Rounds for Januaryhttp://andrewgeller.weebly.com/

Dissection slides adapted from Power Point Presentations from Carol Choe , Alan Braverman et al , Riya Chacko , and Jason

Finkelstein

BLS vs ALS in Cardiac Resuscitation

• A recent review of Medicare records on patients with cardiac arrests revealed the rate of survival was 13.1 % for BLS and 9.2 % for ALS

• The study reviewed 31,292 ALS cases and 1643 BLS cases and looked at survival to discharge and 90 days post discharge.

• Why , what is the difference between ALS care and BLS care ?

Massachusetts Results With CCR• There are currently 26 communities [600,000

people in these communities] performing CCR in the state of Massachusetts under the waiver.

• Out of the 72 people over the past 4 years, who had witnessed vfib , we have 29 who are now alive and well. 40 %

• As a consequence of these results the state has ended the waiver requirement and made CCR a part of the state treatment protocol.

Time to Arrival of EMS

• In a recent retrospective article from North Carolina with 599 cardiac arrest patients every minute of delay in the arrival of EMS led to a 8 % decrease in the likelihood of a shockable rhythm. Again…7-10 % per minute.

Syncope in Children Based on a Talk by Corey Slovis

• Only a small percentage of children with syncope have cardiac syncope. It may be as low as 1.5 %. Why does this matter ? Cardiac syncope can cause sudden death

• Can a rule help differentiate cardiac syncope from vasovagal syncope ?

• An article by JustinTretter and Rae-Ellen Kavey in 2013 examined this issue .

Cardiac vs Vasovagal

• Around activity in 2/3 of cardiac cases and only 8 % of vasovagal cases

• An abnormal EKG was seen in ¾ of the cardiac cases and was not seen in any of the vasovagal cases

• Abnormal cardiac exam was found in ¼ of the cardiac cases and in none of the vasovagal cases

• A family history of sudden death or cardiac disease was found in 2/5 of the cardiac cases and in ¼ of the vasovagal cases.

Syncope in Children [under 18]

• If the syncope occurs around activity, if there is a family history of cardiac disease, if the EKG is abnormal or if the examination of the heart reveals any abnormality these patients are not likely to have a benign cause of their passing out. They need medical care and evaluation.

How to Live to be Old and Healthy

• Eat more fish• Drink 1-2 glasses of wine or ETOH per day• Consume less saturated fats and fried foods• Eat more nuts• Exercise often

Leisure Running and Mortality

• Does Running affect mortality ? How far to get what benefit ?

• 55,137 patients from Texas with 15 years of follow up [mostly college educated , white and middle class age 18-100 mean age 44 both men and women, excluded prior MI, CVA and CA in JACC 2014

• Divided runners into 5 groups based on time running each week

Runners vs Non Runners left 2 bars are non runners, Blue is all

deaths , Red is cardiac deaths

TAKE HOME MESSAGE

Benefits of Exercise

• The benefits of running overcame the risks from smoking , hypertension , hyperlipidemia , obesity. The average increase in lifespan was 3 years in the study for those who exercised .

• Running increased distances or running at a faster pace did not increase lifespan any greater.

A Minimal Amount of Exercise to Prolong Life , JACC 2014

• Run 10 min /day or walk 15 minutes• Walking is safe and very beneficial• Do something physical• Inactivity is dangerous

Calcium and Cardiac Arrest

Only use Under Specific Circumstances

• Do not routinely use• Consider only if hyperkalemia is likely,

especially in patients with ESRD, renal failure• Look for a wide QRS, peaked T waves and

heart block and bradycardias

The Impact of the Perishock Pause on Survival, ROC study

• 2,006 patients with preshock times• 29 % of patients had a preshock pause > 20

seconds• Median time to shock was 15 seconds

Preshock Pause is the Key

• <10 seconds preshock pause increased survival versus > 20 seconds . Only a 10 second difference!

Does Compressing During Charging the Defibrillator Improve Survival

• 129 patients, in a Canadian study• ½ received compressions during charging

Pre Shock PauseYou can decrease hands off from 15

seconds to 3.5 seconds

Minimize Interruption to CPR before and after shock

• Compressing during charging resulted in a 10 % increase in the compression fraction

• It likely will increase survival as well. • This must be a part of CPR training. Hands off

for only a couple of seconds while the shock is occurring.

• Be ready to shock before you cease compressions, stop CPR and shock at the same time.

Precordial ThumpsOnly 16.5 % with any response,4.9 %

ROSC, 9.7 % deteriorate,1.9 % VF

Thumps

• It rarely works and ROSC is seen in only 5 % of cases. If there is no defibrillator available go ahead…. Otherwise shock the patient.

Long Resuscitation Times in Cardiac Arrest

• Even in PEA and in Asystole a short resuscitation time is a marker for possible survival

Good Neuro Outcome

Good Neuro Outcomes

Short Resuscitation Times May Reflect Survivability for Asystole and PEA

PreHospital EKG’s Do They Matter

Prehospital ECG vs No ECG Mortalityred is with ECG , blue is without, left bars

are STEMI, right are Non STEMI

Call To Medical Control with STEMI

Call to Medical Control [Continued]

Why Does the Call Work to Decrease Mortality ?

Calling in 12 Leads , it matters

Beta Blockers in Acute MI

• There is some accumulating data that suggests that IV usage in acute MI may decrease infarct size and mortality. We are not yet ready for prime time use , but be aware . Certainly if a patient is tachycardic with an anterior or lateral MI a call to medical control is wise.

LUCAS

• Lund University Cardiac Arrest System• We recently discussed the multitude of studies that

clearly document that the device is NOT BETTER than your chest compressions. You need to do 4 rounds , 8 minutes of chest compressions prior to placing the LUCAS.

• A recent article reveals perhaps why. The LUCAS was placed correctly but was ineffective [no pulses] . There have been reports of hemopericardium, liver lacerations, and trauma to the right ventricle impairing blood flow.

Cases

• 1.ETCO2 • 2.Rapid Afib and chest pain• 3. Aortic Dissection• 4.Pulmonary Edema• 5.Multiple Trauma

ETCO2

• Extreme values , HIGH or LOW must be considered red flags

• Our Recent Case

A patient with rapid afib and chest pain

• Case

Aortic Dissection

• 49 y/o man with acute onset chest pain from Mansfield [Westwood case]

Overview• Incidence 3/100,000 per year• Men are affected twice as commonly as women• 78% have chronic hypertension• Peak for proximal dissection 50-55, distal 60-70• At least 20% die before arriving at the hospital• Incidence of aortic dissection is at least 2000 new cases per year• Mortality in the first 48 hours is 1% per hour

– Early diagnosis is essential

Pathophysiology

• The chief predisposing factor is degeneration of collagen and elastin in the aortic intima media

• Blood passes through the tear into the aortic media, separating the media from the intima and creating a false lumen

• Dissection can occur both distal and proximal to the tear

PATHOGENESIS

1. Intimal Tear as Primary Event

Propagation of dissecting hematoma within media.

2. Intramural hemorrhage due to rupture

of vasa vasorum in a defective media

- Intimal tear is a secondary event.

- Propagation of cleavage plane by

pulsatile force of blood.

Pathophysiology

• Medial degeneration• Intimal tear

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Aortic Dissection

Jheuser, Wikimedia Commons

Classification

• The Stanford system– Type A

• All dissections involving the ascending aorta

– Type B• All other dissections regardless of the site of the primary intimal

tear

– Ascending aortic dissections are twice as common as descending

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Aortic Dissection

Type A dissection often begins just above the coronary arteries where the aorta is the largest and thinnest. Always a surgical emergency.

Type B dissection involves the distal aorta. Medically managed.

Predisposing factors

• Age, 60-80 yrs old• Long standing history of hypertension

– 80% of cases have co-existing HTN• Takayasu’s arteritis• Giant cell arteritis• Syphilis• Collagen disorders

– Marfan syndrome (6-9% of aortic dissections)– Ehlers-Danlos syndrome

Other Risk Factors• Congenital Cardiac Anomalies

– Bicuspid aortic valve (7-14% of cases)– Coarctation of the aorta

• Cocaine– Abrupt HTN, due to catecholamine release

• Trauma

• Pregnancy (50% of dissections in women <40 yrs)

• Iatrogenic (cardiac cath, IABP, cardiac surgery, s/p valve replacement)

MARFAN SYNDROME

FEATURES• Very long arms, fingers, toes

• Pigeon breast or severe pectus carinatum

• Moderate or severe scoliosis

• Dislocated lenses

• Family history of the Marfan syndrome

PROLONGING LIFE

• Correct Diagnosis

• Medical Management

• Surgical Repair

Clinical Symptoms• Severe, sharp, “tearing” posterior chest pain or back pain

(occurs in 74-90% of pts)

– Pain may be associated with syncope, CVA, MI, or CHF– Painless dissection relatively uncommon

• Chest pain is more common with Type A dissections

• Back or abdominal pain is more common with Type B dissections

Physical Examination

Acutely ill• Hypertension in 80 % [due to catechols and renal

ischemia]• Pulse deficit [60 % in ascending aorta cases]

Weak or absent carotid, brachial, or femoral pulses – these patients have a higher rate of mortality

• Acute Aortic Insufficiency [50 % of ascending aortic dissections]– Diastolic decrescendo murmur– Best heard along the right sternal border

COMPLICATIONS1. Rupture through outer wall of false channel

*typically directly across from entry tear

- pericardial tamponade- mediastinal or pleural rupture- exsanguination

2. Acute Aortic Regurgitation*50% of ascending dissections

- medial split undermines support of aortic valve- may lead to severe CHF

COMPLICATIONS3. Branch Vessel Compromise

- extension of dissection into a branch vessel- compression of orifice by intimal flap

Clinical Scenarios- stroke- paraplegia- HTN-renal failure- visceral ischemia- MI

4. Aneurysmal Dilation and Subsequent Rupture

CLINICAL FEATURES

Most important factor

leading to a correct diagnosis is

a high clinical suspicion!

CLINICAL FEATURES

1. Sudden Onset Severe Pain• May or may not be catastrophic• Ripping, tearing• Migratory• Never experienced before• Restless, sense of doom

2. Look for underlying connective tissue disorder

3. Hypertension (especially moderate or severe)

or known aortic aneurysm

Clinical Signs

• Involvement of the descending aorta– Splanchnic ischemia– Renal insufficiency– Lower extremity ischemia– Spinal cord ischemia

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Signs/Symptoms

Sudden onset of sharp, tearing pain radiating to the back.

Any neurologic complaints associated with pain.

Syncope. Acute CHF. Other vague non-specific symptoms.

61

Aortic Dissection

However, landmark study (International Registry of Aortic Dissection) found: pulse deficit: 15 % aortic murmur: 31.6 % normal chest x-ray: 12 % absence of mediastinal widening: 34 % syncope: 12 % painless: 2.2%

PAIN CHARACTERISTICS

SEVERE PAIN (90%)

• Most Severe at OnsetAnterior Pain: Proximal DissectionPosterior Pain: Distal DissectionMigratory Pain

• Pain in these locations usually due to other more common disorders (MI, pneumonia, pleurisy, pulmonary embolism, pneumothorax, ulcer, cholecystitis, pancreatitis)

• Must consider aortic dissection in cases without other confirmed cause of pain.

Treatment

• Acute dissections involving the ascending aorta are considered surgical emergencies

• Dissections confined to the descending aorta are treated medically

– Unless patient demonstrates continued hemorrhage into the pleural or retroperitoneal space

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Aortic Dissection Treatment

Medical: Morphine Anxiolytics Afterload reduction and β-blockade

Goal SBP 100-110mmHg Goal HR 50-60bpm

Surgical

Surgical Treatment• Operative mortality 5-10%,

higher if complications present

• Goal is to replace the ORIGIN of dissection, not entire involved segment

• Mortality of surgery higher than medical therapy in Type B dissections

• 15% treated surgically require a 2nd operation

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Aortic Dissection

Mortality 1-2% per HOUR for type A dissections. 75% within 2 weeks, 90% mortality at 30

days. With successful initial therapy:

5-year survival rate is 75% 10-year survival rate (if surgically repaired) is

40%-60%.

Pulmonary Edema Patient

• Nice Assessment and care

Multiple Trauma

• Well done, I/O, Lido , Fentanyl IN , permissive Hypotension and a 250 ml bolus once only