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Running Head: CASE STUDY NUR 7201 1&2 1

Case Study NUR 7201 1&2

Ashley Peczkowski

Wright State University

NUR 7201

CASE STUDY NUR 7201 1&2 2

Case Study NUR 7201

Case Study One

Questions:

1. What is the most likely diagnoses for this patient and what are the criteria for this

diagnosis? What is your rationale?

The patient’s most likely diagnosis is pulmonary atrial hypertension (PAH) secondary to

anorexigen pill consumption. Idiopathic PAH is more common in women and remains the most

common type. Primary PAH includes idiopathic, familial, and drug or toxin induced. Other

causes of PAH include congenital heart disease, connective tissue diseases, toxins, drugs, human

immunodeficiency (HIV), portal hypertension, hemoglobinopathies, and myeloproliferative

disorders. These causes are considered Group I PAH; Group II includes PAH with left heart

failure; Group III includes PAH with lung disease or hypoxemia; Group IV, PAH from chronic

thrombotic or embolic diseases; and Group V is miscellaneous PAH. According to the European

Society of Cardiology guidelines (Albert-Barbera et al., 2009), the criteria for a pulmonary atrial

hypertension (PAH) diagnosis is an increase in mean pulmonary arterial pressure of ≥25mmHG

at rest with a normal capillary wedge pressure, left atrial pressure, left ventricular end-diastolic

pressure, and a pulmonary vascular resistance pressure greater than three Wood units. A right

heart catheterization (RHC) is the gold standard for diagnosis. This test has the highest

sensitivity (93%) and specificity (95%) and is important for measuring severity of hemodynamic

impairment, predict prognosis, identify other causes, monitor etiopathology, and evaluate right

ventricular function (Schannwell, Steiner, & Strauer, 2007). During the RHC a vasoreactivity

test can be performed to identify patients who might benefit from long term therapy with calcium

channel blockers. An acute responder has a reduced mean pulmonary arterial pressure by


10mm/Hg to 40mm/Hg without reduced cardiac output (McLaughlin et al., 2009). The current

drug of choice for vasoreactivity testing is nitric oxide. Because this test is invasive, pre-

diagnosis tests are performed to confirm PAH and rule out other differential diagnoses (Albert-

Barbera et al., 2009).

The rational for this patient’s diagnosis came from the physical assessment and the pre-

diagnosis test results. The patient presented with increasing shortness of breath and fatigue, pre-

syncope episodes, dyspneic when walking short distances with relief after sitting, and substernal

chest pain. Advanced disease is suggested through a left parasternal lift, prominent S2, RV S4,

clear lung fields, and an increased jugular a wave indicating elevated right ventricular pressure,

hypertrophy and decreased right ventricular compliance; grade III/VI holosystolic murmur that is

increased with respiration indicates tricuspid regurgitation; hepatojugular reflux shows signs of

high central venous pressures. The cyanotic lips (central cyanosis) and ankle edema suggest

hypoxia and reduced cardiac output. The physical data are suggestive of a cardiopulmonary

disease such as right ventricular heart failure/hypertrophy, pulmonary embolism, severe anemia

or many others. History included use of known toxins such as the fenfluramine and phentermine

which have been indicated in causing primary PAH. Because of this data PAH is suspected; an

electrocardiogram (EKG) and chest x-ray re-confirm this diagnosis. There are many EKG

changes seen in patients with right ventricular hypertrophy (RVH) such as prolonged QRS

duration, right axis deviation, and enlarge right atrium. The diagnosis is suggested through

prominent RSR in lead V1-V6, ST depression, and T wave inversion. Right precordial leads with

ST depression and T inversion indicate that the RVH is severe. An echocardiogram (sensitivity

83%; specificity 72%) will provide the degree of severity. The enlarged pulmonary trunk seen on


the chest x-ray and the absence of left ventricular enlargement on both the chest x-ray and EKG

compliment this conclusion (MacLean, 2007).

Fenfluramine and phentermine use have been associated with increased risk of PAH and

have since been removed from the market. The exact correlation between these types of

anorexigen pills and PAH are not fully understood, however research suggests that these drugs

affects the serotonin receptors in the pulmonary endothelium. Research hypothesis that: While

normal serotonin synthesized by the pulmonary endothelium has a rate-limiting step, the use of

anorexigen pills causes an override initiating unregulated proliferation and/ or constriction

leading to PAH. During this process blood platelets are serotonin depleted while plasma

serotonin is elevated; vasoconstrictors such as endothelin and thromboxane are increased while

vasodilators like prostacyclin are decreased. Proliferation is also increased through endothelial

injury exposing muscle to growth factors and mitogen, and releases proinflammatory cytokines.

This process leads to elevated fibrinopeptide A, plasminogen activator inhibitor-1, and decreased

tissue plasminogen creating a hypercoagulable state (McLaughlin et al., 2009; MacLean, 2007).

This proliferation, apoptosis, and, in some patients, vasoconstriction results in constricted small

pulmonary arterial abnormalities including intimal hyperplasia, medial hypertrophy, adventitial

proliferation, thrombosis in situ, inflammation, and plexiform arteriopathy. Constriction in the

pulmonary arterioles increases the peripheral vasculature resistance increasing the afterload.

Marked increases in after load lead to right ventricular hypertrophy and dilatation. Key features

in Group I are the elevated pulmonary arterial pressure (greater than 25mm/Hg) and a normal

pulmonary capillary wedge pressure (McLaughlin et al., 2009). Based on the patients current

presentation, results of EKG and chest x-ray, and history of fenfluramine and phentermine use,


diagnosis of PAH is most likely. Additional pre-diagnosis testing and conformational diagnosis

though right heart catheterization is recommended.

2. What diagnostic test should be performed? Explain your rationale?

Pulmonary arterial hypertension is a diagnosis of exclusion and therefore the patient

should obtain investigational testing to determine the clinical grouping and etiology of the

diagnosis. Because the clinical presentation of PAH is non-specific and common in other

cardiopulmonary disease states, several pre-diagnosis tests are needed. These tests include an

EKG, chest x-ray, pulmonary function tests (PFT), arterial blood gases (ABG), transthoracic

echocardiography (TTE), ventilation/ perfusion lung scan (VQ scan), contrast computed

tomography (CT) scan, possible pulmonary angiography, cardiac magnetic resonance imaging

(MRI), blood tests including complete blood count (CBC), basic metabolic panel (BMP), thyroid

functioning tests, serological testing for HIV, hepatitis, and connective tissue disease (CTD);

abdominal ultrasound, and finally right heart catheterization and vasoreactivity. The European

Society of Cardiology and the European Respiratory Society have developed a PAH algorithm

guideline to help practitioners accurately diagnosis PAH. If the physical assessment and

presenting symptoms are consistent with PAH then an EKG, chest x-ray, TTE, PFT, ABG, and

chest CT should be ordered. Once other cardiopulmonary diseases and hypoxia are ruled out then

a VQ scan is ordered. Finally once any other causes have been ruled out a right heart

catheterization should be ordered to confirm PAH diagnosis. If diagnosis is confirmed than a

vasoreactivity test can be completed during catheterization to determine if calcium channel

blockers are an effective treatment measure. Further testing to determine clinical grouping and

cause should be considered. The specific diagnostic tests included the CBC, BMP, Liver function

tests, abdominal US, HIV, hepatitis, CTD, and history of drug toxins (Albert-Barbera et al.,


2009). Once the diagnosis is confirmed and the clinical grouping identified then the correct

treatment can be initiated.

3. What is the appropriate therapy for this patient. Include all types of therapy and

rationale for your choices.

A large majority of therapy for this patient is reducing morbidity and prolonging

mortality. There is a high mortality rate of 15% within the first year on medical therapy. Poor

prognosis is predicted through: advanced functional class, reduced 6-minute walking test, high

right atrial pressures, significant right ventricular dysfunction and failure, reduced cardiac index,

elevated brain natriuretic peptide, and an underlying scleroderma disease. The main treatment

goal is to reduce symptoms, improve quality of life, and improve survival. General measure

prevention therapy include physical rehabilitation, pregnancy prevention, social support for

depression and anxiety, flu and pneumonia vaccine for infection prevention, and epidural use for

elective surgeries. Supportive therapy includes oral anticoagulation due to the high risk of

vascular thrombotic lesions, diuretics for fluid retention, oxygen for hypoxemia, and digoxin for

improved cardiac output in acute atrial tachyarrhythmias. Once the vasoreactivity test has been

performed and the test is positive then the patient can be placed on specific calcium channel

blocker therapy. Calcium channel blockers used in treatment for PAH are nifedipine, diltiazem,

or amlodipine (McLaughlin et al., 2009).

For this patient because of her marked dyspnea with minimal activity, fatigue with

resting, right sided heart failure, and her near syncope episode, she is placed in a New York

Heart Association (NYHA) class IV classification. Based on the World Health Organization

functional class (WHO-FC) this patient should be placed on one or a combinations of


Ambrisentan, Bosentan, Sildenafil, Epoprostenol IV, or Iloprost inhaled. These drugs are a 1-A

recommendation. Combination therapy is recommended for PAH patients of advanced

classification. Warfarin is recommended to reduce hypercoagulable state and prevent emboli; a

therapeutic INR is between 1.5-2.5; symptomatic management from right ventricular fluid

overload involves the use of Diuretics; oxygen therapy is initiated to maintain O2 stats greater

than 90%; and lastly calcium channel blockers improves right ventricular compliance for those

with positive vasodilator response. Epoprostenol IV continuous infusion through a port is

indicated for those patients with class IV symptoms (Albert-Barbert et al., 2009). According to

the Ohio Board of Nursing (OBN) an acute care nurse practitioner (NP) may prescribe oxygen,

calcium channel blockers, and diuretics. Warfarin may be prescribed per institutional protocol

and physician initiated or consulted. Epoprostenol may only be prescribed if it has been

physician initiated or consulted and the NP works within the specialty clinic setting (OBN,

2013). Epoprostenol is given 20 to 40 ng/kg/min for optimal therapy benefits. This drug is a

prostacyclin which causes vasodilation and platelet aggregation. There may also be a

cytoprotective and antiproliferative activity. This is the only drug in the treatment on PAH to

show any improvement of mortality rates. Additional pharmacological therapy can be added if

there is no improvement, minimal improvement, or worsening of condition (Albert-Barbert et al.,

2009). Iloprost is an inhaled prostacyclin useful for improvement of exercise capacity and can be

prescribed by an NP (Albert-Barbera et al., 2009; OBN, 2013). Ambrisentan and Bosentan are

both endothelin receptor antagonist that cause vasodilation and release of antiproliferative

substances like nitric oxide and prostacyclin which are helpful in the treatment of PAH (Albert-

Barbera et al., 2009). Endothelin receptor antagonist may only be physician initiated or consulted

prior to being prescribed by a NP (OBN, 2013). Lastly Sildenafil is a Phosphodiesterate type-5


inhibitor that also causes vasodilation and can be prescribed by a NP (Albert-Barbera, et al.

2009; OBN, 2013). Surgical treatment for PAH are reserved for patients with declining

functional capacity despite maximal medical therapy. Surgical treatment involves atrial

septostomy creating a right to left shunt; this allows for decreased right ventricular filling,

improved right sided function, improve left sided filling, and improved cardiac output despite

reduced systemic arterial oxygenation. Atrial septostomy is performed to provide palliation,

restoration, and maintenance until a heart and lung transplant can be performed. Other treatments

include pulmonary thromboendarterectomy and right ventricular assist devices (McLaughlin et

al., 2009).

The objective of medical therapy is to improve functional capacity, stabilize or improve

hemodynamics, and improve survival. The easiest test to perform to evaluate effectiveness of

therapy is the “6 minute walk test”. Improvement in walking is generally indicative of effective

therapy treatment. Other routine tests to monitor drug therapies and PAH disease course include

an EKG, 6 minute walk test, and a BNP every three to six months. If therapy is changed or there

is a clinical worsening of the patient then an EKG, six minute walk test, cardio-pulmonary

exercise test, BNP, echocardiography, and right heart catheterization should be performed every

three to four months (Albert-Barbera et al., 2009).


Case Study Two

Questions:

1. What is your differential diagnosis? Explain.

Differential diagnosis is based on the type of acute renal failure including prerenal,

postrenal and intrinsic renal failure. Differential diagnoses for intrinsic renal failure are acute

tubular necrosis (ATN), glomerulonephritis, and tubulointerstitial nephritis. Based on the

patients recent history of receiving radiographic contrast during coronary angiography within 24

to 72 hours of oliguria, acute tubular necrosis from radiographic contrast, also called contrast

induce nephropathy (CIN), is the most likely cause. CIN is indicated when the serum creatinine

(Cr) is 0.5mg/dl or greater or Cr increases by 25% in 48 hours after radiographic contrast is

given (Adam et al., 2006). Acute tubular necrosis can be caused by nephrotoxic drugs such as

aminoglycosides, radiographic contrast, and chemotherapy or ischemia from hypotension or

vascular occlusions. Glomerulonephritis develops from post infectious, immune diseases,

vasculitis, hemolytic syndromes, or atheroembolic syndrome and presents with proteinuria and

microscopic hematuria (Parmar, 2009). Tubulointerstitial nephritis can be caused by medications

such as cephalosporins, methicillin, and rifampin or infections such as pyelonephritis and HIV

(Gonzalez & Praga, 2010). Based on the patients history and physical both glomerulonephritis

and tubulointerstitial nephritis are a less likely cause than acute tubular necrosis.

Prerenal can be caused by volume depletion, reduced arterial blood flow, medications

such as aspirin, NSAIDs, or ACE inhibitors, and decreased cardiac output. This patient is at risk

for prerenal failure because of his prior medication use of aspirin and ACE inhibitors. Post renal

failure results from an obstruction somewhere in the urinary system from a crystal, stone, or

tumor (Peacock & Sinert, 2011).


2. What is your next step to diagnose the problem? Explain. Of what value is a

urinalysis and urinary electrolytes?

A detailed history and physical is the most beneficial step in diagnosing renal failure

because it allows you to narrow down renal failure type. Obtaining a serum cysteine C level and

serum creatinine level next can show the degree of renal function. A serum cysteine C level is a

more specific test to kidney failure because it shows an accurate glomerular filtration rate and is

less influenced by variables such as age, race, sex, and muscle mass. For prerenal failure the UA

results show a high specific gravity with normal sediment. Finally a urinalysis (UA) and urinary

electrolytes are beneficial in creating a diagnosis. Post renal failure UA results have isosthenuria,

specific gravity of 1.010, and various findings depending on cause such as hematuria or

leukocytes. Intrinsic renal failure however varies greatly depending on cause. Typically all

intrinsic renal failures have isosthenuria and some degree of proteinuria. The differentiating

results are in the casts. Acute tubular necrosis has “muddy brown” granular casts,

glomerulonephritis has hematuria and red blood cell casts, and tubulointerstitial nephritis has

leukocytes, white blood cells, and eosinophil (Peacock & Sinert, 2011).

Urinary electrolytes are less helpful in diagnosis unless the patient has oliguria prerenal

failure or oliguria ATN. Pre-renal failure has a FEna that is less than one percent and urinary

sodium of less than 20mEq/L. In ATN the FEna is greater than two percent with urinary sodium

greater than 20mEq/L. These results vary considerably when the cause of acute renal failure is

different than those stated above (Adam et al., 2006). Other urinary electrolytes can provide

indications of other disease processes. These electrolytes include sodium, potassium, chloride,

and calcium. Sodium can give indication for HTN, glomerulonephritis, hepatic-renal syndrome;

potassium levels indicate diabetic acidosis, ATN, adrenal insufficiency, and


hyper/hypoaldosteronism; chloride levels indicate hypokalemia, tubular acidosis, and acid-base

imbalances; and finally calcium levels can indicate obstructive renal failure and parathyroid

disease (Peacock & Sinert, 2011).

3. What are the indications for dialysis in AKI (acute kidney injury)? Be specific.

The indication for dialysis in acute kidney injury include a BUN > 70 mg/dl in a

symptomatic patient without renal functional improvement, severe metabolic acidosis indicated

by a <7.2 pH, extensive fluid overload causing pulmonary edema, uncontrolled hypertension

greater than 180/110, hyperkalemia greater than 6.5 mEq/L, uremic symptoms, and pericarditis;

all of which are unresponsive to medical therapy (Klarenbach, Manns, Pannu, Tonelli, & Wiebe,

2008). Other variable indications are: Less severe previously stated criteria in combination with

gastritis with hemorrhage, nausea, vomiting, decreased appetite, coma, stupor, severe lethargy or

malaise, asterixis, tremor, seizures, bleeding diathesis, and pericarditis. Drug or toxin ingestion

of dialyzable agents such as lithium, ethylene, glycol, theophylline, barbiturates, and many

others are indications for hemodialysis. Hemodialysis is the preferred choice of dialysis because

it can be done in emergent situations, there is a greater control of hemodynamics, and blood

products can be given if needed (Abrao, Balbi, & Medicina, 2012). Guidelines for dialysis

treatment indications vary and are influenced by the patient’s presentation and the practitioner’s

previous medical experiences. Based on this patient’s lab results and presentation, dialysis would

not recommended. Close monitoring of the patients BNP, EKG, and vitals are necessary.

4. Write a set of admitting orders for the patient. Be specific.

Admission:

Admit: ICU/ CICU, attending Dr. Renal

Consult nephrology


Diagnosis:

Acute renal failure

Secondary diagnosis: Coronary artery disease; diabetes

Condition:

Serious

Vital Signs:

VS every hour with a temperature every four hours.

Continuous cardiac monitor

Record rhythm every shift and with cardiac rhythm changes.

Call practitioner:

BP: SBP <90mmHg or >180mmHg

HR: <50 or >120 BPM

Respirations: <10 or >30

Temperature ≥ 101.5

Obtain stat EKG if a change in cardiac rhythm or patient complains of chest pain.

Call practitioner if EKG is ordered.

Place patient on oxygen for O2 less than 92%. Titrate for O2 greater than 92%.

Allergies:

NKA

Activity:

As tolerated, ambulate in hallways TID

Nursing:

Obtain vital signs every hour


Obtain rhythm strip every eight hours

Monitor arterial line site every four hours for bleeding

Call practitioner if site is bleeding

Titrate oxygen level to maintain oxygen stats greater or equal to 92%

Neuro checks every four hours and as needed. Call practitioner if there is a

change in the patient’s mental condition

POC blood glucose checks AC&HS and at 3am. Call if patients’ blood sugar

is less than 50 or over 400

Obtain daily weights

Strict I&O

Place foley catheter

IS every hour while awake; C&DB every 2 hours while awake

Diet:

Cardiac diet/ Renal diet with low potassium to maintain a heart healthy diet

and to prevent an increase in the serum potassium levels which may lead to

the patient requiring dialysis.

Medications:

IV:

Normal saline 0.9% at 125cc/hr IV continuous

Medications:

Novolog insulin sliding scale SQ ACHS and three am:

Blood Glucose (mg/dL) Dose

<70 Hypoglycemia Protocol


70-130 0

131-180 4

181-240 8

241-300 10

301-350 12

351-400 16

400> Call NP

Aspirin 81mg PO daily

Rosuvastatin 20mg PO daily

Heparin 5,000 units SQ Q8H

Docusate 100mg PO BID

Losartan 50mg PO daily; hold if blood pressure less than 110 systolic

Resume beta-blocker dose and schedule; Hold if BP less than 100 systolic or HR

less than 50 BPM; Call practitioner if medication held.

PRN:

Morphine 2mg IV Q2H PRN minimal pain

Morphine 4mg IV Q2H PRN moderate pain

Morphine 6mg IV Q2H PRN severe pain

Roxicodone 5-10mg PO Q3H PRN moderate pain

Zofran 4mg IV/PO Q6H PRN nausea/ vomiting

Melatonin 5mg PO QHS PRN sleep

Lactulose 10-20g TID PRN constipation


Dextrose 50% 25ml IV as needed of glucose less than 50; recheck POC in 15

minutes. Give OJ if glucose between 70-50 and recheck POC in 15 minutes.

I&O:

Monitor every hour

Place foley for accurate I&O

Call practitioner if urine output is less than 30cc/hr over four hours.

Labs:

Stat CBC, sedimentation rate, serum cysteine C level, BMP, phosphate level,

magnesium level, A1C level, lipid profile, ABG, UA, and urinary electrolytes for

baseline labs

Once MRSA by PCR per ICU protocol

Once 24 hour urine

Obtain CBC daily to monitor hemoglobin and a BMP with magnesium and

phosphorus every six hours to closely monitor potassium and creatinine level

Obtain daily urine FEna, UA, and osmolality.

Special tests:

Stat chest xray to monitor for pulmonary edema

Obtain renal ultrasound with flow studies to rule out post renal obstruction and

hydronephrosis

Consider daily chest x-ray if pulmonary edema or infiltrates present

Consult:

Consult to nephrology for monitoring and to determine if the patient’s condition

or change in condition warrants the need for dialysis. Consult cardiac rehab.


Consult diabetic educator.

At Discharge:

The patient should be referred to an optometrist when discharge for follow up on

the diabetic retinopathy

Rational for medication prescribing include: The patient should be removed off of all

diabetic oral medication especially if he is on metformin as this can increase to amount of renal

damage. Subcutaneous insulin Novolog should be given with each meal after the blood sugar has

been checked to allow for closer monitors of the blood sugar. The patient many remain on their

dose of beta blocker unless the patient’s blood pressure declines in which case the dose should be

reduced by half. Beta blockers should never be stopped as this increases the decline of heart

failure. The aspirin dose should be low dose as a higher dose has not shown to have enhanced

effectiveness. Start normal saline 0.9% at 125cc/hr continuous because studies have shown that

hydration can reduce the severity of acute tubular necrosis from radiographic contrast. Normal

saline is better than half normal saline because the high sodium count allows for better volume

expansion and inhibits the renin-angiotensin pathway (Guo, Li, Wong, & Zhang, 2011).

5. Complete the following chart with values present in prerenal and acute renal

failure. Be certain to reference the chart.

Table 1. Differential Criteria of Pre-renal and Acute Renal Failure.

Laboratory Test Prerenal Acute Renal Failure

FeNa <1% >2%


BUN to creatinine ratio >20:1 <10:1

Urine specific gravity >1.020 1.010-1.020

Urine osmolality, mOsm per kg >500 250-300

Urine sodium concentration, mEq per L

(mmol per L)

<20mmol/L >40mmol/L

Urine sediment Normal or

Hyaline

Casts

Muddy brown Granular Casts

or Renal Tubular Epithelial

Cells

Table 1. Adapted from: (1) Hancock, 2005; (2) Harrison, T. R., & Longo, D. L.

(2013). Harrison's manual of medicine. New York: McGraw-Hill Medical


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