Grand Rounds July 20, 2023 - St. Luke's Bethlehem Emergency Medicine Residency

Acute Heart Failure – Jake Marais, MD (For reference Chapter 53 Tintinalli)

Basic definition of CHF: Functional impairment of ventricular filling or ejection of blood, leading to cardiac symptoms
1. SOB, edema, fatigue, chest pain, exertional symptoms, weight gain, productive frothy cough, syncope
2. Neurohormonal response to poor perfusion- catecholamine surge to compensate leading to sodium and water retention and increased systemic vascular resistance 🡪 worsen myocardial demand
Goals of therapy:
1. Reducing preload is an essential first step in overloaded patient
2. Address afterload reduction – reduce Systemic vascular resistance
3. Find the underlying causes – not necessarily in the ED
4. Consider initiation of beta blockers if HD stable and without signs of low output – less important for ED presentation
5. ** Acute heart failure management (what we do) – largely unchanged and mainly focuses on use of nitrates (preload reduction), diuretics, and positive pressure ventilation
Cardiogenic shock in context of acute heart failure –
1. weak pulses, tachy, cool extremities, JVD, hypoxia, hypotensive, narrow pulse pressure
2. Why tachy? – compensatory
3. Initiate Levophed and Milrinone immediately – Levo usually first, added Milrinone for peripheral perfusion later.
4. Fluid challenge may be harmful in these patients due to cardiogenic shock component of their disease.
5. Diuresis if/when hypotension improved/resolved
Pulse pressure- difference between the systolic and diastolic pressures
1. should be considered an additional vital sign especially in context of CHF.
2. Generally, pulse pressures >40mmHg considered red flag
3. If widened – think aortic insufficiency – backward flow across the aortic valve reduces the diastolic pressure and widens the gap.
4. Poor perfusion in aortic insufficiency – massively reducing diastolic pressure – use nitroprusside, but very temporizing until aortic valve replacement
HTN – #1 cause of heart failure – can be on boards
1. Other risk factors – CAD, Age, diabetes, valvular heart disease, male sex, obesity
One of the hallmarks in chronic decompensated CHF is diuretic therapy
1. Often in the ED we underdose Lasix – onset of action 25-90 minutes
2. In Lasix naïve patient – reach for 40 IV
3. In patient on chronic diuretic therapy – can reach for 80-100 mg IV or use 2.5x the home dose in IV form
  1. i.e. 40 PO BID home furosemide = 80-100 mg IV
Noninvasive ventilation
1. BiPAP or high flow nasal cannula
2. Reduces need for intubation, effect on mortality remains undetermined
3. Improves ventilation by opening alveoli, fluid suppression, and dead space ventilation
4. Requires close monitoring, proper facial anatomy, proper sea
Don’t use Cardizem or Verapemil in acute CHF
1. Negative inotropic action can worsen heart failure
2. If Afib and heart failure, consider Digoxin – get rate control without negative inotrope

Shocking Arrhythmias – Dr. Salen (For reference Chapter 18 Tintinalli)

Criteria for diagnosis of Wide complex tachycardia?
1. QRS >120ms
2. HR >100 for an adult
Causes of wide complex – A LOT
1. Illness
2. Medication effect (sodium channel blockade)
3. Bundle branch blocks
4. Hyperkalemia
5. Ventricular preexcitation syndrome
6. Ischemic heart disease/MI
7. Dilated hypertrophic cardiomyopathy
8. Inherited ion channel abnormalities
4 EKG issues to consider whenever looking WCT
1. Is it truly tachycardic?
2. How wide is it?
3. Is it regular/irregular?
4. Do QRS complexes look the same or different?
Do Wide complex tachycardias originate above or below the AV node?
1. Can be both
  1. Supraventricular tachychardia with aberrant conduction such as a bundle branch block
  2. V-tach
What is the difference between sustained and nonsustaned VT?
1. V-Tach – occurrence of 3 or more consecutive PVCs
2. Sustained – more than 30 PVCs in a row
3. Why is VT bad? – rate is so fast that the LV can’t fill, lose the atrial kick which is responsible for 10-20% of LVEF
Different Types of VT?
1. Monomorphic (70%), Polymorphic (Torsades)
2. Would like to know if they have a pulse with either – stable vs. unstable. But polymorphic VT is inherently very unstable to begin with.
3. Stable 🡪 try rhythm control with meds
4. Unstable 🡪 Cardioversion
What are options for sustained, refractory monomorphic VT?
1. Amiodarone -150 mg with pulse
2. Amiodarone – 300 mg without pulse
3. Lidocaine also an option
4. Procainamide also option – but proarrhythmic, makes you hypotensive
5. Cardioversion (unstable patient) – try to administer Amiodarone before cardioversion, makes it more successful according to multiple studies
Polymorphic VT
1. Torsades – has long QT – give Mg Iv
2. Potentially degenerates into V-fib arrest
Long QT syndrome – beta blockers to slow the HR, get AICD

Further reading: https://litfl.com/ventricular-tachycardia-monomorphic-ecg-library/

Congenital Heart Disease – RJ (For reference Chapter 129 Tintinalli)

The Sick Baby
1. THE MISFITS
2. Have a mantra for panic: “Air goes in and out, blood goes round and round. And that’s really it.”
Review Fetal Circulation
1. Fetal circulation bypasses the lungs cuz they don’t work….yet
2. Oxygenated blood from umbilical vein to the fetus
3. Umbilical vein 🡪 Ductus venosus 🡪 IVC
4. R heart 🡪 Ductus arteriosus or the foramen ovale 🡪 L heart 🡪 systemic circulation
5. In utero, R sided circulation predominates
Changes at birth
1. When newborn takes first breath, everything changes
2. Pulmonary vascular resistance falls as lungs fill with air
3. Rush of blood from the RV to the lungs
4. Blood returns from lungs to the L heart, increasing L heart pressure which subsequently closes foramen ovale to minimize shunting
5. Decreased prostaglandin synthesis at birth (due to loss of placenta) and the ductus arteriosus starts to close
6. Because neonates have noncompliant ventricular walls, they can’t really change stroke volume in response to stress, so they will change HR in response to stress 🡪 sinus tachycardia
7. Ductus arteriosus – closed by 15 hours of life
8. Foramen ovale – closed by 3 months of life
Blue Babies – mixing of deoxygenated and oxygenated blood or R to L shunting
1. Tetralogy
2. Transposition
3. Truncus arteriosus
4. Tricuspid atresia
5. Total anomalous pulmonary venous return
Pink babies – pulmonary overload
1. VSD
2. ASD
3. PDA
4. Coarctation
Many of these lesions you will be unable to fix – your job is to stabilize