Myocardial and Pericardial Disease Flashcards

1
Q

layers of the heart muscle wall and covers

A

inner most
- endocardium
- myocardium (muscle)
- pericardium –> the visceral touches the heart, then theres the pericardial sac, then the parietal)

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2
Q

Myocarditis
- causes
- patho

A

itis = inflammation of the myocardium
Causes
- most common: viral infections : coxsackie, echovirus
- post viral immune mediated cardiac damage occurs
- bacterial: MRSA, strep pyogenes, viridans , rickettsial disease from ticks
- fungal (histo & coccidio)
- parasitic: chagas, toxoplasm.
- toxic: alcohol, chemo
- autoimmune: SLE, RA, ucerative colitis
- systemic: uremia (from kideny failure), hypothyroid
- meds!!: clozapine, INH, phenytoin, ABX.

Patho
- body triggers a severe immune response to teh above issue (usually a viral) which damages the myocytes and results in even more inflammation
- the body will result in: fixing the inflammation and the infection or will fiberosis and scaring of the heart leading to issues
- some genetic component to who develops myocarditis, and who recovers vs. who remains chronic

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3
Q

Myocarditis
- clinical manifestation (3 bigs)
- labs & diagnosis (lots, gold standard)
- treatment

A

Clinical Manifestaions depend on the preceeding factor
- Viral: pt. will complain of viral prodrome (fever, chills, HA, runny nose, sore thorat) or sick contact (kids)

  • Heart Failure: the chronic nature of the disease –> result in redcued ability to properly pump systolic due to the inflammation –> short of breath, chest pain, DOE, tachycardic and pena
    if HF & severe: evidence of SHOCK!! and hemodynamic compromise
  • Concurrent Pericarditis: spreads from the pericardium to the myocardium: fever, chest pain, pleural friction rub (pericardial effusion)

Labs & Diagnosis
- CBC: elevated WBC (infection)
- BMP: see organ dysfunction
- ESR/CRP: systemic disease processes
- Cardiac Enzymes: trops and CK-MB
- culutres: for infection
- EKG: sinuse tachycardia because infection increases HR trying to pump more to get there and help
- EKG: can see signs of arrythmias because problems in the electrica path due to infection
- EKG: if pericarditis: PR depression, ST elevation
- CXR: cardiomegaly
- gold standard dx. tool: endomyocardial bipopsy :shows infiltrates wiht lymphocytes nad necrosis
- TTE/TEE: shows ventrcular dysfunction: reduced EF
- Cardica MRI: most important: detects if its local or diffuse infection

Treatment
- mainstain of treatment is supportive measures, treat underlying cause and reduce inflammation
- Viral: self limting
- bacteriak: ABX
- tick: ceftriaxone/doxy.
- ETOH/drug: stop them
- autoimmune: contorl

… progresses to dilated cardiomyopathy with systolic HF
- treat like HF: ACE/ARB/ARNI, BB, MRA, SGLT2i, dieuretics

…in cardiogenic shock: inotropes (milirone, dubutamine)

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4
Q

3 categories of pericardial diseases

A
  1. pericarditis: inflammation of the pericaridum
  2. pericardial effusion & cardiac tamponade: fluid in the pericardial sac – to the point which it impacts heart beat (tamponade)
  3. constrictive pericarditis: decreased compliance of the pericardium
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5
Q

Pericarditis
- causes/etiology
- clinical manifestations

A

acute pericarditis: fibrinous inflammation of the pericardium

causes
- most commone is idopathic: viral related to some extent
- second most common: Viral (enteroviruses: echovirus and coxsackie)
- Dressler’s Syndrome
- bacterial (TB), fungal
- Autoimmune
- radiation or chemo related
- drugs (procanamide, INH)
- malignancy

Clinical Manifestations
-the 5 Ps of Pericarditis : Chest pain that is…
1. Plueritic
2. Postural (worsen when laying down, better leaning forward) worsen pain in some postions
3. Persistent Pain
4. Pericardial Friction Rub!! : best heard at left sternal boarder, end expiration while upright/leadning forward

  • can have referred neck, back or shoulder pain
  • cough: irritated lining imapcts lungs
  • palpations: due to fevers, inflammation and poor CO
  • HF like symptoms: swelling of LE, ankles and legs with SOB
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6
Q

What is Dressler’s Syndrome

A

post-MI syndrome: pericarditis 2-4 weeks after an MI or cardiac event

  • inflammation of the pericardium as a result of the body’s delayed immune response to the ischmeic or damange that has happened
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7
Q

Pericarditis
- labs
- diagnosis
- treatment

differentiat PERICARD for STEMI

A

Labs and Dx.
- inflammatory markers: CRP, ESR
- Cardiac enzymes: will be elevated
- EKG: will should diffuse ST elevation in precordial leads (V1-V6) , can see PR depression, Knuckle sign!!: avR = PR elevation with ST depression
- CXR: cardiomeg.
- TTE: most helpful for seeing the pericarditis and understanding if therese tamponade or effusion

how to differentiate fromSTEMI?
- difificult: pericarditis will have diffuse ST elevation - stemi might be in jsut one area
- need to get a GOOD hx. of symptoms: stabbing or sharp pain > crushing

Treatment : relieve pain and inflammation
- 1st line: Asprin NSAIDS
- 2nd: colchicine (+ asprin)
- 3rd: steriods if refractory

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8
Q

Pericardial Effusion
- types of effusions
- causes
- clinical findings
- diagnosis

A

types of effusion
transudative: more volume overload in nature: not inflammatory (think liver failure, heart failure, renal failure)

exudative: inflammatory or malignant in nature (think tumor, viral/bacterial/fungal)

hemmorhagic: trauma or ruptured aneurysm

Causes
- same as what triggers pericarditis viral, inflammatory, autoimmune, trauma, etc.

Clinical Findings
- MUFFLED HEART SOUNDS: because fluid is blocking transmission

Diagnosis
- EKG: low voltage QRS because fluid & see electrical alternans
- TTE: fluid seen without any hemodynamic compromise

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9
Q

Cardiac Tamponade
- what is it
- specifics of timing
- clinical manifestations
- diagnosis and treatment

A

so much fluid in pericardium that it impacts the hearts ability to beat
DO NOT MISS: MEDICAL EMERGENCY!!!

results in…
- reduced filling of the heart
- decreased output
- hemodynamic instability

Timing
- normally, there is some fluid in the cavitiy, when a pt. has chornic disease: there could be more (but the rate at which it fills is slow – so it doesnt cause hemodynaic issues)
- in tamponade: the rate of filling is RAPID!!! and this rapid filling is what causes hemodynamic instability
- rate > amount

Clinical Manifestations
- shock: hypotensions, cool extremities, AMS, reflex tachy
- BECKS TRIAD: JVP, muffled heart sounds & hypotension
- ** Pulsus paradoxus: > 10 mmHg drop in systolic when you breath in!!!**

Diagnosis & Treatment
- POCUS can make dx. or a formal TTE
- echo: shows more info too
- Treatmet: pericardiocentesis, pericardial window (remove rib if reoccurance)

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10
Q

what are cardiomyopathies
what do they result in
what do they eventually lead to

three categories of cardiomyopathies

A
  • group of heart muscle tissue disorders
  • these result in abnormal heart structure and function, either ventricualr hypertrophy (big) or dilation (flappy)
  • they eventually lead to a decrease in cardiac function and inability to pump blood effectively —- heart failure can be a result of these over time

categories
1. genetic (HOCM)
2. mixed (DCM, restirtive CM)
3. acquire (frmo infection, stress, etc.)

think… thin walls (dialted) thick walls (HOCM), stiff walls (restrictive)

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11
Q

Dilated Cardiomyopathy
- etiology
- patho
- clinical manifestaions

A

most common type of cardiomyopathy
- ventricualr wall dilation & thinning leads to LV systolic dysfunction (so then it cant pump out)
- males > females, 20-60 years old

Etiology
- idiopathic: assumed viral
- genetic: familial or mutations
- infectious: viral myocarditis of enterovirus
- toxins: ETOH, cocaine
- chemo, pregnancy, autoimmune, metabolic (thyroid), stress induced takotsubo

Patho
- a dilated, weak heart = decreased systolic function
- inability to squeeze by the ventricle –> reduced cardiac output
- LV dilation: resutl of direct myocyte damage
- fiberosis/scarring, damage, remodeling of cells, loss of the integrity of the wall – structural diseas

Clinical Manifestations
- SYSTOLIC HEART DYSFUNCTION: right or left sided
- reduced ejection fraction < 40%
- S3 heart sound (because a dilated ventricle)
- laterally displaced PMI
- MR/TR because they pull the valves

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12
Q

Dilated Cardiomyopathy
- diagnosis and treatmetn

A

Labs
EKG
- sinuse tachycardia
- LV/RV hyertrophy: large QRS complexes
- arrythmias possile

XRAY
- cardiomegaly
- signs of edema: PE, kerly B lines & backflow of fluid

TTE
- see reduced EF < 40%
- left dilation and large ventricles

Treatment
- dictated by underlying causes–> but heart failure treatment systolic
- ACE/ARB/ARNi
- BB
- MRA
- SGLT2i
- Diuretics
- arrythmias : treat with ICD/antiarrythmic

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13
Q

Restrictive Cardiomyopathy
- etiology
- patho
- clincial signs
- diagnosis and treatment

A

imparied Diastolic function: ventricles are stiff & they can’t fill
3 specific points to a restritive cardiomyopathy
1. impaired diastolic function (stiff walls that cant fill, but pump is ok)
2. normal or preserved ventricualr wall thickness (not huge!)
3. normal or preserved EF (mild reduction)

Etiology
- idopathic
- infiltarvie amyloidosis , sarcoidosis, hemochromatosis
- inflamma, autoimmune, environmental

Patho
- infiltrative diseaes: deposit their buildup leading to fiberosis and scarring (but doesnt get big or as big as HOCM)
- the depoists make fiberosis, cant fill as well, reduced CO

Clinical Signs right side: restrictive (R-R)
- RIGHT SIDED HEART FAILURE MOST COMMONLY ASSOCIATED WITH DIASTOLIC DYSFUNCTION: impaired RV filling backs up to the venous system
- S4 heart sound: the blood hitting a stiff wall
- Kussmaul sign: JVP increased with inspiration

Diagnosis
echo:
- ventricles wont be dialted, but the ATRIA will be because the blood is flowing back since ventricles so stiff
- see diastolic dysfunction (inability to fill)
- amyloid: bright speckled myocardium

Treatment
- treat underlying cause
- amyloid: chemo
- ** often treat the HF: right sided diastlic failure with preserved ejection fraction: with MRA and low dose dieurtics: but careful as they are preload dependent**

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14
Q

Hypertrophic Cardiomyopathy
- etiology
- patho
- clinical signs
- diagnosis and treatment

A

chaacterized by…
- THICKENED ventricular walls and septum with small left ventricle
- genetic disease

Etiology
- Obstructive: thickened wall that obstructs outflow HOCM
- Nonobstructive: thickened wall but NO blockage of flow out of the heart

Patho
- LV/RV hypertrophy: thick
- reduces the ability to fill - diastolic issue
- HOCM: subaortic outflow obstruction: the septum is big!!! so there is Systolic anterior motion of mitral valve to try to push blood through

Clinical
- asymptomatic
- HOCM: can have some symptoms due to outflow issue
- sudden cardiac death athletes
- dyspnea is most common complaint
- chest pain, arrythmias

HOCM: SYSTOLIC MURMUR
- HARSH: systolic crescendo-decrscendo murmur
- squat down: gets QUIET (when you increase venous return)
- stand up: gets LOUD (decreased venous return)

Diagnosis
echo: see ASYMMETRICAL wall thickness
- septal wall > 15mm
- outflow obstruction
- SAM of mitral valve
- distolic disfunction

Treatment
- first line: BETA BLOCKERS: to increase the diastolic filling time by slowing HR
- CCBs, HF meds too
- surgical treatment: septal myectomy or alcohol ablation
- ICD: for those prone to arrythmias as a result
- transplant

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15
Q

ENDOcarditis
- what valve MC affected
- except who
- patho
- etiology
- types of endocarditis

A

Infective Endocarditis
- result of bacteremia: most commonely mitral valve
- unless IVDU: tricuspid!!

mitral > aortic> tricuspid > pulmonic

Types
- Acute bacterial: normal valves infected with staph
- subacute bacterial: abnormal valves affecte with strep
- endocarditis IVDU: MRSA, pseudo, candia in tricuspid
- prosthetic valve: < 60 days post transplant

Patho
- damanged heart valves: sticky surface
- bacteria attach to devices, catheters, chronic inflammation creates diease
- bactermia: from IV drugs, CVC, PICC, GI, dental
- valves have no blood supply, cant immune respond

Causes
- STAPH (MRSA) acute
- streph (subacute) – viridans!!
- entercocci (gut)
- HACEK organisms: h flu, actino, cardio, eikinell, kling

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16
Q

Endocarditis
clinical manifestations
diagnosis
treatment

prophylatic tx.

A

clinical
- FEVER!!!
- janeway lesions: “no pain jane” painless lesions on palms and soles
- osler nodes: “ ouch oslers” tender on pads of digits
- roth spots: retinal hemmrrhage
- splinter hemorrhage: nails

Diagnosis
LABS
- CBC
- blood culutres 2-3 1 hr. apart
- TTE is test of choice
- TEE can be used if bacteremia to determien abx use

DUKE CRITERIA
- postitive blood cx. endocaridal involvement from TTE = major criteria
- minor critera: IV drug use, fever, vascular phenomina, immune issue

2 major, 1 major + 3 minor, or 5 minor

Treatment
- Acute: nafcillin + gentamycin (vanco. if PCN allergy or IVDU) bcuz staph
- subacute: PCN/ampicillin + genta (vanco if PCN allergy or IVDU) bcuz strep
- Endocarditis in IV users: vanco + genta
- prostetic valves: vanco + genta + rifampin

Prophylaxis : had endocarditis 1x– we do this
- prosthetic valves, hx. , cogenital dx., transplant
- prior to :dental, respiratory or skin procedure
- amoxicillin 1 hr. before (clind if PCN allergy)