Adults II Exam I 2/21/15 11:47 PM

Blood Components Plasma (55%), RBC/WBC/Platelets (45%)

o Blood cell formation/hemoglobin in bone marrowo 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 Valueso CBC: RBC/WBC/Platelets/Hct/Hgbo 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 acido Removed from circulation by reticuloendothelial cells

in liver/spleen—Hgb is recycled Heme: converted to bilirubin, excreted in bile

Interventionso Nose bleed: high fowler’s, direct pressure to nose, ice

to back of necko Bleeding: direct pressure, call MD if unable to stop in

10 minuteso 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, paino 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 Marrowo 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 diagnosiso 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/cytico Hemolytic: desctruction of RBCs

Sickle cell, thallasemia, heart valveo Blood losso 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/V—give by IV if

can’t 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 minutes—need two RNs, check compatibility, expiration, consent

o Begin within 30 minutes of release from blood banko Infuse within 4 hourso 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 reactiono Common—Chills, >1 C/2 F rise in temp, people more

at risk with multiple transfusionso Stop transfusion, rule out AHTR/infection

Allergic: always stop infusiono Mild: hives, itching, flushing—give anti-histamine,

resumeo Severe (anaphylaxis): anti-histamine, steroids,

vasopressors Fluid overload: infused too fast, too much volume—

diuretic between unitso Cough, dyspnea, crackles, tachy, HTNo Slow infusion, elevate HOB, lower feet, oxygen,

diureticIschemia

irreversible cell injury when tissue demand for oxygen is not met, toxic metabolites accumulate

Treatment: reduce O2 demand, increase O2 supply

Renal 2/21/15 11:47 PM

A+P

Nephron: smallest working unit of kidney

o Filter: water/solutes out of glomerulus into Bowman’s

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

Anuria: <50 ml/24 h

Oliguria: <400 ml/24 h

o BUN to creatinine ratio: 10-20:1

Pre-renal: ratio is >20:1

Intrinsic: normal

Post-renal: decreased/normal

o Creatinine: 0.6-1.2 mg/dl

UTI: lower (bladder, urethra, prostate), upper (kidney)

o Hematuria: >3 RBC

o Proteinuria: >20 mg/dl

o Pyuria: WBC>6-10

o Casts: >4, proteins from damaged tubules

o + nitrites, leukocyte esterase, glucose, ketones

o Culture: women (100,000 cfu per mL), men (10,000 cfu), gram

–

o Acute cystitis

Uncomplicated: oral antibiotic, analgesic, adequate fluid

intake

Complicated: men, diabetes, immunosuppression,

pregnancy, nosocomial, longer course of ATB

o Interventions: pain relief (pyridium/antibiotic, heat, increase

fluid), monitor for sepsis, AKI, chronic kidney disease

o Pyelonephritis: bacterial infection of kidney(s), ascending UTI,

acute or chronic, more frequent in women/DM

Acute: fever, chills, flank pain, N/V/Ana—run

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 (can’t 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

inflammation—thickening 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

Cardiac 2/21/15 11:47 PM

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 Can’t 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, patient’s 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

CHF 2/21/15 11:47 PM

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-angiotensin-

aldosterone system): kidneys release renin to

retain Na/H2O, constrict arteries to maintain BP to

get blood to vital organs, compensates well in

beginning but can’t 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

L eft 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)

Valvular Heart Disease 2/21/15 11:47 PM

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, fatigueo 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, dyspnea—later: angina, HR, syncope

Tests ECHO: TTE, noninvasive, uses sound waves, measures

ejection fraction, size/shape/motion of hearto 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 gago 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/endocardium—alters 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, bypasso 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 2.5-3.5), 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 sick—pulmonary 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