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cushings cause
excess corticosteroid (any of the three)
cushings syndrome
excess prolonged administration of corticosteroids (giving pt the meds)
cushings disease
caused by ACTH secreting tumors of pituitary gland OR direct tumor of adrenal gland
adrenocoticotropic hormone, made in pituitary, stimulates adrenal cortex to produce its hormones
cushings S & S
weight gain, fluid retention, moon face, increase adipose tissue in trunk, face, neck, thin extremities, muscle wasting, thin hair, easy to bruise, sex hormone alteration, glucose intolerance (high BS)
cushings diagnosis
elevated bs, low potassium, 24 hour urine for free cortisol
treatment of cushings DISEASE
removal of pituitary tumor, adrenalectomy if adrenal tumor, mitotane (med to suppress cortisol production),
treatment of cushiness SYNDROME
wean off steroids
addisons disease
adrenocortical insufficiency, primary and secondary
primary addisons disease
secondary addisons disease
from lack of pituitary ACTH
Manifestations of addisons diease
hypotension, vomiting, diarrhea, electrolyte imbalance, weakness, fatigue, anorexia, skin hyperpigmentation
risk of suddenly stopping steroid
severe hypotension and shock, will look like addisons disease
diagnosing addison's disease
low BG, electrolyte imbalance, metabolic acidosis, ACTH stimulation challenge test
ACTH stimulation challenge test
to find out if the problem is with the pituitary gland of the adrenal gland, measures the level of cortisol in your blood before and after an injection of synthetic ACTH. ACTH signals your adrenal glands to produce cortisol.
if adrenal glands are damaged ACTH stim test shows
output of cortisol blunted or non existent
care for addison's disease
replacement therapy with glucocorticosteroids and mineralcorticosteroids, manage underlying problem
clinical syndrome characterized by inadequate tissue person that results in impaired cellular metabolism
types of shock
hypovolemic, distributive, cardiogenic
all shock effects
cardiac output
common to all types of shock
hypoperfusion, hypercoagulability, activation of the inflammatory process
normal 70-105, if not near normal=hypoxia
causes of hypovolemic shock
hemmorhagic, dehydration, burns, most common
excessive loss of whole blood, external loss:GI hemorrhage, surgery, trauma
internal loss: hemothorax, dissecting AA
shift of plasma from vascular to interstitial, direct evaporation loss, rule of nines
nephrotic syndrome (leaky glomerolus), extreme third spacing
fight or flight
distributive shock types
septic, anaphylactic
septic shock
systemic response to infection, may include SIRS and MODS, endotoxins bind with immune cells which initiate an inflammatory response causing severe vasodilatation and capillary permeability
anaphylactic shock
release of histamines leading to massive vasodilation and increased capillary permeability
manifest ions of anaphylactic shock
hives, laryngeal edema, bronchospasm, CV collapse, respiratory failure
cardiogenic shock
instability of the heart muscle to function adequately OR mechanical obstruction to or from the heart resulting in severe decrease of CO and decrease in tissue perfusion. MI, large PE, pericardial tamponade, tension pneumothorax
MI and cardiogenic shock
areas of necrotic tissue impairs the areas ability to contract, usually LV failure, decreased CO
volume x HR/min
normal 1500ml blood/min
PE and cardiogenic shock
increased workload RV>decrease blood to L side of heart >decreased CO
pericardial tamponade and cardiogenic shock
rapid increase in fluid in the pericardial sac which compresses myocardium impairing its ability to pump, decreasing CO
tension pneumothorax and cardiogenic shock
large amount of air in the pleural space which compresses the heart and great vessels > interrupts venous return to the heart > decreased CO
other causes of decreased CO
heart valve insufficiency (aortic stenosis), myocardial aneurysm, ruptured papillary muscles, ventricle rupture, cardiac dysrrhythmias
stages of shock
CO and tissue perfusion is impaired leading to initation, compensated stage, progressive stage, irreversible or refractory stage
stage 1 of shock, initiation
sub-clinical hypoperfusion, no S and S
stage 2 of shock, compensated stage
activation of SNS, decreased blood flow to kidneys, activates RAA system, decreased hydrostatic pressure in the BV causes fluid to move from the interstitial space into the intravascular space, the vasoconstriction keeps the organs perfused
SNS activation
blood flow to heart and brain is maintained, increased heart rate and cardiac output
RAA system
aldosterone causes and increase in NA and water reabsorption
stage 3 of shock, progressive shock
compensatory mechanisms are failing, vasoconstriction is prolonged causing decreased tissue perfusion, tissue hypoxia/anaerobic metabolosm/lactic acid build up, this is the shock cycle
stage 4 of shock, irreversible or refractory stage
compensation is ineffective, cellular death and MODS occurs, pooling and slugging of blood in microcirculation leads to clots, acidosis leading to increased capillary permeability
increased capillary permeability
fluid moves into interstitial (BP drops more, third spacing), hypotension/decreased coronary blood flow/CP arrest and cerebral ischemia
CNS and shock
most sensitive to changes in the supply of O2 and nutrients
CNS S&S of shock
restlessness, agitation, anxiety, unresponsiveness
cardiovascular response to shock
BP is initially maintained do to SNS response of vasoconstriction and increased contractility, and BP decreases systolic pressure will lower first, will see narrow pulse pressure, as shock continues decreased diastolic press will occur
respiratory response to shock
acid base imbalance due to increased CO2, decreased pH, as shock continues-metabolic wastes accumulate and cause generalized muscle weakness leading to shallow breathing and poor gas exchange
respiratory S&S of shock
increased rate and depth following by shallow
renal response to shock
hypo perfusion of kidneys leads to RAA system being activated, aldosterone being released leads to increased sodium and fluid reabsorption, auto regulation attempts to maintain GFR, once systemic BP is too low auto regulation stops, GFR decreases, Renal ischemia starts, decreased blood flow leads to ATN, ARF
renal S&S of shock
pre renal failure r/t hypovolemia, decreased UO and concentrated urine, increased BUN but creatinine may be normal, may lead to ATN
GI response to shock
SNS stimulation decreases the blood flow to GI tract, may lead to ileum, decreased tissue integrity, increased permeability of vessels, GI flora passes into blood stream bacteremia can lead to septicemia, liver is hypo perfused and has decreased ability to detoxify blood
GI S&S of shock
decreased bowel sounds, dissension, nausea, constipation
Hematologic system response to shock
sluggish blood in small vessels causes thrombosis, excessive clotting activates the fibrinolytic system, lysis of newly formed clots, depletes clotting factors and blood looses the ability to clot, stable clot does not form and breakdown of existing clots can lead to hemorrhage
treatment of DIC
heparin and platelets
S&S of DIC
all forms of shock depress
macrophages which leads to a decreased ability to remove bacteria and endotoxins, a decreased ability to fight infection
endocrine systems response to shock (adrenal)
adrenal medulla-releases epinepherine and norepinepherine (SNS)
adrenal cortex-releases glucocoticoids and mineralcorticoids-aldosterone
endocrine systems response to shock (pituitary)
ADH released by posterior pituitary glad to retain water
integumentary system S&S of shock
pallor, cool moist skin
late:mottled or cyanotic
vasoactive substances
catecholamines, histamines, bradykinin, angiotensin
all forms of shock involve
decreased tissue perfusion
hypovolemic shock
initially urine osmolarity and specific gravity are increased, as shock continues the decrease
what I will see in hypovolemic shock
cool clammy skin, cyanotic, decreased urine output, decreased LOC, decreased LOC, decreased BP, increased HR
what I will see in cardiogenic shock
cool clammy skin, cyanotic, decreased urine output, decreased LOC, decreased LOC, EXTREMELY DECREASED BP, increased HR, JVD, chest pain
what I will see in anaphylactic shock
flushed warm skin, headache, dizziness, anxiety, disorientation, loss of consciousness, laryngeal adema, hoarse, dyspnea, stridor, bronchospasm, wheezing, decreased O2 sat, angioedema, hives
fecal/oral hepatitis spread
blood hepatits spread
hep vaccines
A, B, C (B will help), D (B)
no hep vaccine for
Viral hepatitis
cannot live without host cell
bacterial hepatitis
can survive on its own
passive immunity
giving antibodies (breastfeeding)
active immunity
direct exposure or vaccine
protein marker on cell surface, tells body whether its self or foreign
immunoglobulin produced in response to a foreign body. play role in immune system. will attach to foreign body to destroy it
fulminant hepatitis
severe impairment of liver cells, necrosis, leading to liver failure
functional unit of liver
gallbladder function
receives, stores, concentrates bile
liver function
production of bile, bile salts, detoxification and metabolism of drugs, metabolism of alcohol, change ammonia to urea, bilirubin elimination, filtration of blood and removal of bacteria and particulate matter
bile needed for
digestion of fat and absorption of fat soluble vitamins
why do diabetics become hYPOgylcemic when they drink, cannot deal with glucose
the liver is busy detoxifying the alcohol
liver controls clotting factors
prothrombin and fibrinogen, dependent on vitamin K
Liver stores
ADEK, B12, and blood
ammonia is very
toxic to the body, especially the brain
bilirubin elimination
breakdown of RBC's, hemoglobin broken down into heme and globin. heme is converted to bilirubin
unconjugated/indirect bilirubin
before it gets to the liver
direct/conjugated bilirubin
after it gets to the liver, in bile, liver, stool
bilirubin in the intestines converts to urobilinogen/stercobilinogen
gives pt its color
clay stool=
liver problem
S&S of liver problems
clay stool, pruritis (bile salts), flu-like symptoms, bleeding problems, jaundice
(not really liver disease), increased destruction of RBC's, liver can't handle it all, test will show UNCONJUGATED
reasons for increased RBC destruction (hemolysis)
autoimmune of transfusion hemolysis, sickle cell, septicemia, newborns, hemolytic anemia
intrahepatic jaundice
issue within the liver, liver disease. cirrhosis, hepatitis, cancer. blood test will show increased unconjugated or conjugated
posthepatic jaundice
obstructed outflow of bile from liver, blood test will show conjugated bilirubin
accumulation of fluid in the peritoneal space, sodium retention
portal hypertension
blockage of blood flow through the sinusoids to the hepatic veins and vena cava. causes increase in hydrostatic pressure in the portal venous system.
hepatic encephalopathy
r/t increased ammonia levels in the blood, mild confusion to deep coma, anxiety, euphoria, irritability, lack of coordination, factor hepaticus
fector hepaticus
sweet smelling breath
labs and tests for liver problems
viral antibodies for hepatitis, US, CT, Nuclear imagining, EDG, liver biopsy
preicteric phase
approx 2 weeks after exposure, GI issues, flu-like issues, rashes, itching, dark urine, light stool
icteric phase
5-10 days after initial symptoms, jaundiced skin, fever subsides, GI issues continue, hepatomegaly with tenderness. obstruction and inflammation of liver causes bile to be blocked from exiting liver
posticteric phase
4-6 months after initial symptoms, jaundice begins to subside, hepatomegaly continues, disappearance of jaundice does not mean fully recovered.
collaborative care for jaudice
interferon (boost immune system), ribavirin (antiviral), universal precautions
toxic hepatitis
liver injury or death following a toxic insult to the liver, drug induced, alcohol induced. eventually causes the build up of fatter acids (fatty liver)
treatment of idiopathic hepatitis
steroids and immunosuppressive drugs
cirrhosis-late clinical manifestations r/t dilation of BV
jaundice, palmar erythema, spider angioma, decreased body hair, itching, ecchymosis, edema, portal HTN, dysrhythmias, dyspna, esophageal varices, abd pain, anorexia, ascities, light colored stools, hepatic encephalopathy, asterixis, decreased clotting factors, thrombocytopenia, anemia, olgomenorrhea, testicular atrophy, gynecomastia, loss of libido
flapping of hands (neuro problems)
cirrhosis def.
irreversible, progressive deterioration of liver, can be slowed, altered structure and function, fibrosis
alcoholic cirrhosis
fatty liver, can be reversible if ETOH is stopped before fibrosis occurs
postnecrotic cirrhosis
following viral, toxic, or autoimmune hepatitis
biliary cirrhosis
following viral, toxic, or autoimmune hepatitis
biliary hepatitis
due to chronic biliary obstruction and infections
cardiac hepatitis
from long time right sided heart failure
portal HTN
5-10mmHG, bands of fibrotic/scar tissue blocks the sinusoids and blood flow, portal vein to hepatic vein
treatment of portal HTN
TIPS (transjugular intrahepatic portosystemic shunt) stent places btw the high pressure portal vein and the low pressure hepatic vein, shunts some blood away from the portal system
esophageal varices
due to portal HTN, weakened/dilated veins in the esophagus due to backed up pressure from the portal vein, vary susceptible to bleeding, medical emergency
care for esophageal varices
sandostatin-IV med to promote vasoconstriction to reduce bleeding and portal HTN.
banding-variceal ligation-tiny rubber bands around varices
sclerosis-via EGD, injecting varicose with agent that causes vasoconstriction and sclerosing.
beta blockers
sengstaken-blakemore tube or minnesota tube-short term, applies pressure to stop bleeding
hepatic encephalopathy
brain problem r/t increased ammonia levels.
changes in LOC
treatment for high acid levels
lactulose, neomycin, oxazepam
nutrition therapy for cirrhosis
no protein during acute episodes
hepatorenal syndrome
pre renal failure due to liver problems. decreased GFR, ascites, edema
accumulation of fluid in the peritoneal space. low protein in the blood vasculature, meds: aldactone, lasix, albumin.
treatment: paracentesis, TIPS
nutrition: sodium restriction, fluid restriction
acute hepatic failure (fulminant)
medical emergency, severe, acute liver failure.
necrosis and loss of function, many systems involved, treatment is liver transplant
cause of acute hepatic failure
infections, drugs, toxins, hypo perfusion, GI surgeries, may be seen with or without previous problems
Portal HTN
r/t hydostatic pressure and fluid leakage. TIPS shunt
liver problems can lead to
clotting problems
worse case of liver failure
cirrhosis prognosis
can stop progression, can not cure
end stage liver disease effects
all systems
functional unit of lung
alveolar capillary membrane
where issues with gas exchange occur
pulmonary edema
oncotic/ostomic pressure (particles), hydostatic pressure (water), excess fluid in alveoli and further up, pink, frothy sputum.
3 main causes of pulmonary edema
issues with lymphatic system,issues with heart, injury to ac membrane
S & S of pulmonary edema
crackles, dyspnea, tachy, PND, aggitation, frothy pink sputum
VQ mismatch
vent, perfusion-same amount of air and blood should get to A/C membrane=match
increased vent, decreased perf
problem with blood flow (PE, vasculitis)
decreased vent, increased perf
problem with air. COPD, any airway blockage, asthma, mucus plug, bronchospasm, pulmonary edema
pulmonary embolism
pulmonary artery blockage, S&S: sudden onset chest pain, chest petichae, SOB, hemoptysis, tachycardia, tachypnea. Main cause: DVT
tx: heparin
dx: ddimer, spire cat scan
pulmonary HTN
primary: unknown
secondary to LV issues and others
tx: lung transplant
dx: ECHO, R sided heart cath, chest x-ray
anticoagulant won't help
acute respiratory failure
hypoxic-PaO2 less than 60 on 60% O2refractory
not responding
elevated CO2, acidemia (pH less than 7.35) acidosis
decreased O2
tx: O2 ventimask (60%), non-rebreather (100%), ventilator, CPAP
sudden progressive refractory to O2
glomular level
where filtration takes place in kidney
90-120 ml/min = normal
renal tubules
where urine is made
back into blood stream
from blood to tubules
auto regulation
ability of blood flow through glomerulous to stay normal regardless of body's big picture, maintain homeostasis
osmotic diuretic
used for ICP, neuro issues. mantel used to block reabsorption, takes H2O with it
loop diuretic
lasix, HCTZ. Aldosterone antagonist-potassium sparing (hyperkalemia is a risk)
kidneys and fluid balance
kidneys regulate fluid and electrolyte
nurses role with kidney issues
I&O, daily weight, assess edema, labs (BUN), osmolality, H&H
renal calculi
obstruction, back flow-->pressure-->kidney damage
S&S of renal calculi
hematuria, pain, N/V
treatment of renal calculi
treat symptoms, hydrate, pain control, surgery
nephrotic syndrome
leaky glomeruli d/t increased permeability, massive edema, protinuria, decreased BP, hypovolemic
cloudy, foul smelling urine, fever, pain, UTI symptoms, flu-like symptoms
dx:C&S and repeat after treatment
acute renal failure
common post hospital stay, decreased blood to kidney. pre=decreased blood flow to kidney.
intra-direct damage to kidney, acute tubular necrosis (ATN)
post-beyond kidney, renal calculi, tumor, BPH
causes of acute tubular necrosis
gentamycin, NSAIDS, prolonged pre renal failure
stages of renal failure
not progressive, staged according to location
chronic renal failure effects
all systems
direct injury to the lungs
aspiration, near growing, toxic inhalation, pulmonary contusion, pneumonia, oxygen toxicity, transthoracic radiation
indirect injury to the lungs
sepsis, nonthoracic trauma, hypertransfusion, cardiopulmonary bypass, severe pancreatitis, embolism, DIC, shock
risk factors for DVT
Virchow's Triad:
venous stasis, hypercoagulability, damage to vessel wall
SBP and kidney autoregulation
SBP has to be between 80-180
normal GFR
normal excretion rate
kidney function
elimination of waste (urea and creatinine), BP regulation (fluid balance, renin-angiotensis-aldosterone system), erythrocyte production, vitamin D activation, prostaglandin synthesis, uric acid elimination, drug elimination, acid-base balance, fluid/electrolyte balance
most common electrolyte imbalance
potassium, will have hyperkalemia.
diet restriction and kayexalate
inability of the tubules to reabsorb the sodium
magnesium issues
hyper, problem with filtration and excretion.
avoid meds like maalox, MOM, mylanta
metabolic acidosis
d/t kidneys ability to excrete acid
given subQ to help with anemia
reduces potassium, gives pt diarrhea
potassium imbalance
give kayexalate (enema or oral) and insulin/Hco3 IV push
pH of urine
risk factors of urinary calculi
immobility, dehydration, Hx, UTI's, catheter
urinary calculi prevention
inhibit with (magnesium, citrate), hydration, dietary modifications, allopurinol, thiazide diuretics, ATB
nephrotic syndrome
leaky glomerulus. result of increased glomerular permeability, caused by glomerulonephritis, immune response, infective response, inflammatory response
manifestations of nephrotic syndrome
hypoalbumineamia, proteinuria, massive edema, hypovolemia
treatment of nephrotic syndrome
fluid electrolyte balance, reduce inflammation via steroids, try to decrease protein loss
acute pyelonephritis patho
bacterial infection (e. coli), small abscesses form on surface of kidney, repeated infections
S&S of pyelonephritis
flu like, flank pain, CVA tenderness, hematuria, pyuria, foul smelling urine
diagnosis of pyelonephritis
U/A, urine C&S, IVP, US, CT scan, WBC, blood cultures
treatment of pyelonephritis
antibiotics, increased fluid intake, follow up urine culture, symptom control
acute renal failure
manifestation of ARF
abrupt decline in GFR, loss of kidney function, can't excrete wastes and water, BUN elevation, creatinine elevation
sudden rise in BUN and creatinine
<100ml/24 hrs
excessive amount of urine in 24 hrs
100-400ml/24 hours
prerenal failure
happening before the blood gets to the kidneys
reasons for pre renal failure
impaired renal blood flow, happens during big, bad surgeries
intrarenal failure
happening within the renal tissue, damage to kidney cells
acute tubular necrosis, cause of 75% of intrarenal ARF
cause of ATN
prolonged pre renal failure, toxins, meds, NSAIDS, aminoglycosides, contrast materials, systemic diseases
peak too high
dose too high
trough too high
med given too often
post renal failure
problem happening beyond the kidney structure, caused by obstructions
ATN phases
oliguric phase, diuretic phase, diuretic phase, recovery phase
oliguric phase
10-14 days, decreased GFR
diuretic phase
1-3 weeks, unstable period, decreased tubular function, osmotic diuresis
osmotic diuresis
increased urea and creatinine in the tubules, not able to concentrate urine, low BP, low fluid volume,
recovery phase
total recovery, GFR returns to normal, BUN and creatinine begin to stabilize
chronic kidney disease
progressive reduction of functioning nephrons, irreversible, destroyed nephrons replaced by scar tissue, results in uremia (elevated BUN and creatinine), K/DOQI
patho of CRD and CKD
deterioration of nephrons, GFR falls, BUN/creatinine raises, remaining nephrons hypertrophy, inability to concentrate urine
reduced renal reserve
GFR 50% of normal, no S&S yet, still normal kidney function
renal insufficiency
GFR 20-50% of normal, mild azotemia, polyuria and nocturia
renal failure
GFR 20-30% of normal, cannot regulate volume or solute composition, severe azotemia, anemia, lyte imbalances, acidosis, edema
GFR <5%
kidneys can no longer maintain homeostasis, total system manifestations, if left untreated will die, fluid/electrolyte imbalances, cardiac arrhymias, pulmonary edema, cerebral edema, need dialysis or transplant
erythropoietin function
stimulate bone marrow production of RBC
water and fluid removal across a pressure gradient
dialyzer (artificial kidney) designed to provide controllable transfer of solutes and water across a semi permeable membrane
acute indications for dialysis
ARF refractory to treatment, hyperkalemia with ARF, fluid overload not responding to diuretics, drug overdoses, metabolic acidosis
chronic indications for dialysis
CRF, ESRD with low GFR, severe azotemia
subclavian or femoral vein vascular access
short term, ARF, dual lumen, waiting for fistula or graft to mature
palpate thrill and auscultate briut
check for patency
done 3x/wk
dysrhymias, infection, dialysis disequalibrium, hypotension, anemia
dialysis disequalibrium
cerebral edema due to rapid removal of solutes of blood (confusion, h/a, seizures)
palpation of kidney
normally not palpable
most reliable test of kidney function
creatinine 0.5-1.5mg/dl, creatinine clearance test + serum creatine
come from breakdown of muscle
ph of urine
6 range 4.5-8
specific gravity of urine
protein in urine
should not be there, sign of renal disease
sediment in urine
should not be there
leukocytes in urine
sign of infection
secreted by posterior pituitary gland, controls extracellular fluid, acts of distal convoluted tubules to reabsorb water
in the heart dilates these to enzymes are produced, the relax vascular smooth muscle and promote NaCl and water excretion by the kidneys, also activated during high BP
used for neuro reasons, increased ICP, increased intraocular pressure
COPD'er will have
acidemia as a norm
ventilation and perfusion-normal
equal amounts of air and blood reach lungs
oxygen failure
carbon dioxide retention
oncotic/osmotic pressure in the capillaries
pulls fluid back into the capillaries
hydrostatic pressure in the interstitial space
opposes or prevents movement out of the capillary
three main causes of pulmonary edema
heart problems, injury to the capillary, blockage of lymphatic vessels
diagnostic tests for pulmonary edema
CXR (white out), PA value (swan ganz catheter) (normal is 18 mmHg), O2 sat as low as 85%
other causes of pulmonary edema
heart failure, over hydration, decreased albumin in blood, trauma to lung tissue, sepsis, infection, cancer
manifestations of pulmonary edema
change in LOC, elevated RR, elevated HR, cool, clammy, pale, frothy pink sputum, cough, crackles, dyspnea, chest pain, hemoptysis
care in pulmonary edema
high flow mask, CPAP, Vent, reduce preload, reduce afterload
reduce preload
sit up, dangle, diuretics, nitrates, morphine
reduce afterload
calcium channel blocker, antihypertensives, morphine, NTG
support perfusion in pulmonary edema
+ inotropes (dobutamine, digitalize)
figure out what caused problem
V/Q scan
gold standard, will show perfusion and normal ventilation
sudden onset SOB, chest pain, feeling of doom, dyspnea, pleuritic pain, tachycardia, leg swelling, pain, tachypnea, crackles, cough
tests for PE
spiral CT, pulmonary angiography
prevention of PE
prophaylactic anticoagulants, SCD's, ROM or ambulation, assess for DVT
treatment for DVT
oxygen, + inotropes, lower BP, anticoagulation therapy, fibrirolytic therapy, surgery
pulmonary hypertension
increased pressure in the pulmonary arteries, no cure, primary and secondary
primary pulmonary hypertension
rare but more common in women 20-40 years old
secondary pulmonary hypertension-post capillary
distal to the pulmonary capillaries
causes of post capillary HTN
LV failure, mitral stenosis, occlusion of pulmonary vein, septal defect
secondary pulmonary hypertension-pre capillary
problems within the capillaries or alveoli
causes of pre capillary HTN
COPD, stiffness of pulmonary vasculature, pulmonary fibrosis,
diagnostic tests for pulmonary HTN
CXR, doppler echocardiography, right sided heart cath,
MAP in pulmonary HTN
>25mmHg at rest and >30mmHg with exercise
normal MAP
12-16 mmHg
manifestations of primary pulmonary HTN
syncope, dyspnea, fatigue, chest pain, hemoptysis
manifestations of secondary pulmonary HTN
looks like underlying problem but more exaggerated
cor pulmonale
right ventricular hypertrophy leading to RV failure-problem with pulmonary artery
care for pulmonary HTN
double lung transplant, supportive measures
acute respiratory failure
S&S of ARF
tachypnea, deep respirations (acidosis), use of accessory muscles, dysrhymias, confusion, restlessness
correction of acidosis
hyperventilate, bicarb
pulmonary outcome of MODS, non cardiac pulmonary edema, disruption of ac membrane, injury to pulmonary vasculature and or airways, acute, sudden, progressive, refractory to O2, three phases
Acute Respiratory distress syndrome
direct injury to lung, indirect r/t other problems in body, sepsis, aspiration, pneumonia, trauma
exudative phase of ARDS
within 24 hours of initial insult, pt develops pulmonary edema
proliferative phase of ARDS
7-10 days after initial insult, hypoxemia worsens leading to V/Q mismatch, atelectasis, pulmonary hypertension, RV dysfunction, decreased kung compliance
fibrotic phase of ARDS
2-3 weeks after initial insult, pulmonary fibrosis, enlarged alveoli, recovery, lung function returns
diagnosing ARDS
risk factor assessment, ABG's, CXR, "stiff" lung
signs and symptoms of ARDS
crackles, very low PaO2, respiratory distress, tachypnea, tachycardia, dyspnea, restlessness
sub q emphysema
air in tissue
bringing air to the lungs
blood flow to the lungs, actual gas exchange from blood and the AC membrane
bronchi R
shorter and wider, more vertical, more likely to go to the R side for aspiration and intubation
parietal layer of lung
serous membrane that lines the cavity, closest to the chest wall
visceral layer of lung
lining that adheres to and surrounds the lung tissue
pleural cavity
space btw the 2 layers that contains small amount of serous fluid (10-20ml)
peripheral gas exchange
btw blood and cells at tissue/organ level (internal respirations)
perfusion (breathing)
gas exchange at the ac membrane
control of breathing
brain, lung receptors, chemoreceptors
pons/medulla, controls rate and rhythm
lung receptors/breathing
changes in the walls of the airway
located in the carotid arteries and aorta
SA node BPM
60-100 bpm, located in the RA near SVC
AV node BPM
40-60 bmp, in RA behind tricuspid valve
bottom number, resting, ventricles idling, atrium emptying, tricuspid and mitral are open, passive, after lub dub, mitral stenosis, aortic regurg
contracting, ventricles ejecting blood blood to PA or aorta, pulmonic and aortic are open, active, in btw lub and dub. Btw S1 and S2. mitral valve regurg, mitral valve prolapse, aortic stenosis
cardiac cycle
valves open and close
When R Atrium contracts
tricuspid is open and pulmonic is closed
when R ventricle contracts
tricuspid is closed and pulmonic is open
valves on R side
tricuspid and pulmonic
valves on L side
mitral and aortic
when L atrium contracts
mitral is open and aortic is closed
when L ventricle contracts
mitral is closed and aortic is open
lub-dub is
valves opening and closing
lub, closure of mitral and tricuspid valves, start of systole-blood is ejected from ventricles
dub, closure of pulmonic and aortic valves, start of diastole, filling of blood from atria to ventricles
vibrations in the chambers, ventricular gallop, early diastole=heart failure or valve regurg, too much fluid, new heart failure, no compliance
atrial gallop-common in new MI, late diastole, atrial kick, shows resistance to active ventricular filling
pericardial friction rub
inflammation around heart, if pt holds breath and rub stops it is a pleural rub
cardiac enzymes
CK (muscle enzyme), CKMB (cardiac muscle), CKMM (skeletal muscle), CKBB (brain), Troponin (most reliable, specific to heart), Myoglobin (elevates if muscle damage, short half life, non-specific)
other labs in ACS
CBC, Coag, BG, BPM, CMP, Electrolytes, Chest xray
decreased hemoglobin can cause
chest pain r/t decreased o2 to heart
cardiac cath
look for blockage in coronary arteries
R cardiac cath
dx: pulmonary htn, r sided failure, usually through antecubital vein
L cardiac cath
most common, thru femoral or brachial artery
narrowing of cardiac artery r/t stress
stable angina
goes away with rest
unstable angina
pain does not go away
myocardial ischemia
decreased blood and O2. not enough to meet metabolic demands of heart muscle. Causes chest pain
reasons for decreased O2 supply
anemia, hypovolemia, shock, hypotension, increased resistance in coronary vessels, tachycardia
reasons for increased demand
HTN, heavy meals, thickened myocardium, tachycardia
life threatening, formation of localized necrotic areas w/n myocardium, cardiac cells can handle decreased O2 for 20 min (signs seen in 8-10 seconds), decreased O2 converts to anaerobic metabolism increases lactic acid. Acidosis=dysrhythmias
Q wave
>1mm (1 box wide), pathological, transmural MI, tissue death gone completely through myocardium
more severe myocardial injury
Non Q wave MI
Q wave < 1 mm wide, non-stemi
dyspnea during MI
N/V during MI
pain, decreased o2 to brain, Decreased blood to gut
fever during MI
inflammatory response, elevated WBC
sympathetic nervous system
dilated pupils, elevated BP, elevated RR, elevated HR
diagnostics for ACS
12 lead EKG, cardiac enzymes, cardiac cath w/n 90 min
treatment for ACS
salvage the myocardium, increase 02 supply, decrease O2 demand, decrease preload, decrease after load, increase contractility
fibrolinyic therapy
dissolve thrombus, reprofuse the myocardium, given IV within 6 hours of onset of symptoms, must have EKG and enzymes drawn to confirm dx
no fibrinolytics for
recent surgery or trauma, hemorrhagic stroke, pregnant, bleeding disorders, active bleeding, severe chronic illness
heparin given to
prevent future clots
starting fibrinolytic therapy
3 large bore IV's, rectal exam, baseline coag panels
monitoring fibrinolytic therapy
decreased chest pain, return of EKG to normal, repercussion dysrhymias, CKMB's return to normal
Signs of bleeding r/t fibrinolytics
decreased BP, increased HR, changing LOC, oozing from IV, oozing into foley
shaving away plaque
laser angioplasty
vaporizes plaque into particles
improve O2 supply
give O2, chew 325mg aspirin, heparin protocols, PTT (therapeutic range is 2.0-2.5X reference range)
decreased myocardial O2 demand
bedrest, beta blockers (decrease HR, decrease contractility, Decrease BP=decrease pain) soft diet, manage pain (morphine decreased preload and afterload), manage anxiety, stool softener
amount of blood returning to heart
decrease preload
morphine increases vasodilation, NTG (decreased BP causes HA), diuretics
force heart works against
decrease afterload
morphine, NTG, calcium channel blockers, ACE inhibitors
increase contractility
+ inotrope, use with caution, increases contractility but also increases workload
leading cause of death s/p MI
effects contractility
+ inotrope
increases contractility, calcium, digoxin, Epi, dopamine, dobutamine
- inotrope
decreases contractility, beta blockers, diltiazem, verapamil
effects rate
- chronotrope
decreases HR, digoxin, verapamil, beta blockers
+ chronotrope
increases HR, atropine, Epi, dopamine, dobutamine
Epi + inotrope
increases coronary perfusion, increases SVR, vasoconstricts (shunts blood to heart and brain), increases strength of contraction *can exacerbate myocardial ischemia and ventricular ectopy d/t demand on heart
atropine + chronotrope
for symptomatic bradycardia, increases action of parasympathetic NS
antidysrhythmic, decreases ventricular dysrhythmias
antidysrhythmic, decreases cardiac excitability
calcium channel blocker, decreases AV nodal contraction, A flutter/fib, SVT's, angina, HTN, *decrease HR and BP
SVT, *can stop activity for 2-6 seconds, pt will flat line
decrease O2 demand, decrease HR and BP
mag sulfate
decreased may cause VF, may decrease risk of arrest post MI, used for hypomagnesemia, torsades
V Fib
sodium bicarb
incompatible with many meds, metabolic acidosis
a fib/flutter, CHF, normal dig levels 0.5-2
used for a fib, tachyarrhymias or VT with pulse
pulsesless VT or VF
automatic implantable cardioverter-defibrillator, electrodes sense rhythm will shock (cardiovert or defib) if needed
stimulation of myocardium to induce ventricular contraction
external pacemaker
electrical activity delivered through chest wall-external source. Emergency, symptomatic bradycardia, blocks
temporary pacemaker
used after open heart surgery or while waiting on permanent pacer, external generator
permanent pacemaker
symptomatic brady, H. failure with conduction problems, documented asystole
aplastic anemia
decreased RBC's, Decreased WBC's, decreased platelets, decreased tissue perfusion
labs for aplastic anemia
CBC's, H & H, platelets, bone marrow biopsy
meds for aplastic anemia
epotein, neupogen, transfusions, bone marrow transplant
valve cannot close completely, creates back flow of blood
valve cannot open completely, inhibits blood flow forward
auscultatory and possibly placatory assessment made when there is a valve disorder, mitral and aortic valve=most common
assessment of murmurs
problem with valves, harsh blowing sounds, lack of quiet, turbulent blood flow
how to document murmurs
timing, location, how loud is it
murmur I
barley audible in quiet room
murmur II
quiet, but clearly audible
murmur III
moderately loud
murmur IV
loud with thrill
murmur V
very loud, thrill easily palpated,
murmur VI
very loud, thrill palpable and visible
mitral valve stenosis
LA>LV, mitral valve does not open properly, caused by decreased blood flow to LV, causes atrial hypertrophy and pulmonary HTN
mitral valve regurg
blood flows backward in LA, valve does not close properly, regurg during systole, LA diction and hypertrophy, pulmonary congestion, RV failure, LV dilation and hypertrophy
mitral valve prolapse
valve prolapses back to LA, leaflets of valve are compromised, same consequences as M. regurg
aortic stenosis
valve does not open properly, blood cannot move out of LV, blood accumulates in LV, blood does not fully empty from LA, decreased CO, increased blood in LV, incomplete emptying of LA
aortic regurg
valve not closing properly, usually caused from rheumatic fever, blood back flows into LV, LV dilation and hypertrophy
primary unknown, secondary-post viral, alcohol, drug abuse
types of CMP
dilated, hypertrophic, restrictive, debilitating leading to CHF or cardiomegaly
dilated CMP
cardiomegaly with ventricular dilation, impaired systolic function, atrial enlargement, stasis of blood in LV, often follows infectious myocarditis
hypertrophic CMP
treatment of CMP
heart transplant
infective endocarditis
lining of heart, also heart valves, damaged endothelial surface, organisms enter blood stream during surgery or dental work. valves become vegetative, clumps break off, can cause embolization, clumps travel-MI, stroke, PE, valve failure, treated with ATB
outer layer of heart, S/P MI or virus, body responds with inflammatory process, deposits more exudate, causes effusion. s&s: chest pain, pericardial friction rub, fever. Increased risk post MI. Dx: echo tx: nsaids
cardiac tamponade
VERY rapid accumulation of fluid, blood, pus. narrowing of pulse pressure, decreased CO, muffled heart sounds.
normal pulse pressure
pulsus paradoxus
aerial line, decrease in BP with inspiration >10mmHg, JVD distention, SOB, increase in BP
inflammation of actual heart muscle. Causes: myocardial biopsy. S&S: none->failure, cardiomyopathy, dysrhythmias, sudden death
ST elevation
>2mm (two boxes) wide
one small box
= 1mm
Dressler's syndrome
secondary form of pericarditis that occurs in the setting of injury to the heart or the pericardium. triad of features, fever, pleuritic pain and pericardial effusion.
(postmyocardial infarction syndrome)
deterioration in heart muscle
very low metabolic rate, manifestation of hypothyroidism
core temp less than 35
accidental hypothermia
unintentional, prolonged exposure to cold environment, inadequate protective clothing, sudden immersion in cold water, medical conditions (hypothyroidism, adrenal insufficiency, sepsis, alcohol abuse), medications
therapeutic hypothermia
induced during surgeries to slow metabolism, post cardiac arrest to improve neurologic outcomes
mild hypothermia
moderate hypothermia
severe hypothermia
less than 30
S & S of mild hypothermia
confusion, slurred speech, impaired judgement, amnesia, tachycardia, increased cardiac output, SVR, tachypnea, bronchorrhea, increased shivering, increased metabolic rate, hyperglycemia, hematocrit begins to increase, decreased platelet and WBC
moderate hypothermia
lethargy, hallucinations, progressive bradycardia, decreased cardiac output, hypotension, dysrhythmias, hypoventilation, decreased oxygen consumption and CO2, production, loss of cough reflex, cold diuresis, decreased shivering (below 32), muscle rigidity, continued hyperglycemia, coagulopahties, DIC
severe hypothermia
loss of cerebrovascular regulation, decreased EEG activity, coma, hypotension, v. defib., systole, pulmonary edema, apnea, decreased renal perfusion, oliguria, pseudo-rigor mortis, may appear dead, decreased metabolic rate
passive external rewarming
remove wet clothing, cover with blankets, room temp 75
active rewarming
warm blankets, heating pads, heat lamps, warm bath, formed warm air, warm trunk first, IV administration of warm fluids (40-42), warm humidified O2, irrigation of body cavities with warm fluid, cardiopulmonary bypass, hemodialysis
acute freezing resulting in cellular death.
1st degree frostbite
superficial-skin color ranges from pale to bluish/white. Numbness, tingling, burning
2nd degree frostbite
partial thickness, skin frozen and feels hard. Blister formation, edema, hyperemia
3rd degree frostbite
full thickness, hemorrhagic blisters, tissue necrosis
4th degree frostbite
deep injury, skin white, hard, numb. involvement of bone, muscle, tendon. Severe necrosis leads to gangrene.
management of hypothermia
remove clothes and jewelry, handle tissue carefully, do not rub or squeeze, rewarm body part in warm water, rewarming may be painful, elevate after warm, deride blisters and cover with sterile dressings
v fib
no pulse
big box
5X5 little boxes = 0.20 seconds
little box
0.04 seconds
6 seconds=
30 large blocks
what to give with new onset chest pain
morphine, O2, Nitro, aspirin
P wave
atrial depolarization
ventricular depolarization
T wave
ventricular repolarization
P wave
atrial depolarization
P-R interval
.12-.20 seconds
P-R interval is
time it takes electrical activity to go from SA node to AV node, start of the P to start of the R
QRS interval is
0.04-.12, start of the Q to end of the S
T wave
no measurement
ST segment
no measurement, from S to T
acute ischemia
if up or down 2 boxes on ST segment
QT interval
.36-.44, if prolonged places pt at risk for torsades. start of Q to end of T.
R to R
pt heart rate
rhythms originated in SA node
Sinus tachy
document changes with EKG, administer meds, watched for decreased coronary perfusion
sinus brady
atropine, treat underlying problem, pacemaker, watch symptoms
a flutter
meds, cardioversion,
saw tooth appearance
a fib
increases stroke risk, long term anticoagulation, cardioversion, meds
agonal rhythm
cannot defib
acute MI actions
salvage the myocardium, improve myocardial O2 supply, decrease myocardial O2 demand, decrease preload, decrease after load, increase contractility
distributive (neurogenic) shock is the only shock in which
the heart rate drops
distributive shock
decreased HR and BP, loss of SNS stimulation because of spinal cord injury above T6
early: massive vasodilation, skin warm, dry, flushed, "warm shock", late: "cold shock", skin pale, cold, clammy, mottled, ARDS
care for shock
ID and treat underlying cause, give O2, vent, histamine and H2 receptor antagonists, proton pump inhibitors, early feeding, TPN if needed
NG for feeding
used if needed for <30 days, PEG otherwise
care for hypovolemic shock
restore fluid, IV access, fluid challenge, continuous maintenance fluid
Fluid challenge
assess pt response to fluid administration, large amount fast
LR and NS, isotonic, restores fluid in intravascular space
shift fluid from interstitial to intravascular space, used for burns, NOT for anaphylaxis and sepsis
goal of care in cardiogenic shock
increase O2 to myocardium, max cardiac output, decrease LV workload, reverse hypoxemia and acidosis, bicarb
dysrhythmia management
meds (lidocaine) or cardioversion
systemic inflammatory response syndrome, microorganism invades host and inflammatory process is initiated, inflammatory cykokines are released from WBC's, this causes widespread inflammation
septic shock can lead to
SIRS can lead to
MODS, progressive dysfunction of two or more organ systems, result of uncontrolled inflammatory response to severe illness or injury, most common after sepsis
treatment of MODS
treat infection, clean necrotic wounds, pulmonary care, enteral feed, intubate, control fever, decrease O2 demand, dialysis, fluids, + inotropes
three things that contribute to adequate tissue perfusion
heart, cascular tone, blood volume
works independently from rest of circulation
arterial baroreceptors
senses the volume of the circulatory system, if low the SNS causes vasoconstriction (release of epi and norepi), leads to increased CO
atrial receptor
senses fluid volume returning to the right atrium, if it's low it stimulates the SNS to constrict vessels not vital to life.
first line again shock (vasoconstrictor)
juxtaglomerular receptors
in kidneys, active RAA mechanism
normal pH
PCO2 (acid)
HC3O (base)
pt in acidois
depressive effect, lethargic, confused, V fib, asystole, hypercalcemia, hyperkalemia
pt in alkalosis
excitatory effect, restless, paresthesia, thetany, convulsions, tachycardia, arrhythmias, hypocalcemia, hypokalemia
O2 sat is
percent to which the capacity of hemoglobin present in the blood to carry O2 is being used
relaxation or diastole
contraction or systole
electrolytes most important to heart function
K+, Na+, Ca+
inside of cell
way more K+ ions
outside of cell
way more Na+ ions
initiation of electrical activity
can cardiac cell, SA node is target
big box =
5x5=0.20 seconds
little box =
0.04 seconds
calculate heart rate
6 second count, regular rhythm, count number of complexes btw 6 hash marks on EKG paper OR count out 6 seconds 5 large boxes=1 second
P wave
rounded, before QRS, atrial depolarization
tallest part of tracing, ventricular depolarization
Q wave
first downward deflection
R wave
upward deflection above baseline
S wave
negative deflection AFTER R wave
T wave
ventricular repolarization
junctional rhythm
slow, regular, no P wave
v tach,v fib
lethal rhythms
zapping heart to stop activity to reset SA node, used for V tach with a pulse, SYNC mode
no pulse, defibrillate
v fib or pulseless v tach
agonal rhythm
worst case senario
pleural space
btw outside of lung and pleura
water seal for chest tube
prevents atmospheric air from entering pt
bubbles are
BAD in a chest tube (unless there in pneumothorax)
tidaling in chest tube
more movement=more collapsed lung, if on wall suction there is a lot of movement
dissolved CO2 in plasma
low HCO3
met. acidosis
high HCO3
met. alkolosis
Low CO2
resp. alkalosis
High CO2
resp. acidosis
low pH
high pH
dissolved 02 in plasma
outer layer, protection
parietal layer
closest to chest
visceral layer
closest to heart
layer btw
fluid filled space, lubrication, 15-60ml
muscular, middle layer, functional layer
inner layer, closest to heart, lines heart and blood vessels
R side of heart
aorta, tricuspid
L side of heart
pulmonic, mitral
right atrium
receives unoxygenated blood from body
right ventricle
pumps unoxygenated blood to lungs
left atrium
receives oxygenated blood from lungs
left ventricle
pumps oxygenated blood to body
btw R atria and R ventricle
btw R ventricle and pulmonary artery
btw L atria and L ventricle
btw L ventricle and aorta
superior and inferior vena cava
brings unoxygenated blood from body to heart, enters R atrium
pulmonary artery
leaves R ventricle takes blood to lung, only artery that receives unoxygenated blood
pulmonary capillaries
exchange oxygen and carbon dioxide
pulmonary veins
deliver oxygenated blood to left atrium, 2 from each lung
exits left ventricle bringing oxygenated blood to body
coronary circulation
first arteries off of aorta, how heart receives O2, fill during diastole, RCA, LCA, LCA dives into LAD (left anterior descending and circumflex)
coronary artery blockage
L anterior descending blockage
CHF, Edema, sudden death
Circumflex blockage
resting, ventricles filling, atrium emptying
look same, just early
look weird and wacky