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AP III > Pericardial Disease & Cardiac Trauma > Flashcards

Pericardial Disease & Cardiac Trauma Flashcards

1
Q

What are the three most common responses to pericardial injury?

A
  1. Acute Pericarditis
  2. Pericardial Effusions
  3. Constrictive Pericarditis
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2
Q

A stiff, fibrous membrane that attaches to the sternum, mediastinum, and diaphragm.
-Helps maintain hearts position in the thoracic cavity

A

Parietal Pericardium

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3
Q

What is the Pericardial Sac?

A

-Space between layers (Visceral and Parietal Pericardium)
-Pericardial fluid lubricates the heart

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4
Q

Which type of Pericarditis occurs after an MI?

A

Dressler’s Syndrome (!!)
Delayed. Weeks to months after a myocardial event
-Often auto-immune response to damage to pericardium

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5
Q

What causes Acute Pericarditis?

A

Mostly caused by viral infection.
-Usually transient and uncomplicated
-Sometimes follows an MI
-1-3 days post transmural MI

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6
Q

What is Acute Benign Pericarditis?

A

-Acute pericarditis in absence of pericardial effusion
-Does NOT alter cardiac function
-Inflammation for unknown reason.

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7
Q

What are the S/Sx of Pericarditis?

A

Chest pain, friction rub, EKG changes

-Chest pain is acute and worsens with inspiration
-Low grade fever with sinus tachycardia
-Friction rub

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8
Q

How do you diagnose Pericarditis?

A

-Symptoms
-EKG changes in 90% of people (diffuse ST segment elevation and PR segment depression and t wave inversions)
-Caused by inflammation of superficial myocardium

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9
Q

What is the treatment for Acute Pericarditis?

A

1) Aspirin or NSAIDs!!!
-Decrease the inflammation
2) Codeine (for pain relief)
3) Colchicine
-Anti-inflammatory used for Gout
4) Steroids frequently cause relapse once discontinued, so used only if other therapy doesn’t work

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10
Q

What is unique about Relapsing Pericarditis?

A

-Can be relapsing or chronic in nature
-Relapses are rarely life threatening (usually don’t effect cardiac function)
-Two types: Incessant or Intermittent

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11
Q

What is Incessant Pericarditis?

A

Pericarditis that relapses when anti-inflammatory drugs are withdrawn (<6weeks).
-Colchicine is associated with less relapse

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12
Q

What is Intermittent Pericarditis?

A

Relapses after prolonged periods without drug treatments (>6weeks)

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13
Q

What is Resistant Pericarditis?

A

Treated with standard therapies (ASA, Prednisone)
-may respond to Immunosuppressant therapy- azathioprine (Imuran)

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14
Q

What is Pericarditis after Cardiac Surgery?

A

-Postcardiotomy syndrome presents as acute pericarditis
-The cause is infective or autoimmune
-Can occur in any patient who had pericardectomy (all CABG, valve, epicardial pacer implantation, and most congenital surgery)
-Incidence of 10-40% of cardiac surgery patients
-Less common with OHT due to immunosuppression
-More common in pediatric patients
-Treat like pericarditis (ASA or NSAIDS)
-Tamponade is possible, but rare (0.1-0.6%)

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15
Q

What is an effusion?

A

An increase in pericardial volume

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16
Q

How much fluid is usually contained in the Pericardial Space?

A

25-50 ccs

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17
Q

What are causes of Acute Pericarditis & Pericardial Effusion?

A

1) Infection: Viral, Bacterial, Fungal, TB
2) Myocardial Infarction (Dressler’s)
3) Trauma or Cardiotomy
4) Metastatic Disease
5) Drugs
6) Mediastinal radiation
7) Systemic Disease - Rheumatoid Arthritis, Lupus, Scleroderma

18
Q

Define Acute Pericardial Effusion

A

Quick changes as small as 50ml can lead to increased pressure (tamponade).

19
Q

Define Chronic Pericardial Effusion

A

-Gradual increases allow for pericardial stretch
-Up to 2 liters can be accumulated

20
Q

How does Cardiac Tamponade develop from pericardial effusion?

A

As pericardial pressure increases, RAP increases in parallel.
-Atrial and ventricular filling is restricted
-SV becomes fixed, so CO becomes rate dependent
-Remember: CO=HR x SV

21
Q

What are the clinical features of cardiac tamponade?

A

-Acute increases of only 40-50 ml of fluid will cause a rapid rise in pressure and tamponade
-Large effusions compress adjacent structures (esophagus, trachea, lung) leading to anorexia, dyspnea, cough, hoarseness, dysphagia
-Kussmaul’s Sign
-Pulsus Paradoxus
-CVP almost always increased above RVP – this is what maintains forward flow and preserves CO
-Activation of the SNS into overdrive (especially tachycardia) is an attempt to maintain CO and patient survival. CO is HR dependant
-Contractility is great, preload is lacking
-Primary problem is reduced ventricular preload, not failure of myocardial contractility
-Eventual “equilibration of pressures”

22
Q

What is Kussmaul’s Sign?

A

JVD during inspiration

23
Q

What is Pulsus Paradoxus?

A

-Decrease in SBP > 10mmHG during inspiration
-Selective impairment of diastolic filling of the LV
-Present in 75% of patients with acute tamponade vs 30% of patients with chronic pericardial effusion.

24
Q

What do Kussmaul’s Sign and Pulsus Paradoxus reflect?

A

Both Kussmaul’s sign and Pulsus paradoxus reflect dyssynchrony or opposing responses of the RV and LV to filling during the respiratory cycle. Also called Ventricular Discordance

25
Q

What is Beck’s Triad?

A

Seen in 1/3 of acute tamponade patients.
-Muffled heart tones
-Distended neck veins
-Hypotension

26
Q

Describe the pathophysiology of Cardiac Tamponade

A

Transmural pressure = the pressure necessary to distend a chamber.
-In tamponade, the intrapericardial pressure (IPP) is elevated, so RAP must increase to maintain a constant transmural pressure
-Compression of the LV prevents diastolic expansion
-Plateau of pressures is caused by the rise in filling pressures so that eventually: IPP=RAP=RVEDP=PAEDP=PAOP=LVEDP

27
Q

What are the causes of Cardiac Tamponade?

A

-Trauma or iatrogenic (cardiac cath lab, PM insertion….)
-Infection
-Neoplastic disease, uremia, connective tissue disorders
-Acute MI
-Postoperative bleeding
-Aortic dissection

28
Q

What is the tx for Cardiac Tamponade?

A

-Pericardiocentesis at the bedside (CVRU)
-Drainage of pericardial fluid through subxiphoid or mini-thorocotomy incision (in the OR)

29
Q

Describe Anesthetic Mgmt of Cardiac Tamponade

A

Fast, Tight, Full
-Goals are: Tachycardia, vasoconstriction, volume
-Volume expanders, catecholamines (Epi, dopamine)
-In severely hypotensive patient pericardiocentesis can be done at bedside with local anesthesia
-Avoid drugs that depress myocardium. Beta blockade= death
-Ketamine is the drug of choice (etomidate is acceptable)
-Arterial BP monitoring (prior to induction)
-Correct metabolic acidosis from the low CO state
-If general anesthetic is used, the ideal plan is to allow patient to spontaneously breathe until tamponade is relieved
-In reality, paralyze and provide fast RR and low TV (“panting respirations”) until tamponade is relieved
-Surgeon is standing scrubbed and ready as patient is induced in the OR (very much as you do an emergent C-section in OB)
-Quick case with quick resolution; ICU post-op for observation
-Be prepared for post op HTN after release of the tamponade
-Especially important in cases of aortic dissection or aneurysm!

30
Q

What is Constrictive Pericarditis?

A

Characterized by a fibrous scarring and adhesions that obliterate the pericardial space, creating a “rigid shell” around the heart

31
Q

What are the causes of Constrictive Pericarditis?

A

Either idiopathic (most common) or the result of previous cardiac surgery, exposure to radiotherapy or TB.
-Most commonly post cardiac surgery
-Sometimes result of infections

32
Q

What are the S/Sx of Constrictive Pericarditis?

A

-“Soft signs” of progressive dyspnea and fatigue (dec. CO), increased CVP, JVD, edema, ascites, and 25% have atrial fibrillation
-Signs mimic RV failure
-Difficult to diagnose, requires TEE, CT or MRI
-Like tamponade except the restriction to ventricular filling occurs only during last 2/3 of diastole
-SV is maintained
-Right ventricular pressure tracing shows “square root sign”
-Increased CVP without other signs of heart disease
-Kussmaul sign and pulsus paradoxus are present

33
Q

What does the “Square Root Sign” indicate?

A

Rapid early diastolic filling, completed filling in mid-diastole (prolonged diastasis), then leveling off (“dip and plateau morphology”).
-The Ventricle is completely filled by the end of the “rapid filling phase”

34
Q

Describe Anesthetic Mgmt of Constrictive Pericarditis

A

-Acute decompensation is not as worrisome as with tamponade
-Still choose agents to maintain HR, volume, contractility (Ketamine, pancuronium)
-Pericardium is adhered to heart: Can be long case with significant blood loss
-Arrhythmias, hypotension and bleeding common

35
Q

Which part of the heart is most likely to be injured in trauma?

A

RV is directly under sternum and more likely to be injured

36
Q

How does Pericardial Trauma occur?

A

Usually MVA’s but blunt deceleration trauma, shearing, soft tissue crushing, injuries to the aorta, pericardial laceration, valve injury.
-Blunt injuries to the chest can result in CV injury
-Wide range of potential severity (even death within minutes)
-Autopsies reveal that pericardial lacerations are common
-Diaphragmatic rupture and bowel evisceration is possible, Heart can fully or partially herniate into abdomen
-Rib fractures on CXR…. may mean heart injuries
-Unexplained dysrhythmias or HOTN after initial trauma resuscitation could be due to pericardial trauma

37
Q

What are the S/Sx of Myocardial Contusion?

A

Chest pain and palpitations

38
Q

How do you diagnose Myocardial Contusion?

A

ECG, TTE, or TEE
-Elevated CK enzymes
-Very non specific (CK released from damaged skeletal muscle

39
Q

Describe treatment and anesthetic mgmt of Myocardial Contusion

A

-Hemodynamic support
-Avoid depressant drugs and prepare to support circulatory and myocardial function

40
Q

What is Commotio Cordis?

A

A syndrome caused by blunt trauma over the heart, and leading to ventricular dysrhythmias (death if untreated).
-A focused mechanical “thud” during the small window of ventricular polarization causes “R on T” phenomenon

41
Q

What is the Tx of Commotio Cordis?

A

Rapid defibrillation with AED

AP III (20 decks)

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