Non-Pharmacology Heart Failure Flashcards
Framingham Major Criteria of HF
Major criteria:
Paroxysmal nocturnal dyspnea
Neck vein distention
Rales
Radiographic cardiomegaly (increasing heart size on chest radiography)
Acute pulmonary edema
S3 gallop
Increased central venous pressure (>16 cm H2O at right atrium)
Hepatojugular reflux
Weight loss >4.5 kg in 5 days in response to treatment
Framingham Minor Criteria of HF
Minor criteria: Bilateral ankle edema Nocturnal cough Dyspnea on ordinary exertion Hepatomegaly Pleural effusion Decrease in vital capacity by one third from maximum recorded Tachycardia (heart rate>120 beats/min.)
Minor criteria are acceptable only if they can not be attributed to another medical condition (such as pulmonary hypertension, chronic lung disease, cirrhosis, ascites, or the nephrotic syndrome).
Criteria Guidelines for HF
EF lower than 45% AND
2 major OR 1 major + 2 minor criteria met
People can be perfectly normal and functional with an EF of 20% because that is how their body works even though 55% and higher is normal
Most Important Vital Sign for HF
The biggest and most important vital sign in heart failure is the weight
1 liter of water = 1kg
Have patients monitor weight for fluid balance
Clinical Stages of CHF
Normal: no symptoms, normal exercise, normal LV function
Asymptomatic LV Dysfunction: no symptoms, normal exercise, abnormal LV function
Compensated CHF: no symptoms, slightly decreased exercise, abnormal LV dysfunction
Decompensated CHF: symptoms, greatly decreased exercise, abnormal LV function
Refractory CHF: symptoms not controlled with treatment
Medical Therapies for Systolic HF
Many therapies, but standards are:
ACE (preload and afterload reduction)
Beta blockers (decrease sympathetics and recover EF over time)
AICD automatic internal cardiac defibrillator
Aldosterone receptor blockers (decrease hospitalizations and improve mortality)
Ultrafiltration
Ultrafiltration: catheters in veins (one in central and one in peripheral vein); taking water from peripheral vein and putting the leftovers into central vein; results in isotonic aquaresis
Class IIa indication: not enough scientific evidence that every hypervolumic patient
Sympathetic Acute and Chronic Activation
They are initially beneficial by releasing NE trying to increase CO, HR, and contractility, but over time this is not good; people die, ventricular arrhythmias, increased mortality, etc.
Parasympathetic goes down as well due to this; causes increased mortality
Want to oppose these when chronically activated
Experimental Ways of Increasing PNS vs. SNS
Vagal nerve stimulation
Spinal nerve stimulator: inhibits SNS activity to the cardiac region to decrease stimulation on the heart
Carotid Sinus Stimulator: activates parasympathetic NS; stimulate impulses on carotid body to induce vagal response
Single Chamber ICD and Subcutaneous ICD
Single Chamber ICD:
Defibrillator implant
Lead is sitting in R ventricle
Shocking coils to facilitate charge and vectors anywhere in the triangle by setting up polarities to cause shocks
Subcutaneous:
ICD = internal cardiac defibrillator
Doesn’t have to be tunneled into the venous system and only below the skin and above the ribcage
SCD HeFT Study
SCD = sudden cardiac death
Landmark trial for heart failure
Ventricular tachycardia = SCD and people died
ICD implant to see if more people would better survive because need defibrillator within 2-3 minutes to live
Found: showed lowest mortality rate compared to the other two groups; now standard of care
Indications for ICD
Secondary Prevention:
Documented VF (resuscitation from a previous episode)
Hemodynamically unstable VT
Unexplained syncope with LVEF ≤ 35%
Primary Prevention:
LVEF ≤ 40%; with ischemic based etiology & spontaneous NSVT or inducible sustained monomorphic VT
LVEF ≤ 35% (Ischemic or Non-ischemic Cardiomyopathies)
Certain inherited disorders or conditions with structural heart disease: HCM, ARVD, Long QT, Brugada syndrome
Dyssynchrony
As a heart fails, the heart is not pumping in synchrony
As a heart starts to dilate, the walls are not pumping together and get a delay so blood is going back and forth and not pushing it out properly
Heart enlarges and lengthens and remodels = papillary muscles and leaflets are being pulled apart and leads to dyssynchrony
There is a delay between septum and lateral wall beating so blood is not being pumped out effectively
Stages and Classes of HF
Stages = risk factors for heart failure A: high risk but no structural disorders B: structural disorder with no symptoms C: past or current symptoms D: end stage disease
Class I: no limits and no symptoms
Class II: slight limits, comfortable at rest, ordinary activity causes symptoms
Class III: marked limits, comfortable at rest, less than ordinary activity causes symptoms
Class IV: limits due to discomfort, symptoms at rest
CRT
CRT = Biventricular (BiV) Device
3 Lead device in RA, RV, Overlying LV
BBB occurs somehow: must go myocyte to myocyte, so try to restore contraction from this ; septum contracts first and then lateral wall causing widening of QRS
Coordinate contraction: lead in R atrium and find coronary sinus (drains veins into R atrium) and poked a wire into the sinus and go through the vein to pace the L ventricle; have the R ventricular lead fire to stimulate the septum and the lead overlying the L ventricle fire so they fire together; not putting lead in L ventricle because cannot but lead into aortic valve
These leads can cause some minor regurgitation, but no thrombi will form usually; although, infection risk can increase
