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Dr Hernandez 2/25/09 Pathophysiology of Ventilation Problems Upper Airway Trauma Epiglottis Croup FBAO Tonsillitis Lower Airway Trauma Blunt Penetrating Obstructive Lung Disease – (COPD; emphysema and chronic bronchitis, asthma – smooth muscle spasm) Restrictive lung disease – loss of lung compliance causing incomplete lung expansion and increased lung stiffness. Tension Pneumothorax Pneumo/hemo thorax Acute Respiratory Distress Syndrome (ARDS)(bruised lungs, ecchymotic, swelling etc) Airway edema, anaphylaxis, smoke inhalation, APE Empyema – puss purulent material secondary to pneumonia Plural Inflammation – will cause pleuritic chest pain CF, MS Neurologic problems Depressants CVA Head problems Phrenic or spinal nerve dysfunction Airway burns – soot around the mouth Asbestosis Blebs PE –(off plane, long period of immobility, DVT, recent surgery) Interstitial Space Pathophysiology Pulmonary Edema ARDS Near Drowning – freshwater vs. saltwater – Freshwater can be more dangerous than saltwater in secondary drowning. When fresh water enters the lungs it is pulled into the pulmonary circulation via the alveoli because of the low capillary hydrostatic pressure and high colloid osmotic pressure. Consequently, the plasma is diluted and the hypotonic environment causes red blood cells to burst (hemolysis). The resulting elevation of plasma K+ level and depression of Na+ level, due to the hemolysis, alter the electrical activity of the heart. Ventricular fibrilation often occurs as a result of these electrolyte changes. Additionally, if drowning occurs in very cold water ( <10o C), the uptake of cold water into the vascular system can stop the heart. In open heart surgery, the technique of pouring cold saline solution over the heart is used to prevent heart action. If the victim is resuscitated death can occur hours later due to renal failure. During hemolysis, hemoglobin is also released into the plasma which can accumulate in the kidneys leading to acute renal failure. In contrast, salt-water drowning does not lead to uptake of inspired water into the vascular system because it is isotonic to blood. Therefore, no red cell hemolysis occurs and the cause of death is asphyxia. Max Lung Capacity – 6L Dead space – 150ml Tidal volume 5-6 ml/kg – 6-8ml/kg for peds Minute volume Alveolar Volume Inspiratory reserve volume, max amount that can be inhaled Forced Expiratory Volume (FEV) Residual Volume – amt remaining in lung after exhalation Acid Base Balance Normal ph 7.35-7.45 – out of this range normal metabolic process cannot occur properly, acidosis more harmful and more acute than alkalosis (3 mechanisms of H+ removal – kidneys hold on to bicarb) Decreased ventilation = Retention of co2 = acidosis Hyperventilate = blow off co2 = alkalosis = nerve ending malfunction, tingling, carpopedal spasm The Bicarbonate buffering system is the most important buffer solution for maintaining a relatively constant pH in the plasma. It functions via blood buffering with bicarbonate. The enzyme carbonic anhydrase maintains the equilibrium between bicarbonate and H2CO3. This is, in turn, converted into carbon dioxide and water. Most common cause of hemoptysis, chronic bronchitis, blebs, lung CA, TB – The origin of blood can be known by observing its color. Bright red, foamy blood comes from the respiratory tract while dark red, coffee-colored blood comes from the gastrointestinal tract. COPD - Blue Bloaters vs Pink Puffers (The effort made by patients suffering from emphysema during exhalation, causes a pink color in their faces, hence the term commonly used to refer to them, “pink puffers”.) (Patients with advanced COPD that have primarily chronic bronchitis rather than emphysema were commonly referred to as “blue bloaters” because of the bluish color of the skin and lips (cyanosis) seen in them.) Emphysema – destruction of alveolar walls – Chronic bronchitis – too much mucus production The Pores of Kohn are pores between adjacent alveoli, or interalveolar connections. They function as a means of collateral ventilation; that is, if the lung is partially deflated, ventilation can occur to some extent through these pores. The pores also allow the passage of other materials such as fluid and bacteria. Pursed lips breathing – patient is building pressure to alveoli to help breathe. Self PEEPing Asthma Reactive airway disease More common in peds and young-middle adults Triggers – Extrinsic in Peds, Intrinsic in adults Reversible airflow obstruction due to: Bronchial smooth muscle constriction Overproduction of mucus Breath Stacking – can’t exhale complete volume – leads to hyperinflation of alveoli Breath trapping – physical finding, chest gets bigger Bronchiole is obstructed on expiration – mucus plugs Hypertrophy of smooth muscle in asthmatics vs COPD Assessment Inspiratory wheezing – larger airways Expiratory wheezing – Silent chest may mean severe obstruction – flow too low to generate sounds – BAD! As lungs are hyperinflated – cause symptoms of cardiac tamponade – narrow pulse pressure – pulsus paradoxus>20 As they get better they may start wheezing and bringing up mucus – as bronchodilation is occurring Status Asthmaticus – severe and prolonged – taking his meds all day, etc. True Emergency – Up Triage – imminent threat of respiratory failure Role of Magnesium Sulfate in Asthma, Maged A. Zaki, MD in Medscape Magnesium sulfate has been shown to inhibit smooth muscle contraction, decrease histamine release from mast cells, and inhibit acetylcholine release. Studies both in children and adults have shown variable improvement in patients with severe airflow limitation who are unresponsive to standard treatment with beta agonist, anticholinergic, and corticosteroid medications. Ciarallo has shown in 2 studies of children that the optimum dose is 40 mg/kg given as an intravenous bolus with a maximum dose of 2 g. In 1 study, improvement in forced expiratory volume in 1 second (FEV1) was seen within 20 minutes and continued for up to 110 minutes. Up to a 20% improvement in FEV1 may be seen. In adults, a study by Silverman has shown that patients with an initial FEV1 lower than 25% of what was predicted benefited the most from magnesium sulfate therapy. Asthma is classified according to the frequency of symptoms, FEV1 and peak expiratory flow rate.[4] Classification of asthma severity[4] Severity Symptom frequency Nighttime symptoms Peak expiratory flow rate or FEV1 of predicted Variability of peak expiratory flow rate or FEV1 Intermittent < once a week ≤ twice per month ≥ 80% predicted < 20% Mild persistent > once per week but < once per day > twice per month ≥ 80% predicted 20–30% Moderate persistent Daily > once per week 60–80% predicted > 30% Severe persistent Daily Frequent < 60% predicted > 30% Bacterial Pneumonia Fever , chills, pleuritic chest pain, dyspnea Empyema Decreased sounds 02 and transport Some more study resources from Wikipedia Respiratory sounds: Stridor ·Wheeze ·Rales ·Rhonchi ·Hamman’s sign Dyspnea ·Hyperventilation/Hypoventilation ·Hyperpnea/Tachypnea/Bradypnea ·Orthopnoea/Platypnea Biot’s respiration ·Cheyne-Stokes respiration ·Kussmaul breathing Hiccup ·Mouth breathingAsphyxia ·Cough ·Pleurisy ·Sputum Respiratory arrest ·Hypercapnia/Hypocapnia
Dr Hernandez
2/25/09
Pathophysiology of Ventilation Problems
Upper Airway
Lower Airway
Interstitial Space Pathophysiology
Additionally, if drowning occurs in very cold water ( <10o C), the uptake of cold water into the vascular system can stop the heart. In open heart surgery, the technique of pouring cold saline solution over the heart is used to prevent heart action. If the victim is resuscitated death can occur hours later due to renal failure. During hemolysis, hemoglobin is also released into the plasma which can accumulate in the kidneys leading to acute renal failure. In contrast, salt-water drowning does not lead to uptake of inspired water into the vascular system because it is isotonic to blood. Therefore, no red cell hemolysis occurs and the cause of death is asphyxia.
Acid Base Balance
Most common cause of hemoptysis, chronic bronchitis, blebs, lung CA, TB – The origin of blood can be known by observing its color. Bright red, foamy blood comes from the respiratory tract while dark red, coffee-colored blood comes from the gastrointestinal tract.
COPD - Blue Bloaters vs Pink Puffers (The effort made by patients suffering from emphysema during exhalation, causes a pink color in their faces, hence the term commonly used to refer to them, “pink puffers”.) (Patients with advanced COPD that have primarily chronic bronchitis rather than emphysema were commonly referred to as “blue bloaters” because of the bluish color of the skin and lips (cyanosis) seen in them.)
The Pores of Kohn are pores between adjacent alveoli, or interalveolar connections. They function as a means of collateral ventilation; that is, if the lung is partially deflated, ventilation can occur to some extent through these pores. The pores also allow the passage of other materials such as fluid and bacteria.
Pursed lips breathing – patient is building pressure to alveoli to help breathe. Self PEEPing
Asthma
Assessment
Status Asthmaticus – severe and prolonged – taking his meds all day, etc. True Emergency – Up Triage – imminent threat of respiratory failure
Role of Magnesium Sulfate in Asthma, Maged A. Zaki, MD in Medscape
Magnesium sulfate has been shown to inhibit smooth muscle contraction, decrease histamine release from mast cells, and inhibit acetylcholine release. Studies both in children and adults have shown variable improvement in patients with severe airflow limitation who are unresponsive to standard treatment with beta agonist, anticholinergic, and corticosteroid medications. Ciarallo has shown in 2 studies of children that the optimum dose is 40 mg/kg given as an intravenous bolus with a maximum dose of 2 g. In 1 study, improvement in forced expiratory volume in 1 second (FEV1) was seen within 20 minutes and continued for up to 110 minutes. Up to a 20% improvement in FEV1 may be seen. In adults, a study by Silverman has shown that patients with an initial FEV1 lower than 25% of what was predicted benefited the most from magnesium sulfate therapy.
Asthma is classified according to the frequency of symptoms, FEV1 and peak expiratory flow rate.[4]
Classification of asthma severity[4]
Severity
Symptom frequency
Nighttime symptoms
Peak expiratory flow rate or FEV1 of predicted
Variability of peak expiratory flow rate or FEV1
Intermittent
< once a week
≤ twice per month
≥ 80% predicted
< 20%
Mild persistent
> once per week but < once per day
> twice per month
20–30%
Moderate persistent
Daily
> once per week
60–80% predicted
> 30%
Severe persistent
Frequent
< 60% predicted
Bacterial Pneumonia
Some more study resources from Wikipedia
Respiratory sounds: Stridor ·Wheeze ·Rales ·Rhonchi ·Hamman’s sign
Dyspnea ·Hyperventilation/Hypoventilation ·Hyperpnea/Tachypnea/Bradypnea ·Orthopnoea/Platypnea
Biot’s respiration ·Cheyne-Stokes respiration ·Kussmaul breathing
Hiccup ·Mouth breathingAsphyxia ·Cough ·Pleurisy ·Sputum
Respiratory arrest ·Hypercapnia/Hypocapnia
2/18/09 – Dr Hernandez Respiratory Emergencies 1 Control of breathing Involuntary centers start in Pons, Medulla Pons regulates pattern Apneustic center – controls length of inspiration Pneumotaxic center – expiration Central chemoreceptors – separated by blood brain barrier Responds to PaCO2 Diffuses across blood brain barrier Changes PH of CSF Peripheral Chemoreceptors Respond to decreased o2 supply (carotid bodies, aortic arch) Secondary drive – hypoxic drive Low Hb saturation Decreased perfusion Baroreceptors Sense pressure changes respond to low BP hypovolemia hypoxia vs hypoxemia hypoxia – low tissue oxygen hypoxemia – low blood oxygen (sp02 – pulse oximeter) Rate controlled by CO2 level in Medulla Tachypnea vs bradypnea refers to rate Hypopnea vs hyperpnea refers to depth Orthopnea – SOB while lying down Pluerodynia – painful breathing (Platypnea – SOB while sitting up) Dyspnea – subjective description Hyperventilation vs Hypoventilation Hypocarbia – hypercarbia Patient can be tachypneic without hyperventilating Cheyne-Stokes – regularly irregular – alternates between apnea and tachypnea – damage to control centers Biots – Irregular chaotic – severe brain injury or brain stem herniation – abnormal pattern of breathing characterized by groups of quick, shallow inspirations followed by regular or irregular periods of apnea.[ Apneustic Breathing – prolonged inhalation – severe brain injury Kussmaul’s – too much acid, body trying to blow off excess – rapid deep – seen in in DKA, metabolic acidosis Lung Receptors Pulmonary stretch receptors Herring-Breuer Reflex Irritant Receptors Cough receptors Epithelium of tracheal bronchial tree Cause sneeze cough, laryngospasm Vasovagal response (Saddle Embolus – deadly) Normal Spo2 & PaCo2 Spo2 -90-97% acceptable to maintain life, 80s for chronic smokers or COPD – keep neonates, preemies at 93% to prevent o2 damage 35-45mm normal PaCo2 97% of o2 in blood carried by Hb Each Hb takes 4 o2 molecules (a pulse oximeter will read 100% when Hb saturated with 3 o2 molecules) As atmospheric pressure rises you have a higher uptake of 02 – so at high altitudes you will have lower sats You can saturate more o2 in a cold liquid, warm environment requires higher pressure to saturate same o2 70% of co2 transported as bicarbonate, easier to cross membranes, Some Hypercarbia causes – opiates, resp arrest, obstructive diseases, obstructions, etc Any increase in metabolic rate will cause rate to increase and vice versa Initial assessment
2/18/09 – Dr Hernandez
Respiratory Emergencies 1
Control of breathing
Rate controlled by CO2 level in Medulla
Hyperventilation vs Hypoventilation
Patient can be tachypneic without hyperventilating
Lung Receptors
Irritant Receptors
(Saddle Embolus – deadly)
Normal Spo2 & PaCo2
Initial assessment
2/2/09 Functions of the respiratory system Exchange of gases Excretory function (volatile substances – alcohol, garlic, acetone, etc) Acid Base Balance Metabolic and aerobic metabolism Respiratory Physiology Ventilation Hyper/Hypo refers to depth of ventilation and leads to hypo/hyper carbia Eupnea – normal breathing Tachypnea Braydpnea Apnea Dyspnea External Respiration – alveolar capillary membrane (also have bearing on acid/base levels due to transport of co2) Internal Respiration – cellular respiration (also have bearing on acid/base levels due to transport of co2) Transportation of Gases – O2 transported on hemoglobin, (hemoglobin is directly affected by temperature, in cold it picks up O2 but does not release it easily in the tissues – red cheeks because blood is cold O2 stays in the vessels) alkalosis – o2 not given up by Hgb, acidosis- o2 given up by Hgb much faster Regulation – Physics of ventilation Boyle’s Law – describes how air moves in and out of lungs Dalton’s Law of Partial Pressure – distribution of gas Henry’s law of Solubility of gases – describes how gases dissolve in water To be continued….
2/2/09
Functions of the respiratory system
Metabolic and aerobic metabolism
Respiratory Physiology
Physics of ventilation
To be continued….
2/2/09 More on capillaries…lymph, etc Blood pressure would force blood to flow out of capillaries into the interstitial spaces both on arteriole side and venous sides. This couldn’t work obviously. In the plasma you have dissolved proteins (albumins) and electrolytes; they are large molecules and can’t leave the capillaries under normal conditions. Therefore the interstitial spaces are hypotonic with respect to the plasma. Osmosis draws the fluid back into the bloodstream. The movement across the membrane is via osmotic pressure; the pressure caused by the albumin is oncotic pressure (40mm hydrostatic pressure outside – 25mm oncotic pressure inside the arteriole – net 15mm) On the venous side it is net -10mm and pulls fluid back in. Not equal, more pushing out of arteriole side than being pulled into venous side. Excess hydrostatic pressure / excess water is picked up by lymphatic capillaries and returned to circulation by lymphatic system. Lymph has the same composition as plasma except for the proteins. (the result of low oncotic pressure can be edema – excess fluid buildup in the tissues.) Lymph nodes, Spleen & Thymus, filter returning lymph to remove disease and infection. Some complications: If hydrostatic pressure increases on arteriole side, even a little on venous side too. Now you have no movement on venous side because oncotic and hydrostatic pressure are equal. Will result in edema or Pulmonary Edema in the lungs. Blunt Trauma- slashes and cuts cell membranes, capillaries, etc. as a result they bleed into the tissues (hematoma) when you break these capillaries the albumins leak into interstitial spaces. Now they draw fluids out of capillaries – increases swelling, (enough will cause compartment syndrome) Anaphylaxis – one of cells in connective tissues are mast cells don’t do anything unless they are stimulated. Stimulated in injury to the tissue and release histamine. Histamines act directly on the capillary and it makes the capillary more porous to albumins. Now that there are more albumins in the interstitial space you end up with increased fluid in the interstitial spaces, redness caused by leaking RBCs.(ankle, lungs, etc .anywhere there is an injury) In anaphylaxis there is an overstimulation/over production of histamine in every cell in the body due to an allergy, causing the entire body to swell (alveoli, larynx, skin, etc) Burns – 2nd degree have blisters. Blisters contain fluid, interstitial fluid. When you have a partial thickness burn, when you burn the dermis you cause mast cells to secrete, causing fluid to accumulate, large burns = lots of broken capillaries = lots of histamine released causing lots of fluid loss. Dehydration – not taking in enough fluids, results in decreased hydrostatic pressure, thereby pulling fluid from interstitial spaces to maintain homeostasis. Skin can become taut and tented as a result. (Compensatory mechanism to maintain circulation in the core areas of body) Hypovolemia – much faster vs dehydration. Rapid loss of fluid will not have time for decrease in the hydrostatic pressure enough to make up fluid loss like in dehydration. CHF – Right side – pedal edema, left side, pulmonary edema –(cardiogenic shock, failure of both sides – no edema)(Furosemide given as a diuretic and acts as a vasodilator as well, maximize storage of blood, lessens return to heart, same thing for NTG) Cardiac asthma, fluid leaks into bronchioles and alveoli causing lumens to become narrow, causing wheezing – same sound as asthma but different cause (fluid vs bronchoconstriction). Colloid fluids will draw fluids from interstitial spaces; will help make up blood volume, will not diffuse easily like crystalloid solution which would NOT stay in the circulatory system for very long. 3:1
More on capillaries…lymph, etc
Blood pressure would force blood to flow out of capillaries into the interstitial spaces both on arteriole side and venous sides. This couldn’t work obviously. In the plasma you have dissolved proteins (albumins) and electrolytes; they are large molecules and can’t leave the capillaries under normal conditions. Therefore the interstitial spaces are hypotonic with respect to the plasma. Osmosis draws the fluid back into the bloodstream. The movement across the membrane is via osmotic pressure; the pressure caused by the albumin is oncotic pressure (40mm hydrostatic pressure outside – 25mm oncotic pressure inside the arteriole – net 15mm) On the venous side it is net -10mm and pulls fluid back in. Not equal, more pushing out of arteriole side than being pulled into venous side. Excess hydrostatic pressure / excess water is picked up by lymphatic capillaries and returned to circulation by lymphatic system. Lymph has the same composition as plasma except for the proteins. (the result of low oncotic pressure can be edema – excess fluid buildup in the tissues.)
Lymph nodes, Spleen & Thymus, filter returning lymph to remove disease and infection.
Some complications:
If hydrostatic pressure increases on arteriole side, even a little on venous side too. Now you have no movement on venous side because oncotic and hydrostatic pressure are equal. Will result in edema or Pulmonary Edema in the lungs.
Blunt Trauma- slashes and cuts cell membranes, capillaries, etc. as a result they bleed into the tissues (hematoma) when you break these capillaries the albumins leak into interstitial spaces. Now they draw fluids out of capillaries – increases swelling, (enough will cause compartment syndrome)
Anaphylaxis – one of cells in connective tissues are mast cells don’t do anything unless they are stimulated. Stimulated in injury to the tissue and release histamine. Histamines act directly on the capillary and it makes the capillary more porous to albumins. Now that there are more albumins in the interstitial space you end up with increased fluid in the interstitial spaces, redness caused by leaking RBCs.(ankle, lungs, etc .anywhere there is an injury) In anaphylaxis there is an overstimulation/over production of histamine in every cell in the body due to an allergy, causing the entire body to swell (alveoli, larynx, skin, etc)
Burns – 2nd degree have blisters. Blisters contain fluid, interstitial fluid. When you have a partial thickness burn, when you burn the dermis you cause mast cells to secrete, causing fluid to accumulate, large burns = lots of broken capillaries = lots of histamine released causing lots of fluid loss.
Dehydration – not taking in enough fluids, results in decreased hydrostatic pressure, thereby pulling fluid from interstitial spaces to maintain homeostasis. Skin can become taut and tented as a result. (Compensatory mechanism to maintain circulation in the core areas of body)
Hypovolemia – much faster vs dehydration. Rapid loss of fluid will not have time for decrease in the hydrostatic pressure enough to make up fluid loss like in dehydration.
CHF – Right side – pedal edema, left side, pulmonary edema –(cardiogenic shock, failure of both sides – no edema)(Furosemide given as a diuretic and acts as a vasodilator as well, maximize storage of blood, lessens return to heart, same thing for NTG)
Cardiac asthma, fluid leaks into bronchioles and alveoli causing lumens to become narrow, causing wheezing – same sound as asthma but different cause (fluid vs bronchoconstriction).
Colloid fluids will draw fluids from interstitial spaces; will help make up blood volume, will not diffuse easily like crystalloid solution which would NOT stay in the circulatory system for very long. 3:1
