Unit 4

what part of the heart is MC injury in trauma

the Right ventricle due to anterior position 43%

penterating truama catagories

• low velocity- ex knife stab

• medium -

• high - ex rifle or shrapnel injury

primary presentation of cardiac truama

tamponade and hemorrhage, tamponade decreases survival rate

tamponade occurs

when a clot and surrounding pericardial fat partially seals the defect

what if the diagnoist gold standard

subxiphoid window

tx of penetrating cardiac trauma

depends to the stability of the pt, most wounds are repaired through a left thoracotomy

when there is a blunt trauma

might not be able to tell about cardiac injury get and ECG, cardiac markers, holter, CT, or MRI

all pt who have significant mechanism on injury should have a

screening ECG

why are in v tachy and fib uncommon in hospital

cause most do not survive

how to treat trama

treat underlying cause, arrythmias are treated for rate control and suppression of ectopy, hemodynamic instability a definitive echo should be obtained. when there is severe ventricular dysfunction and low cardiac output, inotropic support to aviod a primary ischemic event

pericarditis

inflammation of the pericardium may be due to systemic dx, neoplasm, radiation, drug toxicity, hemopericardium, post cardiac surgery

types of pericarditis

• acute less than 4 weeks

• incessant less than 3 months

• recurrent: after sx free interval

• chronic: greater than three months

acute pericarditis

can be infecious and non infecious

infectious pericarditis

1. viral is MC- enterovirus, coxsackie and echo virus

2. purulent- most common S. aures, s. pneumoniae, other streptococci caused by hematogenous spread or from a close organ or complication from penetrating injury

3. TB

non infectious acute pericarditis

1. uremic, complication of CKD

2. neoplastic

3. early post MI typically occurs within several days of a transmural MI due to inflammation adjacent to myocardial necrosis

4. dressler syndrome: delayed immune-medicated pericarditis occurs weeks to months after MI

6. radiation, autoimmune, drug induced, injury

know the different between dressler and early post MI

sx of pericarditis

• substernal cp: usually sharp and pleuritic that improves with sitting upright, worsen supine and can radiate to neck, shoulder, back, or epigastrium

• friction rub if there is no increase pericardial fluid

what does pericarditis sx require

1. two of the following:

• sharp pleuritic pain

• pericardial friction rub

• consistent changed on ECG

• new or worsening pericardial effusion

what sx occurs pericardial effusion develops in pericardidits

dyspnea, rapid respiratory rate

what sx occurs pericardial temponade develops in pericardidits

pulsus paradoxus, JVD

pericarditis TX

• viral or idiopathic is self limiting used NSAID and colchicine (for 3 months) can sue PPI protection for the high dose NSAID

• if it purulent do an emergency surgical drainage and IV abx

• if TB do regimen

make sure they rest from physical activity

pericardial effusions what should you look for

1. determine to size

• small less than 10mm

• mod: 10-20mm

• severe: greater than 20mm/ 2cm much greater risk for developing tamponade

pericardial effusion to tamponade

is not dependent on size the rate of fluid accumulation determines hemodynamically consequences more than the size alone a rapidly developing smaller effusion can still cause a tamponade

what can echo differentiate on pericardial effusion

differentiate circumferential from loculated effusion

sx for effusion/tamponade

• dyspnea and tachy

• pleuritic CP

• cough/ hiccups

• hoarseness

• syncope

sx are most common associated with rapidly accumulating effusion

PE findings for pleural effusion and tamponade

Normal physical exam is most common unless cardiac tamponade is present

•     Tachycardia can be present without tamponade

•     Hypotension

•     Muffled heart sounds

•     Elevated JVP

•     Pulsus paradoxus

•Electrical alternans

what sx is most concerning for tamponade

syncope

Beck Triad

• hypotension

• JVD

• muffled heart tones

may also have pulsus paradoxus and electical alternans

diagnostics for effusion/ tamponade

slide 29

hallmark finding for effusion on cxr

water bottle configuration

pericarditis

pericarditis

plerual effusion

pericardial treatment

Pain control with:

• NSAIDS and colchicine 

• Treat underlying cause

• Routine diagnostic pericardiocentesis and/or pericardial biopsy are not indicated unless high index of suspicion for a bacterial, fungal, or protozoal infectious etiology or suspicion of cancer.

Pericardiocentesis should be performed:

• Cardiac tamponade 

• Large pericardial effusions

constrictive pericarditis

when a thickened fibrotic pericardium, impedes normal diastolic filling and produces chronically elevated venous pressure

what is MC od constrictive pericarditis

TB in undeveloped countries

echo distinctive finding for constrictive pericarditis

septal bounce that reflects the early filling

sx of con peri

•Slowly progressive dyspnea

•Fatigue, and weakness.

•Chronic edema

•Hepatic congestion ascites

oAscites often seems out of proportion to the degree of peripheral edema.

•Elevated jugular venous pressure

•Kussmaul sign—a failure of the JVP to fall with inspiration

•The apex may actually retract with systole and a pericardial “knock” may be heard in early diastole. 

•Atrial fibrillation is common.

what imaging can you do for constrictive pericarditis

• cxr: can show norm or cardiomegaly

• echo shows septal bounce

• cardiac CT or MRI

• • Invasive hemodynamics are particularly useful when the diagnosis remains uncertain or when distinguishing constriction from restriction..

  •Cath will help differentiate constrictive pericarditis from a restrictive cardiomyopathy

tx

§If inflammatory treat with anti-inflammatory medications

§  Diuretics for venous congestion and edema

§  Diuretics for symptomatic venous congestion — use cautiously to avoid excessive preload reduction., use loop diuretics (oral torsemide or bumetanide, if bowel edema is suspected or intravenous furosemide), thiazides, and aldosterone antagonists

§  If diuretics are no longer working: Surgical pericardiectomy.

oPericardiectomy removes only the pericardium between the phrenic nerve pathways

§  Morbidity and mortality after pericardiectomy are high (up to 15%) 

  Poor prognostic predictors include prior radiation, kidney dysfunction, higher pulmonary systolic pressures, abnormal LV systolic function, a lower serum sodium level, liver dysfunction, and older age

how to differentiate cardiomyopathy and constructive pericarditis

 Restrictive Cardiomyopathy:

◦Diastolic dysfunction → ventricle can’t relax → high filling pressures.

◦Systolic function often preserved until late.

 Pericarditis:

◦Thickened pericardium → abrupt stop in diastolic filling (“square root sign” on catheterization).

◦Myocardial contractility usually normal.

Presentation

Both can present with:

•Right heart failure signs (JVD, peripheral edema, ascites)

•Kussmaul’s sign (↑ JVP with inspiration)

•Pericardial knock (in pericarditis)

jones criteria

• to determine rheumatic fever

• we used revised jones criteria

JONES= joint pain, oh heart (carditis), nodules, erythema marginatum, sydham chorea

infective endocarditis

usually bacterial that cause inflammation of the endocardium and the valves.

I endocarditis usually involves

• mitral valve and aortic valve MC

• TV is most common with IV drug use

usually involves a valve

acute v subacute endocarditis

•Acute = S. aureus + aggressive + can attack normal valve

Subacute = viridans strep + indolent + usually abnormal valve

acute IE

• Infection of previously normal heart valve by highly virulent organism (staphylococcus aureus) that rapidly produces necrotizing and destructive lesions

• Death can occur within days to weeks despite appropriate treatment with antibiotics and surgery 

subacute infective endocarditis

• Infection by organisms of lower virulence (Streptococci viridans) that causes insidious infections of damaged/deformed valves (rheumatic heart disease, congenital bicuspid aortic valve, calcified/degenerative changes) with over all less destruction

• Disease has course of weeks to months and cure can be achieved with antibiotics 

IV drug user usually affects

the tricuspid valve

what destroys the cardiac tissue in infecious endo

the formation of vegetations

IE pathogenesis

1. Endocardial Injury

•Turbulent blood flow from an abnormal valve

•Injury from an intracardiac device/catheter

2. Platelets + Fibrin Deposit

•A small sterile platelet-fibrin deposit forms on the injured surface

3. Transient Bacteremia

•Bacteria enter the bloodstream

•Organisms adhere to the platelet-fibrin surface

4. Vegetation Forms

•Bacteria multiply within the platelet-fibrin material

•Vegetation can cause valve destruction, embolization, and persistent infection

•

Important Exception

•S. aureus is highly virulent and can infect a previously normal valve.

Valve injury → Platelet/Fibrin → Bacteremia → Vegetation

why are the predisposing factor

causes of the IE the bugs for native

•S. aureus

•Streptococci (S. viridans), enterococcus (S. faecalis)

A more rare cause is the gram negative HACEK group

causes of the IE the bugs for IV

•S. aureus (MCC)

•Enterococci, streptococci

•Other organisms: Gram negative (Pseudomonas), Fungi (Candida)

causes of the IE the bugs for prosthetic valve

•Early (<12 months): nosocomial infections: Staphylococci – S. aureus,  S. epidermidis, gram-negative and fungi (Candida).

•Late (>12 months postop)- similar to NVE (SE for early surgery)

figure out

fungal IE

common with heroin that is black tarr cause they have to dissolve in lemon acid

what are risk factors for native valve endocarditis

Mitral valve

•Mitral valve prolapse, mitral regurgitation

•Rheumatic heart disease (now less common)

 Aortic valve

•Calcific aortic stenosis (60-70 year old)

•Bicuspid aortic valve (50-60 year old)

•Rheumatic heart disease (now less common)

 Tricuspid valve (IV drug use)

 Ventricular septal defects (and other congenital heart defects)

CM of IE

• fever MC sx with possible chills, rigors, night

• heart murmur hear in nearly all but might not be heard in right sides (IV drugs)

• fatigue, arthralgia

• anemia

• left sided valve lesions can lead to regurg and new onset of left sided heart failure

stroke pt with fever

ENDOCARDITIS until proven otherwise the cause of the embolism can be broken off parts of the vegetation

new or acute aortic regurg is

IE until proven otherwise

CM of IE

How to dx IE

1. blood culture: obtain 3 from separate venipuncture site before abx when the pt is stable should be more than 10mL

2. echo (TTE is first line can to TEE when need investigate more

3. can looks for septic emboli

• testing for immune complex deposition

• other labs 1.may show anemia, leukocytosis, elevated ESR/CRP

what criteria is used of IE

the Duke must know

tx of IE

1.Multidisciplinary team: Infectious Disease, Cardiology, Cardiothoracic surgery

2.Draw blood culture before giving any antibiotics!!

3.Start empiric IV therapy promptly in acutely ill patients.

4.Tailor therapy to organism, susceptibilities, native vs prosthetic valve and local resistance.

5.Treatment is usually prolonged IV antimicrobial therapy.

6.IV antibiotics:

•2-6 weeks for native valve

• ≥6 weeks for prosthetic valve

7.Consider early surgery when indicated (usually 7-10 days if not better on abx)

what imaging to look for septic emboli

: Chest Xray or chest CTA, MRI of brain, heart, spine, abdominal CT or ultrasound

how to test for immune complex deposition

urinalysis, BMP, rheumatoid factor

empiric tx for IE

Empiric treatment with antibiotics Only if severe/acute.  You want to cover for most common organisms (staph, strep, enterococcus)

Best to consult ID before starting empiric

•NVE(native valve): Vancomycin + ceftriaxone (Cipro if severe PCN allergy)

•PVE: vancomycin + cefepime or piperacillin-tazobactam with antipseudomonal activity

These will change frequently

do you need to use anticoagulation for IE

• not need for native

• CAN NOT use if septic can cause intracerebral hemorrhage

• if they have mechanical valve they will usually get anticoag

when should prophylaxis tx be given

 1. Prosthetic cardiac valve (includes bioprosthetic and mechanical)

 2. Previous infective endocarditis

 3. Congenital heart disease (CHD)

◦Unrepaired cyanotic CHD, including palliative shunts and conduits

◦Completely repaired CHDs with prosthetic material or device during the first 6 months

◦Repaired CHD with residual defects at the site or adjacent to the site of the prosthetic patch or device

 4. Cardiac transplantation recipients in whom cardiac valvulopathy develops

treatment for surgery prophylaxis (like what kind of procedure needs prophylaxis)

•Dental procedures involving manipulation of gingival tissue, periapical area, or perforation of the oral mucosa. (Not for minor procedures)

•Respiratory tract procedures with incision/biopsy of mucosa (e.g., tonsillectomy, adenoidectomy).

•Procedures treating infected skin or musculoskeletal tissue (e.g., abscess drainage), using appropriate antibiotics against staph and β-hemolytic strep.

when is surgery needed for IE

•Acute heart failure unresponsive to medical therapy

•No response to antimicrobial therapy after 7-10 days (persistent fevers, + blood cultures)

•>1 systemic embolus

•Perivalvular leak or myocardial abscess

•Severe valve regurgitation and mobile vegetation > 10 mm

You are doing

great

ambulatory monitoring depends on

frequency of sx

when to do holter

sx that are hours to weeks just records will not be able to react

when to get event/ mobile cardiac telemetry

intermittent sx that are over weeks (they can press a button to get immediate help?)

when to use implantable cardiac monitor (loop recorder)

infrequent or unexplained events - long term monitoring - does not do anything about the rhythm unless put with pacemaker

what can wearable devices detect

possible a fib but cannot establish dx, abnormal findings needs ECG confirmation, performance varies by device and population

what is an EP study

• an invasive catheter-based test that maps the heart electrical activity

• electrode catheters are advanced through vein into the heart and records electrical signals from inside the heart

What does an EP study mmonitor

•Location and mechanism of an arrhythmia

•SA and AV node/conduction system function when clinically indicated

•Presence of an accessory pathway (e.g., WPW)

•Ability to induce an arrhythmia under controlled conditions

when to use EP study

•Recurrent or unexplained SVT

•Suspected AVNRT or AVRT/WPW

•Selected wide-complex tachycardias

•When catheter ablation is being considered

what is catheter ablation

•Minimally invasive procedure used to eliminate abnormal electrical pathways or arrhythmia-producing tissue

•An EP study first maps/localizes the abnormal electrical activity

•Radiofrequency energy, cryotherapy, or other energy sources are then used to ablate the target tissue

common use of cather ablation

•AVNRT → ablate the slow pathway

•AVRT/WPW → ablate the accessory pathway

•Typical atrial flutter → ablate the reentry circuit

•Focal atrial tachycardia → ablate the ectopic focus

•Atrial fibrillation → usually involves pulmonary vein isolation (PVI)

•Ventricular tachycardia → may be used in selected/recurrent VT

what can catheter ablation do for AVNRT

ablate the slow pathway

catheter ablation for AVRT/WPW

ablate the accessory pathway

what will catheter ablation for focal atrial tachy

ablate the ectopic focus

what will catheter ablation do for ventricular tachy

may be used in selected/ recurrent VT

what testing can fing the electrical problem

EP study finds and maps the electrical problem

what can treat electrical problems

catheter ablation

what are the mechanism of arrhythmias

1. abnormal automaticity

2. abnorm impulse conduction

3. reentry

4. triggered activity

why do arrhythmias happen

the impulse starts abnormally, travels abnormally, gets caught in a loop or triggers an extra beat

abnormal automaticity

• cardiac cells fire when they should not

• creates and abnormal/ ectopic pacemakers

ex are PA, PCV, focal tachycardia

abnormal impulse conduction

•Electrical impulse is delayed or blocked

•Examples: AV blocks, bundle branch blocks

reentry

•Electrical impulse travels in a continuous loop, repeatedly reactivating tissue

•Major mechanism of many tachyarrhythmias

•Examples: AVNRT, AVRT/WPW, atrial flutter

triggered activity

•An extra impulse occurs after the normal action potential

•Often associated with electrolyte abnormalities, medications, or prolonged QT

•Example: torsades de pointes

No clear P waves + irregularly irregular

AF

sawtooth flutter waves

a flutter

Regular narrow-complex tachycardia

think SVT a type of AVNRT

Wide-complex tachycardia

VT first, with structural heart dx

Progressively longer PR → dropped QRS

mobitz 1

Fixed PR + sudden dropped QRSs

MObitz II

P waves and QRS march independently

complete heart block