EMS Medical Control Rounds

1. EMS Medical Control Rounds Oct 11, 2012 Domenic Martinello, MD Anna-Jaques Hospital

2. “I Can’t Breathe!” 2 common and different diseases that may cause dyspnea and hypoxia

3. Agenda • New Business • Old Business • Educational Tidbit

4. Old Business • Disclaimer: I have no outstanding old business so will just move on!

5. New Business! • Thank you all for coming! • Thank you to everyone who made possible and attended the EMS Skills lab! • No other current new business at this time • Don’t forget about the wiki • If you need access email me 

6. Educational Tidbits Congestive Heart Failure

7. Congestive Heart Failure • Definition: • Heart Failure: A state in which the heart is unable to provide sufficient “pump” to move adequate amounts of blood and oxygen to the tissues • Congestive Heart Failure: Heart failure that results in pooling of fluid (congestion) • High Output Heart Failure: Is a state in which heart function is adequate but the body’s demand for oxygen is higher than able to be met • Examples: severe anaemia, thyrotoxicosis, sepsis • Fluid Overload is a part of CHF, but many times CHF happens in a euvolemic state, and patients may also develop significant oedema without signs of CHF.

8. Classification of CHF • Side of Failure (left or right heart) • Due to problems with contraction (systolic failure) or relaxation (diastolic failure), or both, of the heart muscle • Failure from increased venous back pressure (preload) or inability to provide arterial perfusion (afterload) • Due to low cardiac output and high vascular resistance (low-output failure) or due to high cardiac output and low vascular resistance with inability to meet tissue needs (high output failure) • By Functional classifications (NYHA classification) • Class I: no limitation is experienced in any activities; there are no symptoms from ordinary activities. • Class II: slight, mild limitation of activity; the patient is comfortable at rest or with mild exertion. • Class III: marked limitation of any activity; the patient is comfortable only at rest. • Class IV: any physical activity brings on discomfort and symptoms occur at rest.

9. Stages of Heart Failure • American College of Cardiology and American Heart Association Stages • Typically progress in a linear fashion • Has loose association with NYHA • Stage A: Patients at high risk for developing HF in the future but no functional or structural heart disorder. • Stage B: a structural heart disorder but no symptoms at any stage. (NYHA Class I) • Stage C: previous or current symptoms of heart failure in the context of an underlying structural heart problem, but managed with medical treatment. (NYHA Classes II and III) • Stage D: advanced disease requiring hospital-based support, a heart transplant or palliative care (NYHA class IV)

10. Pathology of Heart Failure • The pathophysiology requires a massive failure of multiple systems from the subcellular level all the way to the organ level • The primary myocardial response to chronic increased wall stress is myocyte hypertrophy, death/apoptosis, and regeneration • This process eventually leads to remodeling, usually the eccentric type. Eccentric remodeling further worsens the loading conditions on the remaining myocytes and perpetuates the deleterious cycle. The idea of lowering wall stress to slow the process of remodeling has long been exploited in treating heart failure patients • The reduction of cardiac output following myocardial injury sets into motion a cascade of hemodynamic and neurohormonal derangements that provoke activation of neuroendocrine systems (Dopamine, Epinephrine, Norepinephrine)

11. Pathology (2) • The release of epinephrine and norepinephrine, along with the vasoactive substances endothelin-1 (ET-1) and vasopressin, causes vasoconstriction, which increases calcium afterload and, via an increase in cyclic adenosine monophosphate (cAMP), causes an increase in cytosolic calcium entry. • The calcium overload may induce arrhythmias and lead to sudden death. The increase in afterload and myocardial contractility (inotropy) and the impairment in myocardial lusitropy lead to an increase in myocardial energy expenditure and a further decrease in cardiac output. The increase in myocardial energy expenditure leads to myocardial cell death/apoptosis, which results in heart failure and further reduction in cardiac output, perpetuating a cycle of further increased neurohumoral stimulation and further adverse hemodynamic and myocardial responses. pairs myocardial relaxation (lusitropy).

12. Pathology (3) • In addition, the activation of the RAAS (Renin-Angiontensin-Aldosterone System) leads to salt and water retention, resulting in increased preload and further increases in myocardial energy expenditure. Increases in renin, mediated by decreased stretch of the glomerular afferent arteriole, reduce delivery of chloride to the macula densa and increase beta1-adrenergic activity as a response to decreased cardiac output. This results in an increase in angiotensin II (Ang II) levels and, in turn, aldosterone levels, causing stimulation of the release of aldosterone. Ang II, along with ET-1, is crucial in maintaining effective intravascular homeostasis mediated by vasoconstriction and aldosterone-induced salt and water retention.

13. Pathology (4) • In the failing heart, increased myocardial volume is characterized by larger myocytes approaching the end of their life cycle.As more myocytes drop out, an increased load is placed on the remaining myocardium, and this unfavorable environment is transmitted to the progenitor cells responsible for replacing lost myocytes. • Progenitor cells become progressively less effective as the underlying pathologic process worsens and myocardial failure accelerates. These features—namely, the increased myocardial volume and mass, along with a net loss of myocytes—are the hallmark of myocardial remodeling. This remodeling process leads to early adaptive mechanisms, such as augmentation of stroke volume (Frank-Starling mechanism) and decreased wall stress (Laplace's law), and, later, to maladaptive mechanisms such as increased myocardial oxygen demand, myocardial ischemia, impaired contractility, and arrhythmogenesis. • As heart failure advances, there is a relative decline in the counterregulatory effects of endogenous vasodilators, including nitric oxide (NO), prostaglandins (PGs), bradykinin (BK), atrial natriuretic peptide (ANP), and B-type natriuretic peptide (BNP). This decline occurs simultaneously with the increase in vasoconstrictor substances from the RAAS and the adrenergic system, which fosters further increases in vasoconstriction and thus preload and afterload. This results in cellular proliferation, adverse myocardial remodeling, and antinatriuresis, with total body fluid excess and worsening of heart failure symptoms.

14. Pathology (5) • Systolic and diastolic heart failure each result in a decrease in stroke volume. This leads to activation of peripheral and central baroreflexes and chemoreflexes that are capable of eliciting marked increases in sympathetic nerve traffic. • While there are commonalities in the neurohormonal responses to decreased stroke volume, the neurohormone-mediated events that follow have been most clearly elucidated for individuals with systolic heart failure. The ensuing elevation in plasma norepinephrine directly correlates with the degree of cardiac dysfunction and has significant prognostic implications (more = worse). Norepinephrine, while directly toxic to cardiac myocytes, is also responsible for a variety of signal-transduction abnormalities, such as down-regulation of beta1-adrenergic receptors, uncoupling of beta2-adrenergic receptors, and increased activity of inhibitory G-protein. Changes in beta1-adrenergic receptors result in overexpression and promote myocardial hypertrophy.

15. Causes • 4 broad categories: • Underlying causes: Underlying causes of heart failure include structural abnormalities (congenital or acquired) that affect the peripheral and coronary arterial circulation, pericardium, myocardium, or cardiac valves, thus leading to increased hemodynamic burden or myocardial or coronary insufficiency • Fundamental causes: Fundamental causes include the biochemical and physiologic mechanisms, through which either an increased hemodynamic burden or a reduction in oxygen delivery to the myocardium results in impairment of myocardial contraction • Precipitating causes: Overt heart failure may be precipitated by progression of the underlying heart disease (eg, further narrowing of a stenotic aortic valve or mitral valve) or various conditions (fever, anemia, infection) or medications (chemotherapy, NSAIDs) that alter the homeostasis of heart failure patients • Genetics of cardiomyopathy: Dilated, arrhythmic right ventricular and restrictive cardiomyopathies are known genetic causes of heart failure.

16. Causes (2) • Underlying causes of systolic heart failure include the following: • Coronary artery disease • Diabetes mellitus • Hypertension • Valvular heart disease (stenosis or regurgitant lesions) • Arrhythmia (supraventricular or ventricular) • Infections and inflammation (myocarditis) • Peripartum cardiomyopathy • Congenital heart disease • Drugs (either recreational, such as alcohol and cocaine, or therapeutic drugs with cardiac side effects, such as doxorubicin) • Idiopathic cardiomyopathy • Rare conditions (endocrine abnormalities, rheumatologic disease, neuromuscular conditions)

17. Causes (3) • Underlying causes of diastolic heart failure include the following: • Coronary artery disease • Diabetes mellitus • Hypertension • Valvular heart disease (aortic stenosis) • Hypertrophic cardiomyopathy • Restrictive cardiomyopathy (amyloidosis, sarcoidosis) • Constrictive pericarditis

18. Causes (4) • Underlying causes of acute heart failure include the following: • Acute valvular (mitral or aortic) regurgitation • Myocardial infarction • Myocarditis • Arrhythmia • Drugs (eg, cocaine, calcium channel blockers, or beta-blocker overdose) • Sepsis

19. Causes (5) • Underlying causes of high-output heart failure include the following: • Anemia • Systemic arteriovenous fistulas • Hyperthyroidism • Beriberi heart disease • Paget disease of bone • Albright syndrome (fibrous dysplasia) • Multiple myeloma • Pregnancy • Glomerulonephritis • Polycythemia vera • Carcinoid syndrome

20. Causes (6) • Underlying causes of right heart failure include the following: • Left ventricular failure • Coronary artery disease (ischemia) • Pulmonary hypertension • Pulmonary valve stenosis • Pulmonary embolism • Chronic pulmonary disease • Neuromuscular disease

21. Causes (7) • Because of increased myocardial oxygen consumption and demand beyond a critical level, the following high-output states can precipitate the clinical presentation of heart failure: • Profound anemia • Thyrotoxicosis • Myxedema • Paget disease of bone • Albright syndrome • Multiple myeloma • Glomerulonephritis • Corpulmonale • Polycythemia vera • Obesity • Carcinoid syndrome • Pregnancy • Nutritional deficiencies (eg, thiamine deficiency, beriberi)

22. BREATHE! I know that’s a lot of stuff…

23. Heart Failure Presentation • Common Complaints: • Chest Pain • Dyspnea at rest • Orthopnea • Dyspnea on Exertion • Nausea/Vomiting • Frank hypoxia • Paroxysmal Nocturnal Dyspnea • Weakness and fatigue • Increased urine output and increased nocturia • Confusion, Anxiety, sense of impending doom

24. Hart Failure Exam / Workup • May be in no distress at rest! • Look for signs of fluid overload (JVD, peripheral oedema, ascites, pink frothy sputum) • Rales in the lungs • May also have wheezing (formerly called “cardiogenic asthma”) • Post-diastolic heart sound (S3) • May have beat-to-beat pulse variation (pulsusalternans)

25. Important Finding • If a patient has frank CHF and a NEW MURMUR you must consider that patient has a valve dysfunction causing the symptom. Most commonly this is a papillary muscle rupture leaving a free leaf of the mitral valve. This can be a life threatening emergency since the patient will often decompensate RAPIDLY over the next few hours

26. Heart Failure Treatment • Step 1: OXYGENATE (apply supplemental oxygen) • Step 2: VASODILATE (if hypertensive, if BP low see Step 3) • Use NTG, SL if needed, paste if available, drip in the ER • NTG is the only intervention prior to NIPPV to decrease intubation • Step 3: IMPROVE HAEMODYNAMICS • If BP is low you MUST initiate vasopressor drugs • If unstable rhythm you should treat this first • Step 4: OFFLOAD FLUID • Give Lasix (or any other diuretic, I typically use Bumex) • Step 5: If patient is not improving or appears to be decompensating you • should try CPAP or BiPAP! • Step 6: If all else fails, intubate.

27. That’s all that’s to it! Questions?

28. Asthma Asthma is Greek for “panting”

29. What Is Asthma? • Asthma is a chronic inflammatory disease that affects the lungs • It can not be cured and by its nature is variable with frequent periods of asymptomatic existence as well as exacerbations ranging from inconvenient to life threatening • The true cause is unknown but based on epidemiological data is a combination of genetics (often seen in families) and environmental factors (embodied by the cluster of asthma in The Bronx of NY attributed to the high cockroach population) • Is considered a chronic obstructive problem but NOT part of COPD • Can be classified per the following chart • Asthma has a high association with positive allergy tests in 4-15 year olds • Asthma is liked to GERD but not certain which causes the other. • Asthma is common in children of mothers who smoked during pregnancy

30. Interesting correlations • Current data demonstrates a direct correlation (not proper causation) between obesity and asthma rates in children. There is some question about the inflammatory nature of obesity and its ability to generate lung inflammation. • There is also a correlation with hygiene and asthma. Children who live in less hygienic environments have much lower rates of asthma.

31. Classification of Asthma

32. Assessment • Diagnosis of asthma REQUIRES spirometry, not something we do in the ER or prehospital! • Symptoms include: • Wheezing—high-pitched whistling sounds when breathing out—especially in children. (Lack of wheezing and a normal chest examination do not exclude asthma.) • history of any of the following: • Cough, worse particularly at night • Recurrent wheeze • Recurrent difficulty in breathing • Recurrent chest tightness • (see next)

33. Assessment • (cont) • Symptoms occur or worsen in the presence of: • Exercise • Viral infection • Animals with fur or hair • House-dust mites (in mattresses, pillows, upholstered furniture, carpets) • Mold • Smoke (tobacco, wood) • Pollen • Changes in weather • Strong emotional expression (laughing or crying hard) • Airborne chemicals or dusts • Menstrual cycles • Symptoms occur or worsen at night, awakening the patient

34. Acute assessment • Patients typically carry a diagnosis of asthma • Exacerbations are acute episodes of sudden bronchospasm and dyspnea • Examination usually shows: • Wheezing (classic symptom) • Tripod seating position • Increased respiratory rate • Diaphoresis • Sense of impending doom • Prolonged expiratory phase and forcing of exhalation • More severe cases will have short sentences, retractions (intercostal and supraclavicular) • Severe cases progress with inspiratory and expiratory wheezing followed by decreased air movement and respiratory collapse.

35. Treatment (acute) • Prehospital care and emergency department care are not much different • In the ambulance setting the first line drug is albuterol. It is a beta 2 agonist that causes bronchodilation • Second line drugs include Ipratropium bromide which studies note has greatest efficacy in children and older smokers. Is an anticholinergic that dries secretions • Next agents are corticosteroids. They are essentially anti-inflammatory immune modulators. Decrease inflammation, abolish any allergic comorbidities. Take 6-8 HOURS for full effect! • CPAP (and BiPAP) are wonderful new augments for the patient with asthma. Has decreased intubations and helps deliver the nebulized medications deeper into the lungs. • Theophylline (methylxanthine, like caffeine!) is one of the last ditch efforts along with subcutaneous B2 agonists like terbutaline. If you are this far it qualifies for a “bad day”

36. Intubating the Asthmatic • Rule 1: It never goes well • Rule 2: it never goes well • You get the drift • Problem 1: If you intubate the patient your ventilator will have a very hard time with flow rates, plateau pressure management, and will likely cause some degree of barotrauma (pneumothorax and pneumomediastinum being the most severe) • Problem 2: Auto-Peep. Often times after intubation your patient will suddenly crash. STEP 1: DISCONNECT THE VENT/BAG and push moderately hard and slowly on the chest to cause patient to exhale. STEP 2: Decompress or place chest tubes bilaterally. STEP 3: Make sure you bag SLOWLY. • Problem 3: Patients may crash with sudden drops in CO2, lower it SLOWLY • Remember: Intubating an asthmatic is the quickest way to kill them if you aren’t careful

37. Treatment (chronic) • Long term therapy is complex, but begins with identifying stimuli and removing them • Allergy suppression with preferably non-sedating histamine blockers • Inhaled steroids • Long acting B2 agonists • which actually show increased mortality for patients who then go on to have acute exacerbations! • Immune therapy and modulation

38. So, its easy • Identify • Beta agonists (w or w/o anticholinergics) • Steroids • CPAP • Drive fast, try to treat before you need to intubate • If you intubate: breathe slow, long expiratory phase, low pressure, and if they crash remember to disconnect, exhale, decompress

39. That’s it! Thanks for coming, any questions?

40. References available by request if needed They just take too damn long to type… seriously… like all day…