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❧
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)
❧ Lactic acid 8.2 (6.8)
❧ 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)
❧ Lactic acid 3.5 (8.2)
❧ Anion Gap 22 (23)
❧ Creatinine 1.68 (1.62)
❧ 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)
❧ Lactic acid 4.6 (3.5)
❧ Anion Gap 23 (22)
❧ Creatinine 1.98 (1.68)
❧ 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)
❧ Lactic acid 4.2 (4.6)
❧ Anion Gap 25 (23)
❧ Creatinine 3.29 (1.98)
❧ 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
❧Trended labs
❧Trended labs
❧Trended labs
❧Trended labs
❧Trended labs
❧Trended labs
❧❧ Bicarb 12 (15)
❧ Lactic acid 3.7 (4.2)
❧ Anion Gap 24 (25)
❧ Creatinine 3.81 (3.29)
❧ 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)
❧ Lactic acid 4.0 (3.7)
❧ Anion Gap 17 (24)
❧ 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
❧Type B lactic acidosis
❧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.
❧
Type B lactic acidosis
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
❧Type B lactic acidosis
❧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
❧Type B lactic acidosis
❧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.
❧Type B lactic acidosis
❧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
❧
Type B lactic acidosis
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).
❧
Type B lactic acidosis
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