Pulmonary Edema vs Pneumonia

Pulmonary Edema vs Pneumonia
Oregon EMT-Intermediate

Acute Pulmonary Edema, Hypotension, Shock
EMT-Intermediate Acute Pulmonary Edema, Hypotension, Shock Clinical signs: shock, hypotension, congestive heart failure, acute pulmonary edema Most likely problem? Acute Pulmonary Edema Volume problem Pump problem Rate problem First-line Actions Oxygen Nitroglycerine SL Furosemide 0.5 to 1mg/kg Morphine IV 2 to10 mg Administer Fluid Bradycardia? See algorithm Tachycardia? See algorithm Blood pressure

Let’s Review: Cardiac Output 5000-6000 ml/min. HR or SV = CO
Sympathetic effects: HR and SV Parasympathetic: Slows HR Little effect on SV

Review: SV = pressure in ventricle Frank Starling effect
Peripheral vascular constriction increases venous return = Increased RV output. Vasodilation of arteries decreases PVR and diastolic pressure = Decreased CO. The heart has the intrinsic capability of increasing its force of contraction and therefore stroke volume in response to an increase in venous return. This is called the Frank-Starling mechanism in honor of the scientific contributions of Otto Frank (late 19th century) and Ernest Starling (early 20th century). This phenomenon occurs in isolated hearts, and therefore is independent of neural and humoral influences. Increased venous return increases the ventricular filling (end-diastolic volume) and therefore preload, which is the initial stretching of the cardiac myocytes prior to contraction. Myocyte stretching increases the sarcomere length, which causes an increase in force generation. This mechanism enables the heart to eject the additional venous return, thereby increasing stroke volume (SV). The mechanical basis for this mechanism is found in the length-tension and force-velocity relationships for cardiac myocytes. Briefly, increasing the sarcomere length increases troponin C calcium sensitivity, which increases the rate of cross-bridge attachment and detachment, and the amount of tension developed by the muscle fiber (see Excitation-Contraction Coupling). The effect of increased sarcomere length on the contractile proteins is termed length-dependent activation. When venous return is increased, there is increased filling of the ventricle along its passive pressure curve leading to an increase in end-diastolic volume (Figure 3). If the ventricle now contracts at this increased preload, and the afterload is held constant, the ventricle will empty to the same end-systolic volume, thereby increasing its stroke volume. The increased stroke volume is manifested by an increase in the width of the pressure-volume loop. The normal ventricle, therefore, is capable of increasing its stroke volume to match physiological increases in venous return. This is not, however, the case for ventricles that are in failure.

Vital Signs Normal B/P is 120/70 mmHg Increases with age General:
Systolic – age up to 140 At age 50: usually 140 mmHg Increases 1 mmHg/yr after 50.

CHF Causes AMI Left ventricular enlargement Normal heart muscle
“Normal heart muscle” – the left ventricle is slightly thicker than the right “AMI” – the white streak is the area of dead tissue at the interventricular septum and on the anterior surface of the heart. This has taken out at least 40% of the muscle, which will cause difficulty for the heart to eject blood. “Left ventricular enlargement” – The causes of this include atherosclerosis, chronic hypertension, “athlete’s heart” and chronic abuse of stimulants (cocaine, methamphetamine). The left ventricle is considerably thicker than the right side with a much smaller space in the ventricle (compare this to the chamber in the AMI picture). Although the muscle is thicker, it does not contract as well (this is similar to a rubber band – after a point, the distance traveled of the band does not increase even with a greater stretch of the band). Less space for the blood will also reduce cardiac output. Normal heart muscle

Abnormal Cardiac Function
Dispatched as: Man down Chest pain Heart attack SOB Fainted Dizzy Passed out Choking Stroke DFO DRT

Initial Assessment: Brief History Onset Provoking factors Quality
Radiation Severity Time BP changes

Initial Assessment Meds Cardiac rhythm Abnormal breathing Edema Rales
Changes in skin color and moisture

Right and Left Heart Failure
Right Heart Failure Causes COPD Left heart failure Progression Right ventricle cannot eject all of the blood Fluid/pressure backs up Right atrium Venous system Pedal edema, JVD Left Heart Failure Causes High afterload Progression Left ventricle cannot eject all of the blood Fluid/pressure backs up Left atrium Lung tissue Alveoli Pulmonary edema

Acute Left Ventricular Failure
Acute LVF from heart disease: #1 cause of heart failure. Assume the worst, hope for best Pt. with CAD w/ hx of MI(new or old) May develop LVF. Frequently LVF is only manifestation of AMI.

LVF Common causes Systemic HTN Afterload Coronary artery disease
Arteriosclerosis/atherosclerosis Ischemia Local/temporary occlusion

LVF Common Causes Infarction Permanent, necrosis
Significant Sized Infarct Decrease effective wall motion Decreased stroke volume Cardiomyopathy Alcoholism one of main causes

LVF Other Causes Volume overload Bag of Potato Chips Severe anemia
Hypoxemia

LVF and Pulmonary Edema
Incidence of CHF doubles per decade of life > 3 million in US; > 400,000 new diagnoses/yr 5 yr mortality rate /p dx; 60% in men 43% in women CHF is summarized best as an imbalance in Starling forces or an imbalance in the degree of end-diastolic fiber stretch proportional to the systolic mechanical work expended in an ensuing contraction. This imbalance may be characterized as a malfunction between the mechanisms that keep the interstitium and alveoli dry and the opposing forces that are responsible for fluid transfer to the interstitium. Maintenance of plasma oncotic pressure (generally about 25 mm Hg) higher than pulmonary capillary pressure (about 7-12 mm Hg), maintenance of connective tissue and cellular barriers relatively impermeable to plasma proteins, and maintenance of an extensive lymphatic system are the mechanisms that keep the interstitium and alveoli dry. Opposing forces responsible for fluid transfer to the interstitium include pulmonary capillary pressure and plasma oncotic pressure. Under normal circumstances, when fluid is transferred into the lung interstitium with increased lymphatic flow, no increase in interstitial volume occurs. When the capacity of lymphatic drainage is exceeded, however, liquid accumulates in the interstitial spaces surrounding the bronchioles and lung vasculature, thus creating CHF. When increased fluid and pressure cause tracking into the interstitial space around the alveoli and disruption of alveolar membrane junctions, fluid floods the alveoli and leads to pulmonary edema. Etiologies of pulmonary edema may be placed in the following 6 categories: Pulmonary edema secondary to altered capillary permeability–includes acute respiratory deficiency syndrome (ARDS), infectious causes, inhaled toxins, circulating exogenous toxins, vasoactive substances, disseminated intravascular coagulopathy (DIC), immunologic processes reactions, uremia, near drowning, and other aspirations. Pulmonary edema secondary to increased pulmonary capillary pressure–comprises cardiac causes and noncardiac causes, including pulmonary venous thrombosis, stenosis or veno-occlusive disease, and volume overload. Pulmonary edema secondary to decreased oncotic pressure found with hypoalbuminemia Pulmonary edema secondary to lymphatic insufficiency Pulmonary edema secondary to large negative pleural pressure with increased end expiratory volume Pulmonary edema secondary to mixed or unknown mechanisms including high altitude pulmonary edema (HAPE), neurogenic pulmonary edema, heroin or other overdoses, pulmonary embolism, eclampsia, postcardioversion, postanesthetic, postextubation, and post–cardiopulmonary bypass

Basically this happens
Forward or backward ventricular flow. Forward – (LVF) – reduced flow into aorta and systemic circulation Backward – elevated systemic venous pressure

NY Heart Association’s classification of CHF
Not limited by symptoms Class II Fatigue, dyspnea, other sx with ordinary physical activity Class III Marked limitation with normal activity Class IV Symptoms at rest or with any activity

CHF Acute CHF Rapid Chronic CHF Slow Midnight shoppers

Pulmonary edema also results from:
CVA Pulmonary embolism Infection - Sepsis Allergy Inhalation of fumes Narcotic abuse Especially Inhaled (Heroin) Altitude sickness.

Acute Findings History Recent change in sleep patterns
More frequent trips to the bathroom Need to sleep on more pillows at night Recent move to the recliner at nights New episodes of PND Paroxysmal Nocturnal Dyspnea Sudden awakening with acute shortness of breath Relieved after standing or sitting upright for a period of time (Midnight Walmart shoppers)

Acute Findings History
Is more nitroglycerin needed to stop the episodes of chest pain? Have nitroglycerin or oxygen doses increased incrementally in the last few days?

Acute Findings – Critical Patient
General impression/initial assessment Labored respirations Audible sounds Tripod position Frothy sputum Retraction of chest muscles

Acute Findings – Critical Patient
General impression/initial assessment Lung sounds Wheezing, crackles Middle-to-upper lung fields Diaphoresis, change in skin color Severe anxiety or restlessness Tachycardia or bradycardia Severe hypertension may be present

Pulmonary Edema – S/S Tachypnea Orthopnea Paroxysmal Nocturnal Dyspnea
Elevation of pulmonary venous & cap pressures Wakening from sleep

Pulmonary Edema – more S/S
Noisy Labored Breathing Fine crackles/Rales Wheezes Reflex airway spasm “Cardiac asthma” Coarse crackles/Rhonchi (larger airways) Coughing Blood Tinged Sputum Pink Frothy

Normal chest xray

So, What to do? Decide – Sick/NotSick? Vitals Look
Skin – wet/dry, color, temp JVD Peripheral edema Subtle signs

Look Listen Breath sounds Pulse x 6 Skin

Treatment of RVF & LVF CHF a circumstance not a Dx
Treatment objectives Decrease myocardial: Workload Oxygen demand Reduce fluid retention

Treatment Decrease Workload No Physical activity Sitting upright
Oxygen Pt may tolerate BVM CPAP – studies are promising Decreases preload and afterload in CHF Improves lung compliance BiPAP CPAP but also delivers higher pressure during inspiration There is now Level I evidence that CPAP (Continuous Positive Airway Pressure) and BiPAP (Bilevel Positive Airway Pressure) are effective in preventing intubation and decreasing mortality in patients with Acute Respiratory Failure in properly selected patients.1,2,3 This article will attempt to review this evidence. The use of these machines in sleep apnea or chronic respiratory failure will not be explored. The use of positive pressure ventilation dates back to creation: And the Lord God formed man of the dust of the ground and breathed into his nostrils the breathe of life, and man became a living soul. - Genesis CPAP and BiPAP have also been used much of this century and the newer machines are descendants of the IPPB machines that were used from the 40s to the 60s. The current machines are designed to deliver a positive pressure of between 4 and 25 cm H2O. The patient is attached to the machine by either a nasal or a full face mask. Ventilators can deliver this type of non-invasive ventilation, but there are now multiple machines for this express purpose that can be purchased for less than $ for CPAP and about $ for BiPAP. CPAP delivers a continuous positive air pressure, most frequently at about 10 cm of water. This is delivered throughout the respiratory cycle and has been described as being similar to breathing with your head stuck out of a moving car. There are multiple reasons why this might improve breathing. Counteract intrinsic PEEP decrease preload and afterload in CHF improve lung compliance in CHF decrease the work of breathing Intrinsic PEEP (positive end expiratory pressure) is the concept that in patients with severe COPD, the lung does not fully empty due to the obstruction in the airway resulting in a positive pressure in the airways at end expriation. Therefore to breathe in, the COPDer must first overcome this positive airway pressure before he can generate a negative pressure to inhale more air. This is called intrinsic PEEP and in patients with respiratory failure due to COPD it is often about 5 cm H2O, but it can be higher. When CPAP is begun, the usual starting level is 10, though one can start at 5 and work up. Oxygen can be delivered at flow rates high enough to maintain O2 saturation above 90%. BiPAP delivers CPAP but also senses when an inspiratory effort is being made and delivers a higher pressure during inspiration. When flow stops, the pressure returns to the CPAP level. This positive pressure wave during inspirations unloads the diaphragm decreasing the work of breathing. This form of ventilation has been used for years in patients with chronic respiratory failure due to neuromuscular problems or chest wall abnormalities. In patients with respiratory failure, a common technique is begin with the expiratory level at 5 and the inspiratory level at 15. The levels are adjusted based on patient comfort tidal volume achieved and blood gases. As the use of BiPAP machines has increased, their cost has gone down. There are also more types of masks available and this has has improved patient comfort and compliance. The use of BiPAP machines is often called non-invasive face mask ventilation. This is because the trachea is not intubated so there is less trauma to the airway and more importantly there is a lower incidence of nosocomial infections. For acute respiratory failure however, compliance may be a problem. The respiratory technologist should be prepared to stay with the patient, while he/she gets used to the machine. It may be necessary to try several masks to provide effective ventilation that is comfortable for the patient. The patient must always be shown how to remove it in case of panic or vomiting. If the patient has a decreased level of consciousness, copious secretions, can not protect his airway or is unstable hemodynamically, then intubation is warranted. There are now multiple randomized, prospective studies showing the benefit of non-invasive ventilation in respiratory failure. Furthermore, not only has it been shown to be an effective therapy, but there is also evidence that it contributes to less time in hospital, fewer complications and decreased mortality compared to immediate intubation and ventilation.4 One study showed that there is a reduction of intubation from 74% to 16%, major complications were decreased from 48% to 16% and length of stay from 35 days to 23 days. Mortality was decreased from 29% to 9%.3 It should be noted that only 1/3 of the patients could be randomized and only between 50-80% of patients are compliant with treatment. Still there is certainly Level I evidence to support the use of BiPAP in patients with a pCO2>50, a pH<7.35 and a RR>30. There is also evidence from randomized, controlled trials to show that CPAP improves oxygenation, hypercapnia and reduces the rate of endotracheal intubation in pulmonary edema.5,6,7 If tolerated, BiPAP seems even more effective with faster reduction of pCO2, improved pO2, pH and RR. Unfortunately, there was an increased number of MIs in the patients on BiPAP compared to CPAP. Until further studies are done, it is recommended that CPAP be tried first, and if BiPAP is attempted, it should be initiated cautiously, watching for hypotension.8 There is still controversy on how and why CPAP works in CHF. There is no dispute that it reduces the work of breathing by improving atelectasis and V/Q ratios. Some studies have suggested it also improves preload and afterload and that there is actually an improvement in cardiac index. Of even more interest, studies out of Toronto by Bradley suggest that up to 50% of patients with CHF have sleep apnea. In these patients, the use of CPAP not only improves sleep, but leads to an improvement in ejection fraction that lasts into the daytime hours when they are awake. It is postulated that CPAP reduces preload and also afterload. It is possible that obstructive sleep apneas can put a severe strain on the heart by markedly increasing afterload and leading to hypertension. In conclusion, for those patients who present to the emergency department with acute respiratory failure but with normal levels of consciousness, no major secretion problems and who are hemodynamically stable, a trial of BiPAP or CPAP should be attempted prior to considering intubation and a mechanical ventilator. - Scott Rappard

Treatment OMI Oxygen, Monitor, IV MONA - if appropriate
Morphine, Oxygen, Nitro, ASA (Not in that order) Don’t let patient walk! Position of comfort Reassure Positive Pressure Ventilations if necessary

Treatment Vasodilatory Therapy (Nitrates) AMI reperfusion
Container expansion reduces preload Morphine  Reduce Fluid Retention Diuretics Lasix Bumex

Differential Diagnosis
Pneumonia Herpes Zoster Pleurisy COPD Rib fracture Asthma Angina MI Pneumothorax Pancreatitis Hepatitis Salicylate OD Bronchitis Hyperventilation Lung carcinoma Sepsis TB Muscle pain Costochondritis Pericarditis CHF Percardial tamponade

Pneumonia The statistics
Community acquired pneumonia 4.5 million cases annually in US Winter months/Colder climates More men than women 20% require hospitalization 6th leading cause of death Most common infectious cause of death

Viral Upper and lower respiratory infections Untreated, mortality > 30 % 37.7% in elder > 80 y/o Sudden onset of S/S & rapid progression suggest bacterial pneumonia

S/S Productive cough Sputum may be Green Rust-colored Current jelly
Foul smelling Rigor or shaking chills Headache Malaise N/V/D Exertional dypsnea Pleuritic chest pain, friction rub Abdominal pain Abdominal pain is associated with the most severe type of pneumonia (50% of pt with Frank Legionella pn. Have abd. Pn, anorexia), Frank Legionella pneumonia – mortality rate ~ 75% if not treated promptly; elders, smokers, COPD, alcoholics, trauma pt most at risk.

S/S, cont. Fever Tachypnea Tachycardia Cyanosis
Wheezes, coarse & fine crackles Anorexia & weight loss Dullness to percussion Altered mentation

generally resides in the nasopharynx carried asymptomatically
nosocomial pneumonia aspiration or inhalation; ~ 45% of healthy people aspirate during sleep; even higher in severely ill patients; often bilateral typical pneumonia generally resides in the nasopharynx carried asymptomatically in approximately 50% of healthy individuals Pathogenesis of typical pneumonia S pneumoniae generally resides in the nasopharynx and is carried asymptomatically in approximately 50% of healthy individuals. Invasive disease may occur upon acquisition of a new epithelium serotype. A strong association exists with viral illnesses, such as influenza. Viral infections increase pneumococcal attachment to the receptors on activated respiratory epithelium. Once aerosolized from the nasopharynx to the alveolus, pneumococci infect type II alveolar cells. The pneumonic lesion progresses as pneumococci multiply in the alveolus and invade alveolar epithelium. Pneumococci spread from alveolus to alveolus through the pores of Kohn, thereby producing inflammation and consolidation along lobar compartments. Pathogenesis of atypical infection After aspiration or inhalation, the atypical organisms attach to the respiratory epithelial cells by a variety of mechanisms. The presence of pili on the surface of Legionella species facilitates attachment. Once adhered, the organisms cause injury to the epithelial cells and their associated cilia. Many of the pathogenetic mechanisms may be immune-mediated rather than due to direct injury by the bacteria. A host defense is mounted via cell-mediated and humoral immunity. Infection caused by atypical organisms often spreads beyond the lobar boundaries and frequently is bilateral. Pathogenesis of nosocomial pneumonia Aspiration plays a central role in the pathogenesis of nosocomial pneumonia. Approximately 45% of healthy subjects aspirate during sleep, and an even higher proportion of severely ill patients aspirate routinely. Depending on the number and virulence of the pathogenic organisms reaching the lower respiratory tract and on the host defense factors, pneumonia may develop. The oropharynx of hospitalized patients may become colonized with aerobic gram-negative bacteria within a few days of admission. Therefore, nosocomial pneumonia is caused predominantly by the gram-negative bacilli. However, the incidence of Staphylococcus aureus lower respiratory tract infection is increasingly common in the hospitalized and institutionalized patient and must now be considered a possible pathogen for nosocomial pneumonia.

Pneumocystis carinii pneumonia
Bacterial pneumonia Bacterial pneumonia Viral pneumonia

Host Factors DKA Alcoholism Sickle Cell HIV

So – how do we tell the difference?????
Pneumonia Wheezes, Course & fine crackles Febrile, chills Productive cough Hx URI, OM, Conjunctivitis Tachypnea, tachycardia Cyanosis H/A Malaise Abdominal distention N/V/D CHF/Pulmonary Edema Wheezes, fine & course crackles Cardiac history Productive cough ↑ dyspnea suddenly JVD Cyanosis Finger clubbing Prolonged expiratory phase Tachypnea, tachycardia Accessory muscle use Paroxysmal nocturnal dyspnea

Pneumonia Pulm. Edema COPD/Asthma History N/A HTN, Heart problems Lung problems Dyspnea Orthopnea potential Orthopnea Chronic dyspnea Recent Hx Fever, malaise, etc. Acute Wt. gain Edema in legs Gradual Wt. loss Cough Productive, thick, green Foamy sputum Productive (bronchitis) Onset Gradual Rapid BP Normal High Meds Antibiotics, cold medicines Digoxin, antiHTN, diuretics Bronchodilators Steroids Treatment Oxygen, Med-neb, IV fluids High flow O2 NTG, Lasix, MS Oxygen, Med-neb Rx

Treatment summary Pneumonia OMI
Pulmonary Edema OMI MONA if approp. Position of comfort Nitroglycerin 0.4 mg SL per protocol Morphine 2-10 mg Lasix per protocol (commonly 40 mg) CPAP if available Pneumonia OMI Limit IV fluids if hx of cardiac disease CPAP if available

Medications for Pulmonary edema
Nitroglycerine Morphine Lasix

Nitroglycerin Drug Class: Nitrate vasodilator
Relieves myocardial workload Dilates the arterial and venous systems Reduces preload to the already overworked ventricles Reduces blood pressure to reduce afterload Allows pressure and fluid to move into the venous system Sublingual doses start at 0.4mg

Morphine Sulfate Drug Class: Narcotic Analgesic
Relieves myocardial workload as well Dilates the venous and arterial systems Reduces preload and afterload May cause hypotension

Morphine Sulfate: Other Actions
Mechanism of action Binds to opiate receptors throughout the CNS Slows respiratory rate at the medulla Stimulates the nausea center in the brain

Morphine Sulfate Administration
2-4mg over 1-2 minutes, every 5 minutes (usual max dose 10 mg)

Furosemide Class: Loop Diuretic
Moves sodium out of the blood vessels early in the kidney Water follows sodium into the kidney tubules The site pulls out potassium as well Provides some vasodilation within 5 min. Diuresis within min.

Furosemide Reduces preload vasodilation
Pulls the extra fluid out of the circulation Keeps fluid moving out of the kidney Medication effects Effects seen within 5-15 minutes of administration Peaks in 30 minutes after administration

Furosemide Administration
20-40mg IVP over 1-2 minutes Double the dose if the patient is currently taking a diuretic Relief of symptoms should begin within 5 minutes If no relief, consider BVM

SHOPS drugs – CHF patients
Street drugs Herbal drugs OTC drugs Prescription drugs Sexual enhancement

Street drugs may contribute to CHF
Cocaine Meth Inhaled solvents PCP

Herbal remedies Possibly helps High-rite Aqua-rite L-arginine
Possibly hurts St. Johns Wort Ephedra Ginko Biloba Kava Kava Licorice Ginseng Aconite Alisma plantago Bearberry Buchu Couch grass Dandelion Horsetail rush Juniper Herbal remedies Possibly helps High-rite Aqua-rite L-arginine Magnesium Berberine

Over-the-counter drugs (OTC)
Cold Medications

Common Prescription medication for CHF/Pulmonary Edema
(Calcium channel blocker) Amiodarone Norvasc Ace Inhibitors Vasotec Capoten Lotensin Accupril Altace Angiotension II receptor blockers Cozaar Avapro Beta Blockers Coreg

Sexual enhancement drugs
Viagra 24 hours Cialis 36 hours Levitra unknown

Pulmonary Edema vs Pneumonia

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