EHR519 Week 6 Pathophysiology, Chronic Heart Failure PDF

Warning This material has been produced and communicated to you by or on behalf of Charles Sturt University in accordance with section 113P of the copyright act (Act). The material in this communication may by subject to copyright under the act. Any further reproduction or c...

Warning This material has been produced and communicated to you by or on behalf of Charles Sturt University in accordance with section 113P of the copyright act (Act). The material in this communication may by subject to copyright under the act. Any further reproduction or communication of this material by you may be the subject of copyright protection under this act. Do not remove this notice EHR519 Week 6 Pathophysiology, medications, considerations and contraindications for: Chronic Heart Failure 2  Heart failure Occurs when the heart function less effectively Reduced cardiac output and/or elevated intracardiac pressures Result from heart attack, high blood pressure, damaged heart valves or cardiomyopathy Cardiomyopathy is where the entire heart muscle, or a large part of it, is weakened due to disease (CAD, HT, viral) Heart failure and cardiomyopathy commonly occur together Few symptoms in mild HF, severe include dyspnoea, ankle swelling and, fatigue + structural signs = peripheral oedema HF cannot be cured, however, some e.g. valve defects can if treated early Common treatment can improve QAL, reduce hospital admissions, prolong life. In certain end-stage patients, heart transplantation may be used 3  Prevalence Ageing = reduce exercise and functional capacity, disability and impaired QAL HF = final pathway for many CV disorders Australia Self-reported data estimates 102,000 people aged 18 and over had heart failure in 2017–18, 2/3 of these ≥ 65 yrs (men 1.5 x females; 2.5 x in 75-84 yrs) ) Underestimated due to mild symptoms in early stages Review study estimates rates 2-4 x this Hospital rates have increased by 33% men & 13% women since 2002-01, but age-standardised rates fell by around 30% for both males and females Thus, increased incidence likely due to an ageing population and improved treatment Aboriginal and Torres Strait Islander people The rate is 2.9 times higher than non-indigenous Compared to non-Indigenous Australians, the rate is 3.4 times higher in Indigenous men and 2.4 times higher in Indigenous women 4  Classification Inability of the LV to pump adequate blood around the body can be due to systolic or diastolic heart failure. Systolic heart failure; heart muscle is weak, ventricular myofibrils can't contract or against load = reduced ejection fraction, termed HFrEF. However, ~50% with HF have near normal systolic contraction but the ventricle is still stiff from heart failure. The problem is not contraction, rather its inability to expand or relax and fill under pressure. This is diastolic dysfunction and as the EF is normal which is termed HFpEF. Normal EF is > 55% i.e. > 55% of end of diastole filling volume ejected In HFrEF the EF is 100 Enlarged LV pg · mL−1) can be a sensitive index of decompensated HF Echocardiogram – measurement of LV contraction (ejection) Patients with HFrEF may be and relaxation caused by anterospetal MI Sometimes radionuclide test or cardiac Q waves in V1 – V4 catherterisation is completed Unique myocardial characteristics (elevated diastolic filling pressures) Underlying ischemic heart Severity (Level I, II, or III diastolic dysfunction disease Blood tests (BNP) 15  Exercise Capacity Echo, BNP, and other assessments of cardiac function do not quantify the full scope of HF as a disease GXT with gas exchange = determination of peak O2 consumption, ventilator efficiency Indication of 1 year mortality rates: Peak VO2: 70% of predicted peak) = lower (3%) Ventilatory efficiency (slope of the relationship of VE to Figure 16.2 Lower (3%) and higher (10%) risk from carbon dioxide production (VE-CO2) during exercise = mortality at 1 yr in men and women based on achieved predictor of future risk of death Peak VO2 (left axis) and percent predicted peak VO2 (right axis) >30 = moderate increased risk >45 = very high risk 16  Exercise testing Exercise testing patients with HF is similar other types of heart disease Modified Bruce or Naughton 2-3 min per stage steady-state protocol Cycle ramp 10-15W / min Prediction equations to estimate VO2 discouraged as they tend to over-predict functional capacity Ventilatory-derived lactate threshold / gas exchange threshold useful measure V-slope method = plotting VCO2 over VO2 18  Expected responses Compared to healthy, there are a number of central and peripheral differences in HFrEF and HFpEH (tables 16.1 and 16.3 text). The following are all reduced: Power output 30%-40% Q 40% SV 50% (more often observed in HFrEF than HFpEF) HR 20% – If