Heart Failure Flashcards
Heart Failure Classifications
- INTERMACS
- ACC/AHA Stages
- NYHA
- Forrester
INTERMACS patient profiles are important for framing discussion surrounding the appropriateness and timing of mechanical support.
Goes from 7 (Advanced NYHA III) to 1 (Critical cardiogenic shock)
Profile 4 is for those with frequent admissions and recurrent HF relapses.
American College of Cardiology/American Heart Association (ACC/AHA) stages
Stage A; at risk, hypertension, diabetes mellitus, coronary artery disease
Stage B; those with structural heart disease but no HF symptoms
Stage C; patients with current or prior HF symptoms
Stage D; patients with refractory symptoms requiring consideration of advanced therapies such as left ventricular assist device or heart transplantation (stage D).
NYHA functional classification is based on HF symptoms:
Class I is no symptoms
Class II describes slight limitation of physical activities
Class III describes marked limitation of physical activities
Class IV describes the inability to carry out any physical activities without symptoms.
The Forrester classification stratifies patients with HF based on the degree of congestion and hypoperfusion.
Class I is patients who are warm (well perfused) and dry (not congested).
Class II is patients who are warm (well perfused) and wet (congested).
Class III is patients who are cold (poorly perfused) and wet (congested).
Class IV is patients who are cold (poorly perfused) and dry (not congested).
The Killip classification is used for patients with acute myocardial infarction.
Killip class I includes individuals with no clinical signs of HF.
Killip class II includes individuals with rales or crackles in the lungs, an S3, and elevated JVP.
Killip class III describes individuals with frank acute pulmonary edema.
Killip class IV describes individuals in cardiogenic shock or hypotension (measured as systolic blood pressure <90 mm Hg), and evidence of peripheral vasoconstriction (oliguria, cyanosis, or sweating).
Hypertrophic Cardiomyopathy Imaging Diagnosis
- Diagnosis
The diagnosis of HCM can usually be made following echocardiography and/or CMR imaging, and invasive diagnostic assessments are rarely necessary.
Echocardiographic findings : LVH (particularly when asymmetric and involving the septum or anterolateral wall), systolic anterior motion of the mitral valve leaflets, particularly with septal contact resulting in an associated subaortic LVOT gradient.
CMR in all patients with suspected or diagnosed HCM to most reliably assess LV morphology, including maximal LV wall thickness, as well as to further inform risk stratification with assessment of extent of late gadolinium enhancement (LGE).
The majority of patients with HCM have LVOT obstruction under resting conditions or following exercise. Because the identification of a provocable LVOT gradient may result in additional treatment options for heart failure symptoms (ie, disopyramide, septal reduction therapy), we proceed with exercise stress testing in all patients with known or suspected HCM, without resting LVOT obstruction, as part of the initial HCM evaluation. Exercise should be performed as the stress agent rather than using a pharmacologic stress agent, as a maximal treadmill or bicycle exercise stress test provides an objective measurement of functional capacity and information on the integrity of vascular responses and the risk of exercise related ischemia, arrhythmia, and obstruction.
ECG: Narrow, deep, symmetric T wave inversions in lateral precordial leads.
Restrictive Cardiomyopathy Diagnosis
Echo: Normal LVEF. Normal wall thickness. Biatrial enlargement.
Doppler mitral inflow with rapid inflow at the beginning of diastole within first 100 ms. High E low A waves.
Cath Tracings: Elevated filling pressures. Dip and plateau morphology with square Root sign and deep early decent. More problems on the left side of the heart compared with constriction. Ventricular concordance.
Idiopathic Restrictive Cardiomyopathy Treatment
- Cautious Diuresis
- Beta blockers, not as aggressive as DCM
- Cardiac Transplantation
Hypertrophic Cardiomyopathy Treatment
Avoid
- Positive inotropes
- Pure vasodilators
- High-dose diuretic
Do These:
- Decrease contraction
- Increase resistance
- Increase volume
To Decrease Obstruction
- Beta blockers, Verapamil, Diltiazem, Disopyramide
Hypertrophic Cardiomyopathy Genetic Diagnosis
Autosomal dominant disorder.
Most have myosin heavy chain/ binding protein.
First-degree family members of an affected individual should be evaluated for possible inheritance of the disease. Predominately reserved for identifying patients who may have a disease which appears phenotypically similar to sarcomere HCM, such as Fabry disease or a lysosomal/glycogen storage disease, or to help identify family members who may be at risk of developing HCM.
Hypertrophic Cardiomyopathy Screening
If gene is known, genetically test otherwise monitor with imaging.
If engaged in competitive athletics or adolescent screening is annual, as adults screen every 5 years.
HOCM ICD Indications
I- Prior cardiac arrest or sustained VT
IIA- Family history of SCD, LV wall thickness >30 mm, LVEF <50%, Unexplained syncope, LV apical aneurysm
IIB - Nonsustained VT, Extensive LGE on CMR
Hemochromatosis lab findings
serum iron/TIBC of >50%, transferrin saturation >55% and serum ferritin >200 ng/mL in women and >300 ng/mL in men.
Classic triad of hereditary hemochromatosis
The classic triad of cirrhosis, diabetes mellitus, and skin bronzing is variable in HH and often absent.
Genetic mutation in hemochormatosis
due to a genetic mutation (C282Y) in the homeostatic iron regulator (HFE) gene causing increased gastrointestinal iron absorption and resulting in a dilated cardiomyopathy.
Imaging in hemochromatiosis
Cardiac magnetic resonance (CMR) imaging has become the diagnostic test of choice for evaluation of iron-overload cardiomyopathy. Iron shortens the T2 relaxation time and darkens the image more quickly (generally <20 msec, and <10 msec is suggestive of more severe disease).
Serial CMR T2* imaging is also useful to guide response to iron chelation therapy, with significant improvement in prognosis and survival.
Fabry disease
LV hypertrophy and renal dysfunction
In a patient with concentric LV wall thickening, the differential diagnosis includes hypertensive cardiomyopathy, hypertrophic cardiomyopathy, infiltrative diseases (e.g., amyloidosis), metabolic disorders (e.g., Fabry disease), and an athletic heart.
X-linked lysosomal storage disorder resulting from a deficiency in lysosomal hydrolase galactosidase A (alpha-Gal A) that results in the accumulation of globotriaosylceramide (Gb3) in a variety of cells resulting in a broad range of clinical manifestations. Cardiac, renal, and neurologic manifestations tend to be the most common.
When Fabry disease is considered, there are several tests that may be used to make the diagnosis, including genetic testing, an enzymatic assay for alpha-Gal A activity, measuring Gb3 and lyso Gb3 levels, and tissue biopsy. Genetic testing is considered the “gold standard”. If a patient is diagnosed with Fabry disease, genetic testing of family members is also indicated.
