-
Cleanses, warms, & moistens air
LUNGS: Airway Tree
-
Distributes air to deeper parts of the lung
LUNGS: Airway Tree
-
Dilation/constriction of smooth muscle determines ease of air flow; Defense – mucociliary transport system
LUNGS: Airway Tree
-
Site of Gases Exchange
Alveoli/Capillary
-
Defined as the exchange of air between the atmosphere and the alveoli.
Ventilation
-
occurs in three stages: inhalation & gas exchange (between alveoli-capillaries & blood-tissues); oxidative metabolism (in cells) generates CO2 & ATP; Tissue-blood gas exchange & exhalation to remove CO2
Respiration
-
is the airflow in the lungs
Ventilation
-
inhalation & gas exchange (between alveoli-capillaries & blood-tissues).
Respiration
-
- oxidative metabolism (in cells) generates CO2 & ATP
Respiration
-
Tissue-blood gas exchange & exhalation to remove CO2
Respiration
-
resides in Brainstem
Autonomic Respiration
-
originates in cerebral cortex and can override autonomic control.
Voluntary ventilation
-
Diaphragm and accessory muscles; Coordinated through phrenic, intercostal, cranial and cervical nerves; Chemoreceptors and mechanoreceptors
Respiration
-
blood is 100% saturated
Arterial blood
-
blood is typically 75% saturated
Venous blood
-
0-60mmHg -slope
Binding Cooperativity: Steep slope
-
60-100mmHg -slope
Binding Cooperativity: Flat slope
-
provides an inexpensive, noninvasive alternative means of monitoring hemoglobin saturation with oxygen.
Oximetry
-
Affected by: Severe anemia, Abnormal hemoglobin, Presence of intravascular dyes & Lack of pulsatile arterial blood flow
Pulse oximetry is affected by
-
falls with increasing altitude.
Normal arterial Po2
-
Shape and Symmetry: anterior and posterior chest
Inspection
-
Assesses airflow through the tracheobronchial tree
Auscultation
-
soft, low-pitched. Heard over most of lung fields.
Vesicular breath sounds
-
medium pitched. Heard over main bronchus & (R) upper posterior lung.
Bronchovesicular breath sounds
-
loud, high-pitched. Only heard over trachea.
Bronchotracheal breath sounds
-
Inspiration > expiration
Vesicular breath sounds
-
Inspiration = expiration
Bronchovesicular breath sounds
-
Expiration slightly > inspiration
Bronchotracheal breath sounds
-
Added or extra sounds; Are always abnormal and usually indicate underlying respiratory and/or cardiac pathology
Adventitious Lung Sounds
-
discontinuous; heard more often in inspiration; not usually cleared by coughing; dry or wet; fine, medium or coarse
Crackles
-
small airways forced open in disruptive fashion
Crackles physiology:
-
continuous; fog horn or snoring quality usually clear with coughing
Rhonchi
-
air passing through an obstructed airway. thick secretions, tumor
Rhonchi physiology:
-
continuous, musical, high-pitched sound (tea kettle); most commonly heard in asthma and is diffuse and usually bilateral
Wheezes
-
forceful air flow through a constricted airway
Wheezes physiology:
-
in a pediatric patient suggests foreign body aspiration
unilateral wheezing
-
Inflamed pleural surfaces rubbing together
Rub
-
Pleural sound; Like leather rubbing together; Evanescent and depend on amount of fluid in pleural space
Rub
-
transmitted voice sounds
Vocal resonance
-
Assess anywhere on chest where adventitious sounds are heard; Normally voice sounds on auscultation are muffled & unclear
Vocal resonance
-
Increased transmission of voice sounds indicate
airless lung
-
E” is heard as “A”
Egophony:
-
“99” sounds louder, clearer
Bronchophony:
-
whispered sounds are clear
Whispered pectoriloquy:
-
An uncomfortable awareness of breathing, not appropriate to the level of exertion
Dyspnea
-
Chest “tight”; “Can’t get enough air in”; “Wake up in middle of night short of breath”; “Short of breath”; ask for Scale of zero to ten
Dyspnea
-
Dyspnea onset minutes or hours
Dyspnea Acute
-
Dyspnea develops over weeks to months
Dyspnea Chronic
-
Acute MI; Congestive heart failure, Cardiac tamponade
Causes of acute dyspnea: Cardiovascular system
-
Bronchospasm, Pulmonary infection – bronchitis, pneumonia, Pulmonary embolism Pulmonary edema, Pneumothorax, Upper airway obstruction
Causes of acute dyspnea: Respiratory system
-
Asthma, COPD, Interstitial lung disease, Cardiomyopathy
Causes of chronic dyspnea
-
History and physical exam lead to accurate diagnoses in approx 2/3 of patients
Dyspnea – Evaluation
-
Oximetry/ABG; CXR; Spirometry; CBC; ECG
Dyspnea – Evaluation
-
Treat the cause; Oxygen; Pulmonary rehab; Treat anxiety
Dyspnea - Treatment
-
Clears the tracheobronchial tree of mucus, foreign particles, and noxious aerosols
Cough
-
One of the most common reasons for outpatient visits; May impair sleep and social functioning
Cough
-
Cough < 3 weeks
Cough Acute
-
Cough >3 weeks
Cough Persistent
-
women > men to develop
chronic Cough
-
Stimulated cough centers in resp tract send impulses to cough center in
medulla
-
Most commonly associated with URI; Other causes pneumonia, aspiration, pulmonary embolism, pulmonary edema
Acute cough
-
Low-grade chronic bronchitis; Increased intensity and intractability of pre-existing cough – think lung cancer
Persistent cough in Smokers
-
Upper airway cough syndrome (postnasal drip); Asthma; Gastroesophageal reflux (GERD)
Persistent cough in Nonsmokers
-
ACE inhibitor-induced cough
Persistent cough
-
Fatigue, Insomnia, Headache, Urinary incontinence, Rib fractures (ribs 5-7)
Cough - Complications
-
History and physical exam [Timing of cough, Sputum production, Nasal discharge, Frequent throat clearing, Wheezing] Chest x-ray esp in smokers or fever/wt loss patients
Cough - Evaluation
-
Treat underlying cause; Eliminate irritant exposures; Smoke, occupational agents;
Cough - Treatment
-
Persistent cough after URI (think)
asthma
-
Expectoration of blood originating below the vocal cords
Hemoptysis
-
Most likely from bronchial arteries (under more pressure than pulmonary circulation)
Hemoptysis
-
upper resp tract bleeding and upper GI bleed
mimics of Hemoptysis
-
Bronchitis; Bronchogenic carcinoma; Pneumonia
Hemoptysis - Most common causes in U.S.:
-
Infection (TB most common cause of hemoptysis worldwide); Goodpasture’s syndrome, Wegener’s granulomatosis, Auto-immune (e.g., lupus pneumonitis), Iatrogenic (drug-induced, radiation), Cocaine-induced
Hemoptysis -Parenchymal diseases
-
A-V malformation; Pulmonary embolism; Elevated pulm cap pressure (mitral stenosis or LVH); Iatrogenic (Swan-Ganz catheter)
Hemoptysis- Pulmonary vascular disorders
-
History and physical exam; Chest radiograph; Hematocrit; U/A and renal function; Coag profile; Further eval – bronchoscopy/HRCT
Hemoptysis - Evaluation
-
Treat underlying cause; Risk factors for tumor - aggressive workup [ >40 yo, >40 pack yr history of smoking, > 1 week of hemoptysis]
Hemoptysis - Treatment
-
substance that can donate a H+ ion (Lowers pH)
ACID
-
substance that can accept a H+ ion (Raises pH)
BASE
-
Metabolism of carbohydrates & fats generates 15,000 mmol of CO2; CO2 combines w/ water to form H2CO3
CARBONIC ACID
-
Metabolism of proteins forms 50-100 mmol of acid which the kidney must excrete
NONCARBONIC ACID
-
oxidation of sulfur-containing amino acids generates
H2SO4
-
compound that binds H+ when the [H+] rises and releases it when the [H+] falls. The body buffers are primarily weak acids (HPO4-2 + H+ H2PO4-)
BUFFER
-
-
-
-
Help in Diagnosis; Measure Respiratory Function; Make Changes in Treatment, Ventilator Settings, Monitor Acid Base Balance, For Example DKA
Arterial Blood Gas
-
pH Measures
Percent of H+ Concentration
-
pCo2 Measures
Pressure of Carbon Dioxide
-
pO2 Measures
Pressure of Oxygen
-
HCO3 Measures
Bicarbonate
-
SaO2 Measures
Oxygen Saturation
-
-
Arterial Blood Gas Measures
pH, pCo2, pO2, HCO3, SaO2, BE
-
Normal Value: pH
7.35 - 7.45
-
-
-
-
Normal Value: SaO2
80-100%
-
-
CO2 is an acid and reflects lung function; causes
respiratory disorder
-
HCO3 is a base and reflects Kidney function; causes
metabolic disorder
-
exerting opposite effect on pH
CO2 and HCO3
-
are highly reactive especially with proteins
H+ ions
-
There is a change in charge distribution that leads to a change in molecular configuration which leads to a change in protein function
When proteins gain or lose H+ ions
-
The H+ concentration varies little from 40 nanomol/L & is regulated by:
Chemical buffering by IC & EC buffers
-
Control of partial pressure of carbon dioxide is by
ventilation changes (pulmonary)
-
Control of plasma bicarbonate concentration is by changes in
renal excretion of H+
-
maintain the correct balance of substances in the body including H+ and HCO3-
Kidneys and Lungs
-
The vast majority of the acid produced per day is buffered and removed when
CO2 is exhaled. (CARBONIC ACID)
-
Kidneys excrete acid via
titratable acid and ammoniagenesis
-
Kidneys excrete acid via
titratable acid and ammoniagenesis
-
BICARBONATE BUFFERING SYSTEM: Under the control of the kidneys:
metabolic
-
BICARBONATE BUFFERING SYSTEM: Under the control of the lungs:
respiratory
-
+ =hydrogen ion concentration in nmol/L
H+
-
-
-
Compare Bicarb from
Chem7
-
The pH must be defended and maintained near
7.4
-
HOW DOES THE KIDNEY REGENERATE BICARBONATE?
IT ACIDIFIES THE URINE (pH 5-6)
-
URINARY ACIDIFICATION
AMMONIAGENESIS
-
-
-
-
decrease pH; decrease HCO3, decrease CO2
Metabolic Acidosis
-
decrease pH, increase HCO3, increase CO2
Respiratory Acidosis
-
increase pH, increase HCO3, increase CO2
Metabolic Alkalosis
-
increase pH, decrease HCO3, decrease CO2
Respiratory Alkalosis
-
causes Anion Gap METABOLIC ACIDOSIS (AGMA)[MUDPILERS]
Methanol, Uremia, Diabetic/Starvation Ketoacidosis, Paraldehyde/Phenformin Isopropyl Alcohol, Isoniazid, Lactic Acidosis, Ethylene Glycol/Ethyl Alcohol Rhabdomyolysis, Salicylates, Other Causes: Hyperalbuminemia, iatrogenic
-
Anion Gap =
Na – (Cl +HCO3)
-
-
Acid w/o Cl added; H+ buffered HCO3; Anion is added to non measured pool to inc AG
AGMA
-
Uretero sigmoidoscopy, Small Bowel Fistula, Excess Chloride & Diarrhea(Most Common), Carbonic Anhydrase Inhibitor/CRF, Renal Tubular Acidosis, Addison’s Disease, Pancreatic Fistula
METABOLIC ACIDOSIS: Non Anion Gap (NAGMA)
-
HYPERCHLOREMIC METABOLIC ACIDOSIS=
NONANION GAP METABOLIC ACIDOSIS
-
IF YOU GET ACIDOTIC FROM DIARRHEA, WHAT DOES THE KIDNEY DO?
MAKE MORE BICARB!
-
How does the kidney make more bicarb?
INCREASE NH4+ URINARY EXCRETION
-
to differentiate between renal and extrarenal causes of NAGMA.
Calculate Urine Anion Gap (UAG)
-
U[Na] + U[K] – U[Cl]
Urine Anion Gap (UAG)
-
Normal Urine Anion Gap (UAG)
-10 to +10
-
Decreased UAG < -10
Extrarenal NAGMA
-
Increased UAG > +10
Renal NAGMA
-
Kussmaul’s respirations
METABOLIC ACIDOSIS
-
decreased LOC leads to Coma; Weakness, decreased DTRs, Tachycardia( increased CO to decreased CO that leads to Hypotension and Dysrhythmia; Kussmaul’s respirations; Warm, flushed skin & mucous membranes; Anorexia, Nausea and Vomiting, increased K+
METABOLIC ACIDOSIS: Signs and Symptoms
-
Hydration, Correct the underlying cause: Insulin, Antidiarrheal medications, Dialysis. Note: Sodium Bicarb is not routinely given
METABOLIC ACIDOSIS: Treatment
-
Lungs fail to eliminate CO2
ACUTE RESPIRATORY ACIDOSIS
-
CNS Depression: Sedatives, CVA, Head trauma
ACUTE RESPIRATORY ACIDOSIS
-
Neuromuscular Disease: Myasthenia, GBS, Polio, Muscular dystrophy, hypokalemia
ACUTE RESPIRATORY ACIDOSIS
-
Impaired Lung Mechanics: Pleural effusion, pneumothorax, crush injury
ACUTE RESPIRATORY ACIDOSIS
-
Acute airway Obstruction: Foreign body aspiration, tumor, laryngospasm, bronchospasm
ACUTE RESPIRATORY ACIDOSIS
-
Acute Respiratory Disease: Severe Pneumonia, Pulmonary Edema
ACUTE RESPIRATORY ACIDOSIS
-
Lungs fail to eliminate CO2
CHRONIC RESPIRATORY ACIDOSIS
-
COPD, Pickwickian Syndrome, Thoracic Cage, Limitations: Kyphoscoliosis, Scleroderma, Chronic Neuromuscular diseases
CHRONIC RESPIRATORY ACIDOSIS
-
decreased LOC, Weakness, decreased DTRs, Ineffective respiratory efforts, increased [K+] if acute; Tachycardia leads to increased CO to decreased CO to Hypotension and Dysrhythmia
RESPIRATORY ACIDOSIS Signs and Symptoms:
-
Maintain patent airway with enhanced gas exchange: Meds, O2, Pulmonary toilet, ventilatory support, monitor ABGs to make appropriate adjustments in therapy; Assess LOC frequently; Modify diet to Low carbohydrate and high fat
RESPIRATORY ACIDOSIS Treatment:
-
A PRIMARY INCREASE IN HCO3
METABOLIC ALKALOSIS
-
THE PATHOGENESIS OF CHRONIC METABOLIC ALKALOSIS INVOLVES TWO DISTINCT PHYSIOLOGICAL DERANGEMENTS
GENERATION & MAINTENANCE
-
by either an addition of bicarbonate /a loss of acid or /a loss of a fluid containing proportionally more chloride than bicarbonate
A PRIMARY INCREASE IN HCO3 in METABOLIC ALKALOSIS
-
H+ loss from ECF space, HCO3- retention, Contraction alkalosis
GENERATION
-
Decreased ECF/Chloride depletion, Persistent mineralocorticoid excess, Hypercapnia, Potassium depletion(profound)
MAINTENANCE
-
Urine Chloride < than 15 mEq/L; Extracellular Fluid Contraction; Saline responsive (corrects volume contraction)
Chloride Responsive Metabolic Alkalosis
-
Urine Chloride > 15 mEq/L; Associated with excess mineralocorticoid; Associated with Hypokalemia; Saline unresponsive
Chloride Resistant Metabolic Alkalosis
-
Saline responsive (corrects volume contraction)
Chloride Responsive Metabolic Alkalosis
-
Saline unresponsive
Chloride Resistant Metabolic Alkalosis
-
Gastrointestinal Causes: Vomiting, NG suction, Chloride wasting diarrhea, Villous Adenoma
Chloride Responsive Metabolic Alkalosis
-
Renal Causes: Diuretic use, Carbenicillin, Penicillin, Sulfate, Phosphate, Post- hypercapnia
Chloride Responsive Metabolic Alkalosis
-
Exogenous Alkali: Sodium Bicarb, Sodium Citrate, Lactate, Gluconate, Acetate, Transfusion, Antacid
Chloride Responsive Metabolic Alkalosis
-
Cystic Fibrosis & Achlorhydria
Chloride Responsive Metabolic Alkalosis
-
Hypertensive Patient: Adrenal Disease: 1° Hyperaldosteronism, Cushing Syndrome, Liddle Syndrome
Chloride Resistant Metabolic Alkalosis
-
Hypertensive Patient: Exogenous Steroids: corticoids, licorice, carbenoxalone, glycyrrhizic acid, chewing tobacco
Chloride Resistant Metabolic Alkalosis
-
Normotensive Patient: Bartter or Gitelman Syndrome, Hypokalemia, Milk- alkali syndrome, Refeeding alkalosis, excessive alkali administration
Chloride Resistant Metabolic Alkalosis
-
Hallmark sign: increased bicarbonate level with rising PCO2
METABOLIC ALKALOSIS
-
Shallow slow breathing, Anxiety and irritability, (+)Chvostek’s sign (+)Trousseau’s sign, decreased [K+] & [Ca+]; Paresthesias, muscle cramping and weakness; Tetany and seizures; Tachycardia, may be hypotensive, palpitations; increased bicarb & PCO2
METABOLIC ALKALOSIS Signs and Symptoms:
-
Antiemetic medications; Monitor electrolytes and replace as indicated - Potassium sparing diuretic; Seizure Precautions
METABOLIC ALKALOSIS: Treatment:
-
Lungs eliminate Too much of CO2
RESPIRATORY ALKALOSIS
-
Increased Central Respiratory Drive: Anxiety, CNS infection, CVA, Brain tumor, Head trauma Medications: Salicylates, Nicotine, Aminophylline, progesterone, catecholamines, fever, sepsis, pregnancy, liver failure, hyperthyroidism
RESPIRATORY ALKALOSIS
-
Increased Chemoreceptor Stimulation: Anemia, CO poisoning, pulmonary edema, pneumonia, PE, high altitude, restrictive lung disease
RESPIRATORY ALKALOSIS
-
Iatrogenic: faulty settings with the mechanical ventilator
RESPIRATORY ALKALOSIS
-
CNS, Hypotension, Excess mechanical ventilation, Atelectasis, Pain, Cirrhosis Hypermetabolic State, Insufficient, Oxygenation, Psychogenic, Salicylates/Sepsis
RESPIRTORY ALKALOSIS
-
Rapid deep respirations, Anxiety and irritability, + Chvostek’s sign + Trousseau’s sign; decreased [K+] & [Ca+]; Paresthesia, muscle cramping and weakness; Tetany and seizures; Tachycardia, may be hypotensive, palpitations
RESPIRATORY ALKALOSIS: Signs and Symptoms:
-
Monitor ABGs periodically; Decrease respiratory rate: - focused breathing, decrease breaths per minute on ventilator settings, O2 therapy; Antianxiety medications
RESPIRATORY ALKALOSIS: Treatment
-
-
-
For every increase in pCO2 of 10mm, pH decreases by .08
Acute Respiratory Acidosis:
-
For every increase in pCO2 of 10mm, pH decreases by .03
Chronic Respiratory Acidosis
-
For every decrease in pCO2 of 10mm, pH increases by .08
Acute Respiratory Alkalosis:
-
For every decrease in pCO2 of 10mm, pH increases by .03
Chronic Respiratory Alkalosis:
-
-
change in anion Gap (AG)
Patient’s AG – Normal AG (12)
-
Corrected HCO3
change in AG + patient’s HCO3
-
If corrected HCO3 = 24
Pure AGMA
-
If corrected HCO3 = <24
AGMA + NAGMA
-
If corrected HCO3 = >24
AGMA + Additional Metabolic Alkalosis
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