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297 Cards in this Set

  • Front
  • Back
7 dimensions of an illness
PQQRSST: Place, Quality, Quanitity, Regulating/aggrevating factors, Setting, Symptoms, Timing
4 aspects of physical assessment
Inspect, Palpate, Percuss, Ascultate
Patient Goals should be:
Ojective, Measurable, Demonstrable, Realistic, Agreeable, Patient-Centered
Steps to the Nursing Process
ADPIE: Assess, Diagnose/Analyze, Plan, Intervention, Evaluation
"Nursing is...doing for the patient what they would do if they had the knowledge, strength, ability...and helping them not to need your care anymore"
VA Henderson
"nursing is...giving pt whatever they need for their needs to be met...client-centered care, not disease-centered"
Ida Jean Orlando
"Nursing is...the diagnosis and treatment of human responses to actual or potential health problems...combine the art of caring with the science of health care"
ANA
"nursing is...diagnosing human responses to actual or potential health problems, under direction of physician..."
CT Nursing Practice Act
Chief Complaint (cc)
"in quotes in the words of the pt"
9 Human Response Patterns
Communicating, Valuing (spiritual), Relating, Knowing, Feeling, Moving, Perceiving, Choosing, Exchanging
Normal Temp
97-99 F = 37 C
Normal Pulse
60-100
Normal Respiration Rate
12-20 (24 in hospital setting)
Normal BP
120/80 (130/75 for diabetics)
Normal SAO2 (oxygen saturation)
95-100, <90% is hypoxemia
Normal USG
1.002 - 1.028 (high in dehydration, high ADH) (low with DI, low ADH, glomerulosnephritis and pyelonephritis = damage to kidney's tobules and kidney can't absorb water, Renal failure = fixed USG of 1.010)
surgical diuresis
increased urine volume a few days after surgery. In first few days, be aware of fluid retention and avoid FVE
brain surgery and fluid volume
post-surgery = no ADH, so get DI, so NEED urine retention drugs
1oz = x cc
30 cc = 1 oz
molecules
electrically neutral
1 liter = x cc
1000cc = 1 liter
edema is x cc of extra water
edema is 2500cc of extra water
1 lb = x cc
500cc = 1 lb
IVF = x L water
3.5-6
Equation for Cardiac Output
HR x SV = CO
Signs of shock
HR up, Resp Rate up, BP down
sequence of blood flow
heart -> arteries -> arterioles -> capillaries -> venules -> veins -> heart
Capillary action
diffusion of oxygen and nutrients from blood into tissues and diffusion of waste products of metabolism from tissues into blood
4 words to describe fluid of wound
serous, sanguinous, sero-sanguinous, purulent
Normal albumin in blood
3.5-5
Preload
how much blood returns to heart (measured in jugular vein)
CVP
central venous pressure = measurement of R ventricular preload
colloid osmotic pressure
pull of albumin on water and other molecules into the space where colloids are located
Normal serum osmolality
300 (when high, will be THIRSTY)
Liver failure and albumin
can't metabolize albumin, so will have VERY low levels, low venous colloid osmotic pressure, low albumin (high fatality rate)
Heart Failure and fluid
FVE (fluid backs up in system)
IVs for Shock
ALWAYS hypertonic: need to get volume into blood
Measuring Edema
<1/4"=1+, 1/4"-1/2"=2+, 1/2"-3/4"=3+, 3/4"-1"=4+
Formula for Mean Arterial Pressure (MAP)
sBP + 2(dBP)/3
Renin-Angio-Ald System (RAAS) effects on HEART
angio I and II = vasoconstriction; ald = NA and H2O resabsorption
SNS response to heart failure and volume loss
decrease in SV stimulated baroreceptors, incr SNS stim -> incr. HR and force of contraction -> peripheral vasoconstriction -> shunts blood to heart and brain -> incr. venous return
ADH
osmo of IVF high -> ADH secretion -> reabsorbs H20 in kidney tubules -> sm amt of urine with high USG
ANP
when BV or BP incr -> stretches atria -> releases ANP -> incr. vasodilation -> lowers BP, BV, and preload/afterload. ALSO release of ANP -> decr. ADH -> decr. BV, decr. BP, decr. preload/afterload. ALSO release of ANP -> incr. filt rate in kidney -> urine excretion -> decr. BV, BP, preload/afterload
Normal daily Urinary output
1,500cc/day
Calculated Insensible daily loss
1,000cc/day
ADH and stress
increase ADH output, decrease urine output
daily baseline fluid requirement
30cc/kg/day (25 for obese and elderly)
5% albumin solution
Isotonic
Dextran
albumin/blood replacement drug: for every 1cc, pulls 2cc H2O back into blood stream from ICF (great post surgery)
TPN
must be administered via central line (risks of emboli and lung collapse, hyperglycemia, infection)
TPN bag goes dry...
...replace with 10% dextrose to stabalize blood sugar
PPN bag goes dry...
...replace with 5% dextrose
air emboli
Air in IV: put pt in Left Lat position; give 100% O2, and knowthat 50cc 02 = LBP, 100 cc 02 = lethal
Enteral vs. Parenteral
Enteral: GI Parenteral: IV, subcutaneous (non-GI)
NG tubes
single lumen CANNOT be used to decompress the stomach (need double lumen) Salem Sump Tube (sst) used to decompress.
Responding to Aspiration
put head of bed <30degrees, shut off Enteral feeding; use constant infusion (no bolus); monitor and avoid G-distension; feed post pylorically
Responding to Diarrhea
reduce rate of tube feeding; treat with antibiotics; add bulking agents
Responding to High Gastric Residuals (not processing GI food)
high risk = sepsis; hyperglycemia; diabetes; trauma; MI; add prokinetic agents; feed post pylorically; check residuals every 15 minutes
Responding to Dehydration
Monitor I/O and weight; provide free water
Rales
crackles in lungs = L ventricular failure and FVE
SOB
Heart failure or FVE
cough
heart failure or FVE
s3 heart sound
heart failure or FVE
Jugular Vein Distension
Right ventricular failure, FVE, high BP
THIRST
FVD
Orthostatic BP
FVD
Pulse pressure
(diff between s and d pressure) GROSS MEASURE OF SV of <30, FVD
Pulse Quality
full, bounding = FVE

weak, thready, fast = FVD
normal H/H
42-52%
Normal BUN
5-25 (elevated = FVD, renal dysfunction)
Normal Creatnine
0.1-1.2 (elevated = FVD, renal dysfunction)
Azotemia
abnormally high concentrations of urea and nitrogens in blood
Uremia
excess urea in blood; sign of renal failure
USG
<1.010 = FVE; >1.025 = FVD
Normal CVP
2-8; <2=FVD; >12=FVE
Normal PAWP
6-12; >12 = FVE; <6= FVD
FVE Signs/Symptoms
edema, moist tongue/mucosa, full Jugular veins, rales/crackles in lungs, weight up, H/H down, Serum Osm down, pulse bounding and full, BP up
FVD Signs/Symptoms
tenting of skin, tongue is red, beefy, fissured, mucosa dry, jugular veins flat, weight down, H/H high, serum osmo >310, thirsty, pulse is fast weak and thready, BP down, CONFUSION
Formula for Serum Osmolality
2(Na) + Glu/18 + BUN/2.8
USG < 1.010
overhydration, duiretics, DI, CHF
USG > 1.030
dehydration, proteinuria, preeclampsia
Renal Failure and urine output
restrict fluid to 500cc/day for 24 hours
FVD risk factors
burns, blood loss, surgery, vomiting, fever, GI suction, fistulas, Diabetes Melodus, DI, polyuria, laxatives/diuretics, sepsis, liver disease, lymphatic blockage
1st sign of FVD
anxiety
Normal weight loss vs. deficit
Normal = 250cc/day (1/2lb) If loss is 1lb, think FVD.
Necessary Urinary output/day
500cc; if <500cc, BUN and Creatnine in blood goes up, causing toxicity
oliguria
urinary output <400cc/day
FVE risk factors
Cirrhosis (hyperald.), Cushing's disease, IV fluid admin, CHF, renal failure
low Albumin
3rd spacing, water leaves blood and doesn't return (want hypertonic solution
complications of sepsis
expand capillaries, fluid leaves blood stream, edema, no albumin to hold water in blood
fevers and metabolism
every deg over 90 = 15% incr. in metabolism (causes FVD) and incre of Resp. Rate 4/min
Normal Urinary Output
60cc/hr

When <30cc/hr -> TELL PRECEPTOR
Normal MAP
>70-105; when <60 releases renin, shuts down periph vasc. sys., release ald to increase BP
KVO
keep vein open (slow IV)
Causes of Edema (not FVE)
impaired lymphatics, inflammation, clots/venous congestion, liver disease, sepsis
Response to Cardiogenic Shock
PUMP WITH SALINE
reasons to avoid Ald release
heart failure, kidney failure (can't handle increased BV)
Signs of RV failure
edema, jugular vein distension, lung disease
Signs of LV failure
VERY LOW BP, pulmonary edema, shortness of breath, rales/crackles, cough
Hypotonic solutions
<250; 2/3 of H20 will leave ECS for ICS
D5W
considered isotonic, but hypotonic in body (adds H2O to body: 1/3 ECS,2/3 ICS)

Great for pts who are hypernatremic, adds H2O to blood
1/2 Normal Saline
hypotonic, good for dehydration (gives a little salt and water)

problem: swelling (a lot of water leaves bloodstream)
D5 w/1/2 Normal Saline
hypertonic (but Isotonic once glu is released into body) -> contains k+

This is the NORMAL IV fluid usedin hospitals, has: sugar, water, Na+, K+
Full Saline
high Na+ content -> causes hypernatremia, stays extracellular -> 250cc saline stays in bloodstream -> incr BP

GREAT FOR SHOCK

Not good for elderly/weak haearts (can't handle hypernatremia) GIVE WITH DIURETIC (but then will incr. K+ level)
blood makeup
45% RBCs
Obesity and water volume
lower water volume
D5W
isotonic, but hypotonic once glu absorbed, DOES NOT PRODUCE ECFV overload, raises blood sugar, too much can cause ICF edema

Problem: DON'T use with pts with cranial pressure or shock
1/2 Normal Saline
hypotonic; provides free water and Na+. Treats hypertonic ECFV depleted states (good for severe dehydration)

Problem: can cause hyponatremia (sodium leaves blood)
Normal Saline
ECFV replacement. Perioperative. Shock

Problem: ECFV overload in pts with CHF or renal failure.
Ringer's Lactate
iso/mild hyper; provides ECFVreplacement; lactate replacement; perioperative.

GREAT for Burns

contains K+

Problem: ECFV overload in pts with CHF or renal failure.
3% NaCL
HYPERTONIC! treatment of severe hyponatremia


Problem: ECFV overload
D5 1/2 normal saline
hypertonic. Replaces water, sodium, and some sugar (contains K+)
Hypotonic Solutions
<250

Problems: bad for dehydration (takes H2O out of bloodstream); causes edema; volume concentration of bloodstream

NEVER USE WITH: cranial pressure, burns, liver disease, hypoalbuminemia
Isotonic Solutions
250

Problems: expand IVF (risk for FVE)

NEVER USE WITH pts with alkalosis
Hypertonic Solutions
Problems: Need Anal Incontinence bag!!! Puts water into ECF/causes FVE.

ALWAYS ADMIN BY PUMP

NEVER GIVE TO pt with ICF dehydration,or pts with CHF or renal failure
Normal Cardiac Output
4-6 L/minute
Hospital Normal Output/Loss
30cc/hr
Normal BUN:cr
10-15:1
Normal CVP
2-8
pancreatic drain
HCO3 (bicarbonate)
vomiting and electrolytes
decrease K+ and HCl
Signs/Symptoms of Hypokalemia
weakness, cramps, decr. reflexes, paralysis of resp. muscles, paralysis of ileus, nausea, constipation, hypotension, arythmias, drowsiness, dizziness, flat T-wave, U-WAVE

REALLY TIRED
80% of K+ excreted by...

20% of K+ excreted by...
kidney

GI track
Hypokalemia causes
K+ loss: diarrhea, ileostomy, vomiting, GI suction, NG tube, intenstinal drain

low K+ intake: anorexia, alcoholism, fasting, NPO

Fluid/elect shift: ALKALOSIS, vomiting

Drugs that lower K+: diuretics, kayexalate, IV glucose, insulin, steriods, licorice, aldosterone, antibiotics

ALKALOSIS: need acids in blood stream, so K+ leaves blood and goes ICF.
Administering K+
DILUTE! MIX WELL! SALINE FLUSH with GI admin; irrigate with Normal Saline; NEVER BOLUS; never exceed 10meq/hr (in >100cc); MAX is 20 meq/hr IV
Hyperkalemia causes
Increase intake: salt substitutes, K+-sparing meds, crushing injuries/burns, ACE inhibitors, transfusions of old blood

Decreased output: renal disease, adrenal gland failure, hypoaldosteronism

Redistribution: Acidosis (want H+ out of cells, so K+ comes in)
Signs and Symptoms of Hyperkalemia
bradycardia, irregular pulse, decr. CO, Cardiac arrest, PEAKED T-WAVES, PROLONGED PR, numbness of extremeties, muscle weakness, paralysis, GI cramps, diarrhea, oliguria, cell lysing, confusion
Treatment of Hyperkalemia
Dextrose/Insulin, Kayexalate, Ion exchange resin (get Na+ in, K+ out, watch for hypernatremia) , Sodiumbicarb: alkalinizes plasma (K+ into cells)
Calcium gluconate for Hyperkalemia
treats symptoms, not cause

NEVER give to pts with digitalis meds, increases arrhythmias
shortcut formula for Serum Osmolality
2 x Na = approx. of serum osmolality
Causes of Hyponatremia
Dilutional: IV admin, hypotonic solutions, SIADH

Drugs: cytoxan, diabinese, SSRIs, MAO inhibitors

Heart failure, liver failure: nephrosis: decreased Arterial volume and triggers ADH release (pt appears edemic/FVE)

LOSS of Na relative to water: diuretics, burns, vomiting, Ald deficiency
Signs and Symptoms of Hyponatremia
edemic/FVE, low Serum Osmo, USG < 1.010, nausea, abdominal cramping, CNS dysfunction (cell swelling and cerebral edema), lethargy, neuro damage, <115 = seizures, cramps, weakness (may seem FVD if on diuretics)
False pseudohyponatremia
Hyperglycemia: for every 100mg incr. in glu level, the Na level decr. by 1.4
Diff presentaitons of hyponatremia
FVD = diuretic therapy

FVE = CHF and cirrhosis

euvolemia = SIADH
Hyponatremia due to NA loss
urine Na<10meq/L and USG <1.010
Hyponatremia due to NA loss
urine Na<10meq/L and USG <1.010
Hyponatremia due to SIADH/water gain
urine Na >20meq/L and USG >1.012 (continues continue to excrete sodium and retain water
Hyponatremia and IV
cautiously admin. HYPERTONIC solution (3% normal saline has high osmolality)...can they accept additional water loadw/out CHF/pulmonary edema? (give with lasix)
treatment of hyponatremia
plasma Na should raise by only 12 meq in 1st 24hrs.

Problem: osmotic demylination and brain dehydration/injury
Key manifestations of Hypernatremia
"thirst" and renal conc. of urine to conserve H2O
Causes of Hyponatremia
water loss: DI, low ADH, Osmotic diuresis, renal disease (can't concentrate correctly), diarrhea, excessive diaphoresis

Gain of Na+ relative to H2O: problems matching thirst/injesting, hypertonic feedings, hyperaldosteronism
Na reduction in hypernatremia
don't lower Na more than 2meq/hr.
IV for hypernatremia
D5W or 1/2 saline
SIADH presentation
pts do not appear wet or dry...euvolemic! but have dilutional hyponatremia
Treatment of SIADH
fluid restriction

diuretics

tetracycline/demeclocyline (increases water clearance form renal tubules

seizure precautions
Causes of SIADH
cancer (lung especially), chemotherapy, analgesics, antidepressants, nausea
SIADH lab results
serum sodium low

serum osmolality low

urine osmolality high

urine sodium high
DI causes
low ADH secretion, caused by tumor of hypothalamus, kidney non-response to ADH, head trauma, cranial surgery, lithium carbonate and demeclocycline
Signs and symptoms of DI
serum osm high >300

diuresis 5-20L/day

polyuria with low USG

low urine osmolality

FVD

weight loss
DI Interventions
problem is urine output >100cc/hr x 3hrs

exogenous ADH admin
liters body water deficit formula
(.6(kgwt) x serum Na -140)/140
gauges for IVs/catheters
flow rates slow as length increases.
daily K+ intake
20-60mE/day
insulin and K+
when admin insulin, get hypokalemia, need to give K+ with insulin
Hypokalemia and digitalis
makes digitalis more effective and more concentrated in the body
K+ and renal failure
do not give K+ with renal failure
False hyponatremia
hyperglycemia - glu acts as imposter and pull water into bloodstream. FALSE LOW SODIUM. Dilutional.

for every incr of 100g glu = should reflect ACTUAL incre of 1.4-1.6 in Na (add glu level to Na level to get actual Na level)
relat. between CO2 and carbonic acid
need to maintain a 20:1 ratio
major organs of pH buffering
kidneys (metabolic) and lungs (respiratory)
Kidney regulation of pH
slow compensation

when bicarb down, regenerate bicarb OR when bicarb up, reabsorb bicarb from renal tubules
Metabolic Acidosis regulation
low pH

Kidneys excrete H+ and conserve bicarb to restore balance
Renal failure and acid balance
causes metabolic acidosis
Response to Metabolic Alkalosis
pH increases

Kidneys retain H+ and excrete bicarb to restore balance
Response to Pulmonary Acidosis
when CO2 in blood increases, stimulates respiration = greater elimination of CO2 to lower acid load
Response to Pulmonary Alkalosis
CO2 levels down = lowers resp. rate = increases CO2 in blood and raises acid load
three types of blood protein
fibrinogin = clotting

albumin = colloid osmotic pressure

globulin = immunology
use of normal saline
flush wounds/GI tubes
bowman's capsule
role in filtration of molecules into urine...this is the reason we don't pee blood (RBCs are too big)
skin turgor evaluation
use sternum/forehead in elderly, hand in young
Creatinine
normal 0.1-1.4

higher is FVD

lower is FVE
cc equivalent of swelling/edema
2,500cc (five pounds)
pericardium
parietal = outer

serous/visceral = inner
role of lubricating fluid between pericardial tissue layers
keeping the heart tissue from becoming inflamed
vena cava
inferior/superior: large veins where blood enters heart
diastole
heart muscle relaxes (dub)
systole
heart pumps blood out, ventricular muscles contract
Diastole
most of venous blood enters the Right Atrium
pulmonary arteries and veins
arteries carry deoxygenated blood

veins carry oxygenated blood
Left ventricular pressure vs. Right ventricular pressure
LV works harder, walls are thicker, must pump to entire body
blood supply: aorta, coronary arteries
aorta: head, back, and major organs of digestion

coronary arteries: supply the heart muscle
SA node
pacemaker: sends signal to L & R atrium = simultaneous contraction
AV node
received message from SA node, sends to AV bundle
AV bundle
receives signal from AV node and sends to R/L bundles and purkinje fibers
Purkinje fibers
receive message from AV node to R & L ventricles, which contract
Factors that affect Peripheral Resistance
Blood Vessel Diameter (vaso contriction/dilation), length of blood vessel (longer in obese people), viscosity of blood.
Catalysts that increase Peripheral Resistance
vasoconstriction of arteries

lengthening of blood vessels

higher blood viscosity
s/s of CV dysfunction
Right Side: fluid retention

Left Side: dyspnea

both: fatigue, pain (ischemia) (won't see in diabetics, who have less pain reception)
physical exam for s/s of CV dysfunction
postural changes, distress, dyspnea, edema, cyanosis around mouth, clubbing, heaves, JVD (R-side failure), listen for S3 and S4 (ventricular failure), scites, homan's sign (Deep Vein thromboses) pulses, coldness in hands/feet
Tropanin
GOLD STANDARD:

protein that releases from injured/dead heart muscle cells

normal <.5
myocardial injury .5-.8
MI acute >.8

Rises in 4-6 hours after event
Peaks in 10-24 hours
Stays elevated for 10-14 days

Reflect INJURY, not just death, can be used to interrupt MI process
CK-MB
enzyme present when there is tissue necrosis.

ONLY REFLECTS CELL DEATH

returns to normal in 48 hours (missable)

>6% = MI
Lipid Profile
IDs risk factors and influences drug choices

LDL= 80-190
HDL= 30-60

LDL:HDL = 3:1
Angiography/Ateriography
catheter to coronary arteries.

Dye injected, areas of poor perfusion = diminished uptake
Cardio Catheterization
attains injection fraction (normal: 55-65%

detects coronary blockages: where, how much, how occluded?

Checks for backflow and valve function

<40% flow = CARDIAC FAILURE
Nursing care for post-radiological testing
check bleeding at site

avoid hematoma (bruising)

monitor blood flow in peripheral arteries in limb where procedure was done

antiplatelet meds

vasodilation meds

If dye used, increase fluids to flush dye from system
Components of an EKG/cardioelectrical impulse
automaticity

excitability

Conductivity

Contractility
Normal PR interval
.12-.20 sec
Normal QRS interval
.04-.10 sec
Noraml QT Interval
0.34-0.43 sec
demopressin
decreases urine output for pts post neuro surgery
QRS interval <0.12 sec
bundle branch block: PVC
QRS Interval represents
ventricular repolarization
P to P =

R to R =
arterial rate

ventricular rate
small boxes on EKGs represent X seconds
.04
If see a Q-wave, indicates:
previous MI
Sinus bradycardia
HR <60

problems in SA node

all else normal, constant
sinus trachycardia
SA node problem

HR >100-180

P waves encroach on preceding T waves

all else normal, constant

treatement: beta-blockers, calcium channel blockers
Atrial Flutter
Atrial muscle problem

a rhythm regular

v rhythm is reg if block reg; varies if block varies

A rate is 250-350

P wave: flutter (F) waves "saw-toothed"

Treatment: drugs to slow ventricular response: digoxin, calc. chan blockers, beta-blockers.

anti-arrhythmics
normal atrial HR
40-60
atrial fibrillation
problem with atrial muscle

atrial rhythm irregular

v rhythm TOTALLY irregular

NO P-WAVES

BIG RISK OF THROMBOSIS WITH A-fib and A-flutter. NEED ANTI-COAGULATION after 24-48 hrs
Premature Ventricular Contractions
problem with Ventricular Muscle

irregularity, followed by pause

rate varies

P waves inconsistent, unrelated

QRS wider than 0.14

Treatment: treat cause

anti-dysrhythmics

we all feel these when heart "jumps"
PVD
premature ventricular contraction
ventricular trachycardia
three or more PVCs in a row

can't determine atrial rate

v rhythm regular

P-waves not visible

AV dissociation

QRS: wider than 0.14

Treatment: USUALLY AN EMERGENCY: check for pulse.

V-tach = ACLS!
ventricular problems result in:
wide QRS compels

no p-wave
Ventricular Fibrillation
electrical chaos in the ventricles.

ventricular contraction cannot occur

no cardiac output

RAPIDLY FATAL

ACLS!
Asystole
ventricular standstill

complete absence of v rhythm

no QRS

FULL CARDIAC ARREST

ACLS!
SA node firing on EKG is the:
p-wave
from lecture: atrial flutter characterization
saw-toothed waves

p-t buried together

NO ATRIAL KICK! ventricles fill passively and have low CO

atrial does not beat in an organized fashion

atrial doesn't fill ventricle

no PR interval

QRS normal at <.12

A rate: 220-430 pbm
V rate: <300 bpm

No Uniform Regular P-wave
from lecture: a-fib charaterization
no discernable regular p-wave: P-wave looks FLAT

LOSE atrial KICK of 25% of output...ventricles filling passively ONLY

"a-fib of 90" means 90 is V Rate (they don't count A rate)

No PR interval!

A rate: 350-650 pbm

V rate: slow to rapid

rhythm is irregular

QRS normal at <.12
increased risks of rapid a-fib/a-flutter
V rate high

now have poor CO AND high HR

BP will drop

Pulse becomes thready

She's in worse shape because has lower cardiac output AND low BP.
EF warning signs (what % is a red flag)
<40% increases risk
further risks of a-fib and a-flutter
when pts go into a-fib and a-flutter, but CLOTS! Increases risks of emobolism/stroke

give pt blood thinner: heparin
heparin "rule of thumb"
if pt has NEW a-fib/a-flutter for 48 hours, hang HEPARIN!
from lecture: Premature Ventricular Contraction (PVCs)
we all have these.

irregular stim. originating in the ventricular muscle.

TOTALLY irregular

QRS interval: WIDE (>.14)
from lecture: v-tach
ventricular tachycardia: 3 PVCs in a row. Missed heart beats BECAUSE OF CONTRACTION BEFORE VENTRICLES FULL

big risk in situations with ischemia
from lecture:v-fib
ventricular fibrillation: most deadly

electrical chaos in the ventricles

ventricular contraction DOES NOT OCCUR

NO CARDIAC OUTPUT: rapidly fatal (3-5 minutes)

pt is pulseless
from lecture:locations of inflammation of the heart
endocardium (inside)

pericardium (outside)

entire heart
from lecture: causes of infective endocarditis
IV drug use

previous mitral valve procedures

dental procedures

strep

staph

e.coli
from lecture: s/s infective endocarditis
flulike symptoms

fever/night sweats

weight loss

fatigue

cardiac murmurs

back/joint pain

heart failure
pericarditis: leading to cardiac tampynod
inflammation of pericardium: if sac becomes too large and swollen, will start to squish heart and diminish CO and pump action
s/s of pericarditis
friction rub (heard on L sternal border)

pain in inspiration

EKG shows ST segment/T-wave inversion

fever and elevated WBC count
atherosclerosis
build up of plaque (intima) in arteries, leading to coronary artery disease (CAD)

causes ischemia or infarction (necrosis)
s/s of myocardial ischemia
anginal pain (often reversible at rest)

INVERTED T-WAVE
s/s of myocardial injury
ST elevation (double hill)
s/s of necrosis
Abnormal Q
progress up to MI
atherosclerosis -> ischemia/angina -> myocardial injury -> MI
DM and cardiac risk CAD
DM increases the rate of plaque build up
hypertension and CAD
hypertension increases workload on heart, increasing risk of disease
angina pectoris
"strangling of the chest" = ischemia of limited duration, but can -> dysrhythmias -> MI
UNSTABLE angina
preinfarction

anginal symptoms at rest
prinzmetal's/variant angina
spasm of the coronary arteries

(high risk among cocaine users)
risks of angina
could dislodge antherosclerotic plaque
treatment of angina
want supply to equal demand

1. Nitrates: dilate Blood vessels (up supply)

2. Beta-2 blockers: decrease HR (down demand) AND decrease contractility (down demand)

3. Calcium channel blockers: vasodilate (up supply) AND decrease contractility (down demand)

4. Antiplatelet: prevent clots
Beta blockers
decrease HR (down demand) AND decrease contractility (down demand)
Calcium channel blockers
vasodilate (up supply) AND decrease contractility (down demand)
time to full Necrosis of the heart from onset of Ischemia
6 hours
patho changes in MI
hypoxia -> stimulates vasodilation of blood vessels -> acidosis (K+ imbalance) -> suppresses AV node and contractile function -> automaticity and ectopy increase (can lead to arrhythmias)

AND

catecholamines released in response to pain/hypoxia -> increases HR and contraction -> increase O2 demands -> necrosis
anterior wall MI
25% of all MIs w/highest mortality rate

damage to L ventricular wall

L ventricular failure and L ventricular arrhythmias
s/s of heart failure/MI
pain unrelieved at rest

nitro does not releive

nausea

diaphoresis

confusion/irritability

shortness of breath

weakness
s/s of left side failure
sleep dyspnea

high PCWP

blood-tinged sputum

cough

orthopnea

exertional dyspnea

cyanosis
Preload
volume coming into ventricles (end diastolic pressure)

Inreased in: hypervolemia
Afterload
resistance that the left ventricle must overcome to circulate blood

Increased in: hypertension, vasoconstriction

when afterload goes up, cardiac workload goes up

with MI, want to decrease afterload
treatments to decrease oxygen demand to the heart
nitrates: decreases afterload

beta blockers: decrease HR, decrease arrhythmias, decrease contractility

calcium channel blockers: used with ANGINA. Increase myocardial perfusion and dilates coronary arteries. decreases contractility and rate and vasospasm

morphine: dilates arteries to decrease myocardial demand


PUT PT IN SEMI FOWLER's POSITION to reduce CHF
treatments to improve circulation to the heart
antiplatelet meds (heparin)

thrombolytics/TPA: clot busters

PTCA (angioplasty with balloon)

CABG: coronary artery bypass

nitrates: for vasodilation
stroke volume
60-80 spm
pathophysiological changes in heart failure: compensatory mechnisms
increased heart rate-> too fast means cardiac output may fail and heart muscle will tire

improve stroke volume: more stretch inmyocardial fibers (high preload) means greater force of contraction, so CO rises. Too much stretch will decrease cardiac output

Aterial Peripheral vasoconstriction:blood shunted to major organs. too much will cause too great an afterload, which increases 02 demand by left ventricle. This may ultimately decrease stroke volume.

retention of sodium and water: RAAS activated to increase blood volume returning to Left ventricle.

Myocardial hypertrophy: thickening of walls, increasing the force of contraction and increases CO. problem is that blood supply to muscle may not be good enough and will become 02 deprived
digoxin
oral agent that increases contractility of the heart (positive inotropic)
inotropy
influences contractility
% of cardiac output used by kidneys
30%, so if CO is low, will see <30cc/hr of urine
s/s of right sided failure
low stroke volume

peripheral edema

low urine output (no blood volume to kidneys)

distended jugular veins

GI distress

cyanosis

dependent edema
treatment of right-sided failure
NEED MORE PRELOAD

NO diuretics

NO nitrates

give her positive inotropic (enhance contractility on Right side)

give her blood volume
increasing contracility does XXX to 02 demand?
INCREASES 02 demand
s/s of left-sided failure
pulmonary edema

rales/crackles in lungs


low cardiac output

high heart rate

low stroke volume
treatment of left-sided failure
NEED MORE AFTERLOAD

diuretics

positive inotropics to up contractility

sit head of bed up in semi-fowler's

decrease afterload (vasodilate)
starling's Law
the more you stretch the myocardial muscle, the greater the force of contraction, so the better to cardiac output
Norepinephrin
ANS

raises BP through vasoconstriction
Beta 1 Receptors
Baroreceptors

raises BP through increasing cardiac output
Alpha 1 Receptors
Baroreceptors

raises BP through vasoconstriction
Blood vessels and BP
determines peripheral vascular resistance, increase to increase BP
Angiotestin
RAAS

raises BP through vasoconstriction
Parkland's Formula
4cc/kg/% of burn

1/2 in 1st 8hrs

1/2 in next 16hrs
DKA
FVD

hyperkalemic
Digitalis and potassium
dig with low potassium means pt blacks out...bad Drug Interaction
P-Wave
A contraction
QRS
V contraction
lasix and potassium
lowers potassium, check before putting a pt on lasix
ringer's lactate
surgical pts, burns
hospital "normal" IV
D5 1/2 normal saline
Hyperkalemia and EKG
peaked T-waves
Hypokalemia and EKG
U-wave
Hyperkalemia and PH
acidosis
Hypokalemia and PH
alkalosis
CO2 and PH
higher CO2 raises ACID LEVELS, lowers PH
Kayexalate "dog"
ion exchange resin, so gets rid of K+ and BRINGS IN Na+...don't use on pt with poor heart
brown urine
hyperkalemia (cells are lysing)
Bicarb "dog"
cardiac, because increases salt load
NG tube irrigation
ISOTONIC = normal saline
Tube feeding and dehydration
water down IV with H2O
Ischemia and EKG
t-wave changes
how to up O2 supply
vasodilate:

nitrate

morphine

O2
quick formula for serum osmolality
Na x 2
s/s of A-fib
Dizzy/faint

weak
A-Fib EKG
no p-wave

irregular r-r interval
aortic/pulmonic valves are...
semi-lunar valves
mitral/tricuspit valves
AV valves
major organs with:

Potassium

FVE

Na
K+ is heart...think kidney problem

FVE: protest the brain from swelling

Na: think brain
CVP Normal
2-6 mmHg
PCWP Normal
8-12 mmHg