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Semester 2 Case 4: The Downward Spiral
* What is the cardiac cycle?
single cardiac cycle = The period between the start of one heartbeat & the beginning of the next. It includes alternating periods of contraction & relaxation. For any 1 chamber in the heart, the cardiac cycle can be divided into 2 phases: Systole & Diastole. Systole = Chamber contracts & pushes blood into an adjacent chamber or into an arterial trunk. Diastole = Chamber fills with blood & prepares for next cardiac cycle. FLUIDS MOVE FROM HIGHER PRESSURE TO LOWER PRESSURE!
Valves between adjacent chambers help ensure that blood flows in the required direction. The correct pressure relationships are dependent on the careful timing of contractions. Pacemaking & conducting systems normally provide required spacing between atrial &
All 4 chambers are relaxed. Ventricles are partially filled with blood.
Atrial systole (100ms) Atria contract. Ventricles completely fill with blood. Blood from veins can't flow into atria - Patria>Pveins.
Atrial diastole Continues until start of next cycle. Atria are relaxed, but fills with blood.
Phases of Cardiac Cycle
For last 100ms of ventricular diastole, atrial systole restarts.
Ventricular diastole (530ms) Ventricles relax, pressure drops. Blood flows back against semi-lunar valves &
forces them closed. Blood flows into relaxed atria. Ventricles fill passively.
Ventricular systole (270ms) Ventricular contraction pushes AV valves shut. Ventricular pressure then rises & exceeds pressure in arteries, so semilunar valves open & blood is ejected.
This is an example for a heart rate of 75/minute. When heart rate increases, all phases of the cardiac cycle are shortened. The greatest reduction occurs in the length of time spent in diastole. Although pressures are lower in the right atrium & right ventricle, both sides of the heart contract at the same time, and they eject equal volumes of blood. In more detail: Atrial systole - As atria contract, | atrial pressures push blood into ventricles through open right & left AV valves. At start of atrial systole, ventricles are already 70% full due to passive blood-flow during the end of the previous cardiac cycle. As atria contract, | atrial pressures provide remaining 30% by pushing blood through open AV valves. At the end of atrial systole, each ventricle contains the maximum amount of blood that it will hold in this cardiac cycle. This quantity = END-DIASTOLIC VOLUME (EDV). EDV = 130ml in an adult who is standing at rest. Ventricular systole - As atrial systole ends, ventricular systole begins. As | ventricular pressure rises above pressure in the atria, AV valves shut. Ventricles are contracting isometrically (Tension produced doesn't exceed resistance, so muscle length doesn't change) but ventricular pressure isn't yet high enough to force open the semi-lunar valves. This is the period of ISOVOLUMETRIC CONTRACTION. All heart valves are closed, volumes of ventricles remain constant & ventricular pressure rises. Once Pventricles > Parterial trunks, semi-lunar valves open & blood flows into the pulmonary & aortic trunks (beginning of VENTRICULAR EJECTION). Isotonic contraction (Muscle cells shorten & tension production remains relatively constant) occurs. After reaching a peak, ventricular pressures gradually |
near the end of ventricular systole. During ventricular ejection, each ventricle will eject 7080ml of blood, the STROKE VOLUME. Stroke volume at rest is about 60% of the end-
diastolic volume. This is the EJECTION FRACTION. This can vary in response to changing demands on the heart. As end of ventricular systole approaches, ventricular pressure falls rapidly. Blood in aorta & pulmonary trunk now starts to flow back toward the ventricles & this movement closes the semi-lunar valves. As backflow begins, pressure | in aorta. When valves close, pressure begins to rise as elastic arterial walls recoil. (This small temporary rise produces a valley in the pressure tracing called a DICROTIC NOTCH. Amount of blood remaining in ventricle when semi-lunar valve closes = END-SYSTOLIC VOLUME. It's about 50ml at rest: 40% of the end-diastolic volume.) Ventricular diastole - Lasts for the 430ms remaining in the current cardiac cycle &
continues through atrial systole in the next cycle. All heart valves are closed. Ventricular myocardium is relaxing. Pventricular > Patrial, so blood can't flow into ventricles. This is the period of ISOVOLUMETRIC RELAXATION. Ventricular pressures | rapidly over this period because elasticity of connective tissues of the heart & fibrous skeleton helps re-expand the ventricles toward their resting dimensions. When Pventricular < Patrial, AV valves are forced open. Blood now flows from the atria into the ventricles. Both atria & the ventricles are in diastole, but ventricular pressures continue to | as ventricular chambers expand. Throughout this period, pressures in ventricles are so far below those in the major veins that blood pours through the relaxed atria & on through the open AV valves into the ventricles. (Passive mechanism: Primary method of ventricular filling). The relatively minor contribution that atrial systole makes to ventricular volume explains why individuals can survive quite normally when their atria have been so severely damaged that they can no longer function. In contrast, damage to one or both ventricles can leave the heart unable to maintain adequate bloodflow through peripheral tissues & organs. A condition of heart failure then exists. Heart Sounds Auscultation is a simple & effective method of cardiac assessment. A stethoscope is used to listen for normal & abnormal heart sounds. There are 4 heart sounds - S1, S2, S3, and S4.
* S1 = "Lubb" marks the sound of the start of ventricular contraction & is produced as the AV valves close. Lasts a little longer than S2.
* S2 = "Dupp" occurs at the beginning of ventricular filling when the semi-lunar valves close.
* S3 & S4 are usually very faint sounds & are seldom audible in healthy adults. S3 = Blood flowing into ventricles. S4 = Atrial contraction. Heart murmurs: If valve cusps are malformed or there are problems with the papillary muscles or chordate tendinae, the valves may not close properly. Regurgitation then occurs in ventricular systole. The surges, swirls, & eddies that accompany regurgitation create a rushing, gurgling sound known as a heart murmur. Minor heart murmurs are common &
* What is heart failure?
[2, 3] Heart
failure is a complex syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the heart to function as a pump to support a physiological circulation. It is a state that develops when the heart fails to maintain an adequate cardiac output to meet the demands of the body. Epidemiology Incidence increases with advancing age. Average annual incidence: 35-64 years: 2-4%
65+ years: 10%
Prognosis has improved over the past 10 years, but mortality rate is still high. About 50% of patients die within 5 years. Prevalence of heart failure is close to 900,000 in the UK alone, and contributes to 100,000 deaths per year. It costs the NHS PS625million and accounts for 5-10% of hospital admissions. Aggravating Factors
Any factor that increases myocardial work may aggravate existing heart failure or initiate failure. Most common are arrhythmias, anaemia, thyrotoxicosis, pregnancy, obesity, infective endocarditis, pulmonary infection, change of heart failure therapy including poor compliance. Re-admission rates = 29-47% within 3-6months of hospital discharge. Pathophysiology Compensatory physiological changes occur to maintain cardiac output & peripheral perfusion. However, as heart failure progresses, these mechanisms are overwhelmed &
become pathophysiological. Principles:
* Failure of the pump - Damaged muscle contracts or relaxes weakly or inadequately.
* An obstruction to flow - Overworks the chamber behind obstruction.
* Regurgitation flow - Some of the output from each contraction is refluxed back - volume workload to ventricles.
* Disorders of cardiac conduction.
* Disruption of the continuity of the circulatory system. Development of pathological peripheral vasoconstriction & sodium retention in heart failure by activation of the renin-angiotensin-aldosterone system is a loss of beneficial compensatory mechanisms & represents cardiac decompensation. Most Common Causes
- Ischaemic heart disease (35-40%)
- Cardiomyopathy (e.g. diabetes) (30-34%)
- Hypertension (15-20%) Changes
* Ventricular dilation
* Myocyte hypertrophy
* Increased collagen synthesis
* Altered myosin gene expression
* Altered sarcoplasmic Ca2+-ATPase density
* Increased ANP secretion
* Salt & water retention
* Sympathetic stimulation
* Peripheral vasoconstriction Venous Return (PRELOAD) Myocardial failure leads to a reduction of the stroke volume (volume of blood ejected with each heart beat) & an increase in the volume of blood remaining after systole. The increased diastolic volume stretches myocardial fibres & myocardial contraction is restored - Starling's Law. However, the failing myocardium results in depression of the ventricular function curve.
Mild myocardial depression:
- Is not associated with a reduction in cardiac output because it is maintained by an increase in venous pressure.
- However, ejection fraction is reduced early in heart failure.
- Sinus tachycardia also ensures that any reduction of stroke volume is compensated for by increased heart rate - maintains cardiac output. More severe myocardial depression:
- To maintain cardiac output, a largely-increased venous pressure is needed, and/or marked sinus tachycardia.
- Increased venous pressure causes: Dyspnoea due to accumulation of interstitial &
alveolar fluid, hepatic enlargement, ascites, and dependent oedema.
- Cardiac output at rest isn't very depressed.
- Myocardial & haemodynamic reserve is so compromised that a normal increase in cardiac output can't be produced by exercise. In very severe heart failure:
- Cardiac output at rest is depressed, despite high venous pressures.
- The inadequate cardiac output is redistributed to maintain perfusion of vital organs, such as heart, brain, & kidneys, at the expense of skin & muscle. Outflow Resistance (AFTERLOAD) This is the resistance against which the ventricle contracts. It is formed by:
* Pulmonary & systemic resistance
* Physical characteristics of vessel walls
* Volume of blood ejected Increase in afterload = Decrease in cardiac output Results in further increase of end-diastolic volume & dilatation of the ventricle itself, further exacerbating the problem of afterload. Myocardial Contractility (INOTROPIC STATE) Sympathetic nervous system is activated in heart failure via baroreceptors as an early compensatory mechanism - provides inotropic support & maintains cardiac output. Chronic sympathetic stimulation ? Further increases neurohormonal activation & Myocyte apoptosis - Compensated by down-regulation of b receptors. Positive inotropism (increased contractility) occurs due to increased sympathetic drive - Starling's Law. Negative inotropism (decreased contractility) occurs due to myocardial depressants (e.g. hypoxia). Myocardial Remodelling Left ventricular remodelling = Process of progressive alteration of ventricular size, shape &
function due to influence of mechanical neurohormonal & possibly genetic factors in
diseases such as: myocardial infarction, cardiomyopathy, hypertension, & valvular heart disease. Characteristics: Hypertrophy. Loss of myocytes. Increased interstitial fibrosis. Remodelling continues for months after initial insult & the eventual change in shape of the ventricle becomes responsible for significant impairment of overall function of the heart as a
pump. Neurohormonal & Sympathetic System Activation Na+ & H2O retention. Vasoconstriction.
Increased cardiac work. Myocyte damage.
Decreased cardiac output.
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