Adults II Exam I

02/22/2015

Blood Components
Plasma (55%), RBC/WBC/Platelets (45%)
o Blood cell formation/hemoglobin in bone marrow
o Hypoxia causes release of erythropoietin (ERP) from
kidney to turn myeloid stem cell into erythroblast ->
loses nucleus and released into circul9ation as
reticulocyte, matures in blood/spleen to become RBC
o Can give ERP if chronically anemic
Disorders
o Erythrocytes
Too much: Polycythemia
In oxygen deficient disease (COPD, chronic
bronchitis)
Too little: Anemia
Nutritional factors: iron, B12, folic acid
Iron deficiency: Small, low in Hgb
(microcytic, microchromic)
Lack of folate/b12: megaloblastic,
macrocytic
Folic acid deficiency: 1 to 5 mg PO/day,
B12 corrected first/simultaneously to
reduce neuropathy
o Leukocytes
Too much: Leukocytosis, lymphocytosis
Too little: Leukopenia, neutropenia
o Thrombocytes
Too much: Thrombocytosis
Too little: Thrombocytopenia

 Normal Lab Values

o CBC: RBC/WBC/Platelets/Hct/Hgb
o Erythrocytes: Female (4.2-5.4), Male (4.7-6.1)
High reticulocyte count (immature) when
actively bleeding
Hgb: Female (13-14), Male (14-16)
Hct is 3 x Hgb (36-46%) (3:1)
Increased blood volume (fluid retention)
decreases Hct and vice versa
Spontaneous clotting over 60%
MCV (size): 84-96, MCHC (color) 31-35
RDW (variability in size): <14.5
o Leukocytes: 4,000 to 11,000
Majority are granulocytes (neutrophils)
More concerned about increase if elevated after
several days as opposed to right after
Absolute Neutrophil Count > 7,500 is infection
Normal response to stressors, shifts to left
with bacterial infections increased
immature neutrophils/bands)
Want over 2,000 and under 1 % bands
Leukopenia <4,000
Neutropenia <2,000
Can give neupogen to stimulate
granulocytes
o Platelets: 150,000 to 400,000
Primary hemostasis: platelet plug, ASA
interferes

 Secondary: clotting factors form fibrin clot

Thrombocytopenia: <100,000
Decreased production (bone marrow
issue/cancer, toxins, drugs like sulfa,
chemo) and increased destruction
(autoimmune)
Thrombocytosis: >1,000,000
Hypercoagulability leading to
CVA/MI/DVT
Want 50,000 or surgery, bleeding precautions if
under
Replacement therapy if <20,000; will have
petechiae, gum bleeding
Plasma: albumin helps maintain oncotic pressure
o Fresh frozen plasma (FFP): contains Vitamin
K/clotting factors, usually made by liver
RBC
o Hgb binds H+ ions to buffer acid
o Removed from circulation by reticuloendothelial cells
in liver/spleenHgb is recycled
Heme: converted to bilirubin, excreted in bile
Interventions
o Nose bleed: high fowlers, direct pressure to nose,
ice to back of neck
o Bleeding: direct pressure, call MD if unable to stop in
10 minutes
o High INR: give Vitamin K and tell them to watch for
bleeding, give FFP to reduce
2-3 on Coumadin
o Post Op: vital, infection, bleeding, pain
o Anemia: manage fatigue, nutrition/supplements,
oxygen
Renal disease: give ERP to maintain Hgb 10-12,
Check BP before

o Sickle cell crisis: oxygen, fluid replacement, pain,

education
Bone Marrow
o Aspiration: iliac crest/sternum, local anesthetic,
pressure as needle advances, pain when aspiration
(sharp/brief)
o Biopsy: iliac crest, pressure but not pain
Anemia
o Not a diagnosis
o Hypoproliferative: decreased RBC production
Altered DNA synthesis from nutritional
deficiency (megaloblastic)
B12, Folate, Iron, Renal/chronic disease
Renal: decrease RBC life, low ERP, dialysis
loses RBC/iron/folate
Chronic: arthritis, HIV, cancer, few
symptoms, normochromic/cytic
o Hemolytic: desctruction of RBCs
Sickle cell, thallasemia, heart valve
o Blood loss
o Symptoms not apparent until Hgb<10, pallor at <8
Pallor most apparent in oral mucosa
Cyanosis shows unoxygenated Hgb
o Iron deficiency thought blood loss until otherwise
proven
Pica, pagophagia, low serum Fe
Supplements: constipation, N/Vgive by IV if
cant have oral, risk of anaphylaxis, on vent
Vitamin C enhances, liquid stains teeth, stool
dark green/black, take on empty stomach

 No dairy!
o Nutritional deficiency can be caused by faulty
absorption or decreased intrinsic factor in gastic
mucosa (pernicious anemia) so B12 not absorbed
(symptom: glossitis)
Folic: stop drinking alcohol, eat liver/green
vegetables
o Sickle cell: defective Hgb production
HgBSS: disease
HgbAS: trait
Blood therapy
Whole blood: massive blood loss/ hypovolemic (has
anticoagulant)
PRBC: augment O2 carrying, 1 unit will raise Hgb by 1
g/dL
Platelets: active bleeding in thrombocytopenia
o 6 packs raises by 30,000 to 60,000
FFP: correction of coagulopathies (warfarin OD)
Albumin: enhances oncotic pressure
Giving Blood: hang only with normal saline, 3 way tubing
and filter, begin slowly (10 drops/minute), monitor closely
for first 15 minutesneed two RNs, check compatibility,
expiration, consent
o Begin within 30 minutes of release from blood bank
o Infuse within 4 hours
o Change tubing with each unit/per policy
Acute hemolytic transfusion reaction (AHTR)
o Most serious, immune mediated hemolysis,
preformed antibodies to infused blood product
(incompatible)
o Fever, rigor, flank pain, hypotension, nausea, chest
pain, SOB
o Within first 15 minutes

o *Stop infusion immediately, notify MD, disconnect,

keep IV open with N/S, get typing/culture, draw
blood sample, urine
Febrile, nonhemolytic reaction
o CommonChills, >1 C/2 F rise in temp, people more
at risk with multiple transfusions
o Stop transfusion, rule out AHTR/infection
Allergic: always stop infusion
o Mild: hives, itching, flushinggive anti-histamine,
resume
o Severe (anaphylaxis): anti-histamine, steroids,
vasopressors
Fluid overload: infused too fast, too much volume
diuretic between units
o Cough, dyspnea, crackles, tachy, HTN
o Slow infusion, elevate HOB, lower feet, oxygen,
diuretic
Ischemia
irreversible cell injury when tissue demand for oxygen is
not met, toxic metabolites accumulate
Treatment: reduce O2 demand, increase O2 supply
A+P
Nephron: smallest working unit of kidney
o Filter: water/solutes out of glomerulus into Bowmans
o Reabsorption: from renal tubules back into blood
Proximal: water, lytes, glucose
Loop of Henle: Na, Cl, K (ascending), H2O in
descending
Secretion: substances into urine, distal/collecting ducts,
important for acid/base balance
Tubules reabsorb/secrete electrolytes/waste/water

Normal Function
GFR: plasma filtered through glomerulus
o Normal: 125 ml/min or 90
o Determined by age, serum creatinine, gender, ethnicity
o More sensitive than creatinine (byproduct of muscle
metabolism, not reabsorbed)
o Reduces with age, need dialysis between 15-20
Acid/Base balance
o pH: 7.35 to 7.45, 7.4 optimal
o controlled by chemical buffers in body fluids (immediate),
respiratory center (minutes), renal (hours to days)
o HCO3 to H2CO3 ratio of 20:1
Kidney (HCO3), lungs (CO2)
Low pH/high H+ concentration, kidney reabsorbs more
HCO3 and excretes more H+ in the form of ammonia in
urine (vice versa)
Low pH/high H+ concentration, lung blows off more
CO2 through hyperventilation
o Respiratory: acidosis (high CO2, low pH, normal HCO3),
alkalosis (low CO2, high pH, normal HCO3)
o Metabolic: acidosis (normal CO2, low pH, low HCO3), alkalosis
(normal CO2, high pH, high HCO3)
CO2: 35-45
HCO3: 22-26

If either HCO3/CO2 deviate in same direction as pH,

then uncompensated

Urine

o Specific gravity: 1.010 to 1.025

o Volume: 1000 to 2000 ml/24 hours

o

o
UTI:

o
o
o
o
o
o
o

o
o

Anuria: <50 ml/24 h

Oliguria: <400 ml/24 h
BUN to creatinine ratio: 10-20:1
Pre-renal: ratio is >20:1
Intrinsic: normal
Post-renal: decreased/normal
Creatinine: 0.6-1.2 mg/dl
lower (bladder, urethra, prostate), upper (kidney)
Hematuria: >3 RBC
Proteinuria: >20 mg/dl
Pyuria: WBC>6-10
Casts: >4, proteins from damaged tubules
+ nitrites, leukocyte esterase, glucose, ketones
Culture: women (100,000 cfu per mL), men (10,000 cfu),
gram
Acute cystitis
Uncomplicated: oral antibiotic, analgesic, adequate fluid
intake
Complicated: men, diabetes, immunosuppression,
pregnancy, nosocomial, longer course of ATB
Interventions: pain relief (pyridium/antibiotic, heat, increase
fluid), monitor for sepsis, AKI, chronic kidney disease
Pyelonephritis: bacterial infection of kidney(s), ascending UTI,
acute or chronic, more frequent in women/DM
Acute: fever, chills, flank pain, N/V/Anarun
urinalysis/culture, CBC

 Sepsis: low BP, mental status change

AKI: labs, urine output
Acute Kidney Injury
Risk: infection, age, cardiac/respiratory failure, usually caused by
sepsis follower by hypotension/IV contrast
Categories
o Pre-renal: low renal perfusion
Urine sodium low, SF high (concentrated)
o Intrarenal/intrinsic: damage to glomeruli/tubules
Urine sodium high, sediment, SG low (cant concentrate
urine)
o Post-renal: obstruction distal to kidney
Pre-renal: SBP<80 or MAP<60, hypovolemic, impaired cardiac
function, vasodilation, renal artery stenosis/embolism, prevention is
main intervention
Intrinsic:
o acute nephritic syndrome: glomerular membrane
inflammationthickening which causes Na/H2O retention,
reduced u/o, causes volume excess
o Acute tubular necrosis (ATN): ischemia, toxins (avoid
NSAIDS)
Post-renal: mechanical obstruction (renal stone, prostate
enlargement, tumor, kinked catheter), functional (neurogenic
bladder, drugs like anticholinergic to man with BPH)
Best indicators of kidney function: urine output, creatinine
Phases: initiation (initial insult), oliguric (<400 ml/24 h, elevated
BUN/creat/K/Mg, lasts 10-14 days), diuretic (excrete 3-5L in 24
hours, lasts 2-3 days), recovery (takes months)
o Want to avoid further injury, reduce complications
o Weigh daily, 500 ml=1 lb, monitor I/O, assess edema,
maintain MAP >60-70, avoid ACE inhibutors/ARBs/NSAIDs,
high carb and low protein, avoid foods high in K
Temporary dialysis indicated in volume overload, hyperkalemia,
metabolic acidosis, progressive azotemia (BUN>100)
Treat hyperkalemia with insulin, hypertonic glucose, HCO3

A+P
Sa node -> atria -> AV node -> bundle of His -> bundles to R/L ->
pirkinje fibers
o Interruption or slowing causes arrhythmia
P wave: atrial depolarization (contraction), slows down at AV node
to depolarize ventricle
QRS: ventricular depolarization
T wave: ventricular repolarization
PAC (premature atrial contraction)
Irregular rhythm because of interruption, early P wave
Atria tries to control heart
Causes: hypoxia, electrolyte imbalance, CHF/fluid overload,
caffeine/ETOH/smoking/sleep deprivation, surgery, anxiety/pain,
heart disease, COPD
Presentation: usually asymptomatic, may have palpitations
Arrhythmias
Atrial Flutter: regular
o Rate is 250-350, P waves have sawtooth pattern
o Cant measure PR interval
o Caused by pathway in atrium continuously depolarizing
o Causes: hypoxia, heart disease, hyperthyroidism,
CHF/MI/ischemia, acid/base disturbance
o Symptoms: palpitations/angina, CHF, hypotension,
dizziness/syncope, dyspnea, fatigue

o Treatment: slow HR with meds, interrupt reentry pathway (Ca

channel blockers, digoxin, amiodarone, b-blockers),

anticoagulation if lasts >48 hours and cardiovert after 3
weeks
Atrial Fibrillation: irregular
o Rate is >350/min, not measurable; rhythm is irregular, P
wave is absent
o Causes: age related dilation of atria, ischemic HD, CABG,
rheumatic HD (MS), CHF, hyperthyroidism, hypoxia, ETOH
intoxication, HTN
o Presentation: same as a-flutter
o Treatment: control HR or convert back to NSR,
digoxin/amiodarone/Ca channel blockers/ b-blocker,
cardioversion, anticoagulation
PVC (Premature Ventricular Contraction): irregular beats, wide QRS,
t wave in opposite direction of QRS
o Causes: hypoxia, MI, acidosis, hypokalemia +
hypomagnesemia, increased sympathetic stimulation
(caffeine, ETOH, tobacco)
o Intervention needed: occurring at >6/min, couplets/triplets,
R on T
Ventricular tachycardia: regular beat (110-250), no P/PR, wide QRS
o Causes: cardiomyopathy, valvular HD, acid-base disturbance,
cardiac trauma, electrolyte imbalance, increased production of
catecholamines
o Presentation: with pulse (hemodynamic compromise, shock,
chest pain, hypotension, SOB, CHF, AMI, decreased LOC) or
pulseless (unresponsive, apneic)
Treatment: Pulse (cardioversion, antiarrhythmics),
pulseless (CPR, defibrillation, epinephrine, vasopressine,
amiodarone)
o Torsades de Pointes: outline looks like party streamer/Arctic
Monkeys
Ventricular Fibrilation: rapid/chaotic with no pattern, nothing is
discernible
o Causes: increased SNS activity, hypokalemia/magnesemia,
antiarrythmics, electrocution, MI
o Presentation: unresponsive, apneic, pulseless
Complete heart block: third degree
o Rate: normal rate for atria, v rate <60
o Regular rhythm, P wave
o QRS narrow if junctional, wide if ventricular

o Conduction: PR interval random

EKG
5 big boxes is 1 second
count R to R big boxes, divide by 300
Cardioversion is synchronized with EKG, defibrillation is not
Interventions for decreased CO because of dysrhythmia
Monitor BP, rate, rhythm
Auscultate lungs for presence of normal/adventitious lung sounds
Assess peripheral pulses, skin color/temp,
lightheadedness/dizziness/fainting, mental status changes, fluid
balance/weight gain, patients response to activity, chest pain
Obtain EKG, place on tele, monitor oxygen and acid-base/
electrolyte imbalances
Pacemaker: tip of lead/electrode in apex of R V, enters external
jugular vein
ICD detects life threating VT/V fib and shocks heart
Implanted cardiac device: avoid lifting arm above heart for 2
weeks, avoid MRI, report dizziness/infection/hiccups/beeping form
device

Hemodynamics:
CO= HRx SV
o SV: preload, afterload, contractility
Mean Arterial Pressure (MAP)= SBP+DBP (2)/3
Cardiomyopathy
Disease of muscle associated with dysfunction
o Ischemic: underlying CAD, blockages

MI forever damages heart

o Non-ischemic

Dilated: ventricles affected, systolic dysfunction and

possible mitral regurgitation due to virus/ETOH/chemo
Compensatory RAAS (renin-angiotensinaldosterone system): kidneys release renin to
retain Na/H2O, constrict arteries to maintain BP
to get blood to vital organs, compensates well in
beginning but cant manage forever
Hypertrophic: thickening, can be genetic, impaired
filling of LV
restrictive, arrhythmogenic RV, unclassified

Heart Failure
Acute/chronic state where metabolic needs of body not met, heart
fails to pump adequately
o Systolic dysfunction: reduced contractility
o Diastolic: increased resistance to filling
Acute decompensated: abrupt worsening of function by at least one
class with evidence of VO or increased filling pressures
o More symptomatic
o Patient could change: higher than normal Na diet, stopped
taking meds, too much fluid
o Precipitates: clinical conditions (coronary heart disease with
ischemia, acute elevation in BP, acute renal failure),
dysrhythmias, psychological issues, high output, toxins
Hemodynamic profile in decompensated HF
o Wet (pulmonary edema), cold (cardiogenic shock)
o Wet and cold: congestion, poor tissue perfusion (treat with
diuresis, vasodilators)
o Dry and cold: poor tissue perfusion (hypotension), treat with
inotropes
o Wet and warm: volume overload (treat with diuresis)
o Dry and warm: good and normal
Left affects lungs, right affects rest of body (periphery)

o Left: pulmonary edema (frothy, blood tinged sputum),

crackles, dyspnea

o Right: edema in legs, JVD, ascites

Pulmonary edema: accumulation of fluid in interstitial space of

lungs that diffuse into alveoli, impaired gas exchange/severe
hypoxia
Fluid overload signs: weight gain, edema, JVD, SOB, crackles, S3
heart sounds, increased abdominal girth, elevated BNP
o Management: IV loop diuretics, second diuretic type, Na/H2O
restriction, daily weight and I/Os
Hypoperfusion: narrow pulse pressure, resting tachy, cool skin,
altered mentation, decreased U/O, increased BUN/creatinine
o Vasodilators (ACE inhibitors, inotropic therapy, bi-ventricle
pacing, IABP/LVAD/transplant
o Leads to cardiogenic shock: decreased CO
Manage with fluid bolus, inotropic drugs, mechanical
assist
Management of both: oxygen, morphine, diuretic, positioning,
monitoring
Cardiac Transplant
End stage HD class III/IV, suitable physiologic/chronologic age,
emotional stability/social supports, compliance with regimen
o Contraindications: active infection, active/recent malignancy,
severe pulmonary HTN, irreversible hepatic/renal disease,
history of ETOH/drug abuse or mental illness
o Determine stage with ECHO, EKG, heart catheterization
Donor/recipient matching: body/heart size, ABO type
o Maximal time from harvest to transplant is 4 to 6 hours
o Immunosuppression begins in OR (cyclosporine,
corticosteroids)

o
Disorders
Left sided (aortic and mitral) more frequent since it
undergoes more higher pressure
Valves become thicker with age, as well as lipid
accumulation, degeneration of collagen, and calcification

 Mitral valve
o Regurgitation: backflow into L atrium during systole,
high pitched blowing murmur during systole
Symptoms: DOE, orthopnea, PND; acute leads
to severe pulmonary congestion
o Stenosis: obstruction of flow from L atrium to L
ventricle, low pitched rumbling diastolic murmur
Symptoms: DOE, progressive weakness, fatigue
o Prolapse (MVP): prolapse back into L atrium, mid
systolic click
Symptoms: Palpitations, CP, SOB, fatigue,
dysrhythmia
Aortic Valve
o Regurgitation: blood flows back into LV from aorta,
high pitched blowing diastolic murmur
Symptoms: widened pulse pressure, water
hammer pulse
o Stenosis: obstruction from LV to aorta, loud/rough
systolic murmur
Symptoms: decreased exercise tolerance,
fatigue, dyspnealater: angina, HR, syncope
Tests
ECHO: TTE, noninvasive, uses sound waves, measures
ejection fraction, size/shape/motion of heart
o Diagnoses pericardial effusions, cardiomyopathy, wall
motion abnormalities, thrombus, and **valve
function
TEE: transesophageal, passed through mouth with
conscious sedation/topical anesthetic
o View mitral valve and assess function/vegetation,
view atria to identify thrombus in patients with a-fib
o Check vital after to check for bleeding, check gag
o NPO >6 hours before, patient IV, consent
Rheumatic HD

 Rheumatic fever: infection secondary to Group A strep

pharyngitis, bacteria travels in blood and infects
valve/endocardiumalters leaflets and function, give PCN
to treat
VHD Management
Asymptomatic: monitoring, infective endocarditis
prophylaxis
Symptomatic: management of CHF, surgical intervention
o Valve repair/replacement: requires life long
anticoagulation for mechanical valve (not a good
candidate if bleeding d/o, old age)
CABG: blood vessel graft to coronary artery beyond area
of stenosis (>70%) to re-establish blood flow
o General anesthesia, median sternotomy, bypass
o Complications: hypovolemia, persistend bleeding,
cardiac tamponade, dysrhythmia (heart block, a fib,
flutter), HTN, hypothermia, HF/MI, AKI, electrolyte
imbalance, liver failure, infection
Anti-coagulation: mechanical valve (INR 2.53.5), bioprosthetic (INR 2-3 for 3 months, then
ASA)
o Initial post op care: achieving hemodynamic
stability and recovery from general anesthesia
NG tube for stomach decompression, ET tube
for vent assistance, EKG electrodes, chest
tubes, A line
Antibiotics after every dental procedure
Vegetation: can embolize to tissues/through body
o RF: prosthetic cardiac valve, history of infective
endocarditis (rheumatic), congenital heart disease
(repaired or un)
o Infective endocarditis:
Native valve infective endocarditis (NVIE): IV
drug abuse with normal valve
Prosthetic valve (PVIE): more frequent,
bacteremia from dental/GU/GI procedure

o Acute symptoms: normal valve, rapid deterioration,

no time for hemodynamic compensation, most
common on right sided, very sickpulmonary
embolism
High grade fever, chills, dyspnea, JVD,
peripheral edema (right), decreased CO (left)
o Subacute: previously damaged valve, slow
progression, compensation present, left side
embolize to brain/spleen/kidney
Fever, fatigue, weight loss, low grade fever that
waxes and wanes for weeks, night sweats, back
pain, flu
o Physical exam will show fever and murmur, primary
signs
Most prominent on left side due to high
pressure
o IV antibiotics for 2-6 weeks, fever management,
valve replacement