This review article was presented in the 7th International joint cardiovascular congress held on Feb 28-29, 2019, in Convention Center, Shahid Rejaee Heart Hospital, Tehran, Iran
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๏ง Recommendations for
Physiotherapy in the ICU
๏บ Acute lobar atelectasis โฃโฃ
๏บ Positioning in severe ARDS
๏บ Side lying improves 0xygenation
๏บ Continuous rotational therapy
๏บ Facilitating weaning:
๏ decreases length of stay in the ICU or
hospital, and reduces mortality or
morbidity**
๏บ Preventing loss of joint range or soft-
tissue length**
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๏ถThe physiotherapy treatment:
๏ prevents and reduces potential
pulmonary complications:
๏ดHypoventilation,
๏ดHypoxemia,
๏ดInfection,
๏ดRestore muscular and pulmonary
function as fast as possible.
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๏ฑPhysiotherapy should be offered:
๏ to a variety of medical
respiratory conditions:
๏ผ Management of breathlessness
and symptom control,
๏ผ Mobility function improvement
or maintenance,
๏ผ Airway clearance
๏ผ Cough enhancement or support.
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๏ฑ Endotracheal suctioning:
๏ a mean 56% increase inVO2 from
baseline.
๏ฑ Suctioning in the gravity-assisted
drainage position:
๏ Increases in the metabolic stress
๏ Requires an increased effort to cough,
given the altered diaphragmatic and
abdominal muscle position.
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๏ง What should be done during
physiotherapy:
๏บ Monitor hemodynamic status
๏บ Sedation before physiotherapy
๏บ Pre-oxygenation, sedation, and
reassurance before suction
๏บ Monitor ICP and CPP*
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๏ง Contra-indications of CPT:
๏บ Pulmonary edema,
๏บ congestive heart failure,
๏บ Distended abdomen,
๏บ pregnancy, obesity, and ascites,
๏บ Severe surgical emphysema,
๏บ Neuromuscular disease
๏บ Aneurysm or decrease in
circulation of main blood vessels
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๏ง Contra-indications of CPT:
๏บ Untreated tension pneumothorax
๏บ Unstable cardiovascular disorders
๏บ Dyspnea, orthopnea
๏บ Undiagnosed chest pain.
๏บ Chronic obstructive pulmonary
disease with cor pulmonale,
orthopnea, dyspnea on exertion
๏บ Active cases of tuberculosis
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๏ง Accurate and timely
interpretation of ABG and an
acidโbase disorder can be
lifesaving,
๏ง The establishment of a
correct diagnosis may be
challenging
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๏ง ABG interpretation:
๏บ Assessment of Blood
Oxygenation Status
๏บ Assessment of Acid-Base
Status
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๏ง Assessment of ABG
1. careful clinical evaluation
2. assess oxygenation
3. determine pH (Acidosis vs
Alkalosis)
4. consider the respiratory
component
5. consider the metabolic
component
6. consider the possibility of a
mixed acidโbase disturbance
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๏ง signs and symptoms
๏บ vital signs (which may indicate shock or sepsis),
๏บ neurologic state
๏บ signs of infection (e.g., fever),
๏บ pulmonary status (respiratory rate, Kussmaul
respiration, cyanosis, clubbing of the fingers)
๏บ gastrointestinal symptoms (vomiting and
diarrhea)
๏บ pregnancy,
๏บ diabetes,
๏บ heart, lung, liver, and kidney disease,
๏บ medications (e.g., laxatives, diuretics,
topiramate, or metformin)
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๏ง Assessment of ABG
1. careful clinical evaluation
2. determine the primary acidโbase disorder
3. consider the metabolic component
4. consider the possibility of a mixed metabolic
acidโbase disturbance
5. note the serum osmolal gap in any patient with
an unexplained high anion-gap acidosis
6. evaluate the respiratory component
7. determine the cause of the identified processes
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๏ง Assessment of ABG
1. careful clinical evaluation
2. determine the primary acidโbase disorder
3. consider the metabolic component
4. consider the possibility of a mixed metabolic
acidโbase disturbance
5. note the serum osmolal gap in any patient with
an unexplained high anion-gap acidosis
6. evaluate the respiratory component
7. determine the cause of the identified processes
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๏ Based on the iso-hydric principle,
this system characterizes acids as
hydrogen-ion donors and bases
as hydrogen-ion acceptors
๏ The hydrogen-ion concentration
is tightly regulated because
changes in hydrogen ions alter
virtually all protein and
membrane functions
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๏ผ Normal plasma concentration of
hydrogen ions
๏ very low 40 nmol/L
๏ผ pH
๏ the negative logarithm of the hydrogen-
ion concentration, โlog [๐ฏ+
]
๏ used in clinical medicine to indicate acidโ
base status.
๏ผ โacidemiaโ
๏บ Plasma pH is abnormally low (acidic)
๏ผ โalkalemiaโ
๏ Plasma pH is abnormally high (alkaline)
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๏ Respiratory acidosis
๏ถpH <7.35 and ๐ท๐๐ช๐ถ ๐>40 mm Hg
๏ถSecondary (metabolic) response
๏Acute:
๏ผ๐ท๐๐ช๐ถ ๐๏ฉ 10 mm Hg = [๐ฏ๐ช๐ถ ๐
โ
] ๏ฉ 1mmol/liter
๏Chronic:
๏ผ๐ท๐๐ช๐ถ ๐๏ฉ 10 mm Hg = [๐ฏ๐ช๐ถ ๐
โ
] ๏ฉ 2-5mmol/liter
๏ดComplete secondary adaptive response
within 2โ5 days
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๏ Respiratory alkalosis
๏ถpH >7.45 and ๐ท๐๐ช๐ถ ๐<40 mm Hg
๏ถSecondary (metabolic) response
๏Acute:
๏ผ๐ท๐๐ช๐ถ ๐๏ช 10 mm Hg = [๐ฏ๐ช๐ถ ๐
โ
] ๏ช 1mmol/liter
๏Chronic:
๏ผ๐ท๐๐ช๐ถ ๐๏ช 10 mm Hg = [๐ฏ๐ช๐ถ ๐
โ
] ๏ช 2-4mmol/liter
๏ดComplete secondary adaptive response
within 2โ5 days
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๏ง Assessment of ABG
1. careful clinical evaluation
2. determine the primary acidโbase disorder
3. consider the metabolic component
4. consider the possibility of a mixed metabolic
acidโbase disturbance
5. note the serum osmolal gap in any patient with
an unexplained high anion-gap acidosis
6. evaluate the respiratory component
7. determine the cause of the identified processes
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๏ A case report:
๏ถ82 year-old male with diarrhea
๏ถBP: 87/45 mmHg, Chest Pain
๏ถpast medical hx:
๏ผcoronary artery disease,
hypertension,
๏ผCOPD,
๏ผType 2 DM,
๏ผchronic kidney disease,
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๏ A case report:
๏ถAfter being admitted in ER he
vomited and went through cardiac
arrest; BLS and ACLS were done.
๏ถEpinephrine, Bicarbonate, Calcium
๏ถROSC after CPR
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๏ A case report:
๏ถLaboratoryTest Results:
Before CPR After CPR
๐๐+
140 149
๐พ+
6.3 5.2
๐ถ๐โ 101 97
๐ป๐ถ๐3
โ
22 ๐๐ด
๐๐ป 7.21 7.15
๐๐ ๐2 58 120
๐๐ ๐ถ๐2 46 36
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๏ A case report:
๏ถInterpretation:
๏ผ Delta gap = (โAG) - (โ๐ป๐ถ๐3
โ
)
๏ผ Delta gap = = [๐ต๐+
] โ ([๐ช๐โ
] + [๐ฏ๐ช๐ถ ๐
โ
]) โ ๐๐ โ (๐๐ โ ([๐ฏ๐ช๐ถ ๐
โ
])
๏ผ Delta gap = = [๐ต๐+
] โ ([๐ช๐โ
] + ๐๐)
๏ง Interpretation of the generated gap:
๏บ -6 = Mixed high and normal anion gap acidosis
๏บ -6 to 6 = Only a high anion gap acidosis exists
๏บ over 6 = Mixed high anion gap acidosis and metabolic alkalosis
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๏ A case report:
๏ถInterpretation:
๏ถType 2 respiratory insufficiency
๏ถAnion gap metabolic acidosis and
metabolic alkalosis