ACID-BASE IMBALANCE

Prepared by Ms. Jucar

MARIETTA C. JUCAR, RN, MN

ObjectivesAt the end of the session, the students

will define acid-base imbalance; describe the 3 major chemical buffer

system; discuss the roles of lungs and kidneys in

the acid base balance; identify the different types of acid base

imbalances; discuss etiologic factors that cause acid

base imbalances; interpret arterial blood gas values.

OVERVIEW OF ACIDS AND BASESDefinition of terms Acid- any substance releasing a hydrogen ion

when dissolved in water. Base – any substance binding a hydrogen ion

when dissolved in water. Buffer – binds H ion from body fluids (acting as

base) release H ion into body fluids (acting as acid).

Anaerobic metabolism – cellular metabolism occurring without the presence of oxygen.

Chemoreceptors – special cells in the respiratory center of the brain sensitive to changes in the CO2 concentration of ECF.

pH - expresses the acidity or alkalinity of a solution 7.35 to 7.45 is normal >7.45 is alkaline < 7.35 is acidic 6.8 or 7.8 is incompatible w/ life

Acidosis – abnormal H+ or in HCO3 ions

Alkalosis – abnormal in H+ ions & in HCO3 ions

SOURCES OF ACIDS Waste products of CHO,(converted to free

H ions) Protein, and fat metabolism CO2 : waste product of glucose breakdown

and other metabolic reactions (removed by breathing).

Sulfuric acid – CHON breakdown Lactic acid – incomplete glucose

breakdown under anaerobic (no O2) conditions

Ketoacids – incomplete breakdown of FA (under anaerobic

conditions)

SOURCES OF HCO3 IONS Comes from breakdown of carbonic acid, intestinal absorption of ingested HCO3 pancreatic production of HCO3, movement of cellular HCO3+ into the ECF,

and kidney resorption of filtered HCO3Foods that can produce acids & bases. Meats = a dietary source of acids Fruits = dietary source of bases Vegetables = dietary source of acids &

bases

MAGKARIBAL

Activities that produce acids Strenuous exercise Starvation = formation of ketone bodies

d/t fat utilization instead of CHO. Catabolic processes = release organic

acids into the ECF (breakdown)ABG Values Show Amount of O2 in the serum Amount of CO2 in the serum pH, or percentage of H+ in solution

ABG Analysis revealsa. If the patient has enough O2 to maintain perfusionb. If enough CO2 is eliminatedc. The ratio of H+ to HCO3 pH (7.35-7.45)• Reflects H+ concentration• < 7.35- Acidosis• > 7.45 – Alkalosis

PaCO2 (35-45 mmHg)• Partial pressure of CO2 in arterial blood• < 35 mmHg – hypocapnia (R.alkalosis)• > 45 mmHg – hypercapnea (R. acidosis)PaO2 (80-100 mmHg)• Partial pressure of O2 in arterial bloodHCO3 (22-26 mEq/L)• HCO3 concentration in plasma of blood

that has been equilibrated at a PaCO2 of 40 mmHg, and w/ O2 to fully saturate the hgb.

Buffers – chemicals that maintain pH by ensuring a stable H+

concentration. BUFFER SYSTEMSa. H2CO3 – HCO3 buffer systemb. PO4 buffer systemc. Protein buffer system.d. Potassium – Hydrogen exchangee. Respiratory Control of H+ Balancef. Kidneys

a. H2CO3 – HCO3 buffer system

- largest in ECF (plasma & interstitial fluid) Characterized by a series of chemical reactions between

H2CO3 & HCO Takes place in the fluids and renal tubules. Involves electrolytesBufferinga. LUNGS (rapid)

Alkalotic state - Hypoventilation (retains H2CO3)Acidotic state - Hyperventilation (expels CO2 and retain H2O)

b. KIDNEYS (slow)Alkalotic states – reabsorb H+ & excrete alkaline urineAcidotic states – conserve or make new HCO3 & excrete

acidic urine

b. Phosphate Buffer System PO4 are highly concentrated in the ICF. Acts as weak acids/base to buffer a stronger

acid/base takes place in the renal tubules where the

greatest concentration of PO4 exists.BufferingBrings the pH back to normal by moving the

H+ from the plasma to the urine and eliminating the acid through the urine.

c. Protein Buffer System.

Functions as an acid or base (amphoteric). Takes place inside the cell albumin and plasma globulins act as the

primary protein buffers in the ECFBuffering:

When H+ in the blood, protein cross membrane of RBC’s & binds to hgb molecules

d. Potassium – Hydrogen ExchangeNormal: ICF K & H +is > ECF K; H+ Acidosis: ECF H+ exchanges w/ ICF KAlkalosis: ECF K ICF ; H+ ECF K & H

K H K K H

K H K KK K

K H K K

K H K

H K

K H K K

K H H K K

K H K K

K K H K K H

K H K H KK K

K H K K

K K H H

H K H K K

K H H H

NORMAL ACIDOSIS ALKALOSIS

e. Respiratory Control of H+ Balance Quick response to A/B imbalance Hyperventilation and hypoventilation. CO2 : potent stimulus for ventilation. Carried by the RBC’s, the CO2 readily diffuses

across the blood- brain barrier. Reacting w/ H2O to form H2CO3 which in turn splits into HCO3 and H+.

Compensationa. Excess H+ & CO2 RR CO2 pH b. Deficient H+ & CO2

RR CO2 pH

b. Kidneys permanently remove H+ from the body,

reabsorb acids or bases and produce HCO3 ions in the proximal tubule.

Regulates acid or base in the ECF by excreting either acidic or alkaline urine.

Most powerful regulator of acid/base balance

Slowest response, taking hours or days to effectively regulate the pH.

Regulation pH increase renal absorption of HCO3 pH increase renal excretion of HCO3

TYPES OF ACID-BASE IMBALANCES

A. Single Acid – Imbalance1. Metabolic Acidosis (Acute / chronic) 2. Metabolic Alkalosis3. Respiratory Acidosis 4. Respiratory Alkalosis (Acute / chronic)

B. Mixed Acid-Base Disorders (2 or more acid/base imbalances are present)

Metabolic Acidosis

(Base HCO3 deficit < 23mEq/L) accumulation of metabolic acids (e.g.

lactic acid & ketoacids) that rise in proportion to HCO3 resulting in ph.

Secondary to an existing disease.

FOUR PROCESSES IN METBOLIC ACIDOSIS1. Overproduction of H+a. Excessive breakdown of FA: DKA,

Starvation When glucose is not available for fuel , FA are broken for energy w/c release large amounts of H+.

b. Anaerobic Glucose breakdown (Lactic Acidosis)CAUSES

- Trauma, burns, Heavy exercise- Intestinal disorders- Leukemias, lymphomas- Seizure activity, fever, tissue hypoxia, ischemia- Shock, poor liver perfusion, cardiac arrest

c. Excessive intake of acidic substances - floods the body directly w/ H+

Causes1. Alcohol: vomiting, inhibits glucose

synthesis by the liver2. ASA: cross blood-brain barrier & interfere

w/ CHO metabolism w/c production of metabolic acids

3. Methanol ingestion: = absorbed thru skin, lungs or GIT= produces optic nerve & CNS toxicity= organ damage after 24 hrs.= converted to formaldehyde & formic acid

4. Underelimination of H+• Kidney and Acute/Chronic lung disease*Kidneys: inability of the tubules to

excrete H+ into the urine*Lungs: inability to excrete CO25. Underproduction of HCO3+ HCO3 is made in the kidneys, liver,

pancreas; failure cause a base-deficit acidosis E.g. RF, LF, Pancreatitis, Dehydration

4. Overelimination of HCO3+ loss of excessive intestinal secretions

w/c has high HCO3 concentrationCauses diarrhea pancreatic or biliary fistula drainage ileostomy, intestinal suction ileal bladder HCO3 is lost in the urine

Loss of base or production of excess acids

Blood pHHyperventilatio

n Renal Buffering

PaCO2 HCO3 retention

H+ ion excretion

Blood ph returns to

normalNH3 – NH4production

Metabolic Acidosis

Clinical manifestations

Neurological Manifestations Headache Malaise Weakness Fatigue Stupor/coma 

CLINICAL MANIFESTATIONS

SNS Manifestations Vasodilation Warm, flushed skin, dry Decreased skin turgor

Respiratory Manifestations Kussmaul’s respirations Fruity breath – (DKA)

Gastrointestinal Manifestations

Nausea Vomiting Anorexia

What would the nurse expect for

laboratory levels of a client with METABOLIC ACIDOSIS?

LABORATORY RESULTS ABG: pH<7.35, PaCO2 normal, HCO3 <22mEq/L K>5.3mEq/L CL>106mEq/LLung Compensation: increasing RR and depth of respirations

through hyperventilation moving pH to normal

ABG: Normal pH, PaCO2, HCO3<22mEq/L

What could be the possible Nursing Diagnoses for a

Client with METABOLIC ACIDOSIS?

NURSING DIAGNOSES Deficient fluid volume r/t

dehydration Risk for injury r/t skeletal muscle

weakness Decreased cardiac output r/t poor

cardiac contractility and decreased vascular volume.

Impaired memory r/t fluid and electrolyte imbalances.

What is the BEST treatment or the

goal of therapy for clients with

METABOLIC ACIDOSIS?

COLLABORATIVE MANAGEMENT

Goal Correct the underlying problem, and

restoring fluid and electrolyte loss increasing aerobic metabolism, monitoring for change.

MEDICAL INTERVENTIONS

Hydration Calcium supplement Alkalinizing agents (HCO3 <12 mEq/L.)

Hemodialysis or peritoneal dialysis. DKA- Insulin Antidiarrials

What would be the Nursing Interventions

for clients with METABOLIC ACIDOSIS?

NURSING MANAGEMENT Monitor ABG levels Maintain patent IV access Administer drugs as ordered. Monitor I&O Monitor determinants of tissue O2

delivery (e.g. PaO2, SaO2,Hgb, cardiac output)

Monitor loss of HCO3 through GIT OFI, administer fluids Prepare for dialysis Institute seizure precautions.

EVALUATION

ABG returns to normal HR, RR, BP returns to normal Free from injury

Acute/Chronic Respiratory

Acidosis (H2CO3 Excess)

Acute/Chronic Respiratory Acidosis (H2CO3 Excess)

state of relative excess of acid in body fluids resulting from retention or excessive production of CO2.

Hypoventilation CO2 & H+ concentration in the lungs and blood

WHERE and HOW does

COMPENSATION occur in a client

with RESPIRATORY

ACIDOSIS?

Compensation occurs in the kidneys

By: Reducing amount of HCO3+ excreted in the kidneys.

Increased renal absorption of HCO3.

renal excretion of H+

What are the ETIOLOGIES contributing to the development of RESPIRATORY

ACIDOSIS?

ETIOLOGYACUTE CAUSES Cardiopulmoary arrest Pneumothorax or hydrothorax Chest wall trauma Acute abdominal distention Drug overdose (sedatives, anesthesia) Airway obstruction Pulmonary edema/ARDS Atelectasis

Cont. ETIOLOGYACUTE CAUSES Pneumonia Acute neurologic dysfunction from any

cause (cerebral trauma, GBS) Sleep apnea syndrome = reduced

diameter of upper airway during sleep Excessive O2 adm to pt with chronic

hypercapnia (excessive CO2 in the blood)

Electrolyte imbalance Pulmonary emboli

CHRONIC CAUSES Chronic emphysema and bronchitis Myasthenia gravis = weakness of

voluntary muscles Cystic fibrosis COPD CHF Pulmonary fibrosis Muscular dystrophy= progressive

wasting of the skeletal or voluntary muscles.

Respiratory Acidosis

Hypoventilation

Hypercapnia ( PaCO2)

Blood pH

Renal buffering 48-72 hrs

H+ excretion & HCO3 ret

NH3 - NH4 production

Clinical Manifestationsa. Neurological Manifestations Headache Blurred vision Tremors Muscle Twitching Vertigo Irritability Disorientation Lethargy Coma

Cardiac Manifestations

Tachycardia BP Cardiac dysrhythmias Ventricular fibrillation = first sign of

respiratory acidosis for anesthetized patients.

Respiratory Manifestations Initial hyperventilation Eventual hypoventilation result to Acute hypercapnia Acute Hypercapnia

- PR & RR BP (acute)- more serious threat to life than acidemia or hypercapnia - retained CO2 displaces O2 in the alveoli- PR & RR BP (acute)

Rapid PaCO2 eg. 60 mmHg

Cerebral vasodilation

cerebral blood flow causing headache

DX Findings (Resp. Acidosis)ABG= pH, PaCO2, Normal HCO3 pH < 7.35 (acidemia) PaCO2 > 45mmHg (hypercapnia) HCO3 (normal) Cl > 106mEq/L K+ > 5.3Meq/L ECG = cardiac dysrhythmias, K+ CXR to determine respiratory dseRenal Compensation Reabsorbing HCO3 and excreting H+ to

bring pH to normal ABG= Normal pH, PaCO2,HCO3

POTENTIAL NURSING DIAGNOSES Activity Intolerance r/t muscle

weakness Ineffective Breathing Pattern r/t

reduced gas exchange Fatigue r/t altered tissue perfusion Impaired memory r/t fluid &

electrolyte imbalance Risk for injury r/t skeletal muscle

weakness Altered thought process

COLLABORATIVE MANAGEMENTMedical GOAL: Maintain patent airway and enhance gas

exchangea. Pharmacologic agents Bronchodilators Mucolytics Antibiotics Thrombolytics or anticoagulants for pulmonary

embolib. O2 Rx Ventilation support : SaO290, respiratory

muscle fatiguec. Pulmonary hygiene: positioning, tapping,

OFI

NURSING MANAGEMENT Semi-Fowler’s position Administer low flow O2 Monitor ABG levels for changes in pH and CO2 Monitor for symptoms of respiratory failure (PaO2, PaCO2, respiratory muscle fatigue ) Provide low CHO, high fat diet to reduce CO2

production Monitor neurologic status (LOC, confusion) Pulmonary hygiene Monitor V/S Protect pt from injury Provide emotional support and reassurance to

allay anxiety Prevent complications : Monitor RR, and depth,

cyanosis, color of nail beds and mucous membranes for cyanosis (late finding)

COMBINED METABOLIC

& RESPIRATORY

ACIDOSIS (MIXED ACIDOSIS)

COMBINED METABOLIC & RESPIRATORY ACIDOSIS (MIXED ACIDOSIS)

Uncorrected acute respiratory acidosis always leads to anaerobic metabolism and lactic acidosis.

more severe than single A/B imbalance COPD w/ DM Elderly w/ PNA & Diarrhea RF w/ PE ABG: ph (Acidosis) PaCO2 (Respiratory) HCO3 (Metabolic)

METABOLIC ALKALOSIS

(Base HCO3 excess)

METABOLIC ALKALOSIS Occurs when the HCO3 level

rises above the 27mEq/L and the pH above 7.45

increased loss of acid (stomach & kidneys)

Loss of fixed acid decreases H+ concentration

What are the CAUSES

of METABOLIC ALKALOSIS

Etiology: Metabolic Alkalosis1. Increase of base components (Base

Excess)Oral ingestion of bases a. Antacids b. Milk-alkali syndromeParenteral base administration a. Blood transfusion b. NaHCO3 c. TPN

2. ACID DEFICIT Prolonged vomiting Nasogastric suctioning Cushing’s syndrome or disease

Hyperaldosterolism Thiazide diuretics Pyloric stenosis

Metabolic alkalosis

Excess base or loss of acids

Blood pH

Hypoventilation Renal buffering

PaCO2 H retention HCO3 excretion

Blood pH returns to normal

What are the clinical manifestations of a client

with METABOLIC ALKALOSIS

Clinical Manifestations of Met Alkalosis Tingling sensation, carpopedal spasms, tetany

® ionization of Ca++ - more Ca++ combines with S. proteins

RR: lung compensation Apathy, stupor & confusion seizures = CNS

involvement Cardiac dysrhythmias = Na & Mg;

appearance of U wave (K) motility and paralytic ileus Postural hypotension

What could be the Diagnostic Findings of

a client with METABOLIC ALKALOSIS

DIAGNOSTIC FINDINGSABG ph > 7.45 PaCO2 - normal HCO3 > 26 mEq/L/ K – accompanies metabolic alkalosis Ca – Ca binding increases and the blood

level of Ca decreases Chloride levels Compensation: Lungs compensation RR

CO2 = pH or N; PaCO2; HCO3 (no

change)

Potential Nursing Diagnoses Ineffective breathing pattern High risk for injury Impaired thought process AnxietyMEDICAL MANAGEMENTGoal: Acid-base balance and prevention of

complications resulting from serum HCO3 levels higher than desired.

Antiemetics, KCL F/E replacement Carbonic Anhydrase inhibitors (Diamox)= for

patients who cannot tolerate rapid volume expansion (HF,CRF)

Nursing interventions (Met Alkalosis) Monitor ABG, electrolyte levels Maintain patent IV access. Monitor I & O, ensure adequate

hydration. Monitor determinants of tissue delivery

(e.g. PaO2, SaO2, Hgb levels, cardiac output)

Avoid adm of alkaline substances (e.g. HCO3, antacids)

Cont. Nursing interventions (Metabolic alkalosis)

Monitor for electrolyte imbalances associated with metabolic alkalosis (e.g. K, Ca, CL)

Monitor for renal loss of acid (e.g. Diuretic Rx)

Replace ECF w/ Saline , as appropriate. Monitor PR & rhythm Administer KCL

RESPIRATORY ALKALOSIS

(H2CO3 deficit)

RESPIRATORY ALKALOSIS (H2CO3 deficit)

relative excess of base in body fluids resulting from respiratory elimination of CO2.

- may be intentional as with mechanical ventilation

- Or accidental as in panic attack

ETIOLOGY (R. Alk)a. Alveolar hyperventilation Acute hypoxia (early stage): PNA, BA, PE Hypoxemia: Asphyxiation, high altitudes, shock,

pulmonary fibrosis, cyanotic heart disease Anxiety Feverb. Early stages of Salicylate toxicity = cross the

blood-brain barrier & stimulate the respiratory center causing hyperventilation

c. CNS: trauma, seizures, catecholamines, Exercise Gram-negative sepsisd. Excessive mechanical ventilation and

anesthesia= intentional Pregnancy

Respiratory Alkalosis

Hyperventilation

Hypocapnia ( PaCO2)

Blood ph

HypoventilationRenal Buffering 48 – 72

hrs

H+retention

HCO3 exc.

Blood ph returns to normal

Retention of CO2

Clinical Manifestation Light-headedness and dizziness = CO2

crosses the blood-brain barrier causing vasoconstriction and cerebral blood flow

Inability to concentrate Numbness & tingling around the mouth,

fingers and mouth = Ca levels 2° binding of Ca to protein

Dysrhythmias & muscle weakness = K+ & Ca++

Chest pain = 2˚ coronary spasm GIT: nausea, vomiting & diarrhea d/t alkalosis Sweating, palpitation, panic, or air hunger

may also be present.

DIAGNOSTIC FINDINGS (R. Alkalosis)ABG :pH; PaCO2; HCO3 normal ph > 7.42 mmHg: - d/t buffering and renal

compensation cannot maintain the H ions at normal level.

Pa CO2 < 35 mmHg - HCO3 = normal K+ = H+ to ECF; K+ to ICF Ca++ = severe alkalosis inhibits Ca++

ionization carpopedal spasm/tetany PO4 = due to alkalosis causing an increased

uptake of PO4 by the cells Toxicology serum = to r/o salicylate

intoxication

Renal Compensation

Excretion of HCO3 and absorption of H ions.

NURSING DIAGNOSES Ineffective breathing pattern High risk for injury Anxiety Impaired memory Fatigue Activity intolerance Altered thought process

COLLABORATIVE MANAGEMENTGOAL: a. Promotion of A/B balance b. Prevention of complications resulting

from PaCO2 levels lower than desired.Interventions Encourage slow, deep breathing Monitor ABG levels for increased pH level. Monitor for indications of respiratory failure

(PaO2 level, respiratory muscle fatigue,SaO2 level)

Monitor for hyperventilation resulting in respiratory alkalosis (e.g. hypoxemia, CNS injury, hypermetabolic states, GI distention, pain, stress).

Nursing Monitor for CP manifestations of

respiratory alkalosis (e.g. arrhythmias, cardiac output, and hyperventilation).

Provide O2 Rx., if necessary. Reduce O2 consumption to minimize

hyperventilation (e.g. promote comfort, control fever, reduce anxiiety)

Provide ventilatory support, if necessary. Assess patient for respiratory depression Provide emotional support and

reassurance to the patient to reduce anxiety

Evaluation ABG values return to normal Heart rate, rhythm, and blood

pressure return to normal The patient remains injury free.

ARTERIAL BLOOD

ANALYSIS

ABG Interpretation- provide information about alveolar ventilation, oxygenation & A/B balance3 ParameterspHPaCO2HCO3

Pre-testa. No suctioning prior to blood extractionb. Allen’s testc. Pre-heparinized syringed. Container with ice.

Steps

Step 1 Normal Values pH: 7.35 – 7.45 paCO2: 35 – 45 mmHg HCO3: 22-26/23-27 mEq/dl paO2: 80-100%O2 saturation : 95-100%

Step 2: Classify the pH

Normal: 7.35 – 7.45 Acidemia: < 7.35 Alkalemia : >7.45

Step 3: Look at paCO2Normal: 35-45 mmHgRespiratory acidosis: > 45

mmHgRespiratory alkalosis: <35

mmHg Step 4: Look at HCO3Normal: 22-26 mEq/LMetabolic acidosis: <22 mEq/LMetabolic alkalosis: > 26 mEq/L

Step 5: Determine whether Respiratory or Metabolic

ROME

1.Respiratory Opposite: Arrows opposite directions

ph PaCO2 HCO3 7.30 50 28

7.45 20 20

2. Metabolic Equal: Arrows in the same direction

pH PaCO2 HCO3 7.30 20 18 7.45 50 28

Step 6: Degree of Compensation

A.PARTIALLY COMPENSATEDIf CO2 and HCO3 level move towards

the same direction (both are high & both are low)

ph PaCO2 HCO37.30 50 287.45 20 20

B. PARTIAL COMPENSATION -Acid/base balance is compensated

and pH is still ABNORMAL.

pH 7.30 7.30

paCO2 50 33 HCO3 30 20

C. COMPLETE COMPENSATION- Acid/base balance is compensated and

pH returns to NORMAL

pH N 7.36 N 7.36 paCO2 50 33 HCO3 30 20

Compensation absent:One component (PaCO2 or HCO3) is

abnormal, the other normalResp Met

pH 7.33 7.33 paCO2 50 N 38 HCO3 N 24 20

Exception to the rule: in some situations, get the median

MARIETTA C. JUCAR, RN, MN

pH ( 7.35-7.45)

PaCO2 (35-45)

HCO3 (22-26)

Interpretation

Respiratory = pH and PaCO2 moving in opposite direction (RESP, OPPOSITE, RO)

7.20 60 mmHg

24 mEq/L (N)

Resp Acidosis Uncompensated

= no change in HCO3

7.20 60 mmHg

37 mEq/l

Resp acidosis PC= opposite direction;

increase in HCO3 pH is abnormally low

7.42 (N) 60 mmHg

37 mEq/L

Met ALK FC= opposite direction; 1 is

acidotic; 1 is alkalotic; LUNGS RETAINED CO2 moving Ph to normal

Metabolic = pH and HCO3 are moving in the same direction (MET EQUAL,

ME)

7.46 34 mmHg

24 mEq/L (N)

Resp Alkalosis Uncompensated

7.45 34 mmHg

20 mEq/L

Resp Alkalosis PC= opposite direction,1 acidotic,1 alkalotic

7.38 (N)

34 mmHg

20 mEq/L

Met Acidosis FC = Kidneys eliminate HCO3

to balance w/ lowered acid levels, moving pH to normal

7.30 40 mm Hg (N)

20 mEq/L

Met. Acidosis Uncompensated; no change in PaCO2

7.30 32 mm Hg

20 mEq/L

Met Acidosis Partially Compensated

= decrease in PaCO2

7.42 (N) 32 mm Hg

20 mEq/L

Resp Alk FC

7.46 40 mm Hg (N)

28 mEq/L

Met Alkalosis Uncompensated; no change in PaCO2

7.46 48 mm Hg 28 mEq/L

Met Alkalosis PC; retention of PaCO2

7.42 (N) 48 mm Hg 28 mEq/L

Met Alkalosis Fully Compensated

7.30 50 mm Hg 20 mEq/L

Mixed Acidosis

7.48 33 mm Hg 29 mEq/L

Mixed Alkalosis

Get half sheet of paper and interpret the

following for 30 minby

PAIR

s

pH PaCO2 HCO3 pH PaCO2 HCO3

1.7.48 42 30 6. 7.26 50 21

2.7.34 46 24 7. 7.45 30 30

3.7.32 38 20 8. 7.32 32 14

4.7.61 21 20.6 9. 7.37 28 21

5.7.39 49 29.3 10. 7.38 48 29

If you fail to prepare,

You prepared to fail!END