Prepared by Shane Barclay Acute Pulmonary Edema Prepared by Shane Barclay

Acute Pulmonary Edema Two Variations 1. Acute Pulmonary edema with adequate perfusion. Patients usually hypertensive. 2. Acute Pulmonary edema with inadequate perfusion ie cardiogenic shock. Patient’s BP usually low or ‘normal’.

The ‘Old Way’ Traditionally the thought was that CHF was simply extra fluid in the lungs from cardiac decompensation. Treatment of CHF was to give a ton of Lasix IV, then some morphine to ‘open up’ the airways and relax the patient. If they were hypotensive you could use dopamine in low doses to ‘renodilate’ the renal arteries, then give Dobutamine to increase the blood pressure and once that happened then give a ton of Lasix and some morphine. That view has all changed.

Mechanism of CHF/Acute Pulmonary Edema It is now felt that in APE the lungs develop some fluid due to a variety of causes – acute A fib, MI, PE, pneumonia etc. When that happens the body/brain senses fluid in the lungs and the response is that “I am drowning”. This in turn causes a huge catecholamine release – ‘fight or flight response’, which causes massive peripheral vasoconstriction. The vasoconstriction in turn causes more resistance for the heart, which in turn can cause more fluid building up in the lungs and so goes the cycle.

Mechanism of CHF/Acute Pulmonary Edema So now the treatment is to splint the alveoli open to help clear the lungs. This is done with non invasive ventilation and the use of PEEP. This buys you time! Then Nitroglycerin can be given to peripherally dilate the arteries which in turn reduces the afterload. Finally you can give ‘anxiolytics’ usually in the form of Fentanyl to help take away some of the catecholamine surge. As a result, most patients with APE can improve within minutes of having NIV applied.

Treatment of APE The treatment of APE depends on cardiovascular status. Is the patient hemodynamically stable or not? If not, they are usually in “Left Heart Failure”. Left heart failure can be either: - Systolic heart failure - Diastolic heart failure

Types of Heart Failure Systolic and Diastolic Failure Heart failure with reduced ejection fraction, is called systolic failure: The left ventricle loses its ability to contract normally. The heart can't pump with enough force to push enough blood into circulation. Heart failure with preserved ejection fraction, is called diastolic failure (or diastolic dysfunction): The left ventricle loses its ability to relax normally (because the muscle has become stiff). The heart can't properly fill with blood during the resting period between each beat.

Types of Heart Failure Just for completeness there is also Right Sided Heart Failure Right-sided or right ventricular (RV) heart failure usually occurs as a result of left-sided failure. When the left ventricle fails, increased fluid pressure is, in effect, transferred back through the lungs, ultimately damaging the heart's right side. When the right side loses pumping power, blood backs up causing edema and even ascites.

Treatment of APE

Treatment of APE involves Non invasive ventilation Treatment of APE involves Non invasive ventilation. If you are unfamiliar with NIV, it is advised you view the page on REMSTARBC.ca entitled “Ventilators in the ER”

IF Adequate Perfusion (i.e. systolic BP > 100 mmHg, MAP >65) Often these patients are very hypertensive. 1. Oxygen only if hypoxic (most are!), IVs and monitor. 2. Position patient upright (they will want to sit upright!) 3. Non-invasive positive pressure ventilation (NIPPV), start PEEP 6-8, quickly titrate up to 10-12 cm H20. 4. Search for causes (ACS, HTN, arrhythmia, acute aortic or mitral valve regurgitation, aortic dissection, sepsis, renal failure or anemia) and treat appropriately. 5. Intubate ONLY if apneic/agonal respirations.

IF Adequate Perfusion (i.e. systolic BP > 100 mmHg, MAP >65) 6. Vasodilators – Nitroglycerin S/L x 4 sprays, then IV infusion starting at 40 mcg/min, quickly increase by 40-50 mcg/min q 2-4 min up to 200 – 400 mcg/min. 7. If Pt in extremis, bolus Nitro loading dose of 400mcg/min q 2 min up to 5 doses, then drop to 100 mcg/min. Titrate up prn. 8. +/- ACE Inhibitor – sublingual Captopril 12.5 – 25 mg

IF Hypotensive (decompensated CHF) (systolic BP < 100) 1. Oxygen, IVs and monitor. 2. Most of these Pts are complex, call ICU or internist! 3.Provide non-invasive positive pressure ventilation (NIPPV) unless immediate intubation is needed. 4. Search for causes (ACS, HTN, arrhythmia, acute aortic or mitral valve regurgitation, aortic dissection, sepsis, renal failure or anemia) and treat appropriately. 5. Consider Fluid challenge, 250 cc N/S over 5 minutes.

IF Hypotensive (decompensated CHF) (systolic BP < 100) 6. If known systolic heart failure - -Use Inotrope: Dobutamine 2 mcg/Kg/min and increase to a max. 20 mcg/Kg/min. 7. If known diastolic heart failure with signs of hypotension/shock – - Use IV Vasopressor - Phenylephrine 0.5mcg/kg/min and titrate. (NOT inotrope) 8. If unknown cardiac status and signs of hypotension/shock – -Use Inotrope – Dobutamine 2 mcg/Kg/min and titrate up. 9. Once BP restored, then you can add IV Nitroglycerin.

Back to basic pharmacology Why Dobutamine? versus norepinephrine or dopamine or … Any why not a ‘pressor’ for diastolic heart failure?

b1 b1 b1 Drug a1 Inotr Chron Dromo b2 V/C V/D Phenylephrine +++ Epinephrine ++ +++ ++ ++ ++ Norepinephrine +++ ++ ++ ++ + Isoproterenol ++ ++ ++ Dobutamine ++ ++ +

Dobutamine the cardiac ‘squeeze’ drug Has positive inotropic (beta agonist) properties but very little/no vasoconstrictive properties (alpha agonist) Main use is in Cardiogenic Shock (Systolic heart failure) Dose: Start 2 mcg/kg/min

Dobutamine

Dobutamine for Systolic Failure In APE you already have maximal peripheral vasoconstriction, so you don’t want to add another vasoconstrictor. Dobutamine has no alpha adrenergic properties, so it won’t exacerbate peripheral vasoconstriction. Rather it will assist in cardiac inotropic and chronotropic activity to help restore cardiac function.

Phenylephrine for Diastolic Failure In diastolic heart failure, the left ventricle can not relax and becomes ‘stiff’. Adding a beta adrenergic inotrope will only exacerbate this condition. Instead you want to add an alpha agonist (ie phenylephrine) to cause vasoconstriction and therefore increase systemic blood pressure without ‘taxing’ the heart even more.

Systolic and Diastolic Failure If you are interested, the next two slides are You Tube videos explaining more of the systolic versus diastolic heart failure pathophysiology.

Case 1 EHS calls saying 72 year old woman with SOB Vitals: BP 190/110 HR 180/min Sats 82% Resp Rate 35/min Will be arriving in 2 minutes.

Mrs. Heidi Whetlung 78 year old woman with increasing SOB Began with ‘flu’ 3 days ago. History of HTN, RA, Diverticulosis, depression. Medication: Ramipril 2.5 mg od HCTZ 12.5 mg od Quinine 200 mg hs Tylenol ES tid Mirtazapine 15 mg daily

Mrs. Heidi Whetlung

What are you going to do?

Case 2 EHS has brought in a 66 year old female, Noreen Rhales, with acute SOB. Vitals BP 96/40 HR 170 RR 40 Sats 90% on 10 liters by mask.

Ms. Noreen Rhales Increasing SOB for 2 days Felt “unwell”, lethargic for 2 days, noted ‘palpitations’. Awaiting “valve replacement surgery” in 8 weeks Has been in CHF twice in past year. Meds: Ramipril 5 mg bid, Metoprolol 25 mg bid, Lasix 20 mg od, Aldactone 50 mg od, ASA 81 mg od, Synthroid 125 mcg od, Naprosyn 500 bid,

Ms. Noreen Rhales Exam: BP 90/50, HR 170, RR 38, Sats 90%, Looks terrified, can’t speak more than 2 words without gasping for breath. Course creps heard up to upper lung fields.

What are you going to do?

The END