Heart Failure. Acute. Plasma [NE] (pg/ml) 24 Hours. Chronic

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1 Heart Failure Heart failure is the inability of the heart to deliver sufficient blood to the tissues to ensure adequate oxygen supply. Clinically it is characterized by signs of volume overload or symptoms of impaired organ perfusion. Patients with heart failure experience graded difficulty performing everyday tasks, with the grade dependent on the degree of heart dysfunction. Worldwide, it is believed that 2-3% of individuals over 45 years of age have heart failure, with an increasing probability based on age. Acute heart failure Left-heart failure typically begins with a myocardial infarction. The infarction decreases both myocardial contractility and blood flow to the heart. Stroke volume is diminished and this causes decreased cardiac output and arterial pressure. This activates the baroreceptor reflex, which seeks to increase pressure by decreasing arterial compliance and venous compliance, increasing contractility and heart rate. In the period of ischemia, the cardiocentric mechanisms can cause increased damage by adding additional work to already hypoperfused tissues. The immediate response to a left-side myocardial infarction is a shift in blood volume from the peripheral circulation to the pulmonary circulation. This shift increases left heart end-diastolic volume. Increased cardiac filling helps to offset impaired emptying. In addition to the volume shift, increased sympathetic outflow increases left-heart contractility (shown below, data from Griffiths, Cody). This outflow, and in particular the epinephrine associated to it, chronically causes resistance to the increased sympathetic outflow in the heart, dulling the increases in contractility. The increased sympathetic outflow Plasma [NE] (pg/ml) Acute 24 Hours Chronic Normal Myocardial Infarction continues to, for example, the kidney, resulting in altered sodium homeostasis and additional long term damage through the actions of angiotensin II. Multiple mechanisms act to help the body to retain volume in the following period. Hormones such as angiotensin II and aldosterone are elevated in response to

2 reduced glomerular filtration and increased sympathetic outflow. These act to accelerate volume retention in the days following an ischemic episode. Chronically reduced pressure and renal blood flow act to alter body water balance until pressure is restored to a new point below the original stable point of the system, but at the cost of additional work by the heart to keep this volume oxygenated. This additional load taxes the heart and reduces its ability to elevate cardiac output in response to need. This manifests as decreased ability of an individual to exert him or herself. The agents involved in heart failure are shown in Figure 2. Black explosions mark places that can be clamped within the protocol. Hf treatment Heart failure is a complex disease due to the number of systems involved in compensating for decreased cardiac output. Sodium restriction, while not well supported by evidence, is typical because of its low cost and potential effects in salt homeostasis. Angiotensin II blockers (i.e. converting enzyme blockade or renin blockers) improve mortality by decreasing the negative impact of Ang II on reactive oxygen species and inflammatory factors. Beta blockade resensitizes the left ventricle to the effects of sympathetic innervation and catechols. Loop diuretics (e.g. furosemide aka Lasix) decrease volume overload and improve individuals ability to exercise. Aldosterone blockade through Spironolactone or related agents improve sodium handling and improve heart function, improving all-cause mortality in HF patients. Digoxin improves contractile function of the heart in the case of reduced ejection fraction and improves severe symptoms of heart failure.

3 The Heart Failure Protocol Restart to reestablish initial conditions and then record the control data. There are two ways to develop heart failure 1) Immediate by changing heart strength and then turing Immediate failure to ON. A 60% heart strength is a reasonable starting point. This is more like an acute myocardial infarction. 2) Progressive failure whereby a % of heart strength is lost per day. A 5% lost per day is reasonable. We are interested in the effect of the infarction on hemodynamics and the subsequent compensations that help to maintain oxygen delivery. Arterial Pressure (mmhg) Cardiac Output (ml/min) Heart Rate (/Min) Stroke Volume (ml) Left Ventricle EDV (ml) Left Ventricle EDP (mmhg) Ejection Fraction (Left Heart) Sympathetic Nerve Activity Plasma Renin Activity Na+ Excretion (meq/min) Erythropoietin Blood Volume (ml) Red Cell Volume (ml) Plasma Volume (ml) Hematocrit (%) Ejection Fraction The heart s ejection fraction is the ratio of stroke volume to end-diastolic volume. The normal ejection fraction is Ejection fraction is a useful clinical finding, since it decreases in proportion to the severity of heart failure. Decreases are typically due to both decreasing stroke volume and increasing end-diastolic volume. In its early phases, chronic heart failure can present with no reduced ejection fraction. Question: Find the maximal infarct that leaves ejection fraction unchanged to within 1%. Find an infarct level that changes ejection fraction by more than 20 percent. In each case, use clamps to determine the effect of the cardiac

4 sympathetic baroreceptor reflex on pressure, heart rate, and stroke volume, and similarly determine the effect of the vagus on the same quantities. Which is more important on each observable variable (in this case pressure, heart rate, and stroke volume)? Exercise Tolerance Tolerance to exercise is decreased in heart failure (shown below, data from Wilson). 30 Maximum 20 O2 Uptake ((ml/min)/kg) Ejection Fraction (%) Use an exercise stress test to characterize JUSTPHYSIOLOGY s cardiac function at 7 days. Treadmill Speed (MPH) Treadmill Grade (%) Heart Rate (/Min) Time Speed Grade 0% 0% 2% 4% 6% 8% Heart Rate Record the elapsed time and distance when this subject finally gives up. References Cody, R. J., K. W. Franklin, J. Kluger, & J. H. Laragh. Sympathetic responsiveness and plasma norepinephrine during therapy of chronic congestive heart failure with captopril. Amer. J. Med. 72: , 1982.

5 Griffiths, J. & F. Leung. The sequential estimation of plasma catecholamines and whole blood histamine in myocardial infarction. Amer. Heart J. 82: , Wilson, J. R., J. L. Martin, D. Schwartz, & N. Ferraro. Exercise intolerance in patients with chronic heart failure. Role of impaired nutritive flow to skeletal muscle. Circulation 69: , 1984.

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