Aherrera Notes

Aherrera Notes

Dr. Jaime Aherrera’s Internal Medicine Notes 2009

Aher re ra N ot es | TA ABLE O F CO N TE N TS

Aherrera Notes

Dr. Jaime Aherrera’s Internal Medicine Notes 2009

I. Basic Information

II. Cardiology

III. Endocrinology

IV. Gastroenterology

V. Hematology

VI. Infectious Disease

VII. Nephrology

VIII. Neurology

IX. Pulmonology

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GENERAL NOTES

Jaime Alfonso Manalo Aherrera, M.D.

Internal Medicine Notes 2009

WARD NOTES

1) MUST KNOW FORMULAS

I. DOPAMINE DOSAGE COMPUTATION

 Dopamine Drip – used primarily for stabilization of the Hypotensive Patient

 Formulation of Dopamine:

o Dilute 200mg (1 Ampule) in 250cc D5W (Factor used: 13.3) o Drip at 2.5 – 10mcg/kg/min

o Maximum Dose of 20mcg/kg/min (Dopa-Max)

o

If Double Strength: 2 Ampules in 250cc D5W (use 26.6)

Rate (ugtt/min) = . (mcg/kg/min) x body weight . Dose (mcg/kg/min) = . (ugtt/min) x 13.3 .

13.3

body weight

 Dopamine Doses (from Harrisons p1453)

DOSE

MECHANISM OF ACTION

EFFECT

< 2 mcg/kg per min

Stimulate DA1 and DA2 Receptors Vasodilation of Splanchnic and Renal Vasculature

2-4 mcg/kg per minute

Stimulate B1-Receptors Increase in Cardiac Output with little or no change in Heart Rate or SVR

> 5 mcg/kg per minute

Effects on A1-Receptors overwhelm the Dopaminergic Receptors

Vasoconstricion, leading to Increase in SVE, LV Filling Pressures, and Heart Rate

**NOTE:

Dopamine is generally the 1st choice for Tx in situations where Modest Inotropy & Pressor Support are required o It is an Endogenous Catecholamine that stimulates B1, A1 Receptors, and Dopaminergic Receptors (DA1, DA2) in

the heart and circulation

o Dopamine also releases Norepinephrine from nerve terminals, which itself stimulates A1 and B1 Receptors, thus raising Blood Pressure

o Most useful in treatment of heart failure patients who have Depressed Cardiac Output with Poor Tissue Perfusion

Example) Case on Septic Shock: Patient is a 45kg / F, given 2 amps of Dopamine in 250cc PNSS at a rate of 19uggts/min

 In 1 Ampule of Dopamine = 200mg/amp

 In 1 Ampule of Dobutamine = 250mg/amp

NOTE: 19ugtts/min = 19cc/hr

QUESTION: What is the Dose of Dopamine being given to the patient at a rate of 19uggts/min?: Dose Given (in mcg/kg/min) = Rate (in ugtt/min) x 26.6 = 19 uggt/min x 26.6 = 11.23 mcg/kg/min

45 kg 45 kg

ANSWER: 11.23mcg/kg/min is the dose given to the Patient at a rate of 19uggts/min (or 19cc/hr)

Strength Factors:

 1 amp of Dopamine = 13.3

 2 amps of Dopamine = 26.6

Recall the Action of Dopamine at Different Doses (Dr. Magno Notes): 1. At 1-5mcg = RENAL VASODILATOR

 Exerts selective Renal and Mesenteric Vasodilation

 Acts on Dopamine Receptors

 Improve Renal Blood Flow and Urine Output

2. At 6-10mcg = INOTROPIC

 Positive Inotropic Effect

 Acts on Beta-1 Adrenergic Receptors

 Increase Heart Rate

3. At 10-20mcg = VASOCONSTRICTOR

 Peripheral Vasoconstriction

 Acts on A-Adrenergic Receptors

 Increase Systemic Vascular Resistance

 Deleterious for CHF and Low Cardiac Output

Since we are giving 11.23mcg/kg/min, we have a Vasoconstricting

Effect. This is what we want for a patient with Septic Shock. We

can increase the ugtts/min if patient is still Hypotensive up to

34ugtt/min (20mcg/kg/min) for a 45kg patient (Dopa Max). If still

No Response with Dopa Max, we can give LEVOPHED (Norepinephrine).

In the computation, we used 26.6 because 2 ampules of dopamine were used for the patient.

II. DOBUTAMINE DOSAGE COMPUTATION

A. Dobutamine Drip – selectively stimulates Beta-1 Adrenergic Receptors o Direct Inotropic Stimulation with Reflex Arterial Vasodilation o Afterload Reduction and Augmented Cardiac Output

o BP remains constant, HR increases minimally o For patients with Chronic Refractory Heart Failure

o NOT for Heart Failure resulting from Diastolic Dysfunction or High-Output State B. Formulation of Dobutamine

o Dilute 250mg (1 amp) in 250cc D5W (use 16.6) o Drip at 2.5 – 10mcg/kg/min

o Maximum Dose of 20mcg/kg/min

o If double strength: 2 Ampules in 250cc D5W (use 33.2)

Rate (ugtt/min) = mcg/kg/min x body weight mcg/kg/min = . (ugtt/min) x 16.6 . 16.6 body weight C. Action of Dobutamine at Different Doses:

o 0 – 10 mcg/kg/min = INOTROPIC EFFECT

o

10 – 20 mcg/kg/min = VASOCONSTRICTION III. NORADRENALINE (LEVOPHED) – Rounds

 Each ampule has 2mg Noradrenaline per amp

 Usual Starting Dose is at 2-4 mcg/min with a maximum of 15 mcg/min

Notes from Harrisons:

Dobutamine has a Positive Inotropic Action and Minimal Positive Chronotropic Activity at Low Doses (2.5ug/kg/min) but moderate Chronotropic Activity at Higher Doses

Noradrenaline (LEVOPHED) Drip: 2mg Noradrenaline in 2mL Ampule

Usual Preparation: D5W 250mL + 1 Amp (2mg) Levophed to run at 15-60ugtts/min

Concentration = 2mg = 2,000mcg = 8mcg Noradrenaline per cc (this is the concentration of 1 Amp + 250cc D5W)

250cc 250cc

Drip of 2-8mcg Noradrenaline/min is equivalent to 15-60 ugtts/min

Example: We are using 1 Amp (2mg) in 250cc D5W. If we mix 1 Amp with 250cc D5W, the concentration of Levophed will be 8mcg/cc (as

computed above)

1) If Our desired dose to give patient is 2mcg/min (usual starting dose), what is the Rate? Step 1: Convert 2mcg/min to mcg/hour

2mcg/min x 60 mins  120mcg/hr

Step 2: If we desire a dose of 120mcg/hr given a concentration of 8mcg Levophed per cc, compute the rate:

120mcg/hr = 15 cc/hr or 15 ugtts/min **NOTE: cc/hr is equal to uggts/min

8mcg/cc

2) If our desired dose is 8mcg/min  480mcg/hr 480mcg/hr = 60 ugtts/min

8mcg/cc

Example 2) We are using 4 ampules (8mg) in 250cc of D5W. We want to give the patient a dose of 2mcg/min. What is the rate?

Concentration = 8 mg . = 8,000 mcg = 32mcg Noradrenaline per mL (Concentration of 4 Amps + 250cc D5W)

250cc 250cc

Since we initially want to give a dose of 2 mcg/min .2 mcg x 60 min = 120 mcg / hr min hr

120 mcg/hr = 4 cc/hr or 4 uggt/min 32 mcg/cc

III. COMMON FORMULAS USED

A. General Formulas

BMI = kg / m

2

B. Cardiac Output, Mean Arterial Pressure (MAP), Anion Gap, Osmolality, Etc.

Cardiac Output

Heart Rate x Stroke Volume

Mean Arterial Pressure

Systolic BP + (2 x Diastolic BP)

3

Normal Value: 70 – 100 mmHg

Urine Anion Gap

( Na + K ) – Cl

Serum Anion Gap

Na – ( HCO

3

+ Cl )

Urine Osmolality

( SG – 1 ) x 40,000

Plasma Osmolality

[2 (Na + K)] + RBS (mmol/L) + BUN (mmol/L)

or

2 (Na in mmol/L) + (Glucose in mg/dL / 18) + (BUN / 2.8)

Normal Value is 280 – 300 mOsm/L

Normal Value (from Harrisons) = 275-290 mosm/kg

RBS: 1 mmol/L = 18 mg/dL

Effective Plasma

Osmolality

2 Na + RBS in mmol/L

or

2 Na + RBS in mg/dL

18

C. Adequacy of Urine Collection

o

M: 20-23mL/kg

o

F: 15-20mL/kg

D. 24-Hour Urine Collection Adequacy

o Creatinine is produced at a constant rate and in an amount directly proportional to skeletal mass o Creatinine Coefficient = 23mg/kg of IBW (men) and 18mg/kg of IB (women)

o If 24 hr urine creatinine is LESS than IBW x Creatinine Coefficient  INADEQUATE Collected Specimen

o

Unpredictable when Serum Crea > 530umol/L

Underweight < 18.5

Normal Weight 18.5 – 22.9

Overweight 23 – 24.9

Obese I 25 – 29.9

Obese II > 30

Ideal Body Weight:

Females: 100 pounds + (5 pounds per inch over 5 feet) Males: 106 pounds + (6 pounds per inch over 5 feet)

IV. BUN / CREATININE RATIO; CREATININE CLEARANCE A. BUN / Crea Ratio (SI Units)

Conversion Factor for Serum BUN: 1 mmol/L = 2.8 mg/dL B. Fractionated Urine Na (Best test to Diagnose if Renal or Prerenal)

FE

Na

= [ U

NA

x P

CR

] x 100

[ P

NA

x U

CR

]

C. Creatinine Clearance (mL/min): Cockroft and Gault Equation

 IMPORTANT Notes:

o If Female, multiply everything by 0.85

o If Creatinine is NOT in mg/dL, divide it by 88.4  Normal Creatinine Clearance

o 100-125mL/min in Males

o 85-105mL/min in Females

 Staging of Chronic Kidney Disease (CKD)

CKD STAGE DESCRIPTION GFR mL/min / 1.73m2

I Kidney damage with normal / increased GFT 90

II Kidney damage with mildly decreased GFR 60 – 89

III Moderately decreased GFR 30 – 50

IV Severely decreased GFR 15 – 29

V Renal Failure < 15 (for dialysis)

BUN:Crea Ratio = BUN x 247

Crea

Interpretation:

 If < 10: Intrinsic Renal Cause

 If 10-20: Doubtful Cause

 If > 20: Pre-Renal Cause

CreaClearance = . (140 – age) x weight in kg . CreaClearance = . (140 – age) x weight in kg .

72 x Serum Crea in mg/dL

72 x (Serum Crea in umol/L / 88.4)

Interpretation:

< 1 Pre-Renal

V. ELECTROLYTES A. Calcium

1. Corrected Calcium (mg/dL)

[ (40 – Albumin in g/L) x 0.02 ] + Measured Ca

2

in mmol/L

OR

( 4 – Albumin in g/dL x 0.08 ) + Measured Ca

2+

_{in mg/dL}

 LOW in Renal Failure, Hypoparathyroidism, Severe Hypomagnesemia, Hypermagnesemia, Acute

Pancreatitis, Rhabdomyolysis, Tumor Lysis Syndrome, Vitamin-D Deficiency, Pseudohypoparathyroidism; Rarely due to Multiple Citrated Blood Transfusions, critically ill patients, Anti-Neoplastic Agents,

Antimicrobials, Agents used to Treat Hypercalcemia

 Use with Hypocalcemia ONLY if Ionized Calcium cannot be measured

 Make sure that the alteration in Serum Calcium is NOT due to Abnormal Albumin Concentrations  About 50% of Total Calcium is Ionized, and the rest is bound principally to Albumin

 When Serum Albumin Levels are REDUCED, a Corrected Calcium Concentration is calculated by adding 0.2mM (0.8mg/dL) to the Total Calcium Level for every Decrement in Serum Albumin of 1.0g/dL below the reference value of 4.1 for Albumin, and conversely for elevations in Serum Albumin

2. Hypocalcemia

 Calcium Gluconate 10% Solution of 10mL/amp: 1-2amp Slow IV Push (10-15mins) with Cardiac Monitoring then incorporate 1amp Calcium Gluconate to present IV Fluids

 Chronic Treatment:

 Calcium Carbonate 500mg 1 tab BID-TID

 Vitamin-D3 Supplements (Calcitriol 0.25mcg/cap OD-BID)  Treat Hypomagnesemia

3. Hypercalcemia

 Hydrate: 0.9%NSS at 150-600cc/hr (up to 1-4 Liters in 24 hours)  Furosemide 20-40mg IV q8-12 hours

 Bisphosphonates (Pamidronate 30-90mg/day as a single 24-hour Infusion for 3 Days)

A Fall in Serum Albumin of 1gm/dL is associated with a Fall of 0.8mg/dL in Total Calcium

Example:

 Present Total Calcium = 8mg/dL

 Present Serum Albumin = 2.5g/dL (N: 4g/dL)

 Corrected Ca2+ _{= (4 – 2.5) x 0.8 = 1.2}

B. Sodium

1. Corrected Sodium

0.016 (RBS in mg/dL – 100) + Measured Na

+

_{in mmol/L}

 Plasma Na

+

_{Concentration FALLS by 1.4 mmol/L for every 100 mg/dL RISE in the Plasma}

Glucose Concentration

2. Hyponatremia: Sodium Deficit

( Desired Na – Actual Na ) x Body Weight in kg x 0.6

 Target Na+ _{= 125 – 135 mEq/L}

 NOTE: 0.6 is Total Body Water  NaCl 1 Tab = 17 mEq

 NaHCO3 GrX 1 tab = 7 mEq

a. Sodium Correction

 Time needed to Infuse = ( Desired Na – Measured Na ) / 0.5

 Total # of L needed = Na Deficit / 154

 Drip Rate = Total # of L needed / Time needed to Infuse

 Give Patient 50% of Calculated amount of Na+ _{in the first 8 hours, and the other 50% in the next}

16 hours (correct at a Rate NOT > 0.5meq/L/hr) b. Sample Case for Hyponatremia

 A 70-kg male has a Na+_{Value of 105 mmol/L}

 We want to raise the plasma Na+ _{concentration from 105 to 115 mmol/L}  Formula: Deficit in Plasma Na+ _{x Total Body Water (TBW)}

 [115 – 105] x 70 x 0.6 = 420 mmol



Plain NSS (PNSS) has 154 Na+ _{Content per Liter; therefore, we can give 2-3 L of PNSS in one day}

3. Hypernatremia

a. Water Deficit

Water Deficit = Plasma Na

+

Concentration - 140 x 0.6 x BW

(kg)

140

OR

Water Deficit = [ ( Actual Na – Desired Na ) ] x 0.6 x BW (kg)

Desired Na

 TBW is 0.6 mg/kg for MALES



TBW is 0.5 mg/kg for FEMALES

 Desired Na+ _{is 140}

 Total Body Water (TBW) in Hypernatremia is due to water loss

 Should be corrected SLOWLY over at least 48-72 hours, ideally with hourly Serum Na+

determination to target 0.5mmol/L/h, but NOT > 12mmol/L over the 1st _{24 hours}

b. Sample Case on Hypernatremia

 A 50 kg woman with a Plasma Na+ Concentration of 160 mmol/L



Water Deficit = 2.9 L

160 – 140 x 0.4 x 50 kg = 2.9 L

140

Water deficit should be corrected slowly over at least 48-72 hours. Safest route of administration of water is by mouth or via a nasogastric tube. Alternatively, 5% Dextrose in Water of Half-Isotonic Saline can be given IV

4. Water Excess

Water Excess = Normal Na

+

_{x TBW - TBW}

Actual Na

+

C. Potassium

o

Hypokalemia = Plasma K

+

_{Concentration < 3.5 mmol/L}

o

Hyperkalemia = Plasma K

+

_{Concentration > 5.0 mmol/L}

1. Potassium Deficit

(Desired K

+

_{- Measured K}

+

_{) x 100}

0.27



Desired K is 3.5



Target K is 3.5 – 4.9 mEq/L



If K is 2.0 – 3.5 mEq/L, replace 10-20 mEq KCl for

every 0.1 mEq/L Drop in K



Maximum Drip: Max 10 mEqs / hr



Central Line: Max 20 mEqs / hr



Desired K is: 4.0 mEq/L for Cardiac Causes, requiring IV administration of K

3.5 mEq/L for Non-Cardiac Causes, requiring Oral Administration of K



Administer as 10% Solution, 15cc + 20mEqs KCl; 1/2 of the dose given within 24 hours,

then the excess within the next 3 days

Oral Kcl:  15cc: 10 mEqs  30cc: 20 mEqs Kalium Durule:  1 tab = 10 mEqs Hyponatremia

 Plasma Na+ _{Concentration < 135 mmol/L}

 Clinical Manifestations: Brain Swelling or Cerebral Edema

 Stupor, Seizures, and Coma do NOT usually occur unless the Plasma Na+ _{falls below 120mmol/L of Decreases RAPIDLY}

 Goals of Therapy: 1) To raise plasma Na+ _{Concentration by restricting water intake and promoting water loss; and 2) To correct the}

underlying disorder

 Rx: Plasma Na+ _{Concentration should be raised by NO more than 0.5-1.0 mmol/L per hour and by LESS than 10-12 mmol/L over the}

first 24 hours

 For Severe Symptomatic Hyponatremia: Treated with Hypertonic Saline, and Plasma Na+ _{Concentration should be raised by 1-2 mmol/L}

per hour for the first 3-4 hours or until seizures subside. It should be raised by no more than 12 mmol/L during the first 24 hours.

 Osmotic Demyelination Syndrome (ODS): Risk of correcting Hyponatremia too rapidly – Flaccid Paralysis, Dysarthria, Dysphagia

Hypernatremia

 Plasma Na+ _{Concentration > 145 mmol/L}

 Clinical Features: Water shifts OUT of cells, leading to Contracted ICF Volume – Decreased Cell Volume is associated with an Increased

Risk of Subarachnoid or Intracerebral Hemorrhage

 Therapeutic Goals: Stop Ongoing Water Loss and to Correct the Water Deficit

Sample Orders for Hypokalemia: 1. Oral Route

 Kalium Durule 0.75gm (10 meq) TID PO x 2-3 days; or

 Oral KCl Solution 15-30cc TID (1gm KCl = 14meq K+_{, to be diluted in Oral Feeding or Water}

**NOTE: Each Oral Dose should NOT exceed 20-40 meq K+

2. Intravenous Route

 Usual Concentration is 20-40 meq K+ _{in 1L Saline or Dextrose Solution}

 Ex) Add 20-60 meq KCl in 1L Plain NSS x 12 hours

2. Hyperkalemia

Mild (K <5.5) Restrict Potassium Intake Moderate (K = 5.5-6.5) Kayexelate or Sorbisterit 20g; or

Kalmiate 1 Sachet in 50-150cc Water TID x 3 Doses (up to 4-5 Doses/day)

Furosemide 40-80mg IV Stat or Drip 0.5-20mg/hr Salbutamol Nebulization

Severe (K > 6.5) Calcium Gluconate 10mL 1amp in 10% Solution Slow IV Push

 Repeat after 10minutes if no improvement Glucose-Insulin

 D50-50mL + 10 units Humulin R Slow IV stat; then q60 _{x 3 Doses}  500mL 10% Dextrose + 10 Units Insulin over 30-60minutes

 1L 10% Dextrose + 20 Units Insulin with 1/3 solution given in first 30 minutes and the remainder over the subsequent 2-3 hours

Sodium Bicarbonate

 1 amp Dilute in 100cc D5W Slow IV Push > 10 minutes

 Fastest way to decrease Potassium (K+ shift in <15minutes)

D. Bicarbonate

( Desired HCO

3

– Actual HCO

3

) x (Weight in Kg) x 0.4

 For correction of deficit, administer 1/2 of computed value as Bolus, then remaining 1/2 as IV Drip

 Desired HCO

3

of 15 – 18 if patient has Chronic Renal Disease

 For Severe Acidosis: < pH 7.20 in Pure HAGMA, Goal is to Increase HCO

3

to 10 mEq/L and

pH to 7.15

VI. OTHER CONVERSION FACTORS

To mg/dL

RBS:

Multiply by 18

BUN:

Multiply by 2.8

Crea:

Divide by 88.4

Ca

2+

_:

_{Divide by 0.25}

Bilirubin:

Divide by 17.10

Equivalents

1cc Oral KCl:

1.33 mEqs K

15cc Oral KCl:

20 mEqs K

1 K Durule (750mg): 10 mEqs K

NaHCO

3

50mL:

45 mEqs Na

NaHCO

3

Gr X Tab:

7 mEqs Na

Regular requirement for NaHCO3 is 21mEq/day,

VII. TEMPERATURE CONVERSION

 Degrees Fahrenheit to Degrees Celsius: C = (F – 32) x 5/9

 Degrees Celsius to Degrees Fahrenheit: F = (C x 9/5) + 32 VIII. INTRAVENOUS FLUIDS

IV SOLUTION GLUCOSE Na+ _Cl- _K+ _Ca2+ _HCO

3 D5W 50 gm/L D10W 100 gm/L 0.9 NSS 154 154 D5LR 130 109 4 3 28 NM 40 40 13 NR 140 98 5 D50.9 NaCl 50 gm/L 154 154 D5NMK 50 gm/L 40 40 30

IX. PULMONOLOGY FORMULAS

A. Alveolar-Arterial O

2

Difference (PA

O2

– Pa

O2

) or Alveolar-Arterial O

2

Gradient (A-a Gradient)

A – a Gradient

PA

O2

– Pa

O2 or

( FiO

2

x 713) – (PCO

2

/ 0.8) - PaO

2

This formula is derived from:



Alveolar PO2 (PAO2) = FiO2 x (PB – PH2O) – PaCO2/R



In NORMAL Persons:

PA

O2

– Pa

O2

< 15 mmHg

 Four Basic Mechanisms of Hypoxia:

o Decrease in Inspired PO2

o Hypoventilation

o Shunt

o Ventilation/Perfusion (V/Q) Mismatch

A-a Gradient:

1. Normal Gradient (both reduce Alveolar Oxygenation):

 Decrease in Inspired PO2

 Hypoventilation

2. Elevated Gradient:

 Shunting (ie. Intracardiac Shunt): Low PO2 is NOT correctable with Supplemental O2

 V/Q Mismatch: Low PO2 is CORRECTED with Supplemental O2

Shunting VS V/Q Mismatch: 1. Shunt:

 Alveolar Collapse (Atelectasis)

 Intraalveolar Filling (Pneumonia, Pulmonary Edema)

 Intracardiac Shunt

 Vascular Shunt within Lungs

2. V/Q Mismatch:

 Airway Disease (Asthma, COPD)

 Interstitial Lung Disease

 Alveolar Disease

B. Desired FiO

2

Desired FiO

2

[ ( Desired PO

2

/ PAO

2

) + ( PACO

2

/ 0.8) ] x 100

713

Where:

PAO

2

= (FiO

2

x 713) – (PCO

2

/ 0.8)

Desired PO

2

= 80 – ( # of yrs > 60 y/o)

= If < 60y/o = 104 – (0.43 x age)

**NOTE: Desired PO2:

o Instead of 80 (80 is usually used), we can use 80-100 o In COPD, we can use 60

Simplified Version (ER Rounds):

Step I: Compute for PAO2

PAO2 = (FiO2 x 713) – (PCO2 / 0.8)

Step II: Compute for AaO2

AaO2 = PaO2

PAO2

Step III: Compute for Desired FiO2

. Desired PO2 . + PCO2

AaO2 0.8 . x 100

713

EXAMPLE: COPD Patient with the following values (ABG):

pH = 7.365 PCO2 = 42.4

PO2 = 109 HCO3 = 24.4

FiO2 = 60% O2 Sat = 90%

Step I: PAO2 = (0.6 x 713) – (42.4 / 0.8) = 374.8

Step II: AaO2 = . 109 . = 0.29

374.8

Step III: FiO2 = . 60 . + 42.4

0.29 0.8 . x 100 = 36% - therefore, we can decrease FiO2 to 36%

713

2) NUTRITION (DIET)

I. COMPUTATION OF DIET IN NORMAL PATIENTS (Ambulant, etc)

Total Caloric Requirement

(Kcal/day)

Ideal Body Weight x 35 Kcal

CHO (g/day)

. TCR x 0.6 .

4

CHON (g/day)

1gm / kg

Fats

The Rest

Subtract CHO + CHON from the TCR

**NOTE: In DM Patients, we give 3 meals + 2 snacks (to avoid Hypoglycemia)

o

If we want to Up Build Patients (for thin patients), we can give as much as 40 Kcal – 60 Kcal per kg

II. OSTERIZED FEEDING

TCR 1800 Kcal/day (for a 60kg patient)

o

CHO 270g/day

o

CHON 60g/day

Divided into 6 Equal Feeding

o

Fats Rest

1:1 Dilution

III. DM DIET

TCR 1800 Kcal/day (for a 60kg patient)

o

CHO 270g/day

o

CHON 60g/day

3 Meals, 2 Snacks

o

Fats Rest

No Simple Sugars

Low Salt, Low Fat Diet

Na <2g

TC < 200mg

Saturate Fats < 7%

MUFA > PUFA

If CBG >180: give HR 4‟u‟SC

If CBG >250: give HR 6‟u‟SC

CBG Monitoring pre-meals and at bedtime

Example: 70kg Patient

If we use 30 Kcal/kg  Patient will need 2,100 Kcal/day 1. Carbohydrates:

2,100 x 0.6 315g/day

4 2. Proteins:

1gm x 70 = 70g/day

If patient has CKD, we may go down to as much as 0.6g/kg If patient has CKD and is on Dialysis, we can use 0.9g/kg

3. Fats REST

3) NOTES ON INHERITED PATIENTS

I. GBS vs HYPOKALEMIC PERIODIC PARALYSIS



In Hypokalemic Periodic Paralysis = INTACT Deep Tendon Reflexes (DTR)



In GBS, the DTRs are usually disrupted

II. ORGANOPHOSPHATE POISONING

A. Signs of GOOD Atropinization

B. Atropine Toxicity

Dry Mucosa

T > 39

0

C

HR > 60

Flushing

Hypoactive BS

(-) Sweating

Pupils > 4mm

Psychosis, Restlessness

III. ACUTE MYOCARDIAL INFARCTION



CKMB should be > 2x elevated (Normal is 16, therefore, 32 is already MI)



CKMB / CK Total should be > 5%  MI!

IV. HEPARIN DRIP COMPUTATION (Unfractionated Heparin)

A. Initial Therapy

o

Bolus = 60-80 U/kg

o

Infusion = 14-18 U/kg/hr

aPPT (s) Bolus (H) Stop (min) Rate Change (cc/hr) Rpt aPTT (hrs) < 40 s 3000 0 22 6 40 – 49 0 0 1 6 50 – 75 0 0 No Change Next am 76 – 85 0 0 - 1 Next am 86 – 100 0 30 - 2 6 101 – 150 0 60 - 3 6 > 150 0 60 - 4 6

B. Example Case: 60kg male with Massive MI

o

Give 80 „U‟/kg = 4,800 ‘u’ IV Bolus (initial push)

o

Then, maintain on Drip: Add 10,000 Units Heparin with PNSS to make 100cc

o

Infusion is at 18 „u‟/kg/hr, therefore, we are giving 1,080 Units per Hour (U/hr)

o

Give 10.8 cc/hr  10.8 ugtt/min

o

Monitor PTT and make necessary adjustments

C. Example Case 2: PTT: Control is 37.1; then Patient is 33.3

33.3 / 37.1 = 0.9 times

Give 80 Units/kg BOLUS

Then INCREASE the Dose of heparin being given by 4 Units/kg/hr

Computation: 4 x 60kg = 240 Units (therefore, we should ADD 240 units per hour)

**NOTE: In 1 cc, there is 100 „u‟

 Therefore, adjust the Heparin Dose by ADDING 2cc/hr (or 2ugtts/min) to the Baseline Drip

D. Deep Vein Thrombosis

o

DVT Dose = 12 „u‟ UFH BID

o

DVT Prophylaxis Dose = 5 „u‟ BID

Warfarin = Monitor PT (INR) Heparin = Monitor PTT

aPTT CHANGE

< 1.25 times 80 Units/kg/Bolus; then

Increase by 4 units/kg/hr

1.25 – 1.5 times 40 Units/kg/Bolus; then

Increase by 2 units/kg/hr

1.5 – 2.5 times NO Change!

2.5 – 3.0 times Decrease by 3 Units/kg/hr

> 3.0 times STOP for 1 Hour; then

ANTICOAGULANT THERAPY WITH LOW-MOLECULAR WEIGHT AND UNFRACTIONATED HEPARIN

(from Harrisons)

CLINICAL INDICATION HEPARIN DOSE AND SCHEDULE TARGET PTT LMWH DOSE AND SCHEDULE

Venous Thrombosis Pulmonary Embolism

Treatment 5000 U IV Bolus; 1000-1500 U/h

2-2.5x 100 U/kg SC BID Prophylaxis 5000 U SC q8-12h < 1.5x 100 U/kg SC BID

Acute Myocardial Infarction

With Thrombolytic Tx 5000 U IV Bolus;

1000 U/hr 1.5-2.5x 100 U/kg SC BID With Mural Thrombus 8000 U SC q8 + Warfarin 1.5-2.0x 100 U/kg SC BID Unstable Angina 5000 U IV Bolus;

1000 U/hr 1.5-2.5x 100 U/kg SC BID

Prophylaxis

General Surgery 5000 U SC BID < 1.5x 100 U/kg SC BID before & BID Orthopedic Surgery 10,000 U SC BID 1.5x 100 U/kg SC BID before & BID Px with CHF, MI 10,000 U SC BID 1.5x 100 U/kg SC BID

PTT at RECHECK INTERVENTION

Normal (27-35s) 5000 U Bolus; 1300 U/h Infusion

< 50s Rebolus with 5000 U and Increase Infusion by 100 U/h 50 – 60s Increase Infusion Rate by 100 U/h

60 – 85s No Change

85 – 100s Decrease Infusion Rate by 100 U/h

100 – 120s Stop Infusion for 30 minutes and Decrease Rate by 100 U/h at Restart > 120s Stop Infusion for 60 minutes and Decrease Rate by 200 U/h at Restart

V. OTHER DRIPS (A to E from Blue Book) A. Nicardepine Drip

1. D5W 250mL + Nicardepine 20mg Concentration = 0.08mg/mL

Drip of 15-67ugtts/min is equivalent to 1-5mg/hr

OR

2. D5W 90mL + Nicardepine 10mg in Soluset Concentration = 0.1mg/mL

Drip of 10-50ugtts/min is equivalent to 1-5mg/hr

Maximum Dose = 15mg/hr

NOTE: IV Infusion Site must be changed every 12 hours should a peripheral line be used B. Noradrenaline (LEVOPHED) Drip: 2mg Noradrenaline in 2mL Ampule

D5W 250mL + 1 Amp Levophed at 15-60ugtts/min Concentration = 8mcg of Noradrenaline per mL

Drip of 2-8mcg Noradrenaline/min is equivalent to 15-60 ugtts/min

C. Hydralazine (Apresoline) Drip

D5W 250mL + Apresoline 2 Amps (20mg/amp) at 5-30ugtts/min (up to 60 ugtts/min) Maximum Daily Dose = 3.5mg/kg body weight per 24 hours

D. Isosorbide Dinitrate (ISOKET) Drip

1. D5W 90mL + Isoket 10mg in a Soluset

 Drip of 10-50 ugtts/min is equivalent to 1-5 mg/hr

2. If with CHF, may use DOUBLE Dose: D5W 90mL + Isoket 20mg in a Soluset  Drip of 5-25 ugtts/min is equivalent to 1-5 mg/hr

E. Glyceryl Trinitrate (PERLINGANIT) Drip: 1mg/mL in 10mL Vials 1. D5W 90mL + Perlinganit 10mg (1 vial) in a Soluset

 Drip of 10-50 ugtts/min is equivalent to 1-5 mg/hr

2. If with CHF, may use DOUBLE Dose: D5W 90mL + Perlinganit 20mg (2 Vials)  Drip of 5-25 ugtts/min is equivalent to 1-5 mg/hr

F. NTG Drip

o 10mg NTG in enough PNSS to make 100cc in Soluset x 10cc/hr o May increase or decrease by 2cc/hr to achieve Chest Pain-Free State G. Omeprazole Drip

o 80mg IV Bolus

o 40mg + 100cc PNSS to run for 5 Hours (Continuous Drip) H. Somatostatin Drip o 250mg IV Bolus; then 3mg in D5W 250cc x 120 3mg + 500cc PNSS x 42cc/hr (250mg/hr) I. Electrolytes 1. NaHCO3 Drip  150mg NaHCO3 + 250cc D5W x 240 2. MgSO4 Drip  2-4mg in 250cc D5W x 120 3. KCl Drip (Correction)

 Please incorporate 40 meqs KCl to 1L PNSS to run for 80 _{x __ Cycles}

 Repeat K+ _{Post-Correction}

o Formulation: Dilute 20 Units of Insulin in 100cc PNSS to concentration of 0.2 Unit/cc

o Standard Insulin Concentration is 1 Unit Regular Insulin per 10mL Saline (0.1 unit/cc) 1. For Hyperkalemia (from Blue Book) – Glucose-Insulin Drip

a. 50mL of 50% Dextrose in Water + 10 Units Insulin in 2-5 Minutes

 Eg. Mix D50-50 mL + 10 Units Humulin-R Slow IV Stat, then q6 hours x 3 Doses b. 500mL of 10% Dextrose + 10 Units Insulin over 30-60 Minutes

 If Volume Overload is NOT a problem

c. 1000mL of 10% Dextrose + 20 Units Insulin with 1/3 of Solution given in the first 30 Minutes and the remainder over the subsequent 2-3hours

2. For Hyperglycemia a. Loading Dose

 CBG > 200 = 0.075 – 0.1 Unit/Kg IV Push

 CBG > 300 = 0.1 – 0.125 Unit/Kg IV Push

 If DKA = 0.2 Unit/Kg IV Push b. Maintenance Dose

 0.1 Unit/kg/hr, titrate to desired Blood Glucose

3. Dosing Table

a. Intravenous (IV)

CBG

ACTION

< 70 Discontinue for 30 minutes, give 15-20mL of D50-50, re-measure in 30 mins

If > 100, resume drip at 1 unit/hr. Continue glucose infusion

70 – 120 Decrease Rate by 0.3 unit/hr

121 – 180 No Change in Rate

181 – 240 Increase Rate by 0.3 unit/hr

241 – 300 Increase Rate by 0.6 unit/hr

> 300 Increase Rate by 1.0 unit/hr

b. Subcutaneous (SC)

CBG

ACTION

< 80 Discontinue for 30 minutes, give 15-20mL of D50-50, re-measure in 30 minutes

80 – 180 No Change in Rate

181 – 200 Humulin-R 6 Units SC

201 – 300 Humulin-R 8 Units SC

> 300 Humulin-R 10 Units SC

K. Dopamine, Dobutamine, Heparin

o See above discussion

VI. VIRCHOW‟S TRIAD: Encompasses the three broad categories of factors that are thought to contribute to thrombosis

 The triad consists of:

o Alterations in normal blood flow (Stasis) o Injuries to the vascular endothelium

o Alterations in the constitution of blood (Hypercoaguability)

VII. METABOLIC SYNDROME (SYNDROME X, INSULIN RESISTANCE SYNDROME)

 Consists of a constellation of Metabolic Abnormalities that confer in Risk of Cardiovascular Disease and Diabetes Mellitus

 Major Features include: o Central Obesity o Hypertriglyceridemia o Low HDL Cholesterol o Hyperglycemia

o

Hypertension

NCEP:ATPIII 2001 CRITERIA for Metabolic Syndrome: Three or More of the following:

 Central Obesity: Waist Circumference > 102cm (M), > 88cm (F)

 Hypertryglyceridemia: TG > 150mg/dL or specific medication

 Low HDL Cholesterol: < 40 mg/dL and 50 mg/dL, respectively, or specific medication

 Hypertension: BO > 130 systolic or > 85 Diastolic or specific medication

4) ARTERIAL BLOOD GAS (ABG)

I. FORMULA

A. Metabolic Acidosis

Decrease in PCO

2

= 40 – (∆HCO

3

x 1.25) +/- 2

B. Metabolic Alkalosis

Increase in PCO

2

= 40 + (∆HCO

3

x 0.75) +/- 2

C. Respiratory Acidosis

1. Acute Respiratory Acidosis

∆HCO

3

= 24 + [(∆PCO

2

/ 10) x 1] +/- 2

2. Chronic Respiratory Acidosis

∆HCO

3

= 24 + [(∆PCO

2

/ 10) x 4] +/- 2

D. Respiratory Alkalosis

1. Acute Respiratory Alkalosis

∆HCO

3

= 24 – [(∆PCO

2

/ 10) x 2] +/- 2

2. Chronic Respiratory Alkalosis

∆HCO

3

= 24 – [(∆PCO

2

/ 10) x 4] +/- 2

Steps in Interpreting ABGs:

 1) Check pH and Primary Disturbance

 2) Check the Compensatory Mechanism

 3) Check for presence of a Mixed Acid-Base Disturbance

 4) For Metabolic Acidosis: Compute for Anion Gap (AG)

II. COMPENSATORY MECHANISMS

DISORDER PRIMARY

DISTURBANCE COMPENSATORY RESPONSE

Metabolic Acidosis Decrease in HCO3 1.2 mmHg DECREASE in pCO2 for every 1 mEq/L FALL in HCI3

Metabolic Alkalosis Increase in HCO3 0.7 mmHg INCREASE in pCO2 for every 1 mEq/L RISE in HCO3

Respiratory Acidosis

 Acute < 2 weeks

 Subacute 2-6 weeks

 Chronic > 6 weeks

Increase in pCO2 Acute:

1 mEq/L INCREASE in HCO3 for every 10mmHg RISE in pCO2 Chronic

3-5 mEq/L INCREASE in HCO3 for every 10mmHg RISE in pCO2

Respiratory Alkalosis

 Acute

 Chronic

Decrease in pCO2 Acute:

2 mEq/L DECREASE in HCO3 for every 10mmHg FALL in pCO2 Chronic:

5 mEq/L DECREASE in HCO3 for every 10mmHg FALL in pCO2

 Normal Values:

pH

7.4 + 0.3

pCO

2

(mmHg)

40 + 4

HCO

3

(mEq/L)

24 + 2

Anion Gap

12 + 2

Cl (mEq/L)

105

III. CASE: An 50/M, 60kg, intubated patient had the following ABG results, post-intubation



pH = 7.2

decreased



pCO

2

= 18

decreased



HCO

3

= 7

decreased

A. Formula for Metabolic Acidosis:

Decrease in pCO

2

= 40 – (∆HCO

3

x 1.25)

= 40 – ([24 – 7] x 1.25)

*NOTE: 24 is the desired HCO

3

; 7 is the actual HCO

3

= 18.75

Since the Actual Decrease in PCO2 (18) is within +/- 2 of 18.75  COMPENSATED!!!!!

This means that for every decrease in HCO3, there should be a 1.25 Decrease in PCO2

B. Compute for Bicarbonate Deficit:

HCO

3

Deficit = (Desired HCO

3

– Actual HCO

3

) x weight x 0.4

= (18 – 7) x 60 kg x 0.4

= 264 mEq Deficit

= Give half dose as IV Bolus, then the remaining in Drip

= Example: Give 100 mEq IV Bolus NOW, then the remaining 150 mEq as Drip

IV. OXYGEN SATURATION

> 80

Adequate Oxygenation

60 – 80

Mild Hypoxemia

40 – 60

Moderate Hypoxemia

< 40

Severe Hypoxemia

SAMPLE SCENARIO: If the Actual PCO2 is NOT within +/-2:

 If pCO2 is 10  there may be Overcompensation, or a COMBINED Metabolic Acidosis AND Respiratory Alkalosis

V. METABOLIC ACIDOSIS

A. High Anion Gap Metabolic Acidosis

. ∆ AG .

If:

= 1  Pure HAGMA

∆ HCO

3 < 1  HAGMA + NAGMA

> 1  HAGMA + Metabolic Alkalosis

B. Normal Anion Gap Metabolic Acidosis

. ∆ Cl .

If:

= 1  NAGMA

∆ HCO

3 < 1  NAGMA + HAGMA

> 1  NAGMA + Metabolic Alkalosis

VI. ANION GAP

A. High-Anion Gap Metabolic Acidosis (HAGMA) o Methanol o Uremia o DKA MUDPILES o Paraldehyde o Isoniazid o Lactic Acidosis o Ethanol o Salicylates

B. Normal-Anion Gap Metabolic Acidosis (NAGMA) o Renal

o

GI Losses

VII. SOME EXAMPLES OF MIXED ACID-BASE DISORDERS FROM HARRISONS: A. Mixed Metabolic and Respiratory

1. Mixed Acidosis – Respiratory Alkalosis

 Key: High- or Normal-AG Metabolic Acidosis  Prevailing PCO2 BELOW Predicted Value

 Example: Na 140, K 4.0, Cl 106, HCO3 14; AG 20

PCO2 24, pH 7.39

2. Metabolic Acidosis – Respiratory Acidosis

 Key: High- or Normal-AG Metabolic Acidosis  Prevailing PCO2 is ABOVE Predicted Value

 Example: Na 14, K 4.0, Cl 102; HCO3 18; AG 20

PCO2 38, pH 7.3

3. Metabolic Alkalosis – Respiratory Alkalosis

 Key: PCO2 does NOT Increase as Predicted; pH is HIGHER than Expected

 Example: Na 140, K 4,0, Cl 91, HCO3 33; AG 16

PCO2 38, pH 7.55

4. Metabolic Alkalosis – Respiratory Acidosis

 Key: PCO2 is HIGHER than Predicted; pH is NORMAL

 Example: Na 140, K 3.5, Cl 88, HCO3 42; AG 10

PCO2 67, pH 7.42

B. Mixed Metabolic Disorders

1. Metabolic Acidosis – Metabolic Alkalosis

 Key: Only detectable with High-AG Acidosis; ∆ AG >>> ∆ HCO3

 Example: Na 140, K 3.0, Cl 95, HCO3 25, AG 20

PCO2 40, pH 7.42

2. Metabolic Acidosis – Metabolic Acidosis

 Key: Mixed High-AG – Normal –AG Acidosis; ∆HCO3

accounted for by combined change in ∆AG & ∆Cl  Example: Na 135, K 3.0, Cl 110, HCO3 10, AG 15

PCO2 25, pH 7.20

Diseases with HAGMA:

-Lactic Acidosis -Ketoacidosis  Diabetic  Alcoholic  Starvation -Toxins  Ethylene Glycol  Methanol  Salicylates  Propylene Glycol  Pyroglutamic Acid

-Renal Failure (Acute and Chronic)

Diseases with NAGMA

-Renal HCO3 Loss (Proximal RTA Type 2)

-Enhanced NH4 Excretion

-Ingestion of HCl, NH, Cl, Lysine, Arginine

-GI HCO3 Loss (Diarrhea) or Acid Gain

-Impaired NH4 Excretion

-Distal RTA (Type 1) -Diarrhea

-Urinary Tract Obstruction

INTERPRETATION: Lactic Acidosis, Sepsis in ICU INTERPRETATION:

Severe Pneumonia, Pulmonary Edema

INTERPRETATION: Liver Disease and Diuretics INTERPRETATION: COPD on Diuretics

INTERPRETATION: Uremia with Vomiting

INTERPRETATION: Diarrhea and Lactic Acidosis Toluene Toxicity

ECG TEACHING NOTES (PGH, 2008)

1) INTRODUCTION

I. NORMAL VALUES

P-Wave < 0.12 sec

< 0.25 Mv in Limb Leads

< 0.1 Mv Terminal Negative Deflection in V1 PR Interval 0.12 – 0.20 sec (up to 5 small boxes)

QRS Duration < 0.11 – 0.12 sec

T Wave 5 – 10 mm (0.5 – 1.0 Mv)

QTc < 0.44 (females)

< 0.48 (males)



Formula of Corrected QT-Interval (QTc)

Corrected QT Interval = . QT Actual .

√ R-R Interval



Computation of Heart Rate

Rate = . 300 .

= . 1500 .

# of Big Sq

# of Small Sq



Important Notes:

o Significant Q-Wave: > 25% of QRS o Significant ST-Segment Depression: > 1mm

o Significant ST-Segment Elevation: > 1mm Limb Leads; > 2mm Chest Leads

II. AXIS



Computation of Frontal Axis:



Where:

o Avf and I are integers derived by subtracting the Positive Deflection from the Negative Deflection

o The Avf in the numerator is an Integer, while the I and Avf in the Denominator are absolute values of integers

o

If I is a Negative Integer, then adjust the Axis by adding | 90 |



Interpretation:

Right Axis Deviation (RAD)

> 100

0

Left Axis Deviation (LAD)

< -30

0

Normal Axis

-30

0

_{to 100}

0

Extreme Axis Deviation

-90

0

_{to 180}

0

III. NORMAL ECG

Read As: Regular Sinus Rhythm (RSR) Normal Axis (NA)

Within Normal Limits

IV. EJECTION FRACTION ON ECG

Ejection Fraction = (QRS aVr x 2.64) + (Age x 0.645)

Axis = . 90 x aVF .

|I| + |aVF|

ST Depression: Ischemia ST Elevation: Infarction

2) SOME COMMON FINDINGS

I. NON-SPECIFIC ST-T WAVE CHANGES



T-Wave Inversion < 5mm (< 0.5Mv)



ST Segment Depression < 1mm (< 0.1 Mv)



Flattening of ST Segment without the presence of U-Waves

**NOTE: Mention leads where ST-Segment changes and T-Wave inversions occur

II. ISCHEMIA



T-Wave Inversion > 5mm (> 0.5Mv)  read as To Consider Ischemia



ST-Segment Depression > 1mm (> 1Mv) in 2 or more contiguous leads  read as Ischemia

**NOTE: Significant ST-Segment Depression > 1mm in at least 2 contiguous leads (Horizontal or Downsloping)

III. POOR R-WAVE PROGRESSION



In Leads V1-V3 (R-Wave < 3mm or 0.3Mv) AND Normal R-Wave in V4-V6



Do NOT Read as Poor R-Wave Progression in the following conditions:

o

Left Ventricular Hypertrophy

o

Left Bundle Branch Block

o

Wolff-Parkinson-White Rhythm

o

Anteroseptal Wall MI

o

Low-Voltage QRS Complexes

**NOTE: NO Clinical Relevance: Do NOT Write:

o

Early transition / counterclockwise rotation

o

Persistent S V5-V6 or Persistent Posterobasal Forces

IV. ATRIAL ENLARGEMENT

Right Atrial Enlargement

P-Wave with 2.5mm Amplitude (0.25Mv) in any of Lead II, III or Avf

Left Atrial Enlargement

P-Wave Widened > 3mm (> 0.12sec) especially Lead II; OR

Terminal Segment of P-Wave in V1 > 1 small box (>0.04 sec OR 0.1Mv depth)

Do NOT include Notching in Lead II as Criterion

Bi-Atrial Enlargement

RAE

(Tall P-Waves > 2.5mm In Leads II, III, Avf)

PLUS

LAE

(Terminal Segment Of Wave > 1 Small Box (0.04 Sec) In V1 Or Widened

P-Wave, Especially Lead II > 3mm (>0.12sec)

V. VENTRICULAR ENLARGEMENT

A. Left Ventricular Hypertrophy

1. Sokolow-Lyon Criteria

 [S in V1] + [R in V5 or V6] is Greater than 35mm (do NOT use S in V2); OR

 Avl > 11mm

**IMPORTANT Notes:



Cut-Off for LVH, regardless of Age > 35mm



No need to Indicate “By Voltage”

2. Cornell Criteria

 S in V3 + R in AvL



Female > 20mm



Male > 28mm

B. Left Ventricular Strain

C. Right Ventricular Hypertrophy

o

RAD is a Prerequisite Criterion for RVH

o

An Upright V1 or Prominent R in V1 without RAD will NOT be signed out as RVH and need not be

described

D. Biventricular Hypertrophy

Hypertrophy in presence of BBB: RAD + rsR Pattern in V1 (R-Wave Amplitude > 15mm or 1.5Mv)

VI. LOW VOLTAGE COMPLEXES



Chest Leads are more significant



QRS Complexes

< 5mm (0.5Mv) in Limb Leads

< 10mm (1.0Mv) in Chest Leads

Read as Low Voltage Complexes in Limb OR Chest Leads

LVH by Voltage Criteria + Significant Asymmetric ST-Segment Depression with Broad-Inverted T-Wave

Read as LVH with Strain, Cannot Rule Out Concomitant Ischemia

3) ABNORMAL ECG FINDINGS

I. EARLY REPOLARIZATION CHANGES



Embryonic R + ST-Elevation NOT fulfilling criteria for ST-Elevation in MI



Check morphology of ST-Segment if more convex rather than concave

II. BUNDLE BRANCH BLOCKS AND INTRAVENTRICULAR CONDUCTION DEFECT



LBBB



RBBB



Non-Specific Intraventricular Conduction Delay: Widened QRS without Repolarization changes, NOT meeting

the Criteria for LBBB or RBBB



LAFB



LPFB



Bifasicular Block



Trifasicular Block

III. ELECTROLYTE ABNORMALITIES



Low Sensitivity of „U‟ Wave



„U‟ Wave Prominent + Normal T-Wave  Read as Prominent „U‟ Wave



Prominent „U‟ Wave + Flattened T-Wave  Read as T/C Hypokalemia



ST-Segment Depression + „U‟ Wave + Normal T-Wave  Read as Cannot R/O Ischemia; Prominent U Wave



Flattened T-Waves + Normal QRS-Complex  Read as Non-Specific ST-T Wave Changes

QTc Computed to Adjust for Bradycardia (HR < 60bpm) or Tachycardia (HR > 100bpm)

o

Normal Value: Female < 0.48

o

Normal Value: Male < 0.47

**NOTE:

Use the Lead with the longest Absolute QT Interval without Prominent Q-Wave OR Largest Amplitude T-Wave

A. Digitalis Effect

o

Seen in patients without Significant ECG Changes due to Organic Disease

o

Should describe Drug Effects in leads seen

o

Read as Scooping of ST-Segment Depression, Non-Specific ST-T Wave Changes, probably Digitalis Effect

B. Hyperkalemia

o

At least > 2 Contiguous Leads with Peaked T-Waves > 10mm (1.0Mv)

o

Read as Peaked T-Waves, T/C Hyperkalemia

IV. MYOCARDIAL INFARCTION

A. Timing of MI

Acute

Significant ST-Elevation + T-Wave Inversion +/- Q-Waves

Old

Significant Q-Wave + Isoelectric ST Segment + Upright T-Wave

Age Undetermined

ST-T Wave Change +/- Q-Wave not fulfilled by Criteria for Old and Acute MI

B. Definitions

Significant ST-Segment Elevation

> 1mm Limb Leads

> 2mm Chest Leads

Significant Q-Wave

> 25% of the QRS Complex; or

> 0.04 sec

C. Walls of Involvement

LEADS

MYOCARDIAL WALL INVOLVED

V1

Posterior

V1-V2

Septal

V1-V3 or V1-V4

Anteroseptal

V3-V4

Anterior

V5-V6

Lateral

V3-V6

Anterolateral

V1-V6

Massive Anterolateral

II, III, Avf

Inferior

D. Correspondence of Specific ECG Leads (from Medicine Notes)

LEADS

CORRESPONDING LV AREAS

II, III, Avf

Inferior Wall

I, Avl

High Lateral

V1, V2

Septal Wall

V3, V4

Anterior Wall

V5, V6

Lateral Wall

V1 – V3

Anteroseptal Wall

V3 – V6, I, AvL

Anterolateral Wall

V5, V6, II, III, AvF

Inferolateral Wall

Almost All Leads

Diffuse / Global / Massive

Mirror Image V1, V2

Posterior LV Wall

V3R, V4R

RV Wall

V. INTERPRETING ECGs (Rounds)

A. AV Block

Primary AV Block

Prolonged PR interval (More than 5 small squares or more than 0.2msec)

Secondary AV Block I: There is prolonging PR-Interval, then Drop Beat

II: There is a Regular PR-Interval, then Drop Beat

Tertiary AV Block

With AV dissociation (look for P-waves, look for Q waves  DISSOCIATED!)

The PR and QRS Waves are Independent from each other

B. Q-Waves

o

20% of R; Wide  OLD Infarct!

o

In aVr, there is usually a Q-Wave

C. QRS

o

Normal = 0.08 – 0.12

o

If Wider = Bundle Branch Block

D. ST Elevation / Depression

o

ST Elevation = at least 2 small boxes in contiguous leads

o

ST Depression = at least 1 small box

E. T-Waves

o

Peaked T-Waves = 10 boxes in chest leads; 5 boxes in limb leads

o

If Inverted T-Waves = CANNOT rule out ischemia

VI. VENTRICULAR TACHYCARDIA

A. Ventricular Tachycardia can be classified based on its MORPHOLOGY: 1. Monomorphic Ventricular Tachycardia

 Means that the appearance of all the beats match each other in each lead of a surface electrocardiogram (ECG)

2. Polymorphic Ventricular Tachycardia

 Has beat-to-beat variations in morphology

 This most commonly appears as a cyclical progressive change in cardiac axis referred to by its French eponym Torsades de Pointes (literally twisting of the points).

B. Classification Based on Duration of the Episodes:

o Technically, three or more beats in a row on an ECG that originate from the ventricle at a rate of more than 100 beats per minute constitute a ventricular tachycardia

1. Non-Sustained Ventricular Tachycardia

 If the fast rhythm self-terminates within 30 seconds, it is considered a non-sustained ventricular tachycardia

2. Sustained Ventricular Tachycardia

 If the rhythm lasts more than 30 seconds it is known as a sustained ventricular tachycardia (even if it terminates on its own after 30 seconds)

C. Classification Based on SYMPTOMS 1. Pulseless VT

 Associated with NO effective cardiac output, hence, no effective pulse, and is a cause of cardiac arrest  In this circumstance it is best treated the same way as ventricular fibrillation (VF) and is recognized as

one of the shockable rhythms on the cardiac arrest protocol

2. Some VT is associated with Reasonable Cardiac Output and may even be Asymptomatic

 The heart usually tolerates this rhythm poorly in the medium to long term, and patients may certainly deteriorate to Pulseless VT or to VF

VII. PACEMAKER

A. Indications for Permanent Pacemaker Insertion (Pacing)

o Permanent Pacemaker Insertion should be implanted in the following conditions (Class-I Indications) 1. Complete Heart Block with:

 (+) Symptoms due to the AV Block (eg. Syncope, Heart Failure)  Asystole > 3 seconds by Holter Monitoring even if without symptoms  HR < 40 bpm even without symptoms (any escape rhythm < 40 bpm)

2. Second Degree AV Block, Permanent or Intermittent, with Symptomatic Bradycadia 3. Sinus Node Dysfunction with Symptomatic Bradycardia.

 In some patients, this is due to Long-Term Essential Drug Therapy for which there are NO Acceptable Alternatives Eg. Digoxin for Tachycardia-Bradycardia Syndrome

4. Carotid Sinus Stimulation causing Recurrent Syncope or Asystole > 3 seconds in the absence of any medication that depresses the Sinus Node or AV Conduction

B. WOF: Pacemaker Syndrome

o This occurs when Atrium pumps against a Closed Mitral Valve



due to “Asynchronization”

VIII. ECG FINDINGS OF PERICARDITIS



Diffuse ST-Segment Elevations = Concave Diffuse ST-Segment Elevation

A. ECG of Pericarditis

B. ST Elevation in Pericarditis is Different from MI: In Myocardial Infarction, it is CONVEX

o

In MI = ST-Segment Elevation WITH T-Wave Inversion

o

Difference = In Pericarditis, when T-Wave Inversion appears, ST-Segment Elevation disappears

IX. OTHER NOTES (during rounds):

A. ECG Findings of Mitral Stenosis

o

LA-Enlargement = WIDE P-Wave

o

RAD

o

RVH

B. Significant Q-Waves

o

1) Q-Wave > 25% of R-Wave

MECHANICAL VENTILATION

1) BASIC INFORMATION

I. WEANING FROM MECHANICAL VENTILATION

A. Removal of Mechanical Ventilator support requires that a number of criteria be met 1. Upper Airway Function must be Intact for a patient to remain extubated

 If a patient can breathe on his own through an ET Tube but develops stridor or recurrent aspiration once tube is removed, Upper Airway Dysfunction or an abnormal swallowing mechanism should be suspected 2. Weaning Index

 Respiratory Drive and chest wall function are assessed by observation of RR, Tidal Volume, Inspiratory Pressure, and Vital Capacity

 Weaning Index: Ratio of Breathing Frequency to Tidal Volume (breaths per minute per liter), is both sensitive and specific for predicting the likelihood of successful extubation

 If Ratio < 105 with patient breathing without mechanical assistance through an ET Tube, successful extubation is likely

3. Alveolar Ventilation is deemed adequate when:

 Elimination of CO2 is sufficient to maintain arterial pH in the range of 7.35 to 7.40, and an SaO2 > 90% can

be achieved with an FiO2 < 0.5 and PEEP < 5cmH2O

B. Approaches to Weaning

o T-Piece and CPAP Weaning are best tolerated by patients who have undergone MV for brief periods and require little respiratory

muscle reconditioning

o SIMV and PSV are best for patients intubated for extended periods likely to require gradual respiratory-muscle reconditioning

1. T-Piece and CPAP

 Brief spontaneous breathing trials with supplemental O2

 Initiated for 5mins/hour followed by a 1-h interval of rest

 Trials are increased in 5 to 10 minutes/hour increments until patient can remain ventilator independent for periods of

several hours

 Extubation can then be attempted

2. SIMV

 Involves gradual tapering the mandatory backup rate in increments of 2 to 4 breaths per minute while monitoring blood

gas parameters and respiratory rates

 Rates > 25 / min on withdrawal of mandatory ventilator breaths generally indicate Respiratory Muscle Fatigue and the

need to combine periods of exercise with rest

 Exercise periods are gradually increased until a patient remains stable on SIMV at < 4 breaths per minute

 A CPAP or T-Piece Trial can then be attempted before extubation

3. PSV

 Usually initiated at a level adequate for full ventilator support (PSVMax) ie. PSV is set slightly below the peak

inspiratory pressures required by the patient during volume-cycled ventilation

 Level of pressure support is then gradually withdrawn in increments of 3-5cmH2O until a level is reached at which the

RR increases to 25 breaths/min – At this point, intermittent periods of higher pressure support are alternated with periods of lower-pressure support to provide muscle reconditioning while avoiding diaphragmatic fatigue

 Gradual withdrawal of PSV continues until the level of support is just adequate to overcome the reistance of the ET

Tube (~5 to 10cmH2O)

Indications for WEANING:

 Mental Status: Awake, Alert, Cooperative

 PaCO2 > 60mmHg with FiO2 < 50%  PEEP < 5cm

 PaCO2 and pH Acceptable  Spontaneous TV > 5mL

 VC > 10mL/kg

 MIP > 25cmH2O  RR < 30/min

 Rapid Shallow Breathing Index (RBI) < 100



Support can be discontinued and the patient extubated

II. INDICATIONS FOR INTUBATION (Medicine Notes)

 Impending Respiratory Failure; Apnea

 RR > 35  PaCO2 > 50  PaO2 < 60  TV < 3.5mL/kg  VC < 10-15mL/kg  Inspiratory Force < 25cmH2O  FEV < 10mL/kg  VQ/VT > 0.6

 To deliver High FiO2  Absent Gag

 pH < 7.35

III. SPONTANEOUS BREATHING TRIAL (Harrisons)

 Consists of a Period of breathing through the Endotracheal Tube WITHOUT Ventilator Support (both Continuous Positive Airway Pressure [CPAP] of 5cmH2O & an Open T-Piece Breathing System can be used) for 30-120 mins

A. If the Following are Present, Patient has passed the Screening Test and should undergo Spontaneous Breathing Trial o Stable Oxygenation (PaO2/FIO2 > 200) and PEEP < 5cmH2O

o Cough and airway reflexes are intact

o No Vasopressor Agents or Sedatives are being administered

B. Spontaneous Breathing Trial is Declared a FAILURE and STOPPED if any of the following occur: o 1) RR > 35/min for > 5mins

o 2) O2 Saturation < 90%

o 3) HR > 140/min or a 20% Increase or Decrease from Baseline o 4) Systolic BP < 90mmHg or > 180mmHg

o

5) Increased Anxiety ot Diaphoresis

IV. ASSIST CONTROL MODE (Medicine Notes)



Each breath is assisted by the vent even if the RR exceeds the BUR



Parameters: VT

,

PEEP, BUR, PFR/IFR, FiO

2

, Sensitivity Flow Pattern

A

. Tidal Volume o General: 8-10 mL/kg o In ARDS: 6 mL/kg B. PEEP: o 5cm H2O C. Back Up Rate o 16-20

D. Peak Flow Rate:

o 40-60 mL

o Asthma / COPD: Increase to allow more time to exhale

o ARDS: Decrease to Prevent further injury

E. FiO2 – Start at 100%

o If lungs are NORMAL (eg. Trauma patient), start at 50%

o DECREASED to tolerable % as fast as possible (doesn‟t have to be decreased by 10%)

o Non-Toxic FiO2 = 50% (Golden Time to reach this is 4 hours)

F. Sensitivity (Trigger) – 2 L

o Pressure: (-) 1.5 to 2.0 cmH2O (the more negative, the more work patient does)

o Flow: Usually 2L

NOTES on FiO2:

 FiO2 at Room Air = 21%

 O2 via Nasal Prong = # lpm x 0.4 + 20

If at the end of the Spontaneous Breathing Trial, the ratio of the Respiratory Rate and Tidal Volume in Liters (f/VT)

is < 105, the patient can be EXTUBATED

The primary indication for initiation of mechanical ventilation is Respiratory Failure, of which there are 2 basic types:

 Hypoxemic Respiratory Failure

G. Flow Pattern:

o Square Wave

2) BASIC MODES OF VENTILATION

(Mech-Vent Work Shop: Dr.Divinagracia Lecture)

I. ASSIST / CONTROL MODE (A/C MODE)

 The Patient breathes at his OWN Rate and the Ventilator senses the Inspiratory Effort and delivers a Preset Tidal Volume with EACH patient effort

 If patient‟s Respiratory Rate decreases past a Preset Rate, the Ventilator delivers Tidal Breaths at the Preset Rate

 EVERY BREATH is assisted

A. Advantages and Disadvantages

ADVANTAGES DISADVANTAGES

Useful in Patients with Neuromuscular Weakness or CNS Disturbances

The INITIAL Mode usually set upon advent of Mechanical Ventilation

It totally Unloads (“rests”) the Respiratory Muscles requiring NO “Work” on the Patient‟s part

Tachypnea may result in Significant Hypocapnea and Respiratory Alkalosis

Improper setting of Sensitivity to trigger the Ventilator may result in “fighting the ventilator” when sensitivity is set too low

Increases Sensitivity may result in Hyperventilation; Sensitivity is generally set so that an Inspiratory Effort of 2cmH2O will trigger the Ventilation

Since there is almost NO work involved by the Respiratory Muscles, Muscle Tone is NOT well Maintained (Atrophy).

Muscle Atrophy starts within 6 hours

Indications for Mechanical Ventilation:

1. Clinical Assessment

 Presence of Apnea, Tachypnea (>40/min)

 Respiratory Failure that cannot be corrected by any other means 2. Arterial Blood Gases (ABG)

 Severe Hypoxemia (PO2 < 50) despite High-Flow Oxygen  Significant CO2 Retention (PCO2 > 50)

3. Worsening Physiological Parameters

 Are of limited use since patients with Respiratory Insufficiency are unable to perform PFTs and their Respiratory Failure mandates immediate intervention

 However in some cases especially in Neuromuscular Diseases, these parameters can be used as “warnings” that the patient will go into Respiratory Failure sooner rather than later:

o 1) Vital Capacity < 15mL/kg o 2) Inspiratory Force < -25cm H2O

o 3) FEV1 <10mL/kg TWO Main Modes of Ventilation:

 Volume Cycled / Controlled: we set the Tidal Volume (ex. AC Mode)

B. Selection of Ventilator Settings for A/C Mode

SETTING

USUAL VALUE

1) Tidal Volume (V

T

)

 How much volume will the Machine Deliver?

8-10 mL/kg of Ideal Body Weight 6mL/kg for ALI/ARDS

10-15mL/kg for Neuromuscular Dse

2) Back-Up Rate: Number of Tidal Breaths Delivered per Min

 Minimum number of breaths per minute

 Usually set 2 to 4 below the Spontaneous Rate and then the Effect on the patient of Decreasing Rate is noted (this can be adjusted

depending on the desired PaCO2 or pH

 Ex) If set at 8, patient will NOT breath below RR < 8



Faster RR =  Blow of CO2  PaCO2 and pH

16 - 22

3) Oxygen Concentration (FiO

2

)

 Initial FiO2 should be 100% unless it is evident that a Lower FiO2

will provide adequate oxygenation



We can start at 50% if Neuromuscular Disease (ex. MG)

100%

4) Inspiratory Flow Rate (IFR)

 How fast do we deliver the air? 60L/minute is FASTER than

40L/minute (Higher Flow Rates  Higher Peak Pressure)

 This is the Rate air is delivered to the patient to achieve the Tidal Volume set

 Rate needs to be HIGHER (80L/min) in COPD & Asthma

 An IFR LOWER than the patient demand will Increase the work of breathing and is a common cause of Patient-Ventilator Discordance (Fighting or Bucking the Ventilator)

 In Patients with Hypoxemia, deliver the air SLOWER (so that

Inspiration Time is Longer  more time to exchange PO2

40-60 L/minute

5) Inspiratory Flow Pattern (IFP)

 How do you deliver the Air? This is how flow is distributed

throughout the Respiratory Cycle



Normal Person: Sine Wave

Wave Forms usually Available: a. Sine Wave:

 The maximum flow is at Mid Inspiration and resembles a Normal

Spontaneous Tidal Breathing b. Square Wave

 This provides a maximum peak flow throughout the Inspiratory Period

 Fast Delivery  patients prefer it (but has higher pressures)

c. Decelerating Wave



The flow is maximal at the Start and diminishes as Inspiration ends

Square Wave

6) PEEP

 “Physiologic PEEP” of about 5cm H2O should be added regardless

of FiO2 to prevent the Alveolar Injury due to the Shearing Effect

of opening and closing the Alveoli

 Pressure at End Expiration (it is Positive)

 Should be Increased in ARDS

7) Sensitivity

 Ranges anywhere from –5 to –0.5cmH2O (Pressure Sensitivity) or

1 to 5 Liters (Flow Sensitivity)

 The MORE Sensitive (eg. 0.5cm or 1L), the EASIER for the patient to Trigger the Ventilator which may lead to

Hyperventilation



The LESS Sensitive (eg. 5cm or 5L), the HARDER for the patient to trigger the Ventilator which may lead to Increased Work of breathing and thus can cause Patient-Ventilator Desynchrony

a. Pressure Sensitivity

 Ex) If set at –1, the patient has to exert a –1cmHg Pressure for the Vent to

Deliver the Tidal Volume b. Flow Sensitivity

 Ex) If set at 1L, patient has to create a negative pressure



Advantage: Patients with COPD (difficult to empty lungs)  they will

have LESS work

-2.0cm or 2L

Different for PGH Vents

 Sensitivity in PGH Mechanical Ventilators:

o Turn knob Counterclockwise  becomes Less Sensitive o Turn know Clockwise  becomes More Sensitive  I:E Ratio:

o Normal is 1:2

o In COPD, adjust to 1:3 o In ARDS, adjust to 1:1