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Laboratory Interpretation. K.Thornton MSN,RN. Blood Loss. Acute blood loss. Hemolytic anemia. Infection. Acute Infection. Sepsis. Coagulation Tests. HIT. DIC. Nutrition Function. Electrolytes. Sodium. Potassium. Magnesium. Rhabdomyolysis. Drug Monitoring. Lecture Outline.

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Laboratory interpretation

Laboratory Interpretation

K.Thornton MSN,RN


Lecture outline

Blood Loss.

Acute blood loss.

Hemolytic anemia.

Infection.

Acute Infection.

Sepsis.

Coagulation Tests.

HIT.

DIC.

Nutrition Function.

Electrolytes.

Sodium.

Potassium.

Magnesium.

Rhabdomyolysis.

Drug Monitoring.

Lecture Outline


Blood components

Update, 4:55

Blood Components

  • Plasma:55% of whole blood

  • Erythrocytes: 44% of whole blood

  • Leukocytes & Platelets: <1% of whole blood

5:42


Hemoglobin hematocrit

Hemoglobin (Hb):

O2 binds to “heme” of Hb.

Each RBC contains ~ 300 million molecules of Hb.

Combines with 1.39 cc O2.

1 unit PRBC: incr hb by 1gm.

Hematocrit (Hct):

Percentage of RBC in whole blood.

Hct is usually 3X Hb value.

1 unit PRBC: incr Hct by 3-4%

Hemoglobin & Hematocrit

7:10


Acute blood loss

Acute Blood Loss

  • Manifestations are related to loss of blood volume rather than loss of hemoglobin.

    • Blood Volume = plasma + cells

  • Blood Loss: Loss of both plasma & cells.

  • Decrease in Hemoglobin:

    • reflects loss of cells only

  • Decrease in Hematocrit:

    • reflects loss of plasma & cells

    • (Example: Pt has 8hb & 24RBC, then receives 1unit. Now pt has 9hb & 27RBC)


Acute blood loss1

Acute Blood Loss

Plasma is

replaced in a

few hours

 Platelet

count

Internal

Hemorrhage:

 Neutrophil

count

 RBC.  Hb.

 Hct.

Iron recovered

External

Hemorrhage:

Shift from tissues & interstitium to vascular

Presence

of myelocytes,

metamyelocytes &

nucleated RBC in

circulation

Iron is depleted

Shift of

marginated WBC

into circulation

Incr Erythropoiesis


Hemolytic anemia

Hemolytic Anemia

  • Premature, accelerated destruction of RBCs.

  • Accelerated Erythropoiesis (8xnormal):

    • BM’s “bone marrow” response to RBC destruction.

  • CBC: “Complete blood count”

    • Decr RBC count, Hct, & Hb

  • RDW:(Incr RBC Distribution Width- “the size of RBC”)

    • b/c of Anemia, RBC loss, and sickle cell disease

    • Increased in variation


Laboratory interpretation

RBC Destruction & Bilirubin

Spleen

RBC

Hemoglobin

Liver

Globin

Heme

Glucuronide

Indirect Bilirubin

(Unconjugated)

Direct Bilirubin

(Conjugated)

Kidney

Bacteria

Duodenum

Urobilinogen

Urobilinogen

Stool

Urine


Hemolytic anemia1

Hemolytic Anemia

  • Reticulocyte Count: immature cellsincreased

    • Causes: Sickle cells &/or alcoholism

  • s

  • Indirect (Unconjugated Bilirubin): increased

    • An early sign of liver disease/problems

  • Urine Urobilinogen: increased

    • An early sign of liver disease

  • Serum Haptoglobin (Hp): decreased

    • Meaning you have sickle cell & Thaslassemia

  • Sign of bloodloss: 1st see change in consciousness & restlessness. THEN, H&H will be affected/show.


Acute infection inflammation injury

Acute Infection / Inflammation / Injury

ESR

Albumin

C-Reactive

Protein (CRP)

Increases

Elevated

means infection or injury

Decreases

A protein, body

Is using it up for

Energy.

hs-CRP:

Assess risk of MI


Viral infections

Viral Infections

Decreased WBC

Count

Increased

Lymphocytes

Its just the nature of the infection…


Acute bacterial infection inflammation injury

Acute Bacterial Infection / Inflammation / Injury

WBC Count

Recovery:

Acute:

Sepsis:

Towards normal values

Will see

Decrease

b/c you’re

screwed

Will see

increase

Increased

Monocytes (Phagocytes)

= recovery phase of acute infections


Acute infection inflammation injury1

Acute Infection/Inflammation/ Injury

Neutrophil Count

3000 – 7000 /mm3 or

~ 45 - 75% of total WBC Count.

Sepsis:

Decreased

Acute Bacterial:

Increased

Decr Segs

Will see

Incr Bands

Incr Segs

Recovery:

Incr bands

Metamyelocytes

& Myelocytes

Decr Bads. Incr Segs.

0 metas & myelos


Neutrophil maturation see bands then you sick

Neutrophil MaturationSee Bands = then you sick


Shifts in wbcs a shift of cells regenerative means you re getting better

Shifts in WBCsa shift of cells. Regenerative means you’re getting better.

0 Bone

Marrow

Response

  • Degenerative Shift to the Left:

    • Increase in band cells with no leukocytosis.

      • Poor prognosis (Degenerative = Down)

  • Regenerative Shift to the Left:

    • Increased band cells with leukocytosis.

      • Good prognosis

  • Shift to the Right: (Right recovery)

    • Decreased band cells with increased segmented neutrophils.

Bone

Marrow

Response


Response to infection injury

Response to Infection & Injury

Local Inflammatory

Response

Systemic Inflammatory

Response (SIRS).

When SIRS is caused by microorganisms

Sepsis

Sepsis w/ hypoperfusion & organ dysfunction

Severe Sepsis

Sepsis w/ hypotension despite fluid resuscitation

Septic Shock

39:18


Septic shock fluid is the primary treatment for sepsis

Septic ShockFluid is the primary treatment for sepsis.

  • Criteria:(Any 3)

    • Temperature < 36 oC (96.8F)OR > 38 oC (100.4F).

    • HR > 90 bpm.

    • RR > 20 /min OR PaCO2 < 32 mm Hg.

    • WBC count < 4,000 cells/mm3, OR > 12,000 cells/mm3, OR > 10% band forms.

    • Lactate level 4 or greater = sepsis

  • ~ 750,000 new cases/year & 200,000 deaths.

  • Estimated annual cost of Rx > $16 Billion!


Laboratory interpretation

Bacteria. Trauma. Shock

Sepsis

Pathophysiology

Inflammatory Response.

Release of chemical mediators.

Endothelial

damage

 Vascular

permeability

Stimulation of

coagulation. DIC.

 Activated Protein C

Vasodilation.

Peripheral edema.

Hypotension.

Tissue damage.

Organ failure. Decreased

immune function.

Clinical Manifestations:

Tachypnea. Tachycardia.

Fever. Leukocytosis,

followed by leukopenia.


Laboratory interpretation

Later Sepsis:

Hypodynamic 

 CO &  SVR

 Lactic

acid

Tissue /organ

damage

 cellular

oxygenation

Coagulation

cascade

Early Sepsis:

Hyperdynamic 

 CO &  SVR

DIC

Perfusion

Imbalance

Hematological

Alteration

Myocardial

Alteration

Dilated Ventricles

SEPSIS

Broncho-

constriction

Hyperglycemia 2o

insulin resistance

Pulmonary

Alteration

Metabolic

Alteration

Interstitial &

alveolar edema

Impaired

gas exchange

 serum amino

acids.  serum ketones.

 Lactic acid.

Tissue &

organ death

ARDS


Perfusion imbalance

Perfusion Imbalance

Inflammatory mediators

& Bacterial endotoxins

Activation of

coagulation cascade

Vasodilation & increased

capillary permeability

Microthrombi

in capillaries

Activation of

Sympathetic

Nervous system

Low SVR & hypovolemia

Tissue

hypoxia & organ

damage

Vasoconstriction of

splanchnic circulation

& vessels of the skin

with dilation of

skeletal muscle beds

Inadequate cellular

Oxygenation

(Inflam response)

Increased

lactic acid

production

Anaerobic metabolism

Blood flow only to

vital organs


Myocardial alterations

Myocardial Alterations

High CO &

Low SVR

Hyperdynamic

Heart

Early Sepsis

Initial mechanism leading to heart failure!

Low CO &

Increased SVR

Late Sepsis

Hypodynamic

Heart

MYOCARDIAL

DEPRESSION

+

Lactic

Acidosis

Circulating 

Depressants

Dilated

cardiomyopathy


Pulmonary alterations

Pulmonary Alterations

Inflammatory Chemical Mediators &

Bacterial Endotoxins

BRONCHOCONSTRICTION

Increased work

of breathing

Increased capillary

permeability

Pulmonary

Hypertension

Interstitial

edema

Alveolar edema

Shunting

Medium for

bacterial growth

Impaired gas

exchange

ARDS

Hypoxemia


Metabolic alterations

Metabolic Alterations

Excessive

Catecholamines

“Your body’s

natural

Adrenaline”

Stimulates

gluconeogenesis

Hyperglycemia

Glycogen stores

are depleted

Insulin resistance

Cells unable to use

glucose, protein & fat

Protein used

for energy

Fats used

for energy

Increased

ketones

Increased serum

amino acids

Cellular

pumps fail

Lactate

production

TISSUE & ORGAN DEATH


Hematological alteration coagulation cascade in septic shock

Hematological Alteration: Coagulation Cascade in Septic Shock

APC

Micro-

organism

Activation of

Coagulation

Inactivation

Endotoxin

Release

Tissue Factor

Factor VIIa

Factor Va

Stimulates

Thrombin activation

Inhibits

Inhibits

Fibrin clot

formation

Fibrinolysis

APC

Depletion of clotting factors

DIC

Tissue Factor

Endothelial cells

Hemorrhage


Sepsis labs

Sepsis: Labs

  • Cultures: From wound, UA, Catheter

  • CBC: Will see an incr or decr in WBC (so look for the words early or late)

    • Bands will incr, meaning sepsis.

  • Chemistry: will develop into hyperglycemia.

    • Steroids may be given which is another reason for insulin drip.

  • ABG: Metabolic acidosis b/c of impaired gas exchange.

  • Lactate Levels (Normal 0.5-2.0): Will incr & incr SVR.

54:50


Laboratory interpretation

Sepsis: Labs Continued…Note: Xigris is a protein replacement. Has anti-thrombotic, anti-inflammatory, and profibrinolytic properties. To prevent DIC & to treat sepsis.

  • Hemodynamic Monitoring: Fluids to treat hypovolemia.

    • Decr CardOutput and incr SVR

  • CXR & Abdominal X-rays:

    • infiltrates

  • CT Scans:

    • Abscesses and anything that can be infectious or cause an infection.

1:01:10, break


Laboratory interpretation

COAGULATION CASCADE- what happens to make a clot

Intrinsic Pathway

Extrinsic Pathway

XII

XIIa

VIIa

VII

XI

XIa

Tissue Factor

IX

IXa

X

Xa

X

XIII

V

Va

Prothrombin

Thrombin

XIIIa

Fibrinogen

Soluble Fibrin

Insoluble Fibrin


Platelet count life span of platelet is 7 5days

Platelet CountLife span of platelet is 7.5days

  • Normal Counts: 140 - 400 x 103/mm3.

  • 2/3 ( circulating in blood ) & 1/3 ( spleen ).

  • Drugs Affecting Platelet Function:

    • Plavix, aspirin, Coumadin & NSAID (ibuprofen)

  • Thrombocytosis:

    • increased risk of clot

      • Seen in CA, splenectomy, chronic pancreatitis

  • Thrombocytopenia:

    • increased risk of bleeding

1:07:30


Bleeding time measures the primary stage of hemostasis

Bleeding TimeMeasures the primary stage of hemostasis.

  • Phase: Interaction of platelet with blood vessel wall & formation of hemostatic plug.

  • Best screening test for platelet function disorders.

    • Prolonged: means thrombocytopenia, no clotting factor, leukemia, and/or DIC.

  • Common meds for surgery:

    • Protonix- To reduce gastric acid. A prophylaxis to protect GI Tract. Since they’re taking a blood thinner. Its to protect from stomach ulcers.

    • Lovenox- to prevent & treat deep vein thrombosis or pulmonary embolism.


Hit heparin induced thrombocytopenia

HIT- Heparin Induced Thrombocytopenia

  • HIT Type II or White Clot Syndrome:

    • Heparin-dependent antibodies develop after a patient has been on heparin for 5 or > days or previous heparin exposure.

    • Presence of Factor 4 can induce Heparin Induced Thrombocytopenia.

    • Normal person

  • Non-immune Heparin Associated Thrombocytopenia (non-immune HAT):

    • Absence of heparin-dependent antibodies.

    • HIT Type I.

    • Not common


Hit pathophysiology of

HIT: Pathophysiology of

Heparin-PF4 complex formation

Antibody generated against

Heparin-PF4 complex

“Antibody-Heparin-PF4”

attaches to platelets

Activation of platelets  releases

microparticles (procoagulant)

Activates coagulation cascade


Hit diagnosis

HIT: Diagnosis

  • Normal platelet count before commencement of heparin therapy.

  • Onset of thrombocytopenia 5 - 14 days after initiation of heparin therapy. (“hmm, works too well”)

    • Platelets drop, so then start to consider Lovenox.

  • R/O other causes of thrombocytopenia.

  • Occurrence of thromboemboli during heparin therapy. (Here nurse says, “this aint right!?!”)

  • Platelet aggregation assay/panel. Common, cheaper.

  • Serotonin release assay/panel. Definitive test, but expensive.


Hit treatment

HIT: Treatment

  • Avoid use of heparin.

    •  Heparin drips (IV).

    •  Lovenox (SQ).

    •  Heparin flushes.

    •  Heparinized dialysate.

  • Warfarin (???) a: no.

  • Anticoagulants.

    • ARGATROBAN.

      • Advantage:

  • Monitor: Thrombosis. Platelet counts.

Venous Limb Gangrene

Would the physician order platelet transfusions?

1:17:18


Prothrombin time pt

Prothrombin Time (PT)

  • Protein produced in the liver – depends on Vitamin K intake & absorption.

  • Results are reported as:

    • Time (seconds): Normal 12-15 seconds

    • INR:2.0 to 3.5

  • Effectiveness of Coumadin Therapy.

    • ***Maintain PT 2 to 2.5 times normal range.

    • Prolonged: will bleed

    • Shortened: will form clots

    • Antidote: Vitamin K. NovoSeven. ($7,800-10,000/dose)


Partial thromboplastin time ptt

Partial Thromboplastin Time (PTT)

  • Normal PTT: 60-70 seconds (Varies!)

  • Activated Partial Thromboplastin Time (APTT)

    • Normal: 21-35 seconds

  • Prolonged PTT:

    • You will see this w/ heparin treatment, decr of Vitamin K, Liver disease, DIC

  • Shortened PTT:

    • Immediately after an acute hemorrhage, and/or Early DIC


Heparin therapy

Heparin Therapy

  • When rapid anticoagulation is desired.

  • Monitor:

    • PTT: 1.5 to 2.5 times normal.

      • Desired therapeutic range: 40-70 seconds

      • Too much heparin: If > 90 seconds

    • aPTT: 1.5 to 2.5 times normal.

      • Desired therapeutic range: 70 seconds

      • Too much heparin: > 100 seconds

  • Antidote: Protamine Sulfate. Given slowly.


Iv heparin guidelines

IV Heparin Guidelines

  • Baseline Wt (kg), PTT, INR, CBC with Platelets.

  • Heparin: 25,000 units in 500 ml D5W

    • Concentration:

  • Bolus: 80 units/kg.

    • Maximum Bolus:

  • Infusion: 18 units/hg/hr

    • Maximum Rate:

  • Lab:

    • PTT (CHS: 24.1 – 37.3 sec) every 6 hours x 48 hours.

      • If 2 consecutive PTT in therapeutic range after 1 day  PTT daily.

    • H & H daily.

    • Platelet count every 24 hours.


Iv heparin dose adjustments

IV Heparin Dose Adjustments


Fibrinogen d dimers

Fibrinogen:

Converted to fibrin.

Fibrin + Platelets → Clot.

 in injury & inflammation.

Normal: 200-400mg/dL

Decreased:

Liver disease & DIC

Panic value:

Cryoprecipitate

>700 mg/dL: MI/CVA risk

D-Dimers:

To check if pt is going into DIC.

Produced by action of plasmin on fibrin. (Will see an incr in fibrinogen)

Normal:

< 250 ug/L

Increased:

Renal/Liver failure, sepsis.

Fibrinogen & D-Dimers

1:29:26


Fdps protein c

Fibrin Degradation Products (FDP):

Used to dissolve clots.

Fibrin is split by plasmin → fibrin degradation (split) products.

Normal: 0 or <10mg/L

Critical value: > 40mg/L

Increased:

Primary: fibrinolysis

Protein C:

Produced by the liver.

Prevents thrombosis (anticoagulant).

Enhances fibrinolysis.

Decreased:

Means you have DIC, Liver disease, Vit K deficiency, ARDS, & CA

FDPs & Protein C

Thrombin

Plasminogen

Plasmin

Fibrin

FDP


Laboratory interpretation

DIC

  • Inappropriate triggering of the coagulation cascade & breakdown in normal feedback mechanisms in body that allow for distribution of clots.

  • Common causes:

    • Surgery. Obstetric emergencies. Liver cirrhosis, Trauma/crushing injs,. Transfusion reactions. Burns. Septicemia. Shock or low flow states.


Dic pathology 1 36 20

DIC Pathology- 1:36:20

  • Exessive bleed  shock  death.

1:37:30


Dic assessment

DIC: Assessment

  • S/S of inappropriate clotting:

    • Thrombosis

    • Gangrene

    • Altered LOC. CVA

    • PE

    • Bowel ischemia & infarction

    • ARF

  • S/S bleeding:

    • Bleeding from various sites

    • Hematuria

    • Petechial reashes

    • Oozing from IV acess sites

1:40:00


Dic labs

DIC: Labs

  • Massive Intravascular Clotting & Secondary Depletion of Essential Clotting Factors:

Platelet Count

Decreased

Fibrinogen Level

Decreased

Prothrombin Time (PT)

Prolonged

Early- Shortened

Partial Thromboplastin

Time (PTT)

Late- Prolonged

Protein C Level

Decreased


Dic labs1

DIC: Labs

  • Excessive / Accelerated Fibrinolysis:

Fibrin Degradation

Products (FDPs)

increased

increased

D-dimer Assays

decreased

Antithrombin III Level


Dic labs2

DIC: Labs

  • Clinical effects of microvascular clotting / cell destruction:

    • Schistocytes in peripheral smear: Present

  • Serum Bilirubin: increase b/c of the fibrolysis & hemolysis

  • BUN: incr b/c of the fibrolysis & hemolysis


Dic treatment

Treat underlying cause.

Correct Effects:

Oxygenation (ischemia)

replace fluids

Electrolyte balance

Vasopressors

In Severe Bleeding:

cryoprecipitate.

Fresh frozen plasma

platelet transfusions

Heparin Infusion:

Interrupts thrombosis process.

Controversial.

DIC: Treatment

1:27:40

Case study- 1:51:40


Metabolic cart b c of everything incr calorie expendature

Metabolic Cart-b/c of everything  incr calorie expendature.

  • Calculates REE (Resting Energy Expenditure).

    • Exact calorie consumption.

      • Temp incr of 1degreeF, - incr calorie demand 500kcal/day.


Prealbumin to reflect status today

Prealbumin- to reflect status TODAY.

  • Short Half-life: 2-3 days

    • Responds QUICKLY to decreased nutritional intake & nutrition restoration.

  • Normal: 19-38mg/dL

  • Severe protein depletion: 0-5

  • Moderate protein depletion: 5-10

  • Mild protein depletion: 10-15


Urine urea nitrogen

Urine Urea Nitrogen

  • 24-hour Urine Collection.

    • Measures degree of catabolism.

    • The more protein catabolized = the more urea present in the urine.

  • Normal: 5gm/24hrs

  • Severe:above 18gm/24hrs

  • Pts w/ bad Kidneys/Renal, this won’t work.


Albumin

Albumin

  • Most abundant plasma protein.

  • Function:

    • Nutrition status.

    • Maintenance of colloid osmotic pressure.

      • I.O.W. to maintain hydrostatic pressure

    • Buffer system (acid-base balance).

  • Half-life: 21days

    • SLOW to respond to recent change in nutritional status. If low thn pt has been malnourished for 7days.

  • Normal Levels: 3.4 – 5.0g/dL


Albumin helps to hold h2o

Albumin- helps to hold H2O

  • Increased albumin:

    • edema

  • Decreased albumin:

    • Acute and chronic inflammation, liver disease,, burns, and starvation/malnutrition

  • Serum Calcium*:

    • 50% bound to albumin.

    • Look at both together


Osmolality adult

Osmolality (Adult)

  • Normal Serum Osmolality: 280 - 303mOsm/L

  • Normal Urine Osmolality: 300 - 900mOsm/L

  • Calculated Osmolality:

  • Always look at sodium & glucose together.

    • Increased glucose means decr Na+ means incr risk of dehydration

2 Na + BUN + Glucose

3 18


Osmolality

Hyperosmolality:

Cells Shrink:

Disorders:

Severe brain cell dehydration.

Hypernatremia- too much Na+ in blood makes cells shrink.

> 320 concern. > 350 Neuro deficits will be seen. (seizures, confusion)

Hypoosmolality:

Cells Swell:

Disorders:

Hyponatremia- too little salt in cells. Fluid shifts into the cell.

Poss cause: Diuretics, Renal failure, Hyponatremia, overhydration, diabetes insipidus.

Osmolality


E g calculate osmolality

E.g.: Calculate Osmolality

  • Labs:

    • Sodium: 140 mEq/L

    • Glucose: 108 mg/dL

  • BUN: 9 mg/dL

A: 289

Pt is normal.


Hemodilution overhydration

Hemodilution / Overhydration

RBC. HCt. Hb.

decr

decr

Serum Osmolality

Sodium

Hypothermia

Creatinine

decr

BUN

decr

Albumin

decr


Dehydration

Dehydration

RBC. Hct. Hb.

incr

Serum Osmolality

incr

Sodium

hypernatremia

Potassium

incr

Creatinine

incr

BUN

incr

Albumin

incr


Sodium na 136 145 meq l

Sodium (Na+) (136-145 mEq/L)

  • Extracellular cation – osmotic pressure.

  • Hypernatremia:

    • Excess Na+ in relation to water.

    • Causes:

      • Diabetes Insipidus, Cushing's syndrome, Dehydration.

    • Clinical Manifestations:

      • Restless, weakness, muscle irritability

    • Treatment:

      •  Fluid Loss:Water (D5W, 4.5% NS). Check Osmoality.

        • Over a period of 48hrs. (meaning: give slowly)

      •  Na+ Intake:Decr or restrict Na+


Hyponatremia hopefully caught before pt goes in to seizure or coma

HyponatremiaHopefully caught before pt goes in to seizure or coma.

  • Too little Na+ in relation to water.

  • Causes:

    • Severe burns. Fluid loss. Hyperglycemia.

  • Clinical Manifestations:

    • Depends on rate of drop in Na+ levels.

      • > 125 mEq/L: Asymptomatic (usually).

      • 120 – 125 mEq/L: Nausea. Malaise.

      • 115 – 120 mEq/L: Headache. Lethargy. Obtundation.

      • < 110 – 115 mEq/L: Seizures. Coma.


Hyponatremia

Hyponatremia

  • Treatment:

    • Fluid replacement & Rx cause.

    • Diuretics.

    • 3% Hypertonic Saline (513 mEq/L Na).

      • RULE: Never correct hyponatremia faster than 0.5 mEq/L/hr to 1 mEq/L/hr & Not > 12 mEq/L/24 hrs.

      • Central pontine demyelination.

      • ***Correct to 130mEq/L rather than 140mEq/L.


Potassium k

Potassium (K+)

  • Normal Levels: 3.5 – 5.5 mEq/L.

  • 98% intracellular. 2% extracellular

  • Neuromuscular transmission.

  • Acid-Base Balance:

    • Alkalosis: decr serum K+ levels (drives K+ into cells)

    • Acidosis: incr serum K+ levels (drives K+ out of cells)

  • Hyperkalemia Causes:

    • Renal disease. Acidosis. Salt substitutes, potassium supplements.Blood draws (hemolysis). Stored blood  washed PRBC. transfusions.

2:16:35


Hyperkalemia ekg changes

Hyperkalemia & EKG Changes

K+ (6-7 mEq/L):

Tall, peaked, narrow T waves.

K+ (7-8 mEq/L):

Flat P wave & wide QRS

K+ (> 8 mEq/L):

Bradycardia, no P wave, wide QRS, tall T wave (“Sine wave”)

K+ (> 9 mEq/L):

Cardiac Arrest.

K+ (> 11 mEq/L):


Hyperkalemia 5 5 meq l

Treatment:

depends on severity

< 6 mEq/L:

Stop meds  K+.

> 6 mEq/L:

Loop diuretics. Kayexalate.

> 7 mEq/L:

Glucose & Insulin. Sodium Bicarb.

Albuterol. S/E:

Extreme Cases:

Treat w/ Dialysis & Calcium gluconate

2:17:12

Hyperkalemia (> 5.5 mEq/L)

1 Amp Na+ Bicarb

1 Amp D50

10 Units Regular Insulin


Hypokalemia 3 5 meq l too little k

Hypokalemia (< 3.5 mEq/L)Too little K+

  • Causes:

    • Diarrhea, alkalosis, diuretics, NG tube (can suction it out of them), vomiting

  • Clinical Manifestations:

  • EKG Changes:

  • Depressed ST segment.

  • Flat / inverted T wave.

  • Prominent U wave.

  • PVCs. VT. V Fib.

Cardiac Patients: K+ at 4.0 mEq/L


Hypokalemia treatment

Hypokalemia Treatment

  • OralPotassiumSupplements.

  • K-Lyte:

    • If K+ < 3.0: 50mEq in 6-8oz of fluid

    • If K+ < 3.5: 25mEq in 6-8oz of fluid

  • Potassium Chloride Tablets:

    • Unable to tolerate K-Lyte.

    • 40 mEq (10 mEq x 4).

  • Recheck Serum K+: 4hrs for PO route

  • Repeat PO Bolus: PRN to maintain K+ level


Hypokalemia treatment1

Hypokalemia Treatment

  • IV Potassium (KCL):

    • Always dilute (50 – 100 cc NS).

      • Not mixed in dextrose: Will shift K+ into cells.

    • Standard Dose: 20mEq/100 cc over 1-2hr

    • Rapid Administration: Cardiac standstill & death

    • Painful in Peripheral Administration.

      • Add NaHCO3 (NEUT 5 ml vial) to IV bag. (pharmacist!)

    • Recheck Serum K+:

    • Repeat IV K+ Bolus:

  • Remember to correct Hypomagnesemia!

1hr afterIV bolus is infused.

1:22:50


Hypomagnesemia

Hypomagnesemia

  • Normal Magnesium: 1.6 – 2.1 mEq/L

    • Cardiac patients: Treat < 2mEq/L

  • Hypomagnesemia Causes:

    • Vomiting, diarrhea, poor nutrition, Diuretics, or from Suctioning

  • Clinical Manifestations:

    • Anorexia, tremors, confusion

  • EKG Changes:

  • Treatment (Ø in Renal patients):

    • IV Magnesium 2 gm in 100 ml NS over 1 hour.

    • Recheck Serum Mg: 1hr after infusion. Repeat if needed.

    • Slo-Mag 64 mg tablets (Ø IV access): 2PO TID x 2days


If magnesium is low than calcium is low so s s hypocalcemia

27:35

If Magnesium is low, than Calcium is low.So… S/S Hypocalcemia

  • Laryngeal spasm

  • + Trousseau’s

  • + Chvostek’s


Hypermagnesemia

Hypermagnesemia

  • Hypermagnesemia Causes:

    • Renal failure (rare, b/c renal provides Mg)

  • Clinical Manifestations:

    • Muscle weakness and incoordination (Loss of deep tendon reflexes

  • EKG Changes: (Present, but will be covered in cardiac)

  • Treatment:

    • Dialysis

    • IV calcium gluconate


Rhabdomyolysis rhabdo myo lysis rod muscle breakdown

RhabdomyolysisRhabdo-myo-lysis = “rod-muscle-breakdown”

  • Definition: Condition caused by skeletal muscle injury & release of muscle cell contents into circulation.

  • Skeletal Muscle:

    • 40-50% of total body wt

  • Those at risk:

    • Trauma, ETHOL, DO, Viral infections

  • Manifestations:

    Muscle hurt, Pee tea-color, HypoVolemia, altered LOC

1:28:50


Pathophysiology rhabdomyolysis

Pathophysiology: Rhabdomyolysis

Causative agent

Hypocalcemia

Increased cell membrane permeability

Release of muscle

components into circulation

Accumulating of Na+ & Ca++

into muscle cytoplasm

Compartment

Syndrome

Further damage

to muscle cell

Damages

mitochondria

Hyperkalemia

Hyperphosphatemia

Hyperuricemia

  • Creatine kinase (CK)

  • Serum myoglobin

  • Aldolase (muscle injury)

  • Serum creatinine & BUN

  • Urine myoglobin

Muscle cell

necrosis

 ATP

production

Profound hypovolemia

Cardiac arrest

& dysrhythmias

Acute Renal

Failure


Rhabdomyolysis labs

Rhabdomyolysis: Labs

  • Serum creatine phosphokinase (CK):

    • Elevated meaning muscle damage. (CK-MM iso-enzyme predominates)

  • Serum Myoglobin: Elevated

  • Myoglobinuria: Discolored urine

  • Electrolytes:

    • Hypocalcemia. Hyperkalemia. Hyperuricemia. Hyperphosphatemia.  Aldolase.

  • Metabolic Acidosis: Release of uric acid & lactic acid from muscle cell.

1:30:40, case study


Drug monitoring

Common specimens:

Blood. Urine. Gastric contents.

Testing for Vancomycin/Gentomycin. Adjust if needed.

Therapeutic management:

Estimation of appropriate drug dose requirements.

Monitor potential for drug toxicity.

Toxicology:

Suspected poisoning or overdose (homicide/suicide).

Suspected date rape situations.

Accidental poisoning (kids).

Child abuse cases.

Illicit drug use.

Exposure to anticoagulants, heavy metals & iron.

Vehicle accident cases – alcohol involved.

Drug Monitoring


Drug monitoring1

Drug Monitoring

  • Therapeutic Range:

    • Range of plasma [ ] that produce desired drug effect w/out toxicity.

  • Peak:

    • highest plasma [ ] attained from a dose.

  • Trough (Minimal Effective Concentration):

    • Lowest [ ] that produces the desired effect.

  • Toxic Levels:

    • plasma [ ] at which the drug produce a serious adverse effect.


Plasma drug levels

Commonly Monitored Drugs for Therapeutic Ranges:

Fosphenytoin (Cerebyx).

Phenytoin (Dilantin).

Theophylline (Aminophylline).

Digoxin (Lanoxin).

Salicylates.

Acetaminophen.

What would you do if the therapeutic range in too high?

Pull the dose and give antidote.

What would you do if the therapeutic range is too low?

Incr the dose

Either way give it slowly to check for AR.

Plasma Drug Levels


Vancomycin

Vancomycin

Peak:

3rd Dose

Trough:

2nd Dose

1st Dose


Labs to monitor w these drugs

Labs to Monitor: w/ these drugs

K+, Electrolytes

Lasix

PT, INR

Coumadin

PTT, APTT, ACT

Heparin

Insulin

(sliding scale/infusion)

Accudata/blood glucose

Serum electrolytes

Electrolytes


Drug screening

Drug Screening

  • ***Screening for unknown drugs: blood*, gastric contents & urine* samples.

    • Noninvasive procedure.

    • Drug conc. more elevated in urine.

    • Metabolites are excreted for longer period through urine (indicating past drug use).

  • Common Urine Drug Tests:

    • Amphetamines. Barbiturates. Benzodiazepines. Opiates. Marijuana. Cocaine metabolites. Methadone. Heroin. Methaqualone. Phecyclidine (PCP). Propoxyphene. Tricyclic antidepressants.

  • Must confirm ALL POSITIVE results.


Blood alcohol concentration

Blood Alcohol Concentration

  • Blood Alcohol Concentration (BAC): Amount of alcohol in bloodstream.

  • BAC specimens: via Breath, blood*, or urine.

    • Living: venous, 5mls Dead: 5mls of arterial

  • For determining the role of alcohol in:

    • Car crashes, and others injuries.

  • Legal standard in ALL STATES for drunkenness: 0.08% ( 0.08 BAC Per Se Law)


All done whew

All Done Whew!


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