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Congestive Heart Failure and Pulmonary Edema
Nestor Nestor, MD June 21, 2006
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Goals and Outline Pathophysiology of Congestive Heart Failure (CHF)
Recognizing CHF and Pulmonary Edema (PE) Prehospital Treatment
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1. Pathophysiology
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Terminology Heart Failure: The inability of the heart to maintain an output adequate to maintain the metabolic demands of the body. Pulmonary Edema: An abnormal accumulation of fluid in the lungs. CHF with Acute Pulmonary Edema: Pulmonary Edema due to Heart Failure (Cardiogenic Pulmonary Edema)
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The Heart is Two Pumps in Series
CO2 LA RV tissue
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Like any pump: The heart generates pressure to deliver blood to the body Therefore it also must…
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Pull blood out of the veins
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Fluid (and some cells) from stagnating blood leak out…
alveolus lymphatic capillary
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Three Pathophysiological Causes of Failure
Increased work load (HTN) Myocardial Dysfunction (ASCVD) Decreased Ventricular Filling (Valvular, cardiomyopathy, etc.)
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Normal Heart LV RV
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Myocardial Infarction
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Hypertension
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Dilated Cardiomyopathy
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Heart Failure - Concepts
Cardiac Output (L/min) Afterload (BP) Primarily arterial and systolic function Preload (volume) Primarily a venous and diastolic function Frank-Starling Length: Tension Ratio Why preload effects output
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CHF: A Vicious Cycle Low Output
Increased Preload Increased Afterload Norepinephrine Increased Salt Vasoconstriction Renal Blood Flow Renin Angiotension I Angiotension II Aldosterone
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Airway flow CO2 O2 no gas exchange Gas exchange
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Infiltration of Interstitial Space
Normal Micro-anatomy Micro-anatomy with fluid displacement
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Perivascular cuffs in early pulmonary edema
Normal lung Early pulmonary edema
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The ultimate insult: alveolar flooding
flow
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Precipitating Causes Non-Compliance with Meds and Diet
Increased Sodium Diet (Holiday Failure) Acute MI Arrhythmia (e.g. AF) Infection (pneumonia, viral illness) Pregnancy
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2. Recognizing CHF and Pulmonary Edema
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Acute Pulmonary Edema
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History, History, History
Acute or chronic onset Prior episodes Weight gain Medications
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Symptoms Fatigue Nocturia DOE PND GI Symptoms Chest Pain Orthopnea
Profound Dyspnea
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Vitals Tachypnic Tachycardic Hypoxic
Hypertensive (even “normal” may be too high) or Hypotensive in severe failure
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Physical Exam Anxious Pale Clammy Confusion Edema Diaphoretic Rales
Rhonchi S3 Gallop JVD Pink Frothy Sputum Cyanosis
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Pitting Edema
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JVD
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3. Prehospital Treatment
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EMS Management Sit upright High Flow O2
Nitroglycerine (If SBP > 100) Morphine Diuretics (furosemide) Ventilatory Support CPAP BVM Intubation and ventilation
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Pharmacological Treatment:
Nitroglycerine (NTG) Relaxes arteries and veins 0.4 mg sub lingual or 1 spray Repeat x2 every 5 min if SBP > 100 Consider 1” NTG paste to CW
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Pharmacological Treatment:
Morphine Also relaxes arteries and veins Reduces anxiety and O2 demand 2-4 mg IV
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Pharmacological Treatment:
Furosemide (Lasix) A diuretic, reducing fluid overload Requires good enough cardiac output to reach the kidneys 40mg IV May require more if already taking Lasix
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Beta Blockers (Lopressor)???
Pharmacological Treatment: Beta Blockers (Lopressor)??? Not useful in acute CHF Decrease HR and output, worsening failure May cause/worsen bronchoconstriction However they are used in stable, compensated failure so they may be on a pt’s med list
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Continuous Positive Airway Pressure
Ventilatory Support: CPAP Continuous Positive Airway Pressure CPAP: Continuous Positive Airway Pressure The term ‘continuous positive airway pressure’ was coined in 1971 by Gregory et al to describe an elevated airway pressure therapy for spontaneously breathing, intubated neonates. Current application has expanded to include adults and more recently patients without an artificial airway. ‘The application of positive airway pressure throughout the whole respiratory cycle to spontaneously breathing patients’ (Keilty et al. 1992).
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CPAP is oxygen therapy in its most efficient form.
Simple Masks Venturi Masks CPAP CPAP IS OXYGEN THERAPY IN ITS MOST EFFICIENT FORM Medium concentration oxygen mask: Unable to deliver an accurate oxygen % since the patient inspiratory flow is not taken into account. Venturi mask: Deliver accurate concentrations at 24%, 28%, 35%, 40%, 60%; however, the higher the % the greater the necessity to humidify especially long term use. Humidified Oxygen: Able to deliver up to 60% O2, but only accurate up to a Peak Inspiratory Flow Rate (PIFR) of 22 Lpm above which the % is diluted according to the patient’s demand. CPAP: The only system capable of delivering up to 100% humidified oxygen at flow rates of up to 140 Lpm, thus satisfying all clinical requirements.
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Why does oxygen pass into the blood?
The Pressure Gradient Deoxygenated blood has a lower partial pressure of oxygen so oxygen transfers from the air into the blood. The blood supply arriving at the alveoli carries deoxygenated blood. This means that the oxygen has been used as the blood has been circulated round the body. Oxygen passes from the alveolar air into the blood because the partial pressure of oxygen in the alveolar air is higher than that in the blood arriving at the lungs It also applies the other way too! Blood arriving at the lungs has a higher partial pressure of carbon dioxide than the alveolar air, hence CO2 leaves the blood and is expired.
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CPAP and Patient Airway Pressure
PATIENT AIRWAY PRESSURES This slide illustrates simulated breath traces at atmospheric pressure (0cm H2O), and at 5cm H2O CPAP. Note that for inhalation of air to occur when breathing without assistance (0cm H2O), the generation of a pressure gradient is required: the pressure within the lungs is negative compared to that in the atmosphere, and consequently air is drawn into the lungs. Conversely, during exhalation, the passive elastic recoil of the ribcage elevates the intrathoracic pressure to above the atmospheric level and is therefore positive, consequently forcing air out of the lungs. The larger the drop in pressure on inhalation (i.e. the more negative it gets) the greater the patient work of breathing. When breathing with the aid of CPAP, the pressure within the lungs always remains positive. ‘The application of positive airway pressure throughout the whole respiratory cycle to spontaneously breathing patients.
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CPAP increases the pressure gradient
7.5cm H2O CPAP increases the partial pressure of the alveolar air by approximately 1%. This increase in partial pressure ‘forces’ more oxygen into the blood. Even this comparatively small change is enough to make a clinical difference. 1 cm H2O is equal to mm Hg. A 7.5cm H2O C.P.A.P. valve increases atmospheric pressure at sea level by 5.51mm Hg, and this in turn increases the partial pressure of the alveolar air by approximately 1%. This increase in partial pressure ‘forces’ more oxygen into the blood. Even this comparatively small change is enough to make a clinical difference.
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Physiological Effects Of CPAP
Increases the volume of gas remaining in lungs at end-expiration CPAP distends alveoli preventing collapse on expiration Greater surface area improves gas exchange Reduces work of breathing PHYSIOLOGICAL EFFECTS OF CPAP. Increases FRC Reduces Patient Work of Breathing Reduces V/Q Mismatch and Shunt The positive pressure increases the volume of air left in the lungs at the end of expiration. CPAP provides an increase in FRC (Gherini 1976). As a result of the increase in FRC additional areas of lung are recruited into the gas exchange process and allows an improvement in blood gas values. Since CPAP shifts the lung volume along the compliance curve it reduces the patient work of breathing. In addition, as more alveoli now participate in the gas exchange process the V/Q mismatch is corrected and the fraction of shunt is reduced.
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Application
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CPAP And Pulmonary Edema
CPAP increases transpulmonary pressure CPAP improves lung compliance CPAP improves arterial blood oxygenation CPAP redistributes extravascular lung water CPAP AND PULMONARY odema. Severe pulmonary odema is a frequent cause of respiratory failure. CPAP increases FRC. CPAP increases transpulmonary pressure. CPAP improves lung compliance. 10 cm CPAP improves arterial blood oxygenation. CPAP redistributes extravascular lung water.
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Redistribution Of Extravascular Lung Water With CPAP
REDISTRIBUTION OF EXTRAVASCULAR LUNG WATER WITH PEEP. The application of PEEP to the edematous lung decreases intra-alveolar fluid volume, increases interstitial lung water, and facilitates the movement of water from the less compliant interstitial spaces where gas exchange occurs to the more compliant interstitial spaces. This redistribution of interstitial water improves oxygenation, lung compliance, and ventilation/perfusion matching when applied in either cardiogenic or non-cardiogenic pulmonary odema.
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CPAP And Acute Respiratory Failure
CPAP prevents airway collapse during exhalation CPAP overcomes inspiratory work imposed by auto-peep (pursed lip breathing) CPAP may avoid intubation and mechanical ventilation CPAP AND ACUTE RESPIRATORY FAILURE. CPAP overcomes inspiratory work imposed by auto-PEEP. CPAP prevents airway collapse during exhalation and has the effect of ‘splinting the airways’ CPAP improves arterial blood gas values. CPAP may avoid intubation and mechanical ventilation. (Miro 1993)
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Caution COPD and Asthmatic patients do not respond predictably to CPAP
Higher risk of complications such as pneumothorax
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When Not To Use Mask CPAP
Pneumothorax (evolve into tension) Hypovolemia (further limit preload) Severe facial injuries Patients at risk of vomiting CONTRA-INDICATIONS OF MASK CPAP. Hypercapnic patients may have a reversed respiratory drive, and rely on low levels of oxygen to trigger a breath rather than the much more sensitive trigger of CO2 active in normal subjects. A patient whose respiratory drive is now sensitive only to low levels of oxygen must not therefore be administered oxygen as this will knock out the respiratory drive and as a result lead to a reduction of the respiratory rate, with the consequent elevation of PaCO2. CPAP should not be used with patients with an undrained pheumothorax. An emphysematous bulla within the lungs presents a risk when any type of positive airway pressure is applied to the lungs. A bulla is a large area of the lungs that has broken down to form a hole. Bullae are very brittle and present a risk of bursting. Hypovolemia is a low blood volume. Administering CPAP may reduce both blood pressures and cardiac output. Although no true contra-indications have been identified in the literature, CPAP should not be administered to patients with unstable facial fractures, excessive facial lacerations, laryngeal trauma, or a recent tracheal or esophageal anastomosis. Patients at risk of vomiting (those with gastrointestinal bleeding or ileus) may also need to be excluded.
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Common Complications With CPAP
Gastric distension Pulmonary barotrauma Reduced cardiac output Hypoventilation COMMON COMPLICATIONS ASSOCIATED WITH CPAP. 1. Pressure Sores - Since the advent of soft, self-sealing masks, these complications are usually limited to nasal-bridge pain and erythema at the site of application. However these symptoms can be reduced by the prior application of materials such as “Granuflex”. Another less serious complication of the mask is patient discomfort or intolerance. 2. Gastric Distension - The most significant potential complication cited by early critics were aerophagia and aspiration of gastric contents. However, the levels of CPAP used (<10 cm H2O) are usually not associated with gastric distension. If this complication occurs, it is easily remedied by naso-gastric intubation, with regular aspiration. Gastric aspiration related to CPAP via face mask has never been reported in the literature. 3. Pulmonary Barotrauma - With mask CPAP, as with any positive-pressure therapy, the potential for distension and pulmonary barotrauma is always present. However, in investigations cited by Branson (1985) only one of 196 patients developed evidence of barotrauma (pneumomediastinum), representing a complication rate of 0.5%. The low incidence of barotrauma in these patients may be attributed to the use of spontaneous breathing as the method of ventilatory support. To further minimise this risk the status of the patient’s lung disease should be considered when prescribing CPAP. 4. Reduced Cardiac Output - Positive-pressure therapy has been associated with a decrease in cardiac output by Gong (1983). However, heamodynamic embarrassment in patients treated with the levels of CPAP described in that report was most often due to hypovolemia. In Branson’s report cardiovascular depression did not occur in patients with adequate volume status. 5. Hypoventilation - A potentially lethal complication of mask CPAP is hypoventilation, which may occur with excessive levels of CPAP. Overdistension of normal lung units can increase the ratio of dead space to tidal volume and result in CO2 retention. Hypoventilation may also occur in patients who become lethargic and weak. All patients receiving CPAP therapy should be closely monitored, and if CO2 retention is identified, intubation and mechanical ventilation should be instituted. 6. Fluid Retention - The application of CPAP causes a reduction in urine output secondary to reduced renal perfusion, redistribution of renal blood flow and increased antidiuretic hormone secretion. It is often necessary to modify fluid therapy or employ diuretics when applying positive airway pressure if fluid retention and odema are to be avoided. Alternatively, the depression of cardiovascular and renal function which may occur with CPAP may be treated successfully with inotropic agents.
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CPAP Flow Sheet No Exclusion Criteria Present
-Respiratory/Cardiac Arrest Pt.unable to follow commands Unable tp maintain patent airway independently Major Trauma Suspicion of a Pneumothorax Vomiting or Active GI Bleed Obvious signs/Symptoms of Pulmonary infection 2 or more of the following Respiratory Distress Inclusion Criteria Retractions of accessory muscles Brochospasm or Rales on Exam Respiratory Rate > 25/min. O2 Sat. < 92% on high flow O2 Administer CPAP using Max FIO2 Stable or Improving Reassess Patient Deteriorating Continue CPAP Continue COPD/Asthma/Pulmonary Edema Protocol Contact Medical Control with a Report -Contact Medical Control with report Discontinue CPAP unless advised by Medical Control Continue Asthma/COPD/Pulmonary Edema Protocols ,
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Ventilatory Support: Intubation
Definitive (but not first) treatment of pulmonary edema Positive pressure redistributes edema fluid as in CPAP but to a greater extent Mechanical ventilation greatly reduces O2 demand Sedation/paralysis also reduces O2 demand and increases compliance CPAP: Continuous Positive Airway Pressure The term ‘continuous positive airway pressure’ was coined in 1971 by Gregory et al to describe an elevated airway pressure therapy for spontaneously breathing, intubated neonates. Current application has expanded to include adults and more recently patients without an artificial airway. ‘The application of positive airway pressure throughout the whole respiratory cycle to spontaneously breathing patients’ (Keilty et al. 1992).
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Ultimate Therapies If pt stabilizes: long term therapy with beta blockers and ACE inhibitors If cardiac output remains unacceptable: Beta agonists LVAD Transplant
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In Summary Heart failure is the result of an acute event (MI, AF) or chronic decompensation Pulmonary edema frequently results from cardiac failure but may also result from other disease processes (ARDS) or direct insult Correct diagnosis is crucial and depends on good history and exam Therapy is both pharmacological and ventilatory support
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Thank You
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