What is the respiration rate?
What is the normal respiratory rate?
What are the effects of increased respiratory rates?
What is the respiration rate?
The respiration rate is the number of breaths a person takes per minute. The rate is usually measured when a person is at rest and simply involves counting the number of breaths for one minute by counting how many times the chest rises. Respiration rates may increase with fever, illness, and with other medical conditions. When checking respiration, it is important to also note whether a person has any difficulty breathing.
Normal respiration rates for an adult person at rest range from 15 to 20 breaths per minute. Respiration rates over 25 breaths per minute or under 12 breaths per minute (when at rest) may be considered abnormal.
Respiratory rate
Respiratory rate (Vf, Rf or RR) is also known by respiration rate, pulmonary ventilation rate, ventilation rate, or breathing frequency is the number of breaths taken within a set amount of time, typically 60 seconds. A normal respiratory rate is termed eupnea, an increased respiratory rate is termed tachypnea and a lower than normal respiratory rate is termed bradypnea.
MeasurementHuman respiration rate is measured when a person is at rest and involves counting the number of breaths for one minute by counting how many times the chest rises. Respiration rates may increase with fever, illness, or other medical conditions. When checking respiration, it is important to also note whether a person has any difficulty breathing.
Inaccuracies in respiratory measurement have been reported in the literature. One study compared respiratory rate counted using a 90 second count period, to a full minute, and found significant differences in the rates.[citation needed] Another study found that rapid respiratory rates in babies, counted using a stethoscope, were 60–80% higher than those counted from beside the cot without the aid of the stethoscope.[citation needed] Similar results are seen with animals when they are being handled and not being handled—the invasiveness of touch apparently is enough to make significant changes in breathing.
Normal range
Average respiratory rate reported in a healthy adult at rest is usually given as 12-18 breaths per minute (Vf) [1][2] but estimates do vary between sources, e.g., 12–20 breaths per minute, 10–14,[3] between 16–18,[4] etc. With such a slow rate, more accurate readings are obtained by counting the number of breaths over a full minute.
By AgeAverage resting respiratory rates by age[5][6]
birth to 6 weeks: 30-60 breaths per minute
6 months: 25-40 breaths per minute
3 years: 20-30 breaths per minute
6 years: 18-25 breaths per minute
10 years: 15-20 breaths per minute
adults: 12-20 breaths per minute
Minute volumeRespiratory minute volume is the volume of air which can be inhaled (inhaled minute volume) or exhaled (exhaled minute volume) from a person's lungs in one minute.
Diagnostic valueThe value of respiratory rate as an indicator of potential respiratory dysfunction has been investigated but findings suggest it is of limited value.
One study found that only 33% of people presenting to an emergency department with an oxygen saturation below 90% had an increased respiratory rate.[citation needed] An evaluation of respiratory rate for the differentiation of the severity of illness in babies under 6 months found it not to be very useful. Approximately half of the babies had a respiratory rate above 50 breaths per minute, thereby questioning the value of having a "cut-off" at 50 breaths per minute as the indicator of serious respiratory illness.
It has also been reported that factors such as crying, sleeping, agitation and age have a significant influence on the respiratory rate.[citation needed] As a result of these and similar studies the value of respiratory rate as an indicator of serious illness is limited.
Abnormal respiratory rates
Apnea
Dyspnea
Hyperpnea
Tachypnea
Hypopnea
Bradypnea
Orthopnea
Platypnea
Biot's respiration
Cheyne-Stokes respiration
Kussmaul breathing
What are the effects of increased respiratory rates?
When we breathe more than the medical norm, we lose CO2 and reduce body oxygenation due to vasoconstriction and the suppressed Bohr effect caused by hypocapnia (CO2 deficiency). Hence, overbreathing leads to reduced cell oxygenation, while slower and easier breathing (with lower respiratory rates) improves cell-oxygen content.
Respiratory rate is a critical indicator of performance in various professions. The health and safety of fighter pilots during high altitude flights is monitored closely.
Arterial Blood Gases
|
Arterial blood gas analysis provides information on the following:
1]
Oxygenation of blood through gas exchange in the lungs. 2]
Carbon dioxide (CO2) elimination through respiration. 3]
Acid-base balance or imbalance in extra-cellular fluid (ECF).
Normal Blood Gases
|
| |
Arterial |
Venous |
| pH |
7.35 - 7.45 |
7.32 - 7.42 |
| Not a gas, but a measurement of acidity or alkalinity,
based on the hydrogen (H+) ions present. The pH of a solution is equal
to the negative log of the hydrogen ion concentration in that solution:
pH = - log [H+]. |
| PaO2 |
80 to 100 mm Hg. |
28 - 48 mm Hg |
The partial pressure of oxygen that is dissolved in
arterial blood.
New Born – Acceptable range 40-70 mm Hg. Elderly: Subtract 1 mm Hg
from the minimal 80 mm Hg level for every year over 60 years of age:
80 - (age- 60) (Note: up to age 90) |
| HCO3 |
22 to 26 mEq/liter
(21–28 mEq/L) |
19 to 25 mEq/liter |
| The calculated value of the amount of bicarbonate in the
bloodstream. Not a blood gas but the anion of carbonic acid. |
| PaCO2 |
35-45 mm Hg |
38-52 mm Hg |
| The amount of carbon dioxide dissolved in arterial
blood. Measured. Partial pressure of arterial CO2.
(Note: Large A= alveolor CO2). CO2 is called a “volatile acid”
because it can combine reversibly with H2O to yield a strongly acidic H+
ion and a weak basic bicarbonate ion (HCO3 -) according to the following
equation: CO2 + H2O <--- --> H+ + HCO3 |
| B.E. |
–2 to +2 mEq/liter
Other sources: normal reference range is between -5 to +3. |
|
The base excess indicates the amount of excess or
insufficient level of bicarbonate in the system.
(A negative base excess indicates a base deficit in the blood.) A
negative base excess is equivalent to an acid excess. A value outside of
the normal range (-2 to +2 mEq) suggests a metabolic cause for the
abnormality. Calculated value. The base excess is
defined as the amount of H+ ions that would be required to return the pH
of the blood to 7.35 if the pCO2 were adjusted to normal.
It can be estimated by the equation:
Base excess = 0.93 (HCO3 - 24.4 + 14.8(pH - 7.4))
Alternatively: Base excess = 0.93×HCO3 + 13.77×pH - 124.58
A base excess > +3 = metabolic alkalosis a base excess < -3 =
metabolic acidosis |
| SaO2 |
95% to 100% |
50 - 70% |
| The arterial oxygen saturation. |
Step by Step ABG Analysis
|
Step One - Assessing pH
|
Look at pH and determine if it is acidotic (<7.35),
normal (7.35 - 7.45), or alkalotic (>
7.45).
pH is the best overall indicator in determining the acid-base status of
the patient. |
Step Two - Determine respiratory
involvement
|
Review the PaCO2 to assess respiratory involvement [The lungs
control the level of carbon dioxide in the arterial blood]. The PaCO2
must be evaluated in light of the arterial pH. That is, if the pH is
abnormal, we then ask ourselves: would this observed PaCO2, by itself,
cause this pH abnormality? For example, suppose that the pH is below
7.35 (denoting acidosis) and the PaCO2 is above 45 mmHg. According to
the Henderson-Hasselbalch equation, a high PaCO2 would indeed cause a
low pH (i.e., acidosis). Therefore we know that the respiratory system
is at least in part, if not entirely, responsible for the acidosis. On
the other hand, if the pH is less than 7.35 and the PaCO2 is in the
normal range, then we know that the acidosis must be of non-respiratory
(metabolic) origin.
PaCO2:
Normal: 35 - 45 mmHg (4.6 - 6 kPa)
Respiratory acidosis: > 45 mmHg (> 6 kPa)
Respiratory alkalosis: <35 mmHg (< 4.6 kPa)
|
|
Step Three - Determine metabolic involvement
|
Review the plasma [HCO3-] or B.E. (Base excess) to determine
metabolic involvement (both controlled by non-respiratory factors.)
Each of these components must be evaluated based on the current pH.
If the pH is abnormal, we ask: would this observed [HCO3-] by itself,
cause this pH abnormality? For example, suppose that the pH is
less that 7.35 (denoting acidosis) and the [HCO3-] is below 22 mEq/L.
Indeed, according to the Henderson-Hasselbalch equation, the low [HCO3-]
is consistent with acidosis. Thus, we know that non-respiratory factors
are in part, if not entirely, responsible for the acidosis. If [HCO3-]
were in the normal range in the presence of this acidosis, then we would
know that the acidosis must be of respiratory origin.
HCO3-
--------------------------
Normal: 22 - 26 mEq/L
Metabolic acidosis: <22 mEq/L
Metabolic alkalosis: > 26 mEq/L
[Standard Bicarbonate: Calculated value. Similar to the base
excess. It is defined as the calculated bicarbonate
concentration of the sample corrected to a PCO2 of 5.3kPa
(40mmHg).
|
BE (Base Excess):
--------------------------
Normal: -2 to +2 mmol/L
Metabolic acidosis: < -2 mmol/L
| Mild |
-4 to -6 |
| Moderate |
-6 to -9 |
| Marked |
-9 to -13 |
| Severe |
to < -13 |
Metabolic alkalosis: > +2 mmol/L
| Severe |
> +13 |
| Marked |
9 to 13 |
| Moderate |
6 to 9 |
| Mild |
4 to 6 |
[Base excess (BE) is the mmol/L of base that needs to be removed
to bring the pH back to normal when PCO2 is corrected to 5.3 kPa
or 40 mmHg. During the calculation any change in pH due to the
PCO2 of the sample is eliminated, therefore, the base excess
reflects only the metabolic component of any disturbance of acid
base balance.] |
|
Step Four - Assess for compensation
|
Look at the pH, PaCO2, and B.E. / HCO3-
to decide whether compensatory mechanisms are at work.
Once the acid-base disorder is identified as respiratory or metabolic,
we must look for the degree of compensation that may or may not be
occurring. we know that the system not primarily responsible for the
acid-base abnormality must assume the responsibility for returning the
pH to the normal range. This compensation may be complete (pH is brought
into the normal range) or partial (pH is still out of the normal range
but is in the process of moving toward the normal range.) In pure
respiratory acidosis (high PaCO2, normal [HCO3-], and low pH) we would
expect an eventual compensatory increase in plasma [HCO3-] that would
work to restore the pH to normal. Similarly, we expect respiratory
alkalosis to elicit an eventual compensatory decrease in plasma [HCO3-].
A pure metabolic acidosis (low [HCO3-], normal PaCO2, and a low pH)
should elicit a compensatory decrease in PaCO2, and a pure metabolic
alkalosis (high [HCO3-], normal PaCO2, and high pH) should cause a
compensatory increase in PaCO2. All compensatory responses work to
restore the pH to the normal range (7.35 - 7.45)
[ See sample problems near the bottom of the page] |
Step Five - Further analysis in cases of
METABOLIC ACIDOSIS
|
Metabolic acidosis:
1] Calculate the anion gap:
Anion gap = Na+ - [CL- + HCO3-]
Difference between calculated serum anions and cations.
Based on the principle of electrical neutrality, the serum
concentration of cations (positive ions) should equal the serum
concentration of anions (negative ions).
However, serum Na+ ion concentration is higher than the sum of
serum Cl- and HCO3- concentration.
Na+ = CL- + HCO3- +
unmeasured anions (gap).
Normal anion gap: 12 mmol/L (10 - 14 mmol/L) |
2] Based on the anion gap and patient history - review potential
causes:
Normal anion gap (hyperchloremic) metabolic acidosis:
Normal anion gap acidosis: The most common causes of normal
anion gap acidosis are GI or renal bicarbonate loss and impaired renal acid excretion.
Normal anion gap metabolic acidosis is also called hyperchloremic acidosis,
because instead of reabsorbing HCO3- with Na, the kidney reabsorbs Cl-.
Many GI secretions are rich in bicarbonate (eg, biliary, pancreatic, and intestinal
fluids); loss from diarrhea, tube drainage, or fistulas can cause acidosis. In
ureterosigmoidostomy (insertion of ureters into the sigmoid colon after
obstruction or cystectomy), the colon secretes and loses bicarbonate in exchange for
urinary Cl- and absorbs urinary ammonium, which dissociates into NH3+ and H+.
Loss of HCO3 ions
is accompanied by an increase in the serum Cl- concentration. The anion
gap remains normal. Disease processes that can lead to normal anion gap
(hyperchloremic) acidosis. Useful mnemonic (DURHAM):
a) Diarrhea (HCO3- and water is lost).
b) Ureteral diversion: Urine from the ureter may be diverted to the
sigmoid colon due to disease (uretero-colonic fistula) or after bladder
surgery. In such an event urinary Cl- is absorbed by the colonic mucosa
in exchange for HCO3-, thus increases the gastrointestinal loss of
HCO3-.
c) Renal tubular acidosis: dysfunctional renal tubular cells causes an
inappropriate wastage of HCO3- and retention of Cl-.
d) Hyperalimentation
e) Acetazolamide
f) Miscellaneous conditions: They include pancreatic fistula, cholestyramine, and calcium chloride (CaCl) ingestion, all of which can
increase the gastrointestinal wastage of HCO3-.
Increased anion gap metabolic acidosis
High anion gap acidosis: The most common causes of a high anion
gap metabolic acidosis are ketoacidosis, lactic acidosis, renal failure, and
toxic ingestions. Renal failure causes anion gap acidosis by decreased acid
excretion and decreased bicarbonate reabsorption. Accumulation of sulfates, phosphates, urate, and
hippurate accounts for the high anion gap. Toxins may have acidic metabolites
or trigger lactic acidosis.
In increased anion gap metabolic acidosis, the nonvolatile acids are
organic or
other inorganic acids (e.g., lactic acid, acetoacetic acid, formic acid,
sulphuric
acid).
The anions of these acids are not Cl- ions. The presence of these acid
anions,
which are not measured, will cause an increase in the anion gap.
Useful mnemonic (MUD PILES):
Methanol poisoning:
Methanol is metabolized by alcohol dehydrogenase in the liver to formic
acid.
Uremia:
In end-stage renal failure in which glomerular filtration rate falls
below
10—20 ml/min, acids from protein metabolism are not excreted and
accumulate in blood.
Diabetic ketoacidosis: incomplete oxidation of fatty acids causes a
build up
of beta-hydroxybutyric and acetoactic acids (ketoacids).
Paraldehyde poisoning.
Ischemia: causes lactic acidosis.
Lactic acidosis:
Lactic acid is the end product of glucose breakdown if pyruvic acid, the
end
product of anaerobic glycolysis, is not oxidized to CO2 and H2O via the
Tricarboxylic Acid Cycle. (Causes: hypoxia,
ischemia,
hypotension, sepsis).
Ethylene glycol poisoning:
Ethylene is metabolized by alcohol dehydrogenase to oxalic acid in the
liver. Usually there is also a coexisting lactic acidosis.
Salicylate poisoning
|
Causes of common acid-base disturbances:
|
Metabolic acidosis (non-respiratory)
|
High anion gap.
Ketoacidosis (diabetes, chronic alcoholism,
malnutrition, fasting).
Lactic acidosis.
Renal failure.
Toxins metabolized to acids:
Methanol (formic acid)
Ethylene glycol (oxalate)
Paraldehyde (acetate, chloracetate)
Salicylates
Toxins causing lactic acidosis
CO2
Cyanide
Iron
Isoniazid
Toluene (initially high gap, subsequent excretion of metabolites
normalizes gap)
Rhabdomyolysis (rare)
Loss of base -
Normal anion gap (hyperchloremic acidosis)
GI HCO3- loss (diarrhea, ileostomy, colostomy, enteric fistulas, use of
ion-exchange resins)
Ureterosigmoidostomy, ureteroileal conduit
|
Renal HCO3- loss:
Tubulointerstitial renal disease.
Renal tubular acidosis, types 1, 2, 4.
Hyperparathyroidism.
Ingestions (acetazolamide, CaCl2, MgSO4) Others
Hypoaldosteronism, Hyperkalemia
Parenteral infusion of arginine, lysine, NH4Cl.
Rapid NaCl infusion. Toluene (late).
Formulas (Compensation):
pCO2 decreases 1.2 for each mEq/L change in HCO3 or
pCO2 = last two digits of pH
Compensation
Ventilation of the lungs
increases through stimulation of central chemoreceptors (H+ ion receptors)
in the medulla and peripheral chemoreceptors in the carotid and aortic
bodies. Consequently PCO2 falls below normal, and H+ ion concentration
falls. Respiratory compensation increases the acidic
pH towards normal. The respiratory system responds
to metabolic acidosis quickly and predictably by hyperventilation, so
much so that pure metabolic acidosis is seldom seen. |
Respiratory Alkalosis:
|
CNS disorders or lesions, hypoxia
[Hypoxia-causing conditions], pulmonary receptor stimulation (asthma,
pneumonia, pulmonary edema, PE),
Pulmonary vascular disease, anxiety, fear, pain, drugs (ASA,
theophylline), liver failure, sepsis.
Formulas (Compensation):
- Acute: HCO3 decreases 0.22 for every mmHg change in pCO2
- Chronic: HCO3 decreases 0.5 for every mmHg change in pCO2 |
Compensation:
In the presence of respiratory alkalosis the kidneys compensate for the
increase in pH by retaining H+ ions and excreting HCO3 - ions. As a
result, pH falls towards normal and HCO3 - concentration falls below
normal. Renal compensation to respiratory alkalosis is a slow process
and the pH does not completely return to normal. |
Metabolic (non-resp) alkalosis:
|
Respiratory Acidosis:
|
Increase in base
Administration/ingestion of HCO3-
Hypochloremia (HCO3 retained).
Diuretic therapy
Contraction of blood volume.
Loss of fixed acid.
Severe vomiting (loss of H+).
Nasogastric suction.
Hypokalemia - Potassium deficiency.
Corticosteroid administration.
Formulas (Compensation):
pCO2 increases 0.6 for each mmol/L change in HCO3
Compensation:
The respiratory response to metabolic alkalosis is hypoventilation. PCO2
rises above normal. Respiratory compensation to metabolic alkalosis is
variable and unpredictable. It is unlikely that a conscious patient
breathing spontaneously will hypoventilate to a PCO2 > 7.3 kPa (55 mmHg)
to compensate for metabolic alkalosis. |
Central nervous depression: sedatives etc.
Neuromuscular disease (Guillain-Barr, myasthenia gravis).
Trauma.
Severe restrictive disorders: scoliosis.
COPD.
Acute airway obstruction: choking etc.
CVA,
pneumothorax, chest wall disorder,
tumor. Acute and chronic lung disease.
Formulas (Compensation):
- Acute: HCO3 increases 0.1 for every mmHg change in pCO2
- Chronic: HCO3 increases 0.35 for every mmHg change in pCO2
Compensation: In the presence of respiratory acidosis
the kidneys compensate for the fall in pH by excreting H+ ions and
retaining HCO3 - ions. As a result, pH rises towards normal and HCO3 -
concentration rises above normal. Renal compensation (also called
metabolic compensation) to respiratory acidosis is a slow process.
Compensation is not obvious for several hours and takes 4 days to
complete. |
Sample Problems - Arterial Blood Gases
|
Respiratory alkalosis
(chronic alveolar hyperventilation) |
pH:
PaCO2:
HCO3:
BE: |
7.44
24
16
-6 |
Respiratory acidosis.
Chronic ventilation failure |
pH:
PaCO2:
HCO3:
BE: |
7.38
76
42
+14 |
| Uncompensated metabolic alkalosis |
pH:
PaCO2:
HCO3:
BE: |
7.56
44
38
+14 |
(Respiratory acidosis.
acute ventilation failure |
pH:
PaCO2:
HCO3:
BE: |
7.26
56
24
-4 |
| uncompensated metabolic alkalosis |
pH:
PaCO2:
HCO3:
BE: |
7.56
40
34
+11 |
| Respiratory alkalosis (chronic alveolar
hyperventilation) |
pH:
PaCO2:
HCO3:
BE: |
7.44
26
18
-4 |
Respiratory acidosis.
Chronic ventilation failure |
pH:
PaCO2:
HCO3:
BE: |
7.40
56
34
+7 |
Respiratory alkalosis.
Chronic alveolar hyperventilation |
pH:
PaCO2:
HCO3:
BE: |
7.44
20
16
-7 |
| Uncompensated metabolic acidosis |
pH:
PaCO2:
HCO3:
BE: |
7.24
36
14
-13 |
| Respiratory alkalosis (acute alveolar
hyperventilation) |
pH:
PaCO2:
HCO3:
BE: |
7.52
28
22
+1 |
| Acute Respiratory Acidosis |
Dx - heroin overdose.
Breathing - shallow, slow.
ABGs:
pH: 7.30
PaCO2: 55 mm/Hg
HCO3-: 27 mEq/L |
| Chronic Respiratory Acidosis |
Hx/Dx: 73yo, emphysema, labored
breathing at rest.
ABGs:
pH: 7.36
PaCO2: 64 mmHg
HCO3-: 35 mEq/L |
| Acute Respiratory Alkalosis |
Hx/Dx: 77yo, anxiety,
psychosomatic origin. Rapid breathing and slurred speech.
ABGs:
pH: 7.57
PaCO2: 23 mmHg
HCO3-: 21 mEq/L |
| Compensated Respiratory Alkalosis |
Persistent bacterial
pneumonia. Mild cyanosis and labored breathing.
ABGs:
pH: 7.44
PaCO2: 26 mmHg
HCO3-: 17 mEq/L
PaO2: 53 mmHg |
| Metabolic Alkalosis |
80 yo with heart disease.
RX: diuretic
ABGs:
pH: 7.58
PaCO2: 48 mmHg
HCO3-: 44 mEq/L
BE: + 19 mEq/L
Serum CL- 95 mEq/L |
|
