STOMACH LINING only
generally lasts from 2-10 days
etiology - irritating substances, drugs, and infectious agents (H pylori)
Chronic Gastritis: def, etiology, and complications
def - progressive disorder with chronic inflammation of the stomach
can last weeks to years
Etiology - autoimmune (attacks parietal cells) and H pylori
complications - PUD, bleeding ulcers, anemia, and gastric cancers
H pylori
gram - bacteria that thrives in acidic environments
destructive pattern with PERSISTENT INFLAMMATION
transmitted by saliva, fecal matter, or vomit and by contaminated food or water
CM of Acute and Chronic Gastritis
maybe none, anorexia, n/v, postprandial discomfort (after eating), intestinal gas, hematemesis, tarry stools, and anemia
Acute GastroENTERITIS: def, etiology, CM, and complications
inflammation of the stomach AND SI
caused by stomach viruses (norovirus, rotavirus, E coli, salmonella, and campylobacter)
usually lasts 1-3 days (could be up to 10)
CM - watery diarrhea, abd pain, n/v, fever, malaise
complications - FVD, risk for dehydration
PUD: def, etiology, RF, and patho
def - ulcerative disorder of the upper GI tract (esophagus, stomach, or duodenum)
etiology - develops when the GI tract is exposed to acid and H pylori, injury causing substances, NSAIDS*, ASA, alcohol, excess secretion of acid, smoking, family history, and stress
RF - age, higher dose of NSAIDS, PUD, use of corticosteroids and anticoagulants, serious systemic disorders, and H pylori
Patho - mucosa is damaged and histamine is secreted which results in increased acid and pepsin secretion which causes further tissue damage (if blood vessels are destroyed, it causes bleeding)
PUD: classifications
duodenal ulcer - most common type, happens the most in early adulthood
gastric/peptic ulcer - happens the most between 50-70 due to increased use of NSAIDs, corticosteroids, anticoagulants, and other serious illnesses
PUD: CM and Complications
CM - sometimes none, n/v, anorexia, weight loss, bleeding, burning pain (middle abdomen)
gastric - pain 1-2 hours after eating
duodenal - pain 2-4 hours after eating
Complications - Hemorrhage, Obstruction, Perforation and Peritonitis
Appendicitis
inflammation of the appendix, caused when the appendix is obstructed which causes inflammation
can cause gangrene, abscess formation, and peritonitis
Key CM of Appendicitis
RLQ pain
rebound pain
sudden pain relief - could indicate burst
peritonitis: def, causes, and CM
def - inflammation of the peritoneum, can cause third spacing (could lead to hypovolemic shock), decreased peristalsis, and paralytic ileus
causes - perforated ulcer, ruptured gallbladder, pancreatitis, ruptured spleen, ruptured bladder, and ruptured appendix
CM - sudden and severe, severe abd pain, tenderness, board-like abdomen*, n/v, fever, increased WBC, increased HR, and decreased BP
IBS: def, symptoms, and relationship with stress
def - chronic condition characterized by alterations in bowel pattern due to changes in intestinal motility (chronic constipation and/or diarrhea)
symptoms - vary for everyone, distention, fullness, flatus, bloating, pain relieved by defecation, urgency, intolerance to certain foods, non-bloody stool (may contain mucous)
stress - never the result of psycho. causes but can be exacerbated by stress
IBD: def, RF, conditions, and etiology
def - chronic inflammation of the intestines with exacerbations and remissions
RF - women, Caucasians, Jewish descent, and smokers
conditions - Chron’s and Ulcerative Colitis
Etiology - autoimmune activated by an infection
Chron’s: def, complications
def - lymph structures of the GI tract are blocked causing tissue to become engorged and inflamed, causes deep liner fissures and ulcers (skip lesions and cobblestone appearance)
complications - malnutrition*, scar tissue and obstructions, fistulas, cancer
Ulcerative Colitis: def, RF, patho, CM, complications
Def - inflammation of the mucosa in the RECTUM and COLON
Usually develops in the third decade of life
RF - white people of European descent, Jewish descent
Patho - inflammation begins in the rectum and continues in a CONTINUOUS segment that may involve the entire colon (crypt abscess - necrosis of epithelial tissue resulting in abscess) then, the colon and rectum try to repair the damage with new granulation tissue (tissue is fragile and bleeds easily)
CM - abdominal pain, BLOODY DIARRHEA, weight loss, no appetite, fever, hemorrhage, perforation, colon cancer
Complications - malnutrition, anemia, strictures, FISSURES, ABSCESSES, toxic megacolon, liver disease, fluid/electrolyte imbalances
Diverticulosis: patho, CM
Patho - development of diverticula (small couching in lining of colon that bulge outward through weak spots), can be congenital or acquired, could be caused by a low fiber diet with chronic constipation
Usually located in the descending colon
CM - usually asymptomatic, could be discovered accidentally over with flare up of acute diverticulitis
Diverticulitis: def, CM, complications
Def - inflammation of one or more diverticula pouches, usually from retained fecal material
CM - abdominal pain, fever, increased WBC, constipation or diarrhea, large quantity of frank blood (acute), could resolve spontaneously
Complications - perforation, peritonitis, and obstruction
What are the two ways that GI disorders can be treated with pharmacotherapy?
increasing protective factors - antacids, sucralfate
Decrease aggressive factors - treat H pylori, H2 blockers, and PPIs
How do we treat H pylori?
Several antibiotics with gastric acid inhibitor (minimizes resistance - H pylori likes acidic environment)
Very low adherence due to high cost and many pills to take
What are the two ways that drugs can target gastric acid production?
Block H2 receptors
Inhibit the proton pump
Cimetidine: class, MOA, indications, AE, interactions, and safety alert
Class - H2 receptor agonists
MOA - block H2 receptors in the stomach, reduce gastric acid secretion by 60-70%
*Give at least 1 hour apart from antacids
Indications - GERD, PUD, ulcer prophylaxis, heartburn, and dyspepsia
AE - well tolerated, CNS effects in the elderly, slight risk for pneumonia in the elderly
Interactions - inhibits CYP450 (newer generations do not)
Safety alert - can increase the levels of warfarin, phenytoin, and theophylline
*Give slow IV to avoid bradycardia
-prazole: class, MOA, indications, AE, interactions, nursing implications
Class - PPI
MOA - binds to proton pump, inhibits hydrogen potassium ATPase enzyme system, inversely inhibits the secretion of HCl
More effective than H2RA
Indications - short term treatment of GERD and PUD
AE - safe (short term), increase risk for pneumonia, bone loss, and stomach CA (long term)
Interactions - few
Nursing implications - short terms use only
Sulcrafate:class, MOA, indication, AE, Interactions
Class - Mucosal protectant
MOA - alters when exposed to gastric acid, creates a sticky and thick gel (protective barrier)
Indication - duodenal ulcers and gastric ulcers
AE - no major
Interactions - *decreased drug absorption (do not take before you take other drugs - take 2 hours apart)
Antacids: MOA, Indication, AE, Interactions
MOA - neutralizes acid by approximately 50%
Indication - PUD, GERD, stress ulcers, possibly heartburn and indigestion
AE - diarrhea or constipation, acid rebound
Interactions - chelation (alter the absorption of other drugs), altered gastric absorption, separate from other drugs by 1-2 hours
Ondansetron: MOA, use, AE
Zofran
MOA - blocks serotonin receptors in the trigger zone in the brain and the afferent vagal nerves in the stomach and SI
AE - common, usually mild headache, diarrhea, and dizziness (serious - serotonin syndrome*)
Dimenhydrinate, meclizine, hydroxyzine : class, MOA, indication, AR
Antihistamines
MOA - block the release of histamine 1 receptors in the inner ear
Indication - treatment of dizziness and nausea, antiemetic and anti vertigo associated with motion sickness
AE - sedation, drowsiness, dizziness, and anticholinergic effect
FALL RISK
Metoclopramide: MOA, indications, SE
Dopamine antagonist
MOA - blocks dopamine receptors increasing the tone of the LES (GERD) and increases peristalsis in both the stomach and intestine (diabetic gastroparesis)
Indications - n/v associated with chemo/radiation, GI motility issues, and paralytic ileus SE- sedation, severe = extra pyramidal symptoms, restlessness, neuroleptic malignant syndrome
Extra pyramidal symptoms
Akathisia - may feel restless, tense, constant desire to move, acute dyskinesia - involuntary muscle contractions, Parkinsonism, tardive dyskinesia, and neuroleptic malignant syndrome
Diphenoxylate with atropine
Loperamide
Drug therapy for diarrhea
MOA - decrease intestinal peristalsis and reduce intestinal effluent
AE - drowsiness and constipation, fall and driving precautions, anticholinergic effects, serious (cardiac arrest/arrhythmias)
Sulfasalazine
5-amino salicylates (IBD)
MOA - converts intestine into 5-amino salicylic acid and sulphapyridine
SE - nausea, fever, rash, headache, hematologic disorders
Precaution - do not give to patients allergic to sulfa or have certain types of anemias, caution for use with comorbidities
Infliximab
DMARDs (IBS)
MOA - monoclonal antibody which neutralizes TNF alpha
SE - immune suppression*, infection *, cancer, HF, infusion reactions, neutropenia
Often require therapeutic drug monitoring and bio marker monitoring for inflammation
Must be screened and vaccinated before administering
Pituitary Gland Hormone Secretion
Anterior - TSH, ACTH
Posterior - ADH, oxytocin
ADH
Released in response to high serum osmolality and or hypotension
Causes water retention in kidneys
Adrenal glands
Secrete epinephrine and norepinephrine
In response to ACTH, it secretes cortisol, aldosterone, and androgens
Adrenal Cortex steroid hormones
Regulate body’s response to normal and abnormal levels of stress
Sugar, Salt, Sex
Glucocorticoid/Cortisol Function
Raise blood sugar, protect against physiologic effects of stress, suppress inflammatory and immune processes, release muscle stores of proteins, and increase blood cholesterol
Mineralcorticoids
Aldosterone
Regulated by RAAS
Maintain salt and water balance
Promotes secretion of K
When triggered by angiotensin II, aldosterone promotes sodium retention and thus water retention
T3 and T4
T3 - active form, converted from T4
T4 - two forms: one attaches to proteins when they’re not needed and free T4 enters the tissues when they are needed
Parathyroid gland
Glands produce and secrete parathyroid hormone in response to hypocalcemia and break down bone to reestablish normal calcium in the blood
Promotes vitamin D production
Adrenal Hormone Disorders
Low - addison’s disease
High - Cushing syndrome
Cushing’s Syndrome - def and CM
Collection of S/S associated with hypercortisolism
Caused by: disease of the adrenal cortex (syndrome), disease of the anterior pituitary (disease), and exogenous steroids (syndrome)
CM - glucose intolerance, hyperglycemia, hypertension, capillary friability, muscle wasting, muscle weakness, thinning of skin, osteoporosis, bone pain, redistribution of fat to abdomen, shoulders and face, impaired would healing and risk for infections, mood swings, and insomnia
Aminoglutethimide
MOA - blocks synthesis of all adrenal steroids
Indication - temporary therapy to decrease cortisol production, reduces cortisol levels by 50%
AE - drowsiness, nausea, anorexia, rash
Ketoconazole
MOA - anti fungal drug that also inhibits glucocorticoid synthesis
Indication - adjunct therapy to surgery or radiation with Cushing’s
Safety Issues - do not take with alcohol or other drugs that harm the liver, do not give during pregnancy
Addison’s Disease
Disease of the adrenal cortex that causes hypo-secretion of all 3 hormones (cortisol, aldosterone, and androgen)
Most severe effects come from a lack of cortisol
Etiology - idiopathic, autoimmune, or other
Patho - adrenal gland destroyed, symptoms arise when it is 90% nonfunctional, and ACTH is secreted in large amounts
CM - anorexia, weight loss, weakness, malaise, apathy, electrolyte imbalances (hyperkalemia), and skin hyperpigmentation
Addisonian (Adrenal Crisis)
Acute adrenal insufficiency, body doesn’t have cortisol to combat stress
Medical emergency
Cause - sudden insufficiency of serum corticosteroids, results from sudden loss of adrenal gland or sudden increase in chronic stress or sudden cessation of corticosteroid drug therapy
How to treat Addison’s
All patients require a glucocorticoid
Some patients require a mineralcorticoid
Dosing mimics the release of natural hormones - timing is important and doses are small
NEVER abruptly stop therapy (3x3 rule)
Pheochromocytoma
Rare tumor of the adrenal medulla that produces excessive catecholamines (epi and norepinephrine)
Benign
Rare, could happen from young to middle age
Tumor cells secrete catecholamines due to SNS activation
CM - HTN*, headache, diaphoresis, tachycardia
Pheochromocytoma Treatment
Preferred - surgery to remove the tumor
Alpha adrenergic blockers may be used on inoperable tumors and preoperatively to reduce the risk of HTN
Phenoxybenzamine
Alpha blockers in Pheochromocytoma
MOA - long acting, irreversible, blockage of alpha adrenergic receptors
Drug effects - lowers blood pressure due to blood vessel widening
AE - orthostatic hypotension, reflex tachycardia, nasal congestion, sexual side effects in men
Antidiuretic Hormone Disorders
Low - diabetes insipidus
High - SIADH
SIADH
Syndrome of inappropriate antidiuretic hormone
Abnormal production or sustained secretion of ADH
Characterized by fluid retention, serum hypoosmolality and hyponatremia and concentrated urine
SIADH Etiology
Malignant tumors
Central nervous System Disorders - trauma
Drug Therapy - morphine, SSRI, chemo
Misc - hypothyroidism and infection
SIADH Patho
Increased ADH
Increased water reabsorption in the renal tubules
Increased intravascular fluid volume
Dilutional hyponatremia and decreased serum osmolality
SIADH Osmolality
Serum Osmolality - low
Urine osmolality and specific gravity - high
Serum sodium - low
Urine output - low
Weight - gain
SIADH CM
Depend on severity and rate of onset
Dyspnea, fatigue, dulled sensorium, confusion, lethargy, muscle twitching, convulsions, impaired taste, anorexia, vomiting, and cramps
Severe - possible irreversible neurological damage
Can die of water intoxication
Demeclocycline
Tetracycline broad spectrum antibiotic
MOA - interferes with renal response to ADH
AE - photosensitivity, teeth staining, and nephrotoxicity
Diabetes insipidus - def and etiology
A deficiency of ADH or decreased renal response to ADH
Characterized by excessive water loss in urine
Neurogenic and nephrogenic
Neurogenic DI
Neuroleptic origin
Caused by hypothalamus or pituitary gland damage
Associated disorders - stroke, TBI, brain surgery, and cerebral infections
Sudden onset and usually permanent **
Nephrogenic DI
Renal origin
Cause - loss of kidney function, often drug related
Associated with CKD
Slow onset and progressive **
DI Patho
Decreased ADH, decreased water reabsorption in renal tubules, decreased intravascular fluid volume, and increased serum osmolality and excess urine output
DI osmolality
Serum osmolality - high
Urine osmolality and specific gravity - low
Serum sodium - high
Urine output - high
Weight - loss
DI CM
Polyuria, polydipsia, dehydration
Based on severity - hypovolemic shock to electrolyte imbalances
Treatment of DI
Neurogenic - synthetic ADH replacement
Nephrogenic - thiazide diuretics
Desmopressin
Neurogenic DI treatment
MOA - synthetic ADH replacement therapy, anti diuretic effects
AE - irritation from nasal spray, and large doses can cause hyponatremia and water intoxication
thyroid negative feedback loop
hypothalamus releases TRH
causes the anterior pituitary to release TSH
causes the thyroid gland to raise the level of thyroxine (T4)
(feeds back to anterior pituitary and hypothalamus)
goiter
enlargement of the thyroid gland with or without symptoms of thyroid dysfunction
excess pituitary TSH
low iodine levels
hypothyroidism
insufficient levels of T3 and T4
primary - increase release of TSH from pituitary
hashimotos - autoimmune disorder, most common cause of hypothyroidism (creates thyroid receptor antibodies, antithyroglobulin antibody, and antithyroperoxidase antibody*)
hypothyroidism RF
female, older than 40, caucasian, pregnancy, history of autoimmune disorders, family hx, medications, treatment for hyperthyroidism
early vs late CM of hypothyroid
early - cold intolerance, weight gain, lethargy, fatigue, memory deficits, poor attention span, increased cholesterol, muscle cramps, raises carotene levels, constipation, decreased fertility, puffy face, hair loss, and brittle nails
late - below normal temp, bradycardia, weight gain, decreased LOC, thickened skin, and cardiac complications
What does hypothyroidism do to the rest of the body?
raises cholesterol
raises carotene levels
causes anemia
decreases filtration by the kidneys
can cause hoarse voice
myxedema
severe hypothyroidism (coma), describes the dermatological change that occurs with hypothyroidism
how to diagnose hypothyroidism
high TSH level
low free T3
low free T4
antithyroglobilin
antithyroperoxidase antibodies
low hormone secretion by the thyroid gland
treatment of hypothyroidism
replace hormone with levothyroxine (converts to T3 in the body) or surgical intervention if necessary
hyperthyroidism
excess secretion of T3 and T4
primary - graves
secondary - pituitary
tertiary - hypothalamus
hyperthyroidism RF
family history of graves, age above 40, women, caucasian, medications, excess iodine intake, pregnancy
graves disease
autoimmune disorder with excess levels of T3 and T4
includes thyroid stimulating antibodies
CM - nervousness, insomnia, sensitivity to heat, weight loss, gland is usually enlarged, audible bruit, atrial fibrillation, myxedema, exophthalmos
exopthalmos
wide eyed stare associated with increased sympathetic tone and infiltration of the extra ocular area with lymphocytes and mucopolysaccharides
preorbital edema and bulging of the eyes termed = graves ophthalmopathy
women are more effected than men
diagnosis of grave’s disease
low TSH, high T3 and T4, antithyroglobulin, antithyrotropin receptor antibody, ultrasound with color doppler evaluation, radioactive iodine scanning and measuring of iodine uptake
treating hyperthyroidism
antithyroid hormone medication
radioactive iodine
surgery
thyrotoxic crisis
overwhelming release of thyroid hormones that exert an intense stimulus on the metabolism
life-threatening condition that is most commonly precipitated by surgery, trauma, or infection
parathyroid gland function
controls calcium levels in the body
promotes vitamin D production by kidney
hypoparathyroidism
result of insufficient PTH secretion and the resultant hypocalcemia
CM - muscle cramps, irritability, tetany, convulsion, hypocalcemia
treat - replace PTH, normalize serum Ca and vitamin D
hyperparathyroidism
CM - muscle weakness, poor concentration, neuropathies, HTN, kidney stones, metabolic acidosis, osteopenia, pathological fractures, constipation, depression, confusion, or subtle cognitive deficits
caused by excessive secretion of PTH with resulting hypercalcemia, and bone breakdown
treat - reduce calcium, diuretics, calcitonin, bisphosphonates, vitamin D, and surgery
end diastolic volume
blood volume at the end of relaxation
end systolic volume
residual volume of blood remaining in the ventricle after ejection
three factors that effect stroke volume
preload
afterload
contractility
preload
stretch of cardiac muscle cells before contraction
chamber volume before contraction
frank starling law
increase in resting muscle fiber strength results in greater muscle tension
hydrostatic pressure
force that attempts to push fluid out of the capillary pores and into the interstitial and intracellular spaces
oncotic pressure
force that attempts to pull fluid from the interstitial and intracellular spaces into the capillary
starlings law on capillary forces
oncotic pressure forces and hydrostatic pressure forces oppose each other at every capillary membrane and attempt to balance each other out
afterload
resistance that must be overcome in order to eject blood from the chamber
increase leads to a decrease in SV
contractility
contractile force of the heart muscle cells
determined by the amount of free calcium within the myocardial cell
LVF backward effect
creates buildup of hydrostatic pressure in the left atrium, pulmonary veins, and pulmonary capillaries
LVF forward failure
decreased perfusion of the brain, kidneys, and other organs
CAD
coronary arteries branch from the aorta
they become clogged due to atherosclerosis
LV determines perfusion to the body
CAD nonmodifiable vs modifiable RF
non-modifiable - age, family history, gender, ethnicity, genetics
modifiable - HTN, smoking, DM, obesity, inactivity, diet, hyperlipidemia*
endothelial dysfunction
vessels aren’t necessarily blocked but become narrowed when they are supposed to dilate
causes - DM, HTN, HPL, smoking
angina
main symptom of CAD
includes anxiety, dizziness, chest pain, heartburn, irregular HR, weakness, anxiety, nausea, cold sweat, and burning sensation
stable angina
coronary blood flow is diminished but not blocked
there is an imbalance between oxygen supply and demand
brought on by exertion and relieved with rest
lasts 2-5 minutes
caused by atherosclerosis
atypical angina in women
discomfort - hot, tenderness
location - not always the chest
other - indigestion, heart burn, nausea, fatigue, weakness, lightheadedness, dyspnea
Angina Pectoris with Myocardial Infarction
chest pain that is not brought on by exertion, could radiate to other areas, not relieved in 2-5 minutes
often accompanied by n/v, SOA, and diaphoresis
risk for MI increased
radiating pain areas: neck, jaw, upper abdomen, shoulders, and arm
Stable angina treatment
educate! - remember the rest and relax, decrease bodily demand
nitrates
prevent and treat further atherosclerosis
teach about MIs
cardiomyopathy
disease of the myocardium (heart muscle)
usually idiopathic but can be caused by ischemia, HTN, inherited disorders, infections, toxins, myocarditis, and autoimmune conditions
leads to HF
heart failure
chronic and progressive condition in which the heart muscle is unable to pump enough blood to meet the body’s needs for blood and oxygen
the heart can’t keep up with the workload
can’t meet the body’s demands
what does heart failure result in?
decreased CO
decreased myocardial contractility
increased preload
increased afterload
pathological changes that can occur in developing HF
volume overload
impaired ventricular filling
weakened ventricular muscle
decreased ventricular contractile function
major causes of HF
repeated ischemic episodes*
MI
chronic HTN
COPD
valve disorders
pulmonary embolus
risk factors for HF
HTN*
DM
within 6 months of MI
men and postmenopausal women
black/african americans
genetics
age
ethnicity
ischemic heart disease
obesity
lifestyle factors
COPD, severe anemia
congenital heart defects
viruses (myocarditis)
alcohol/drug use
kidney conditions
right vs left HF
right - blood backs up into PULMONARY circulation
left - blood backs up into SYSTemic circulation
left sided HF
LV increases in size
backflow into pulmonary veins
congestion in LUNGS
findings - cough, crackles, wheezes, frothy sputum, may be blood tinged, paroxysmal nocturnal dyspnea, and orthopnea
right sided HF
often due to COPD
RV increases in size
backflow into the vena cava, decreased to the lungs
congestion of jugular veins, liver, and lower extremities
findings - JVD, dependent edema, weight gain, hepatosplenomegaly
reduced ejection fraction (systolic HF)
<40%
caused by impaired contractile function, increased afterload, cardiomyopathy, and mechanical problems
left ventricle loses the ability to generate pressure to eject blood
weakened muscle cannot generate stroke volume and then lowers CO
LV fails, blood backs up and causes fluid accumulation
preserved ejection fraction (diastolic HF)
inability of ventricles to relax and fill during diastole
HTN is primary cause
RF - female, older age, DM, obesity
leads to high filling pressures and decreased SV and decreased CO
reduced CO leads to fluid congestion
EF is normal or only slightly decreased
ventricular remodeling in HF
a weakened heart muscle
secretes molecular substances (angiotensin 2, endothelin, TNF alpha, catecholamines, insulin-like growth factor, growth hormone)
promotes genetic changes, apoptosis, and hypertrophy of cardiac myocytes as well as collagen deposits and myocardial fibrosis
**lead to enlargement and dilation of the LV
S3
low pitched sound heart after S2
during rapid filling of the ventricle in the early part of diastole
fluid is left in the ventricle after each contraction
increased pressure within the ventricles
indicative of HF in those over 40
automacity
ability to generate an electrical impulse
excitability
ability to respond to an outside impulse (chemical, mechanical, electrical)
conductivity
ability to receive an electrical impulse and conduct it
contractility
ability of myocardial cells to shorten in response to an impulse
depolarization
light switch turns on, contractions that occur in atrium and ventricles during systole, when atrial cells polarize they squeeze
repolarization
heart ramps back up
in what part of the heart rhythm is atrial depolarization?
p wave
in what part of the heart rhythm is ventricular depolarization?
between r and s
in what part of the heart rhythm is ventricular repolarization?
t wave
normal electrical conductivity of the heart
60-100 bpm
regular rhythm
pr interval - 0.12-0.20
QRS - <0.12sec
sinus arrhythmia
a degree of variability in the heart rate
common in young people
HR fluctuates with respiration or autonomic nervous system
dysrhythmia
abnormality of the heart rhythm
problem with impulse generation or conduction
when we alter rhythms, CO is impacted
what are the causes of dysrhythmias?
inappropriate automaticity - a cell initiates AP’s when it isn’t supposed to
triggered activity - extra impulse generated during or just after repolarization
re-entry - cardiac impulse in one part of the heart continues to depolarize after the main impulse has finished
sinus bradycardia
originates in the SA node
<60bpm
normal rhythm
normal PR and QRS intervals
causes of sinus bradycardia
hyperkalemia
vagal response
dogoxin toxicity
late hypoxia
medications (beta blockers)
myocardial infarction
S/S of sinus bradycardia
lightheadedness
easily fatigue
syncope
dyspnea
chest pain or discomfort
confusion
treatment of symptomatic bradycardia
atropine (anticholinergic)
pacemaker if not effective
sinus tachycardia
originates in SA node
100-150bpm
p waves may be partially hidden
causes of sinus tach
catecholamines
fever
fluid volume deficit
meds (epi, albuterol)
substances (caffeine)
hypoxia (early)
treatment for sinus tach
based on cause
hypovolemia - fluids
fever - antipyretics
pain - analgesics
beta blockers can lower HR and myocardial oxygen consumption
paroxysmal supraventricular tachycardia (PSVT)
HR 159-250bpm
originates in AV node
usually no P wave
normal QRS
usually caused by a re-entry phenomenon
typically begins and ends suddenly
“my heart is racing”
(intermittent above ventricle)
causes of PSVT
over exertion
emotional stress
stimulants
digitalis toxicity
rheumatic heart disease
CAD
WPW
RHF
PSVT S/S
palpitations
chest pain
fatigue
lightheadedness
dyspnea
premature atrial contractions (PAC)
early P waves that look different
normal PR
QRS follows PAC
usually has no consequences (frequent can put them at risk for another dysrhythmia)
CHECK ELECTROLYTES
may need O2
atrial flutter
originates in the AV node (overrides SA node)
reentry impulse that is repetitive and cyclic
atrial rate of >250 (faster than ventricles)
“sawtooth”
narrow QRS
causes of a flutter
CAD, cardiomyopathy, heart valve disease, congenital heart disease
inflammation of the heart
high BP
lung disease or overactive thyroid, electrolytes
a fib
multiple irritable spots on atria
IRREGULAR
100-175bpm
no identifiable P wave
fibrillation waves
a fib CM
palpitations
racing heart
fatigue
dizziness
chest discomfort
SOA
or asymptomatic
causes of a fib
electrolytes
hypoxia
CVD
complications of a fib
decreased CO
HF
embolus / stroke
treatment of a fib
rate control - beta blockers
stroke prevention
cardioversion, abalation
premature ventricular contractions (PVC)
contractions come from an ectopic focus in the ventricles
comes earlier than the QRS should come
doesn’t follow normal rhythm or p wave
wide and distorted shape compared to normal
causes of PVC
stimulants, ELECTROLYTES, hypoxia, fever, exercise, emotional stress, and CVD
TREAT CAUSE
bigeminy
PVC every QRS
trigeminy
PVC every third beat
quadrigeminy
PVC every 4th beat
v tach
3 or more PVCs together
ectopic focus in ventricles takes control and fires repeatedly (no atrial contractions)
seriously decreases CO
DEADLY RHYTHM
150-200bpm
no p wave, PR not measurable
v tach treatment
anti-dysrhythmic medication (beta blocker or CCB)
electrolyte replacement
CHECK PULSE
vfib
irregular wave forms of varying shapes and sizes
ventricles quivering
NO CARDIAC OUTPUT
PVD
umbrella term describing several circulatory diseases
PVD patho
related to atherosclerosis processes in the extremities
thrombus, inflammation, or vasospasm
RF PVD
SMOKING
DM
high cholesterol
heart disease
stroke
increased age
PAD CM
calf or butt pain
wounds that don’t heal
diminished sensation in extremities
trophic skin changes (skin, loss of leg hair, diminished pulses, elevation pallor, cyanosis, reactive hyperemia, erectile dysfunction)
intermittent claudication
consistent pain precipitated by consistent level of exercise
CEASES WITH REST
pain depends on site of plaque buildup and collateral circulation
intermittent claudication S/S
cramping of the lower extremity or buttocks caused by arterial flow obstruction
pain usually starts after walking a certain distance
“angina” of the lower extremities
common site for PAD
femoral artery
lack of circulation
ischemia of muscle in lower leg, cellular hypoxia
5 P’s of PAD
pain
pulselesness
palpable coolness
paresthesias
paresis
diagnosing PVD
compare BP in the arm and leg
ankle pressure should be greater than arm pressure
*severe PAD - ABI =0.5
PVD arterial vs venous
*arterial - intermittent claudication pain
no edema
no pulse or weak pulse
round and smooth sores
black eschar
sores on toes and feet
*venous - dull and achy pain
lower leg edema
pulse present
sores with irregular borders
yellow slough or ruddy skin
sores on ankles
chronic venous insufficiency
occurs when the venous walls or valves in the leg veins are not working effectively
blood pools in veins
chronic
S/S of venous insufficiency
lower extremity edema
achiness or tiredness in legs
leathery looking skin
stasis ulcers
flaking or itching skin
new varicose veins
non pharm treatment of PVD
reduce contribution factors
smoking cessation
increased PA
weight reduction
stress reduction
DM management
HTN control
pharm treatment of PVD
antiplatelet agents
anticoagulants
thrombolytics
lipid lowering agents
cilostazol
intermittent claudication treatment
MOA - platelet inhibitor, vasodilation
AE - headache, dizziness, diarrhea, abnormal stools, palpitations, peripheral edema
*metabolized by cytochrome P450
pentoxifylline
vasoactive agent, treat intermittent claudication caused by PVD
MOA - relieves leg pain by increasing blood flow and oxygen through blood vessels, helps increase walking distance and duration
AE - n/v, dizziness
what is the big deal with valve abnormalities?
very tight and hard for blood to get through
lose and the blood flows backward with increased pressures
aortic stenosis triad
chest pain
lightheadedness
SOA
mitral regurgitation
causes fatigue and SOA
may require valve replacement surgery
infective endocarditis
infection of valve
vegetation - ineffective mass on the valve
pieces can break off and enter the blood stream which can cause an occlusion
ineffective endocarditis RF
prosthetic valve
pacemaker associated bacteria
IV drug use
Caused by - strep or staph
symptoms of ineffective endocarditis
fever, chills, anorexia, weight loss, pain in muscles, joint pain, heart murmur, signs of ischemia of extremities
septic emboli in ineffective endocarditis
microorganisms travel to the heart and adhere to damaged endothelial tissue, stimulate coag cascade which eventually develops vegetation
vegetations are carried into the bloodstream which can initiate infection and ischemia
classic CM of IE
petechiae
splinter hemorrhages
janeway lesions - nontender lesions of palms and soles
osler’s nodes - subq nodules in pulp of fingertips
roth spots - oval retinal hemorrhages with pale centers
duke criteria for IE
requires 2 major criteria, one major and three minor, or five minor
major criteria of IE
positive cultures from at least two separate cultures
echocardiogram showing vegetation, abscesses or valve perforation
new murmor
minor criteria of IE
predisposing heart condition such as mitral valve prolapse, rheumatic or congenital heart disease or IV drug abuse
temp greater than 100.4
presence of embolic disease or hemorrhage
presence of immunological phenomena
positive culture
positive ECG
pharm for IE
antibiotics
prolonged therapy
lengthy hospital stay
goals of therapy for stable angina
relieve chest pain
reduce HL
improve morbidity and mortality
antifungals for stable angina
nitrates - dilates veins, decreases preload
beta blockers - decreased HR and contractility
CCB - dilate arteroles which decreases afterload, decreases HR and contractility
ranolazine - helps the myocardium generate more efficiently
pharm for stable angina
antifungals
beta blockers
CCB
statins
aspirin
nitroglycerin
organic nitrate
MOA - dilates veins, decreases preload
AE - related to vasodilation, tolerance
rapid acting, short acting, and long acting
monitor for headache, take only as many tablets as needed, rotate patch sites, taper long acting forms
ranolazine
antifungal
MOA - unknown, possibly helps the myocardium use energy more effectively
prolongs QT interval *
AE - headache, dizziness, nausea, constipation
CYP340 inhibitor - avoid grapefruit and other inhibitors
pharm treatment for HF
ACE inhibitors
beta blockers
MRAs
SLGT inhibitors
angiotensin recetor neprilysin inhibitor
MOA - decreases preload and afterload, suppresses aldosterone, favorably impact, cardiac remodeling
use highest dose possible
AE - hypotension, hyperkalemia, cough
carvedilol
beta blockers
MOA - protect against SNS activation and dysrhythmias, reverses cardiac remodeling
AE - fluid retention or worsening HF, fatigue, hypotension, bradycardia
spironolactone
PSD
suppress sodium and water retention to help with offloading in the LV
associated with decreased hospitalizations and cardiac death
must watch carefully for hyperkalemia
dapaflifozin
SLG2 inhibitor for HF
decreases readmissions, mortality, and morbidity
diuretics in HF
loop diuretics
for volume overload
AE - hypokalemia, hypotension, dogoxin toxicity
mainly for symptom relief*
inotropic drugs (digitalis)
cardiac glycosides
second line due to increased risk for dysrhythmias
MOA - inhibits sodium potassium ATP pump causing calcium to collect within the cells of the heart helping to increase myocardial contractility (increases flow to kidney, decreases SNS action and increases parasympathetic action, decreases HR)
AE - cardiac dyshythmias, digitalis toxicity
digitalis toxicity
highest risk - age, women, combination drugs
prevent toxicity - reduce dose, serum digitalis levels (periodic monitoring levels), supplemental potassium
nursing implications when giving digoxin
monitor serum K
take apical pulse for a full minute before giving
monitor cardiac rhythm
antidote for digoxin
digoxin immune fab (digibind) IV
medicines for rate and rhythm control
beta blockers
CCB
amiodarone
andenosine
atropine
dofetilide
amioderone
MOA - prolongs the activation potential duration and effective refractory period in all cardiac tissues
many AE - thyroid alterations, corneal microdeposits, pulmonary toxicity*, BBW - pulmonary toxicity, hepatotoxicity, and pro arrhythmic effects
contraindicated with severe bradycardia
amioderone drug interactiosn
digoxin and warfarin
extremely long half life
atropine
sinus brady treatment
MOA - poisons the vagus nerve
given IV push only for bradycardia
AE - xerostomia, blurry vision, photophobia, tachy, flushing, hot skin
*need to be on cardiac monitoring
adenosine
MOA - slows down the conduction time through the AV node
very short half life*
only given IV*
always follow with rapid normal saline flush
dofetilide
antidysrhythmic
converts afib or flutter to NSR
MOA - selectively blocks the rapid cardiac ion channel carrying potassium currents
SE - torsades, SVT, headache, dizziness, chest pain
ECG monitoring
don’t give to someone with long QT intervals or other drugs that can lengthen QT
