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AP III > Cardiomyopathies > Flashcards

Cardiomyopathies Flashcards

1
Q

T/F: Cardiomyopathy is usually related to CAD, HTN, or a Valve Disorder.

A

False.
Usually due to a genetic condition.
-Associated with mechanical and/or electrical dysfunction
-Hypertrophy or Dilation

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2
Q

What is Primary Cardiomyopathy?

A

Genetic, mixed or acquired.
-Exclusively confined to heart muscle
-Ex: HCM, DCM, peripartum

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3
Q

What is Secondary Cardiomyopathy?

A

Usually in context of multiorgan dysfunction.
-Amyloidosis, drug induced, sarcoidosis
-Something has caused it.

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4
Q

-The most common genetic CV disease
-An autosomal dominant disorder
-LV hypertrophy in the absence of any other cardiac disease
-Can affect people of all ages
-Prevalence of 1 in 500 people

A

Hypertrophic Cardiomyopathy aka
Idiopathic hypertrophic subaortic stenosis (IHSS)

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5
Q

Describe the pathophysiology of Hypertrophic Cardiomyopathy.

A

-Myocardial Hypertrophy leads to large interventricular septum.
-Dynamic LVOT obstruction: accelerated blood flow through narrowed LVOT leads to Venturi effect.
-Systolic Anterior Movement (SAM) of Mitral valve: During systole, piece of the Mitral Valve flips back and can cause obstruction. decreases blood flow leading to sudden death.
-Diastolic Dysfunction
-Myocardial Ischemia: Abnormal coronaries, large ventricular mass, inc. LVEDP->dec. Subendocardial coronary perfusion. Coronaries cannot perfuse these thick muscles.
-Dysrhythmias: exacerbated by exercise. Can lead to sudden death.

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6
Q

What are the S/Sx of Hypertrophic Cardiomyopathy?

A

Usually go from asymptomatic to sudden death.
-If they do have symptoms, will be S/Sx of HF
-Angina, fatigue, syncope, tachydysrhythmias, HF
-Lying down relieves symptoms (dec. LVOTO)
-Valsalva aggravates them
-Murmur present, gallop rhythm
-Sudden death most likely aged 10-30 years
-No competitive sports

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7
Q

How do you diagnose Hypertrophic Cardiomyopathy?

A

-ECG shows LVH, QRS and ST alterations
-Echo shows hypertrophy, LVOTO, SAM, cavity obliteration during systole, MR, EF >80% (EF is high because no blood is left behind in the heart after it beats)
-SAM- Systolic anterior movement of anterior leaflet of mitral valve (MR from Venturi effect)
-Histology features hypertrophied myocardial cells and areas of patchy scarring
-Definitive diagnosis with endomyocardial biopsy and DNA analysis

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8
Q

What key words diagnose Hypertrophic Cardiomyopathy on an endomyocardial biopsy?

A

Myofibrillar Disarray

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9
Q

What are the treatment goals for Hypertrophic Cardiomyopathy?

A

-improve diastolic filling
-reduce LVOT obstruction
-decrease myocardial ischemia

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10
Q

What is the treatment for mild symptoms of Hypertrophic Cardiomyopathy?

A

-Beta blockers
-Calcium Channel Blockers
-Possible diuretics if S/Sx of CHF

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11
Q

What are the interventions for high risk patients with Hypertrophic Cardiomyopathy?

A

-Amiodarone (afib is common)
-ICD

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12
Q

What are the treatments for HF due to Hypertrophic Cardiomyopathy?

A

1) Non-obstructive – drug therapy or transplant
2) Obstructive – drug therapy, surgical myomectomy or pacing (desynchronize the heart to dec LVOTO)
3) Alcohol sclerosing of the septal perforating arteries (cath lab)

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13
Q

What is the surgical treatment for Hypertrophic Cardiomyopathy?

A

Considered in 5% of patients with SEVERE disease
-Myomectomy (remove pieces of ventricle/septum inside of heart)
-MV replacement (mechanical valve - can’t have LVOT obstruction with a mechanical valve)

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14
Q

What is the prognosis of Hypertrophic Cardiomyopathy?

A

-Overall annual mortality is 1%
-If there is family history of malignant arrhythmias or sudden death it is 5%

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15
Q

How can you minimize LVOT obstruction?

A

-decrease contractility
-increase preload
-increase afterload

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16
Q

What things worsen LVOT obstruction?

A

SNS stimulation, hypovolemia and vasodilation

17
Q

What should you assess preop for a patient with HCM?

A

-Cardiac eval, ECG, echo, continue meds, turn off ICD, apply R2 pads
-Ask all patients if they or family members have hx of sudden death
-Systolic murmur should raise suspicion of HCM
-Anxiolytics to blunt SNS

18
Q

Describe HD goals for management of HCM

A

Slow, Tight, Full, Dec Contractility

19
Q

Describe anesthetic management of HCM

A

-Blunt SNS to DL (deep on gas, consider BB with DL)
-Beta antagonists are good at decreasing SNS stimulation and slowing HR
-Invasive BP and echo (depending on case)
-Use NEO!
-Avoid Beta agonists (ephedrine, dopa) due to increasing contractility and HR will worsen LVOTO
-NO Vasodilators (dec. SVR will worsen LVOT obs. )
-Maintain NSR, Treat SVT quickly
-PPV can dec. Preload and worsen LVOTO
-Smaller TV and inc. RR
-Avoid Peep
I-nsufflation can worsen LVOT obstruction (dec. Preload)
-Insuflate slowly and dec. Insufflation pressure

20
Q

Describe HCM in a parturient patient.

A

-Pregnancy is usually well tolerated
-Challenge with labor - usually get scheduled C/S
-Pain increases catecholamine release
-Bearing down (valsalva) increases LVOT obstruction
-Regional is OK
-Euvolemia or slight hypervolemia is helpful
-Use Neo for HOTN
-Use care with oxytocin due to vasodilating effects
-Pulmonary edema post delivery can be seen (Delicate fluid balance)

21
Q

Describe postop mgmt of HCM

A

All factors that stimulate SNS must be avoided:
-Pain, shivering, anxiety, hypoxia, hypercarbia

Maintenance of euvolemia and prompt treatment of HOTN.

22
Q

What is Dilated Cardiomyopathy?

A

The most common type of CM.
-A primary myocardial, LV or biventricular dysfunction, systolic dysfunction, normal wall thickness
-Many different causes

23
Q

What are the different causes of Dilated CM?

A

-genetics
-viruses
-ETOH
-cocaine
-peripartum
-HIV
-Duchenne’s MD
-thyroid
-chemotherapy, radiation
-hypertension, CAD, valve disease

24
Q

What are the S/Sx of Dilated CM?

A

-Heart failure, exertional angina
-Functional Mitral or tricuspid regurgitation: Ventricular dilation leads to valve regurg
-SVT and ventricular dysrhythmias common
-Sudden death can occur
-Systemic embolization: Mural thrombi form in hypokinetic chambers (leads to TIA, strokes, etc)
-Diagnosed by EKG, Chest xray, Echo showing global hypokinesis and sometimes thrombi

25
Q

What is the prognosis of dilated CM?

A

-5 year mortality of 50%
-Alcoholic is reversible with abstinence

26
Q

Describe Anesthetic Mgmt of Dilated CM?

A

-Same as that of CHF
-AICD and OHT common
-Regional anesthesia is well tolerated (check anticoagulation status)

27
Q

What is Apical Ballooning Syndrome?

A

-Stress induced cardiomyopathy, “broken heart” syndrome
-Physical (acute asthma, surgery, stroke) or emotional stress
-Temporary disruption of contractility at LV apex
-Apical ballooning seen on ECHO
-SxS: chest pain and dyspnea
-Treatment is supportive (medical mgmt, IABP)

28
Q

What is Peripartum CM?

A

-Rare form of Dilated CM of unknown cause
-Usually in 3rd trimester-5 months after delivery
-Women with no history of heart disease
-Risk factors: obese, multiparity, >30 years of age, twins , preeclampsia, AA
-Symptoms like normal pregnancy-DOE, ankle swelling
-Diagnosis – Echo; EF <45% around delivery
-Prognosis: mortality of 25-50% within 3 months of delivery

29
Q

Describe Mgmt of Peripartum CM

A

-Treat like HF- diuretics, vasodilators, hydralazine and nitrates. Mechanical support or OHT if severe
-Manage as you would HF; regionals are well-tolerated

30
Q

What is Restrictive CM due to?

A

Due to myocardial infiltration and cause severe diastolic dysfunction (can’t relax)
-Mostly amyloidosis, as well as sarcoidosis, or carcinoid
-Stiffness of the myocardium due to deposition of abnormal substances
-Rigid heart that can’t fill
-Similar to restrictive pericarditis
-Affects both R & L heart; systolic fxn usually nml; thromboembolism may occur, conduction disturbances are common

31
Q

How do you diagnose Restrictive CM?

A

Diagnosis best via echo – shows diastolic dysfunction, and “speckled” ventricle (amyloid plaque); endomyocardial biopsy confirms

32
Q

How do you treat Restrictive CM?

A

Diastolic dysfunction WITHOUT cardiomegaly
-Treat like diastolic HF – diuretics, ICD (digoxin may cause dysrhythmias), maintain NSR (SV fixed)
-OHT is not an option with sarcoid, amyloid because plaque will recur in donated heart
-Prognosis is poor
-Treat like tamponade (fixed SV so inc HR)

33
Q

What is Cor Pulmonale?

A

Severe Pulm HTN -> R HF.

Causes:
-COPD (most common), restrictive lung disease, obesity-hypoventilation syndrome, or primary pulmonary htn
-Chronic hypoxia causes the lung changes (pulmonary vascular remodeling)
-Hypoxia->inc. PVR->RV hypertrophy->RV failure

34
Q

How do you diagnose Cor Pulmonale?

A

-EKG shows RAD, RBBB, and peaked P waves in leads II, III, aVf (P pulmonale)
-TEE shows increased PAP

35
Q

What is the treatment for Cor Pulmonale?

A

Dig, lasix, O2 (goal PaO2 >60), sildenafil, lung or heart-lung transplant

36
Q

Describe Anesthetic Mgmt of Cor Pulmonale

A

-Optimize respiratory function
-Volatiles and bronchodilators help
-Avoid respiratory depression (too much narcotic)
-Lines as needed
-Maybe TEE
-ICU after

AP III (20 decks)

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