shortness of breath a symptom not always understood of breath – a symptom not always understood...

❧

Shortness of breath –

a symptom not

always understood

Case Conference

March 18, 2014

Andrea Caballero

❧❧ DOE x 1 week

Chief Complaint

❧54 year-old woman with PMHx of HIV (CD4 count 485; 30.6%), DM2, HTN and CKD stage 3 who presented with DOE. Four days prior to presentation, she experienced an episode of SOB while walking in the Dollar Store. She returned to her car and sat down for a while and her SOB resolved. Dyspnea progressively worsened => exacerbated with exertion and improved with rest. ❧ No CP, diaphoresis, headache, dizziness, N/V ❧ At baseline she could ambulate a little over a block before

getting SOB. On presentation she would get SOB after 50ft. ❧ Baseline 3 pillow orthopnea; no PND❧ Decreased PO intake, but still urinating 5-6 times/day due to

the furosemide she takes for pedal edema (at baseline). ❧ No fever, chills, cough or calf pain/redness/swelling.

HPI – 1st presentation

❧❧ Earlier that day:

❧ Pt was seen at diabetes clinic and metformin was

discontinued due to increase in Creatinine from

baseline of 1-1.4 (GFR 50-59) to 2.6 (GFR<30).

❧ Patient did not complain of any symptoms

HPI

❧❧ HIV (diagnosed on 3/2013– CD4 391 / 24.3% and on 7/13-

485 / 30.6%). ❧ Hypertension

❧ Diabetes mellitus type 2 (A1C 7.8 on day of admit)

❧ CKD stage 3

❧ Dyslipidemia

❧ Iron Deficiency Anemia

❧ Vitamin D deficiency

❧ Central Retinal Vein Occlusion with Cystoid Macular Edema

Past Medical History

❧❧ Cone biopsy

❧ Hysteroscopy w/ polypectomy

Past Surgical History

❧❧ Lamivudine-Zidovudine

150-300mg BID❧ Raltegravir 400mg BID❧ Metformin 1000mg BID❧ Insulin Glargine 42Units BID❧ Insulin Aspart 16Units QAC❧ Amlodipine 10mg Qday❧ Clonidine 0.2 TID❧ Labetalol 300mg TID❧ Lisinopril 40mg Qday

Medications

❧ Furosemide 40mg Qday❧ Spironolactone 50mg Qday❧ Pravastatin 40mg QHS❧ Esomeprazole 40mg Qday❧ Colace 100mg prn

constipation❧ Ferrous Gluconate 240mg

Qday❧ Loratidine 10mg Qday❧ Timolol 0.5% opth BID

❧❧ NKDA

Allergies

❧❧ DM2 and HTN in several first degree relatives

Family History

❧❧ Negative for tobacco, alcohol, and illicit drug use

❧ Lives alone and works as a bus driver and hall

monitor at a school in the lower 9th ward

❧ 3 heterosexual partners; partner 9 months prior to

HIV diagnosis likely source

Social History

❧❧ Up to date on influenza vaccine

❧ Up to date on Tdap vaccine

❧ Received 1st dose of Hepatitis B vaccine

❧ No pneumococcal vaccine

❧ Up to date on PAP

❧ Mammogram > 1yr

❧ Colorectal cancer screen - FOBT neg x 3

Health Maintenance

❧❧ Gen: No weight changes

❧ HEENT: no visual changes/sore throat/rhinorrhea

❧ CV: per HPI

❧ RESP: per HPI

❧ GI: per HPI

❧ Neuro: No numbness

❧ Skin: No new rashes

❧ GU: No complaints

ROS

❧Physical Exam

❧Vitals

❧Triage

❧ BP 111/59 P 107 RR 26 T 96.8 O2 100% on RA

❧ 5’0” 126kg BMI 54

❧Exam

❧ BP 93/57 P 94 RR 16 T 98.8 O2 98% on RA

❧❧ Gen: Alert, appears stated age and cooperative, obese,

uncomfortable but in no distress. Could speak in full sentences

❧ Head: Normocephalic, without obvious abnormality, atraumatic❧ Eyes: Conjunctivae/corneas clear. PERRL, EOM intact. ❧ Throat: Lips, mucosa, and tongue normal; teeth and gums

normal ❧ Neck: No adenopathy, no carotid bruit, unable to assess JVD

secondary to body habitus, supple, symmetrical, trachea midline

❧ Lungs: Clear to auscultation bilaterally, no w/r/c❧ Heart: Tachycardic, regular rhythm, S1, S2 normal,

no S3/S4/m/r❧ Abdomen: Obese; bowel sounds normal; soft, non-tender; no

organomegaly could be appreciated

Physical Exam

❧❧ Extremities: Extremities normal, atraumatic; no cyanosis or

edema ❧ Pulses: 2+, symmetric radial and DP pulses bilaterally.

❧ Skin: Dry skin, no rashes

❧ Neuro: Awake, alert, and oriented x4. Sensation intact to

light touch; biceps, patellar reflexes 2+. Strength is 5/5

bilaterally in the upper and lower extremities. Cerebellar

function intact as demonstrated by finger to nose evaluation.

CN II-XII: intact

Physical Exam

❧Labs Admit

135 101 48

5 17 2.66

204

AG 19

Ca 9.1 Mg 2.1 Phos 3

TP Alb TB AST ALT ALP

7.4 3.2 1.0 35 29 114

(65-99)

(0.5-1.10)

(7-25)

(24-32)

(3.4-5)

(1.2)6.8 23410

30.3

N 60 L 21 M 16 E 3

113.5

17.2

(10-11)

(40-51)

(13.5-17.5)

(80-100)

(11.5-14.5)

(5-6)

(4.5-11)

(25-28)

(33-34)

(20-25)

❧Labs cont’d

Trop <0.01

BNP 29

D-dimer 2519

Lactic acid 4.4

CK 460

PT 12.5/NR 1.2/PTT 27

ABG on RA 7.25/35/80/94.4%

(0.3-2.4)

UA:

Sg

pH

Prot

Glu

Ket

Blood

Nitrite

Urobil

1.020

5.0

Neg

Nml

5

25

Neg

1.0

RBC 6-10

WBC 3-5

Sq >100

Bact Rare

Casts Neg

Utox - negative (35-45)(7.35-7.45)

❧❧ DOE - negative trop, BNP 29. CXR clear. D-dimer 2519,

VQ scan negative. TTE with normal systolic function (EF

>55%). ABG 7.25/35/80/15. Believed to be partly 2/2

body habitus.

❧ AGMA - thought to be 2/2 metformin and ART. Both

discontinued. Lactic acid 4.4 on admit, 4.3 on discharge.

AG improved (15)

❧ AKI on CKD3 - FeNa 0.25%, no eos. CK 460. Creatinine

decreased to 1.5 by discharge with IVF. Thought to be

from dehydration and over diuresis. Stopped ACEI,

spironolactone and furosemide.

Hospital Course

138 107 35

5.2 18 1.5

204

❧❧HIV - ART stopped. CD4 432 (27.2%)

❧DM2 - A1C 7.8. Basal insulin decreased to 25 Units

BID

❧Patient was discharged home and followed up with

her PCP at HOP 3 days later.

Hospital Course cont’d

❧❧ Re-presented to ED 5 days after discharge stating that

her DOE was not improved❧ Since the time of discharge she had also been

experiencing lower abdominal pain (unable to point to exact location), present all the time, 10/10. She was not able to keep any food or liquids down, despite feeling hungry. She would vomit whenever she attempted to eat or drink anything. ❧ Non-bloody, non-bilious, usually whatever food/drink

she had just consumed. ❧ No alleviating factors.

❧ Denied subjective fevers, chills, night sweats, dysphagia, changes in BM quality/color (last BM morning of presentation), dysuria/hematuria, discharge.

HPI – 2nd presentation

❧❧Vitals

❧Triage

❧ BP 136/73 P 98 RR 24 T 97.8 O2 99% on RA

❧ 5’0” 126kg BMI 54

❧Exam

❧ BP 111/47 P 99 RR 22 T 98.5 O2 100% on

RA

Physical Exam

❧❧ Gen: Alert, appears stated age and cooperative, obese,

uncomfortable but in no distress. Could speak in full sentences but appeared tired.

❧ Head: Normocephalic, without obvious abnormality, atraumatic

❧ Eyes: Conjunctivae/corneas clear. PERRL, EOM intact. ❧ Throat: Lips, mucosa, and tongue normal; teeth and gums

normal ❧ Neck: No adenopathy, no carotid bruit, unable to assess JVD

secondary to body habitus, supple, symmetrical, trachea midline

❧ Lungs: Clear to auscultation bilaterally, no w/r/c❧ Heart: Tachycardia, regular rhythm, S1,S2 normal, no

S3/S4/m/r❧ Abdomen: Obese, bowel sounds normal; soft, pain with deep

palpation and manipulation of RL pannus, no erythema;; no masses, no organomegaly could be appreciated.

Physical Exam

❧❧ Extremities: Atraumatic, no cyanosis or edema ❧ Pulses: 2+, symmetric radial and DP pulses bilaterally. ❧ Skin: Dry skin, no rashes

❧ GU: No lesions on labia, vaginal canal without erythema, scant

white discharge, not foul smelling. Cervix closed, no discharge,

purple in color. No tenderness with speculum. Could not

perform bimanual 2/2 body habitus. Wet prep - no trich, <50%

clue cells

❧ NEURO: Awake, alert, and oriented x4. Sensation intact to light

touch. Reflexes are 2+ in biceps, patellar. Strength is 5/5

bilaterally in the upper and lower extremities. Cerebellar function

intact to finger to nose. CN II-XII: intact

Physical Exam

❧Labs

134 103 43

5.8 12 2.25

166

AG 22

Ca 9.5 Mg 2.6 Phos 3.0

TP Alb TB AST ALT ALP

7.3 3.0 2.0 43 33 264

(24-32)

(65-99)

(7-25)

(0.5-1.10)

(3.4-5) (<1.3) (20-120)

(1.5)11 311

10.6

43.2

N 70 L 10 M 3 E 1 B 1 bands 7

114.6

18.9

(13.5-17.5)

(10-11) (80-100)

(11.5-14.5 )

(4.5-11)

(35-46)

(25-28)(5-6)

(20-25)

(33-34)

❧Labs cont’d

Beta-OH 1.87

Trop 0.02

BNP 81

Lactic acid 4.9

ABG on RA 7.25/27/95/95.8%

(<0.3)

(0.3-2.4)

UA:

Sg

pH

Prot

Glu

Ket

Blood

Nitrite

Urobili

1.024

6.5

25

Neg

15

250

Neg

8.0

RBC 51-99

WBC 6-10

Sq >100

Bact Neg

Casts 6-10

Utox - negative

(35-45)(7.35-7.45)

❧❧ Patient admitted to LSU Medicine

❧ CXR clear.

❧ ABG 7.25/27/95/11.8.

❧ BNP 80, recent ECHO normal.

❧ AGMA – anion gap 22. Likely from renal function

and medications (recently stopped). Lactic acid 4.9.

❧ With leukocytosis and abdominal pain, cultures sent

and empirically started on Vancomycin/Piperacillin-

Tazobactam/Ciprofloxacin (renally dosed)

Admission

❧❧ AKI on CKD3 - Creatinine increased at 2.2 (1.5 on

discharge). FeNa 0.18%, no eosinophils. Started

IVF.

❧ Elevated AP/Tbili, N/V - lipase 48. RUQ ultrasound

was limited by patient’s body habitus, showed

hepatomegaly (diameter of 19cm, CBD 2.9mm)

Admission cont’d

❧❧ Blood Pressures low/nml with Tachycardia (90s-100s),

oxygen saturations wnl

❧ DOE - unchanged

❧ Nausea and vomiting with minimal improvement.

❧ Pannus still TTP.

❧ Alk Phos and Tbili continued to increase.

❧ On broad spectrum abx, all cultures NGTD.

❧ Still on continuous NS IVF. Cr improved - 1.64 from 2.25

❧ Renal consulted

Day 2

❧❧ CT abd with PO contrast

- hepatic steatosis. No

bowel wall thickening or

adjacent changes

indicating inflammation

❧ ABG on RA

7.29/30/125/14.4

❧ On IVF, improving

creatinine 1.47 (1.64)

Day 3

❧ Labs:

❧ Bicarb 17 (12)

❧ Lactic acid 6.8 (4.9)

❧ AG 19 (22)

❧ CK 176

❧ AST 48 (43)

❧ ALT 30 (33)

❧ Tbili 2.9 (2.0)

❧ AP 276 (264)

❧ Hepatotoxic meds

discontinued - abx, statin,

protonix.

❧❧ Labs:

❧ Bicarb 12 (17)


❧ Anion Gap 23 (19)

❧ Creatinine 1.62 (1.47)

❧ AST 53 (48)

❧ ALT 30 (30)

❧ Tbili 3.4 (2.9)

❧ AP 290 (276)

❧ Given 3 amps of bicarb in D5 ½N

❧ L-carnitine, Vit B complex, Thiamine, Vitamin C

supplementation started

Day 4

❧❧ Labs:

❧ Bicarb 15 (12)




❧ AST 85 (53)

❧ ALT 35 (30)

❧ Tbili 3.6 (3.4)

❧ AP 290 (290)

❧ GI consulted - recommend HIDA

Day 5

❧Day 5 cont’d

❧ WBC 15.5, 3% bands. Afebrile.

❧ Piperacillin-Tazobactam restarted

❧ Blood Glucose readings

❧ Day prior: 147-186 on 15U Lantus and SSI

❧ Day 5: Elevated at 342 that afternoon

❧ Patient placed on BIPAP overnight

❧❧ Labs:

❧ Bicarb 15 (15)




❧ AST 130 (85)

❧ ALT 47 (35)

❧ Tbili 4.9 (3.6)

❧ AP 332 (290)

❧ WBC 14.9 (15.5), 0% bands (3%)

❧ ABG - 7.28/32/75/15

Day 6

❧❧ ICU consulted

❧ Blood Glucose readings 261-342

❧ UA shows persistent ketone

❧ Pulmonary consulted, no new recommendations

Day 6 cont’d

❧❧ First episode of hypotension, 89/39 with a repeat

read of 95/50

❧ WBC 23.6, 12% bands. Afebrile.

❧ Linezolid started for possible panniculitis.

❧ Dermatology consulted for punch biopsy

❧ HIDA scan showed diffuse hepatocellular

dysfunction.

❧ Autoimmune workup pending - AMA, ANA

Day 7

❧❧ Bicarb 15 (15)




❧ AST 141 (130)

❧ ALT 58 (47)

❧ Tbili 6.9 (4.9)

❧ AP 365 (332)

❧ ABG - 7.23/29/86/12.1

❧ Blood Glucoses: 280-301

❧ UA with 15 ketones, beta OH 7.3

Day 7 cont’d

❧Trended labs

❧❧ Bicarb 12 (15)




❧ AST 151 (141)

❧ ALT 63 (58)

❧ Tbili 7.9 (6.9)

❧ AP 384 (365)

❧ WBC 22.5 (23.6), 10% (12%) bands

Day 8

❧❧ Blood Glucose 204-316

❧ Continued to titrate insulin

❧ UA with 15 ketones, beta OH 7.76

❧ Ammonia 218

❧ ABG 7.16/30/80/10.7

❧ BP 84/65, HR 117, Blood Glucose 316

❧ Trialysis catheter placed in Right Internal Jugular

❧ Transferred to ICU

Day 8 (cont’d)

❧❧ Pt confused and tachypneic

❧ CRRT initiated – creatinine improved to 1.64 (3.81)

❧ Continuous BiPAP

❧ Insulin drip started - beta OH 4.96 (7.76)

❧ Lactulose started - ammonia improved to 107 (218)

Day 8/9 -ICU

❧❧ Bicarb 16 (12)



❧ AST 131 (151)

❧ ALT 66 (63)

❧ Tbili 8 (7.9)

❧ AP 424 (384)

❧ WBC 23.8 (22.5), 13% (10%) bands. Afebrile.

Day 8/9 cont’d

❧❧Patient went into asystole and was unresponsive

❧Code was called and several rounds of ACLS were

performed with multiple amps of NaHCO3 given due

to her profound metabolic acidosis

❧Patient never regained ROSC

❧Patient died

❧Autopsy was not performed per the family’s request

Day 9

❧❧Metabolic Acidosis

❧Lactic acidosis => ? mitochondrial dysfunction

due to antiretroviral therapy

Final Diagnosis

❧

Thank You

❧❧Most common cause of metabolic acidosis

in hospitalized patients.

❧Associated with:

❧Elevated anion gap

❧Plasma lactate > 4 meq/L

❧Leads to:

❧Impaired tissue oxygenation

❧Cause increased anaerobic metabolism

❧Source of rise in lactate production

LACTIC ACIDOSIS

❧Pathophysiology

❧Factors that accelerate

pyruvate production and

simultaneously impair

mitochondrial oxidation,

thereby increasing pyruvate

and lactate generation

include:

❧Inadequate oxygen

delivery or utilization

❧Rapid oxidation of

certain substrates

❧Such as ethanol.

❧❧ When lactic acid accumulates in body fluids and its concentration increases

❧ Hydrogen ions are almost completely buffered by extracellular bicarbonate.

❧ When lactate is utilized a hydrogen ion is also consumed.

❧ Whether by oxidation to CO2 and water or conversion to glucose or alanine

❧ Thus utilization of the lactate will restore the bicarbonate concentration.

❧ Excess lactate can accumulate as a result of increased production and/or diminished

utilization

❧ Three mechanisms can cause this accumulation:

❧ Increased pyruvate production

❧ Reduced entry of pyruvate into mitochondria, where it would be converted to

either carbon dioxide and water or to glucose precursors

❧ A shift of the cellular redox state such that NADH accumulates, which drives the

pyruvate/lactate ratio toward lactate

Pathophysiology Cont.

❧❧The causes of lactic acidosis can be divided into:

❧Those associated with obviously impaired tissue

oxygenation (type A)

❧Those in which systemic impairment in

oxygenation does not exist or is not readily

apparent (type B)

Causes

❧TYPE A Lactic acidosis

❧Type A lactic acidosis

❧Most cases d/t marked tissue hypoperfusion in:❧Shock

❧due to hypovolemia, cardiac failure, or sepsis

❧Or during a cardiopulmonary arrest.

❧Concurrent respiratory acidosis can contribute to the acidemia

❧Prognosis generally poor unless tissue perfusion

rapidly restored.

❧Initial serum lactate level is a strong predictor of

survival in patients with septic shock

❧Type B lactic acidosis

❧Evidence for systemic hypoperfusion is not apparent

in type B lactic acidosis.

❧Mechanisms that may be involved include

❧Toxin-induced impairment of cellular

metabolism

❧Regional areas of ischemia


❧Metformin induced

❧Risk very low

❧More common with phenformin

❧Symptoms nonspecific and may include:

❧Anorexia, nausea, vomiting, abdominal pain,

lethargy, hyperventilation, and hypotension.

❧Serum lactate usually < 2 mmol/L

❧More serious lactic acid accumulation occurs w/:

❧Superimposed shock or

❧Presence of predisposing conditions to

metformin toxicity below

❧

Type B lactic acidosis

Metformin induced

❧Has high fatality rate.

❧Most cases have occurred in patients with shock or tissue

hypoxia or in the presence of several other predisposing

conditions❧ Impaired renal function

❧ Cr of 1.4 mg/dL in women and 1.5 mg/dL in men

❧ Concurrent liver disease or alcohol abuse

❧ Heart failure

❧ Use has been common and well tolerated

❧ Decreased tissue perfusion or hemodynamic instability due to infection or other

causes

❧ Past history of lactic acidosis

❧ Of these factors, impaired renal function is of greatest concern

❧ Heart failure least worrisome.

❧


Metformin induced

❧Treatment❧ Role of bicarbonate therapy in patients with lactic acidosis and shock or tissue hypoxia

is not well established

❧ Concern about possible worsening of intracellular acidosis.

❧ Limit use to patients with:

❧ Severe metabolic acidosis (arterial pH below 7.10 to 7.15)

❧ Aim being to maintain the pH above 7.15,

❧ Until the acute toxicity resolves.

❧ In patients with concurrent renal failure, bicarbonate hemodialysis can both correct

the acidosis and remove metformin

❧ HD should be used in patients who are:

❧ Critically ill

❧ Severe metabolic acidosis (pH <7.1)

❧ Fail to improve with supportive care or

❧ Renal insufficiency is present


❧Malignancy

❧Pathogenesis is unclear

❧Rarely occurs with rarely leukemia, lymphoma, and solid malignancies

❧ removal of the tumor (by chemotherapy, irradiation, or surgery) usually

corrects the acidosis

❧ETOH

❧ Mild degree may develop in chronic severe alcoholism.

❧Lactate production usually normal

❧Lactate utilization may fall as a result of hepatic dysfunction.

❧Oxidation of ethanol can increase NADH levels and reduce the

NAD+/NADH ratio.

❧This will shift pyruvate toward lactate.

❧ Lactate levels do not exceed 3 meq/L in these patients.

❧Alcohol ingestion can potentiate the severity of other disorders that

cause overproduction of lactate


❧Antiretroviral medication-induced mitochondrial dysfxn

❧Typically occur in absence of systemic hypoperfusion

❧Without intervention, leads to a fatal outcomes

❧Most often due to liver failure and cardiac arrhythmias.

❧Risk Factors:

❧Associated with exposure to dideoxynucleosides (NRTI’s)

❧Female gender

❧Advanced immunosuppression

❧Hepatic steatosis

❧ Possibly ethnicity.


❧Symptoms may be nonspecific and include: ❧Nausea, vomiting

❧Abdominal pain or liver failure

❧Aminotransferases are only mildly abnormal in most cases

❧Weight loss

❧Severe fatigue

❧Extertional dyspnea

❧Hyperventilation

❧Arrhythmias

❧Usually follows a minimum of six months of

treatment❧May occur precipitously

❧


ART-induced

❧ Gold standard for the diagnosis of nucleoside-

related mitochondrial toxic effects (Lactic Acidosis,

etc) is a muscle or liver biopsy

❧Tx for Asxs Lactic acidosis

❧Substitution of the implicated nucleoside analogue w/

alternative drug in the same class that has less

mitochondrial toxicity is recommended.

❧ lactate levels slowly normalized

❧Can consider:

❧An all together alternate regimen or

❧ART may be discontinued temporarily

❧Treated with medications, which may have a benefit on

mitochondrial function (eg, riboflavin, carnitine, thiamine,

coenzyme Q).

❧


ART-induced ❧Tx for Sxs for Lactic Acidosis

❧ALL HIV meds should be stopped immediately and

❧Close monitoring in a hospitalized setting

❧ For potential clinical progression, despite ART discontinuation

❧Resolution of lactic acidosis after discontinuation can be extremely slow

❧Reported experience is from 4 to 28 weeks

❧ Lactate level itself may be a risk factor for mortality

❧No controlled trials to prove benefit but meds that support mitochondrial

function should be given

❧Anecdotal success has been described for combinations of:

❧riboflavin (50 mg daily)

❧L-carnitine (1000 mg twice daily),

❧thiamine (100 mg daily).

❧Easily available (also intravenously) and relatively harmless.

❧Survival also described with uridine (1000 mg three times daily)

❧Not easily available and cannot be given intravenously

❧

ART Induced Lactic Acid

❧❧ The following general approach applies to the use of bicarbonate therapy:

❧ Who should be treated

❧ Lactic acidosis and severe acidemia (pH less than 7.1, but generally not those

with higher values)

❧ may treat/prevent the following adverse clinical effects of acidemia, each of which

can produce hemodynamic instability:

❧ Reduced left ventricular contractility

❧ Arrhythmias

❧ Arterial vasodilation and venoconstriction

❧ Impaired responsiveness to catecholamine vasopressors

❧ Goals of therapy

❧ Primary aim of therapy is reversal of the underlying disease (eg, shock).

❧ When using bicarbonate therapy in patients with lactic acidosis

❧ the aim is to maintain the arterial pH above 7.1 until the primary process

causing the metabolic acidosis can be reversed.

Bicarb Therapy

❧❧ Potential harms

❧ Rapid infusions of sodium bicarbonate may:

❧ Increase the PCO2

❧ Bicarbonate must undergo several metabolic steps

❧ Generates CO2 that must be removed by circulation and respiration

❧ Adequate perfusion and ventilation is a prerequisite

❧ Even with adequate ventilation, PCO2 likely to rise at the local tissue

❧may worsen intracellular acidosis even as arterial blood pH inc

❧ In CSF

❧ At baseline a rise in arterial pH diminishes the drive for hyperventilation

❧Causing systemic PCO2 to increase.

❧Any systemic and/or local inc in PCO2 quickly reflected within CSF.

❧ Increased bicarbonate concentration is slowly transmitted to the CSF.

❧"paradoxical" CSF acidemia results from infused bicarb

❧ may be associated with neurologic deterioration

Bicarb Therapy

❧❧ Potential harms

❧ Accelerate the production of lactate

❧ by reactivating glycolysis (which can produce LA) with inc pH

❧ Lower the ionized calcium

❧ Secondary to inc pH

❧ Can effect cardiac membranes

❧ Expand the extracellular space, and

❧ Raise the serum sodium concentration.

❧ Approach

❧ In adequately ventilated patients with lactic acidosis and severe academia:

❧ Give 1 to 2 meq/kg sodium bicarbonate as an intravenous bolus.

❧ repeat this dose after 30 to 60 minutes if the pH is still below 7.1.

Bicarb Therapy

ssann1

Text Box

References: Emmett, M; Causes of lactic acidosis; UpToDate; 4/2014. Brinkman, K; Mitochondrial toxicity of HIV nucleoside reverse transcriptase inhibitors; UpToDate; 1/2013. Chu, J, Stolbach A; Metformin poisoning; UpToDate; 3/2014. Wiederkehr, M, Emmett, M; Bicarbonate therapy in lactic acidosis; UpToDate; 1/2014.

shortness of breath a symptom not always understood of breath – a symptom not always understood...

Documents