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Acute congestive heart failure: pathophysiological alterations
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when compensatory haemodynamic and neurohormonal mechanisms are overwhelmed or exhausted (Packer 1992).
PATHOPHYSIOLOGICAL ALTERATIONS ASSOCIATED WITH ACUTE CHF Pathophysiological alterations associated with acute C H F can be divided into two categories: cardiac compensatory dysfunction and excess neurohormonal stimulation.
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Rebecca Dahlen and Sharon L. Roberts
The goal of a healthy heart is to transfer blood coming to the ventricles from the low pressure venous system into the high pressure arterial system. In acute congestive heart failure (CHF), impaired cardiac function leads to failure to empty venous reservoirs and therefore to reduce delivery of blood into the arterial circulation (Michaelson 1983). Once heart failure occurs it has a high mortality rate. According to the Framingham Heart Study, 50% of patients with New York Heart Association class II or III heart failure died within 5 years. With class IV patients, 50% survived less than I year (Cupples 1987). The purpose of this article is first to define acute CHF. Secondly, the pathophysiological alterations that occur as a result of strained and misdirected compensatory mechanisms will be discussed to help critical care nurses to recognise why certain patients are at risk of developing acute CHF. Rebecca Dahlen RN, MSN, CNS, Assistant Professor Sharon L. Roberts RN, PhD, FAAN, Professor, California State University, Long Beach, Department of Nursing, California, USA
(Requests for offprints to SLR) Manuscript accepted 14 June 1995 Nursing management of congestive heart failure Parts I and 2, by the same authors, will appear in the next two issuesof the journal
Cardiac compensatory dysfunction Cardiac compensatory dysfunction includes six factors: reduced myocardial contractility; cardiac dilation; myocardial hypertrophy; loss of positive-inotropic mechanism; biochemical changes and myocardial oxygen supply/ demand imbalance.
Reduced myocardial contractility Acute C H F patients with systolic dysfunction have reduced myocardial contractili W due to prolonged pressure or volume overload. Loss of muscle as in myocardial infarction causes an additional volume and wall stress overload in the remaining normal myocardium, which is why patients with AMI are at risk of developing heart failure. Reduced myocardial contractility is manifested by: • Decreased force development • Decreased rate o f force development • Decreased veloci W of shortening at a given loading condition • Decreased relaxation (Parmley 1983). A disturbance in the contractile state can diminish ejection fraction and stroke volume. There is also a shift downward in the ventricular function curve with an increase in atrial pressure. The acute CHF patient can have a low ejection fraction (EF)_0.5 indicating excessive myocardial dilation with respect to stroke volume (XVeeks 1986, Benz 1994).
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D E F I N I T I O N OF T E R H S Myocardial failure exists when the heart fails due to an intrinsic abnormality of the heart muscle. Heart failure includes myocardial failure and exists when demands are made on normal heart muscle that exceed its capability to perform (VCeeks 1986). Acute C H F patients have structural cardiac damage that adversely affects systolic or diastolic function. Heart failure can develop when the heart is injured and
Intensiveand Critical CoreNursing (I 995) I I, 210-216 © 1995PearsonProfessional/td
Cardiac dilation Normally, the left and right ventricles each respond in their own way to the cardiac workload placed upon them. Figure 1 is a summary of these responses. The right ventricle is an efficient volume pump. Increases in right ventricular blood volume can be accommodated as long as right ventricular filling pressure remains low. Increased left ventricle volume in the failing heart, however, causes increased diastolic and systolic ventricular size or dilation. N o r -
Acute congestive heart failure: pathophysiological alterations
Ventricular failure I
I Left ventricle
I Right ventricle
I
I Configuration
Can eject blood volume against high outflow pressure
I
I I Small internal diameter
Due to ventricular configuration I Cylindric shape
21 I
Has a large surface area
I Requires
I
I Thick wall
High levels of myocardial tension to generate high intrachamber pressure
I
I
J
Result
I Moves large volume of blood when outflow pressure remains low
Fig. I Responses of right and left ventricles to cardiac workload.
really, the left ventricle is distensible and adapts to increased diastolic volume or reload without significantly increased tilting pressure. Optimum contractility occurs at a fibre length of 2.2 blrn or 12-18 m m H g (Forster, Armstrong 1990). With cardiac dilation, the muscle cell stretches. The relationship between the cardiac output and the length of the heart muscle cell at the end of diastole is expressed as the FrankStarling relationship. This relationship states that as the end-diastolic filling length increases so does the cardiac output (CO). However, cardiac dilation can be self-limiting whereby the stretching of the muscle cell leads to reduced CO. The change is explained by the Laplace relationship, whereby the tension in the wall of a chamber such as the left ventricle is related directly to the p r e s s u r e o n that chamber and its radius (Benz 1994). Dilation results in an increased capacity of the cardiac chamber for work and stroke output. The degree to which dilatation must adapt to this increased workload increases with the severity of C H F as a result of reduced contractility. With cardiac dilation less fibre shortening is required to eject a given amount of blood during systole than is required in the normal heart. However, as the ventricle fails, increased enddiastolic volume and pressure is required to generate tension equal to that of a normal heart with normal end-diastolic volume (Weeks 1986). Myocardial hypertrophy In the presence of chronically increased volume loads, the ventricle hypertrophies. The number of individual myocardial fibre increases, resulting in greater ventricular mass (Weeks 1986). Hypertrophy is a significant compensatory mechanism for a failing heart and is accompanied by an increase in connective tissue which may stiffen the diastolic properties of the heart.
The myocardial ceils adapt to a sustained elevated workload by hypertrophy with increased muscle mass and altered geometrical configuration (Michaelson 1983). See Figure 2 for a summary of pathological factors involved in hypertrophy. Each hypertrophied cell requires more energy because of its increased mass and has less contractile force. As a result the heart is likely to fail under prolonged stress (Michaelson 1983). Hypertrophy is due to myocellular enlargement and initiates a sequence of adaptive responses affecting ventricular function. Hypertrophy due to ventricular failure involves ventricular wall remodelling. As the diastolic volume enlarges, the following cellular processes of remodelling are initiated: • • • •
Myocytes elongate Myocytes increase in diameter Myocytes are displaced relative to one another Reduction in the number ofmyocytes across the wall • Increased wall tension per cell (Cupples 1987). Myocellular hypertrophy is determined by two factors. The first factor is a segmental loss of myocardium resulting in hypertrophic growth of non-ischaemic myocytes. The second factor involves a reduction in the number ofmyocytes across the ventricular wall associated with lateral slipping of cells (Cupples 1987). When the number of myocytes is reduced there is an increased tension per cell which requires that myocytes hypertrophy. Augmented diastolic ventricular volume can result in increased hypertrophy. Therefore, diastole (with ventricular wall remodelling) and systole (with increased systolic tension) combine to augment the amount of hypertrophy required to normalise tension and balance the Laplace relation-
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Myocardial hypertrophy
I I Hypertrophy compensates for the pressure overload induced by dilation
Two factors I
I Hypertrophy normalised systolic and diastolic stress regardlessof increased pressure load
I Effective in I
How?
L
I Systolic pressure overload
By sharing the load over a greater number of fibres
I
I Contractile disturbances
I
I
Increase in muscle mass can create problem of
I
Oxygen supply/demand imbalance even with normal coronary circulation Fig. 2 Summary of pathological factors involved in hypertrophy.
ship. Should there be a marked increase in diastole volume and pressure with CHF patients, remodelling with side-to-side slippage and myocyte elongation dilate the left ventricular chamber with thinning of the wall. Eventually the ratio of wall thickness to chamber radius decreases. When this occurs hypertrophy cannot compensate, leading to acute ventricular failure (Cupples 1987). The hypertrophied heart increases in size according to two structural patterns. The patterns include eccentric hypertrophy and concentric hypertrophy. Eccentric hypertrophy occurs when the heart enlarges due to dilation and ventricular wall thickness. The structural change occurs when increases in ventricular end-diastolic volume cause total intraventricular volume to increase. The following changes occur in eccentric hypertrophy: • Chamber enlarges to accommodate the increased filling volume • Muscle mass is increased to maintain normal wall thickness • Total mass ofventricular volume is increased (Weeks 1986). With eccentric hypertrophy there is an increase in diastolic tension due to elevated volume and preload which stimulates elongation or synthesis of myocardial cells. T h e C H F patient with eccentric hypertrophy has an increased end-diastolic volume with normal filling pressure due to chamber enlargement reflecting an increase in ventricular compliance. Concentric hypertrophy produces an increase in the thickness of the ventricular wall without dilation of the ventricular chamber. It occurs in response to pressure overload. Therefore an increase in systolic wall tension associated with elevated pressure or afterload
stimulates the synthesis of myocardial cells in parallel (Michaelson 1983). The C H F patient with concentric hypertrophy develops a less compliant or distensible ventricle due to increased wall thickness. The ventricle requires a higher diastolic filling pressure to develop normal filling of the heart. Regardless of the specific type of hypertrophy in CHF, the compensatory mechanism is effective when the alteration in ventricnlar mass and geometry are sufficient to decrease the stress on the ventricle and maintain its functional capacity (Michaelson 1983). See Table 1 for a summary of physical findings associated with left and right ventricular hypertrophy.
Loss ofpositive-inotropic mechanism With CHF, the heart loses its load-reducing mechanism. During failure, the heart becomes dependent on endogenous inotropic processes to maintain cardiac function. Activation of inotropic mechanisms leads to a two-fold loss of their effects in myocardial contractility. Firstly, in CHF, the heart loses its ability to enhance its inotropic state in response to elevated ventricular volume. At this time, increases in preload fail to enhance systolic ejection. Secondly, in heart failure, the heart loses its ability to respond to the positive inotropic effects of endogenous and exogenous catecholamines (Packer 1994). Ventricular dilatation coupled with sympathetic activation leads to loss of positive-inotropic effect on cardiac contractihty. Furthermore, an enlarged ventricular size depresses cardiac function in heart failure, since the failing heart is resistant to increases in preload but susceptible to increases in afterload (Packer 1992). The failing heart is associated with a loss of responsiveness to ~-adrenergic stimuli in the heart; however, it is characterised by increased
Acute congestive heart failure: pathophysiological alterations
2.13
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responsiveness to 0~-adrenergic stimuli on peripheral vessels (Forster, Armstrong 1990).
Biochemical changes Biochemical changes are accompanied by changes in the mechanism o f contraction. Reduced contractility is accompanied by a shift in myosin isozymes, such that rapidly contracting V1 forms with high adenosine triphosphatase (ATPase) activity are converted into slower contractility V3 form with slower ATPase activity (Entman, Michael 1988). Biochemical changes in C H F include the following: • Increase in connective tissue • Calcium overload • Decreased function ofsarcoplasmic reticulum • Decreased stores o f myocardial norepinephrine • Decreased production ofnorepinephrine • Decreased beta-receptors (Parmley 1983). Biochemical changes also cause mechanical changes in contraction. These changes include the following: • • • •
Slower rate o f contraction Prolonged time to peak tension Slower rate of relaxation Reduced velocity of shortening (Michaelson 1983, Parmley 1989).
W h e n relaxation is slowed, the normal elastic recoil of the ventricle in early diastole is reduced. The overall response is restricted diastolic filling.
Myocardial o x y g e n s u p p l y / d e m a n d imbalance Continuous mixed venous oxygen saturation (SVO2) monitoring is an invasive procedure that demonstrates the body's ability to meet tissue oxygen demands. A normal SVO2 is 60% to 80% whereas a value of_<60% signifies cardiac decompensation or oxygen demand greater than supply. There are two factors affecting SVO2: oxygen supply/delivery and oxygen demand/consumption. Oxygen supply is the amount o f oxygen delivered to the tissues each minute. The goal o f the cardiovascular system is to deliver adequate oxygen to meet tissue
arterial oxygen content (CaO2) and the amount of blood delivered to the tissues which includes C O and cardiac index (CI). W h e n oxygen supply is reduced it may be due to decreased oxygen content (decreased Hgb, PaO 2 or arterial oxygen saturation (SaO2)) or to decreased cardiac output (Mims 1992). The normal oxygen transport is approximately 640 to 1400ml/min or 5006 0 0 m l / m i n / m 2. For the C H F patient inadequate oxygen supply/delivery is due to reduced C O secondary to myocardial dysfunction. The thickened, elongated myocardial fibres are inefficient with respect to oxygen diffusion. The diffusion rate of oxygen through tissue varies inversely with the square o f the distance the oxygen must travel. If a myocardial fibre doubles in size, it takes four times longer for oxygen saturation to occur than if the fibres were not hypertrophied. The oxygen disadvantage is even greater in a hypertrophied heart that is tachycardiac (Weeks 1986). Oxygen demand/consumption is the amount of oxygen used by the tissues each minute. The amount o f oxygen consumed can be an indicator o f the adequacy o f oxygen supply. The normal oxygen consumption is approximately 180 to 380ml/min or 110 to 1 6 0 m l / m i n / m 2 (Mims 1992). W h e n oxygen supply is insufficient, a greater proportion of the oxygen delivered will be extracted from the blood, thus lowering the oxygen content in the venous end of the circulation. Should oxygen demand/consumption increase, the C H F patient may be unable to increase C O to provide sufficient supply. During CHF, the oxygen requirements o f the hypertrophied heart are increased. The blood vessels do not correspondingly increase or dilate adequately to meet oxygen demand. Continuous mixed venous oxygen saturation is an indicator o f oxygen supply/demand status. A reduced SVO2 <60% may indicate that oxygen demand exceeds supply. In order to compensate, oxygen supply must be increased by increasing C O , Hgb or SaG 2 and oxygen demand must be reduced (Mims 1992). As mentioned earlier, patients with C H F may have insufficient myocardial reserve to increase C O in order to meet the body's need for oxygen. Patients with acute C H F have increased tissue oxygen extraction. The percentage o f oxygen extracted by the tissues becomes a useful indication of the balance between oxygen delivery and consumption. The normal extraction ratio is 25%. The ratio increases in pathologic conditions showing an imbalance between oxygen supply and oxygen demand (Gardner 1989). When, as in acute CHF, the cardiac reserve is not sufficient to
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maintain tissue perfusion, the increased tissue oxygen extraction is associated with a decline in the affinity of haemoglobin for oxygen. A shift of the oxyhaemoglobin dissociation curve to the right increases oxygen requirements to bind with haemoglobin and risk of lactic acidaemia (Ganong 1981). Excess
neurohormonal
stimulation
Excess neurohormonal stimulation includes sympathoadrenergic hyperactivity, renin-angiotensin-aldosterone system, sodium retention and peripheral vascular changes.
Sympathoadrenergic hyperactivity An immediate physiological response to acute CHF is increased sympathoadrenergic stimulation which maintains adequate circulation when there is cardiac dysfunction or decreased intravascular volume. Stimulation of the sympathetic nervous system (SNS) is caused by a sudden decrease in cardiac output. The overall goal of sympathoadrenergic stimulation is to increase cardiac output and to effect a redistribution of peripheral blood flow to preserve circulation to vital organs (Weeks 1986). See Figure 3 for a summary of factors involved in sympathoadrenergic stimulation (Michaelson 1983). Sympathetic hyperactivity results in an increased production of norepinephrine which can cause the following adaptive response: • • • • •
Increase heart rate Increase contractility Increase stroke volume Increase cardiac output Redistribution of blood flow through vasodilation and vasoconstriction • Retention of sodium and water to raise blood volume (Weeks 1986)
The sympathetic compensatory redistribution of blood flow occurs in response to a failing heart. The normal shunting of blood from the mesenteric vascular system to the vital organs is increased in a patient with acute CHF. A 90% reduction in the total concentration of norepinephrine (noradrenaline) stores occurs in the failing myocardium. A reduction in the total amount of norepinephrine release may contribute to worsening heart failure. As a compensatory response, the level of circulating catecholamines is increased and the neurotransmitters become the source of cardiac stimulation (Weeks 1986). The sympathetic compensatory redistribution of blood flow occurs in response to a failing heart. The normal shunting of blood from the mesenteric vascular system to the vital organs is increased in a patient with acute CHF. A 90% reduction in the total concentration of norepinephrine (noradrenaline) stores occurs in the failing myocardium. A reduction in the total amount of norepinephrine release may contribute to worsening heart failure. As a compensatory response, the level of circulating catecholamines is increased and the neurotransmitters become the source of cardiac stimulation (Weeks 1986). The failing myocardium, in response to norepinephrine, becomes hypersensitive and dependent on sustained sympathoadrenergic stimulation and elevated levels of exogenous norepinephrine. The result is compensatory tachycardia. As CHF progresses, tachycardia can decrease coronary artery perfusion leading to myocardial supply/demand imbalance (Michaelson 1983). In addition, depletion of endogenous or cardiac stores ofnorepinephrine interferes with sympathetic augmentation of contractility which further reduces cardiac reserve (Rutenberg, Spann 1976).
genin-Angiotensin-Aldosterone Reduced cardiac output
I Depresses I
I
Arterial pressure
[
I
I Which stimulate I
Baroreceptors
I Atrial stretch receptors I Goal
I
Emit afferent nerve impulse to cardioregulatory centre in the brain
Fig. 3
i
Cardiac
Pulse pressure filling
Stroke volume
Factors involved in sympathoadrenergic stimulation.
I Myocardial receptor
sites
I
With CHF, the renin-angiotensin-aldosterone (RAA) system is stimulated by the catalyst renin. The RAA system promotes proximal and distal tubular reabsorption of sodium and water, and the kidneys are unable to excrete any increase in sodium load. RAA can be activated in patients with CHF by three primary mechanisms whereby renin production is increased: • Reduced serum sodium • Increase in sympathetic tone • Decreased blood pressure perfusing the macula dense (Parmley 1989). Renin is secreted by the juxtaglomerular cells that surround the afferent renal arterioles as they enter the glomerulus. The hypersecretion of renin in CHF potentiates sympathetic
Acute congestive heart failure: pathophysiological alterations
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vasomotor tone to produce increased vascular resistance. The resulting increase in arterial pressure and left ventricular afterload can alter cardiac pump function (Michaelson 1983). Renin converts into angiotensin I, which is finally converted into angiotensin II, which serves as a primary stimulus for aldosterone release from the adrenal cortex for action in the kidney. Angiotensin II has significant implications for patients in CHF. Angiotensin II is a potent vasoconstrictor which can lead to excessive systemic vascular resistance, facilitate sympathetic outflow contributing to further elevated levels o f plasma catecholamines, and release aldosterone, which further contributes to the increased salt retention in patients with CHF.
Firstly, there is a decrease o f effective arterial blood volume and augmented sodium reabsorption. Secondly, in moderate failure, elevated aldosterone may cause increased sodium reabsorption in the distal nephrons while there is a reduction of natriuretic hormone. Finally, in severe failure, both circulatory and neurohormonal stimuli are intense so that extracellular fluid volume become diflScult to obtain (Weeks 1986). The development o f sodium retention in heart failure can signify a shift in circulatory response with the cardiovascular system moving from a state of compensation to a state of decompensation. Sodium retention therefore plays a role in the progression o f CHF.
Sodium retention
Peripheral vascular changes
Decreased renal perfusion plays a significant role in the abnormality of sodium excretion by a C H F patient. Besides the R A A system, there are two other mechanisms involved in abnormal sodium reabsorption in the renal tubules. The first is diminished glomemlar filtration rate. The primary site for sodium transport is in the proximal tubule. W h e n the C H F patient experiences reduced cardiac output, renal blood flow is decreased while sodium is reabsorbed from a decreased filtrate flow (Parmley 1989). Secondly, hormonal substances promote reabsorption. The following hormones are involved in sodium reabsorption:
W h e n cardiac output falls, systemic perfusion pressure is maintained by peripheral vasoconstriction. Peripheral vasoconstriction is produced by the interrelationship of haemodynamic and neurohormonal factors (Packaer 1992). The sympathetic nervous system is activated in heart failure when ventricular dilatation occurs. Furthermore, the release o f endothelium-derived relaxing factor is decreased in patients with C H F (Goldstein et al 1993). Because o f vasodilation factor, the action of vasoconstriction is left unopposed. Loss of vasodilation factor leading to vasoconstriction, and related factors, are summarised in Figure 4. Because neurohormonal activation causes peripheral vasoconstriction, mechanical factors can also lead to increased peripheral resistance. Sodium retention may impair the vasodilation capacity of peripheral blood vessels due to an increase in the sodium content of peripheral vessels or to the compression of perivascular tissue from oedema (Packer 1992).
• Extra-adrenal sodium-retaining factor or natriuretic hormone • Antidiuretic hormone (ADH) • Adrenergic effect of decreased cardiac output (Weeks 1986). A reduction of the natriuretic hormone may lead to oedema in CHF. The antidiuretic hormone's major effect is to increase nephron permeability to water, thus enhancing reabsorption. The adrenergic effects involve the results of redistribution of cardiac output which indude the following: • Diminished renal blood flow • Increased venous hydrostatic pressure • Augmented renin release (Weeks 1986). Angiotensin has a two-fold effect. First, angiotensin has a vasoconstrictor effect in the efferent arterioles. This causes an increase in the filtration fraction which alters the peritubular balance ofoncotic forces. The overall response is the enhancement o f proximal tubular sodium reabsorption. Secondly, angiotensin causes water retention by stimulating the thirst centre to increase water intake and by enhancing the release of vasopressin to decrease water excreuon (Packer 1992). The kidney's response in C H F is three-fold.
SUMMARY Heart failure is primarily the result of two pathologic problems: myocardial failure leading to dysfunction o f the left ventricle and congestive failure which develops as a consequence o f impaired left ventricular function (Sonnenblick, LeJenkel 1993). To understand better how various treatments are used to support a failing heart, it is important for critical care nurses to examine pathological alterations associated with CHF. These alterations are categorised into cardiac compensatory dysfunction and excess neurohormonal stimulation. Knowing the two categories of pathological alteration can alert health care providers to those patients who are at risk of developing
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Intensive and Critical Care Nursing
Loss of vasodilating factor
I
Vasoconstriction
I Enhanced by process of
I Mural neurohormonal amplification
I Such as
I
I
Activation of the sympathetic nervous system
I
Angiotensin
I
Enhances the release of two factors
I Increase release of renin
I Noradrenaline
l
I Vasopressin
Fig. 4 Responses to loss ofvasodilating factor. progressive
or decompensatory
and mobilise interventions more
h e a r t failure q u i c k l y to
alleviate o r lessen its o c c u r r e n c e . REFERENCES BenzJJ 1994 Heart failure. In: Hudak C M, Ballo B M, eds. Critical Care Nursing. J B Lippincott, Philadelphia Cupples L A, D'Aqostino R B 1987 Framingham Study Monograph. Section 34. An epidemiological investigation of cardiovascular disease. Some risk factors related to the annual incidence of cardiovascular disease and death using pool of repeated biennial measurements: 30-year follow-up. In: Kannel W B, WolfP A, Garrison R J, eds. NIH Publication, No. 87-2703, US Department of Commerce. National Technical Information Service, Springfield, VA.
Entman M L, Michael L H 1988 Molecular and cellular basis for myocardial failure. In: Parmley W W, Chatterjee R, eds. Cardiology. J B Lippincott, Philadelphia Forster C, Armstrong P W 1990 Pacing-induced heart failure in the dog: evaluation of peripheral vascular alpha-adrenoreceptor subtypes. Journal Cardiovascular Pharmacology 16:708-716 Ganong W F 1981 Review of medical physiology. Lange Medical, Los Altos, CA Gardner P E 1989 The pulmonary circulation and gas exchange. In: Underhill S G, Woods S L, Froelicher E S, Halpenny C J, ed. Cardiac nursing, 2nd ed. J B Lippincott, Philadelphia, pp. 80-85 Goldstein R E, Boccuzzi S J, Cmess D, Nattel S 199? The adverse experience committee and the multicenter diltiazem post-infarction research group. Diltiazem increases late-onset congestive heart failure in postinfarction patients with early reduction in ejection fraction. Circulation 88:52-60 Michaelson C R 1983 Pathophysiology of heart failure: a conceptual framework for understanding clinical indicators and therapeutic modalities. In: Michaelson CR, ed. Congestive heart failure. C V Mosby, St Louis, pp 44-84 Mims B C 1992 Imbalance of oxygen supply and demand. In: Huddlestrom V B, ed. Multisystem organ failure. Mosby Year Book, St Louis Packer M 1992 Pathophysiology of chronic heart failure. Lancet 340:88-92 Parmley W W 1989 Pathophysiology and current therapy of congestive heart failure. American College of Cardiology 13 (4): 771-785 Rutenberg H L, SpannJ F 1976 Alteration of cardiac sympathetic neurotransmitter activity in congestive heart failure. In: Mason D T, ed. Congestive heart failure mechanisms, evaluation and treatment. York Medical Book, New York Weeks L C 1986 Advanced cardiovascular nursing. Blackwell Scientific, Boston
Acute congestive heart failure:
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when compensatory haemodynamic and neurohormonal mechanisms are overwhelmed or exhausted (Packer 1992).
PATHOPHYSIOLOGICAL ALTERATIONS ASSOCIATED WITH ACUTE CHF Pathophysiological alterations associated with acute C H F can be divided into two categories: cardiac compensatory dysfunction and excess neurohormonal stimulation.
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Rebecca Dahlen and Sharon L. Roberts
The goal of a healthy heart is to transfer blood coming to the ventricles from the low pressure venous system into the high pressure arterial system. In acute congestive heart failure (CHF), impaired cardiac function leads to failure to empty venous reservoirs and therefore to reduce delivery of blood into the arterial circulation (Michaelson 1983). Once heart failure occurs it has a high mortality rate. According to the Framingham Heart Study, 50% of patients with New York Heart Association class II or III heart failure died within 5 years. With class IV patients, 50% survived less than I year (Cupples 1987). The purpose of this article is first to define acute CHF. Secondly, the pathophysiological alterations that occur as a result of strained and misdirected compensatory mechanisms will be discussed to help critical care nurses to recognise why certain patients are at risk of developing acute CHF. Rebecca Dahlen RN, MSN, CNS, Assistant Professor Sharon L. Roberts RN, PhD, FAAN, Professor, California State University, Long Beach, Department of Nursing, California, USA
(Requests for offprints to SLR) Manuscript accepted 14 June 1995 Nursing management of congestive heart failure Parts I and 2, by the same authors, will appear in the next two issuesof the journal
Cardiac compensatory dysfunction Cardiac compensatory dysfunction includes six factors: reduced myocardial contractility; cardiac dilation; myocardial hypertrophy; loss of positive-inotropic mechanism; biochemical changes and myocardial oxygen supply/ demand imbalance.
Reduced myocardial contractility Acute C H F patients with systolic dysfunction have reduced myocardial contractili W due to prolonged pressure or volume overload. Loss of muscle as in myocardial infarction causes an additional volume and wall stress overload in the remaining normal myocardium, which is why patients with AMI are at risk of developing heart failure. Reduced myocardial contractility is manifested by: • Decreased force development • Decreased rate o f force development • Decreased veloci W of shortening at a given loading condition • Decreased relaxation (Parmley 1983). A disturbance in the contractile state can diminish ejection fraction and stroke volume. There is also a shift downward in the ventricular function curve with an increase in atrial pressure. The acute CHF patient can have a low ejection fraction (EF)_0.5 indicating excessive myocardial dilation with respect to stroke volume (XVeeks 1986, Benz 1994).
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D E F I N I T I O N OF T E R H S Myocardial failure exists when the heart fails due to an intrinsic abnormality of the heart muscle. Heart failure includes myocardial failure and exists when demands are made on normal heart muscle that exceed its capability to perform (VCeeks 1986). Acute C H F patients have structural cardiac damage that adversely affects systolic or diastolic function. Heart failure can develop when the heart is injured and
Intensiveand Critical CoreNursing (I 995) I I, 210-216 © 1995PearsonProfessional/td
Cardiac dilation Normally, the left and right ventricles each respond in their own way to the cardiac workload placed upon them. Figure 1 is a summary of these responses. The right ventricle is an efficient volume pump. Increases in right ventricular blood volume can be accommodated as long as right ventricular filling pressure remains low. Increased left ventricle volume in the failing heart, however, causes increased diastolic and systolic ventricular size or dilation. N o r -
Acute congestive heart failure: pathophysiological alterations
Ventricular failure I
I Left ventricle
I Right ventricle
I
I Configuration
Can eject blood volume against high outflow pressure
I
I I Small internal diameter
Due to ventricular configuration I Cylindric shape
21 I
Has a large surface area
I Requires
I
I Thick wall
High levels of myocardial tension to generate high intrachamber pressure
I
I
J
Result
I Moves large volume of blood when outflow pressure remains low
Fig. I Responses of right and left ventricles to cardiac workload.
really, the left ventricle is distensible and adapts to increased diastolic volume or reload without significantly increased tilting pressure. Optimum contractility occurs at a fibre length of 2.2 blrn or 12-18 m m H g (Forster, Armstrong 1990). With cardiac dilation, the muscle cell stretches. The relationship between the cardiac output and the length of the heart muscle cell at the end of diastole is expressed as the FrankStarling relationship. This relationship states that as the end-diastolic filling length increases so does the cardiac output (CO). However, cardiac dilation can be self-limiting whereby the stretching of the muscle cell leads to reduced CO. The change is explained by the Laplace relationship, whereby the tension in the wall of a chamber such as the left ventricle is related directly to the p r e s s u r e o n that chamber and its radius (Benz 1994). Dilation results in an increased capacity of the cardiac chamber for work and stroke output. The degree to which dilatation must adapt to this increased workload increases with the severity of C H F as a result of reduced contractility. With cardiac dilation less fibre shortening is required to eject a given amount of blood during systole than is required in the normal heart. However, as the ventricle fails, increased enddiastolic volume and pressure is required to generate tension equal to that of a normal heart with normal end-diastolic volume (Weeks 1986). Myocardial hypertrophy In the presence of chronically increased volume loads, the ventricle hypertrophies. The number of individual myocardial fibre increases, resulting in greater ventricular mass (Weeks 1986). Hypertrophy is a significant compensatory mechanism for a failing heart and is accompanied by an increase in connective tissue which may stiffen the diastolic properties of the heart.
The myocardial ceils adapt to a sustained elevated workload by hypertrophy with increased muscle mass and altered geometrical configuration (Michaelson 1983). See Figure 2 for a summary of pathological factors involved in hypertrophy. Each hypertrophied cell requires more energy because of its increased mass and has less contractile force. As a result the heart is likely to fail under prolonged stress (Michaelson 1983). Hypertrophy is due to myocellular enlargement and initiates a sequence of adaptive responses affecting ventricular function. Hypertrophy due to ventricular failure involves ventricular wall remodelling. As the diastolic volume enlarges, the following cellular processes of remodelling are initiated: • • • •
Myocytes elongate Myocytes increase in diameter Myocytes are displaced relative to one another Reduction in the number ofmyocytes across the wall • Increased wall tension per cell (Cupples 1987). Myocellular hypertrophy is determined by two factors. The first factor is a segmental loss of myocardium resulting in hypertrophic growth of non-ischaemic myocytes. The second factor involves a reduction in the number ofmyocytes across the ventricular wall associated with lateral slipping of cells (Cupples 1987). When the number of myocytes is reduced there is an increased tension per cell which requires that myocytes hypertrophy. Augmented diastolic ventricular volume can result in increased hypertrophy. Therefore, diastole (with ventricular wall remodelling) and systole (with increased systolic tension) combine to augment the amount of hypertrophy required to normalise tension and balance the Laplace relation-
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Myocardial hypertrophy
I I Hypertrophy compensates for the pressure overload induced by dilation
Two factors I
I Hypertrophy normalised systolic and diastolic stress regardlessof increased pressure load
I Effective in I
How?
L
I Systolic pressure overload
By sharing the load over a greater number of fibres
I
I Contractile disturbances
I
I
Increase in muscle mass can create problem of
I
Oxygen supply/demand imbalance even with normal coronary circulation Fig. 2 Summary of pathological factors involved in hypertrophy.
ship. Should there be a marked increase in diastole volume and pressure with CHF patients, remodelling with side-to-side slippage and myocyte elongation dilate the left ventricular chamber with thinning of the wall. Eventually the ratio of wall thickness to chamber radius decreases. When this occurs hypertrophy cannot compensate, leading to acute ventricular failure (Cupples 1987). The hypertrophied heart increases in size according to two structural patterns. The patterns include eccentric hypertrophy and concentric hypertrophy. Eccentric hypertrophy occurs when the heart enlarges due to dilation and ventricular wall thickness. The structural change occurs when increases in ventricular end-diastolic volume cause total intraventricular volume to increase. The following changes occur in eccentric hypertrophy: • Chamber enlarges to accommodate the increased filling volume • Muscle mass is increased to maintain normal wall thickness • Total mass ofventricular volume is increased (Weeks 1986). With eccentric hypertrophy there is an increase in diastolic tension due to elevated volume and preload which stimulates elongation or synthesis of myocardial cells. T h e C H F patient with eccentric hypertrophy has an increased end-diastolic volume with normal filling pressure due to chamber enlargement reflecting an increase in ventricular compliance. Concentric hypertrophy produces an increase in the thickness of the ventricular wall without dilation of the ventricular chamber. It occurs in response to pressure overload. Therefore an increase in systolic wall tension associated with elevated pressure or afterload
stimulates the synthesis of myocardial cells in parallel (Michaelson 1983). The C H F patient with concentric hypertrophy develops a less compliant or distensible ventricle due to increased wall thickness. The ventricle requires a higher diastolic filling pressure to develop normal filling of the heart. Regardless of the specific type of hypertrophy in CHF, the compensatory mechanism is effective when the alteration in ventricnlar mass and geometry are sufficient to decrease the stress on the ventricle and maintain its functional capacity (Michaelson 1983). See Table 1 for a summary of physical findings associated with left and right ventricular hypertrophy.
Loss ofpositive-inotropic mechanism With CHF, the heart loses its load-reducing mechanism. During failure, the heart becomes dependent on endogenous inotropic processes to maintain cardiac function. Activation of inotropic mechanisms leads to a two-fold loss of their effects in myocardial contractility. Firstly, in CHF, the heart loses its ability to enhance its inotropic state in response to elevated ventricular volume. At this time, increases in preload fail to enhance systolic ejection. Secondly, in heart failure, the heart loses its ability to respond to the positive inotropic effects of endogenous and exogenous catecholamines (Packer 1994). Ventricular dilatation coupled with sympathetic activation leads to loss of positive-inotropic effect on cardiac contractihty. Furthermore, an enlarged ventricular size depresses cardiac function in heart failure, since the failing heart is resistant to increases in preload but susceptible to increases in afterload (Packer 1992). The failing heart is associated with a loss of responsiveness to ~-adrenergic stimuli in the heart; however, it is characterised by increased
Acute congestive heart failure: pathophysiological alterations
2.13
demand. The oxygen delivery (D02) is deter~i~i~i~iii~iii~i~i~i~i~iii~i~iii~i~iiiiiiiiiiiiiiii!iii!i!iiiii!iiiiiiiiiii~ii!ii~iii~iii~ii!~i~iiiii~iiiii~iii~i~i~i~i~iii~iii~iii~!iiiiiiiii!iii!i!i!i!iii!iiiiiiiiii~iiii~iii~!~!~i~!ii~i~i~iii~iiiiiii~i~i~iiiii~iiii~i
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Left ventricular hypertrophy
Right ventricular hypertrophy
Left ventricular heave palpated at
Palpation of right ventricular heave
the apex of the heart
over the lower central chest
$3, ventricular gallop
Right sides S3
$4, atrial gallop related to decreased ventricular compliance
S4, atrial gallop
responsiveness to 0~-adrenergic stimuli on peripheral vessels (Forster, Armstrong 1990).
Biochemical changes Biochemical changes are accompanied by changes in the mechanism o f contraction. Reduced contractility is accompanied by a shift in myosin isozymes, such that rapidly contracting V1 forms with high adenosine triphosphatase (ATPase) activity are converted into slower contractility V3 form with slower ATPase activity (Entman, Michael 1988). Biochemical changes in C H F include the following: • Increase in connective tissue • Calcium overload • Decreased function ofsarcoplasmic reticulum • Decreased stores o f myocardial norepinephrine • Decreased production ofnorepinephrine • Decreased beta-receptors (Parmley 1983). Biochemical changes also cause mechanical changes in contraction. These changes include the following: • • • •
Slower rate o f contraction Prolonged time to peak tension Slower rate of relaxation Reduced velocity of shortening (Michaelson 1983, Parmley 1989).
W h e n relaxation is slowed, the normal elastic recoil of the ventricle in early diastole is reduced. The overall response is restricted diastolic filling.
Myocardial o x y g e n s u p p l y / d e m a n d imbalance Continuous mixed venous oxygen saturation (SVO2) monitoring is an invasive procedure that demonstrates the body's ability to meet tissue oxygen demands. A normal SVO2 is 60% to 80% whereas a value of_<60% signifies cardiac decompensation or oxygen demand greater than supply. There are two factors affecting SVO2: oxygen supply/delivery and oxygen demand/consumption. Oxygen supply is the amount o f oxygen delivered to the tissues each minute. The goal o f the cardiovascular system is to deliver adequate oxygen to meet tissue
arterial oxygen content (CaO2) and the amount of blood delivered to the tissues which includes C O and cardiac index (CI). W h e n oxygen supply is reduced it may be due to decreased oxygen content (decreased Hgb, PaO 2 or arterial oxygen saturation (SaO2)) or to decreased cardiac output (Mims 1992). The normal oxygen transport is approximately 640 to 1400ml/min or 5006 0 0 m l / m i n / m 2. For the C H F patient inadequate oxygen supply/delivery is due to reduced C O secondary to myocardial dysfunction. The thickened, elongated myocardial fibres are inefficient with respect to oxygen diffusion. The diffusion rate of oxygen through tissue varies inversely with the square o f the distance the oxygen must travel. If a myocardial fibre doubles in size, it takes four times longer for oxygen saturation to occur than if the fibres were not hypertrophied. The oxygen disadvantage is even greater in a hypertrophied heart that is tachycardiac (Weeks 1986). Oxygen demand/consumption is the amount of oxygen used by the tissues each minute. The amount o f oxygen consumed can be an indicator o f the adequacy o f oxygen supply. The normal oxygen consumption is approximately 180 to 380ml/min or 110 to 1 6 0 m l / m i n / m 2 (Mims 1992). W h e n oxygen supply is insufficient, a greater proportion of the oxygen delivered will be extracted from the blood, thus lowering the oxygen content in the venous end of the circulation. Should oxygen demand/consumption increase, the C H F patient may be unable to increase C O to provide sufficient supply. During CHF, the oxygen requirements o f the hypertrophied heart are increased. The blood vessels do not correspondingly increase or dilate adequately to meet oxygen demand. Continuous mixed venous oxygen saturation is an indicator o f oxygen supply/demand status. A reduced SVO2 <60% may indicate that oxygen demand exceeds supply. In order to compensate, oxygen supply must be increased by increasing C O , Hgb or SaG 2 and oxygen demand must be reduced (Mims 1992). As mentioned earlier, patients with C H F may have insufficient myocardial reserve to increase C O in order to meet the body's need for oxygen. Patients with acute C H F have increased tissue oxygen extraction. The percentage o f oxygen extracted by the tissues becomes a useful indication of the balance between oxygen delivery and consumption. The normal extraction ratio is 25%. The ratio increases in pathologic conditions showing an imbalance between oxygen supply and oxygen demand (Gardner 1989). When, as in acute CHF, the cardiac reserve is not sufficient to
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maintain tissue perfusion, the increased tissue oxygen extraction is associated with a decline in the affinity of haemoglobin for oxygen. A shift of the oxyhaemoglobin dissociation curve to the right increases oxygen requirements to bind with haemoglobin and risk of lactic acidaemia (Ganong 1981). Excess
neurohormonal
stimulation
Excess neurohormonal stimulation includes sympathoadrenergic hyperactivity, renin-angiotensin-aldosterone system, sodium retention and peripheral vascular changes.
Sympathoadrenergic hyperactivity An immediate physiological response to acute CHF is increased sympathoadrenergic stimulation which maintains adequate circulation when there is cardiac dysfunction or decreased intravascular volume. Stimulation of the sympathetic nervous system (SNS) is caused by a sudden decrease in cardiac output. The overall goal of sympathoadrenergic stimulation is to increase cardiac output and to effect a redistribution of peripheral blood flow to preserve circulation to vital organs (Weeks 1986). See Figure 3 for a summary of factors involved in sympathoadrenergic stimulation (Michaelson 1983). Sympathetic hyperactivity results in an increased production of norepinephrine which can cause the following adaptive response: • • • • •
Increase heart rate Increase contractility Increase stroke volume Increase cardiac output Redistribution of blood flow through vasodilation and vasoconstriction • Retention of sodium and water to raise blood volume (Weeks 1986)
The sympathetic compensatory redistribution of blood flow occurs in response to a failing heart. The normal shunting of blood from the mesenteric vascular system to the vital organs is increased in a patient with acute CHF. A 90% reduction in the total concentration of norepinephrine (noradrenaline) stores occurs in the failing myocardium. A reduction in the total amount of norepinephrine release may contribute to worsening heart failure. As a compensatory response, the level of circulating catecholamines is increased and the neurotransmitters become the source of cardiac stimulation (Weeks 1986). The sympathetic compensatory redistribution of blood flow occurs in response to a failing heart. The normal shunting of blood from the mesenteric vascular system to the vital organs is increased in a patient with acute CHF. A 90% reduction in the total concentration of norepinephrine (noradrenaline) stores occurs in the failing myocardium. A reduction in the total amount of norepinephrine release may contribute to worsening heart failure. As a compensatory response, the level of circulating catecholamines is increased and the neurotransmitters become the source of cardiac stimulation (Weeks 1986). The failing myocardium, in response to norepinephrine, becomes hypersensitive and dependent on sustained sympathoadrenergic stimulation and elevated levels of exogenous norepinephrine. The result is compensatory tachycardia. As CHF progresses, tachycardia can decrease coronary artery perfusion leading to myocardial supply/demand imbalance (Michaelson 1983). In addition, depletion of endogenous or cardiac stores ofnorepinephrine interferes with sympathetic augmentation of contractility which further reduces cardiac reserve (Rutenberg, Spann 1976).
genin-Angiotensin-Aldosterone Reduced cardiac output
I Depresses I
I
Arterial pressure
[
I
I Which stimulate I
Baroreceptors
I Atrial stretch receptors I Goal
I
Emit afferent nerve impulse to cardioregulatory centre in the brain
Fig. 3
i
Cardiac
Pulse pressure filling
Stroke volume
Factors involved in sympathoadrenergic stimulation.
I Myocardial receptor
sites
I
With CHF, the renin-angiotensin-aldosterone (RAA) system is stimulated by the catalyst renin. The RAA system promotes proximal and distal tubular reabsorption of sodium and water, and the kidneys are unable to excrete any increase in sodium load. RAA can be activated in patients with CHF by three primary mechanisms whereby renin production is increased: • Reduced serum sodium • Increase in sympathetic tone • Decreased blood pressure perfusing the macula dense (Parmley 1989). Renin is secreted by the juxtaglomerular cells that surround the afferent renal arterioles as they enter the glomerulus. The hypersecretion of renin in CHF potentiates sympathetic
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vasomotor tone to produce increased vascular resistance. The resulting increase in arterial pressure and left ventricular afterload can alter cardiac pump function (Michaelson 1983). Renin converts into angiotensin I, which is finally converted into angiotensin II, which serves as a primary stimulus for aldosterone release from the adrenal cortex for action in the kidney. Angiotensin II has significant implications for patients in CHF. Angiotensin II is a potent vasoconstrictor which can lead to excessive systemic vascular resistance, facilitate sympathetic outflow contributing to further elevated levels o f plasma catecholamines, and release aldosterone, which further contributes to the increased salt retention in patients with CHF.
Firstly, there is a decrease o f effective arterial blood volume and augmented sodium reabsorption. Secondly, in moderate failure, elevated aldosterone may cause increased sodium reabsorption in the distal nephrons while there is a reduction of natriuretic hormone. Finally, in severe failure, both circulatory and neurohormonal stimuli are intense so that extracellular fluid volume become diflScult to obtain (Weeks 1986). The development o f sodium retention in heart failure can signify a shift in circulatory response with the cardiovascular system moving from a state of compensation to a state of decompensation. Sodium retention therefore plays a role in the progression o f CHF.
Sodium retention
Peripheral vascular changes
Decreased renal perfusion plays a significant role in the abnormality of sodium excretion by a C H F patient. Besides the R A A system, there are two other mechanisms involved in abnormal sodium reabsorption in the renal tubules. The first is diminished glomemlar filtration rate. The primary site for sodium transport is in the proximal tubule. W h e n the C H F patient experiences reduced cardiac output, renal blood flow is decreased while sodium is reabsorbed from a decreased filtrate flow (Parmley 1989). Secondly, hormonal substances promote reabsorption. The following hormones are involved in sodium reabsorption:
W h e n cardiac output falls, systemic perfusion pressure is maintained by peripheral vasoconstriction. Peripheral vasoconstriction is produced by the interrelationship of haemodynamic and neurohormonal factors (Packaer 1992). The sympathetic nervous system is activated in heart failure when ventricular dilatation occurs. Furthermore, the release o f endothelium-derived relaxing factor is decreased in patients with C H F (Goldstein et al 1993). Because o f vasodilation factor, the action of vasoconstriction is left unopposed. Loss of vasodilation factor leading to vasoconstriction, and related factors, are summarised in Figure 4. Because neurohormonal activation causes peripheral vasoconstriction, mechanical factors can also lead to increased peripheral resistance. Sodium retention may impair the vasodilation capacity of peripheral blood vessels due to an increase in the sodium content of peripheral vessels or to the compression of perivascular tissue from oedema (Packer 1992).
• Extra-adrenal sodium-retaining factor or natriuretic hormone • Antidiuretic hormone (ADH) • Adrenergic effect of decreased cardiac output (Weeks 1986). A reduction of the natriuretic hormone may lead to oedema in CHF. The antidiuretic hormone's major effect is to increase nephron permeability to water, thus enhancing reabsorption. The adrenergic effects involve the results of redistribution of cardiac output which indude the following: • Diminished renal blood flow • Increased venous hydrostatic pressure • Augmented renin release (Weeks 1986). Angiotensin has a two-fold effect. First, angiotensin has a vasoconstrictor effect in the efferent arterioles. This causes an increase in the filtration fraction which alters the peritubular balance ofoncotic forces. The overall response is the enhancement o f proximal tubular sodium reabsorption. Secondly, angiotensin causes water retention by stimulating the thirst centre to increase water intake and by enhancing the release of vasopressin to decrease water excreuon (Packer 1992). The kidney's response in C H F is three-fold.
SUMMARY Heart failure is primarily the result of two pathologic problems: myocardial failure leading to dysfunction o f the left ventricle and congestive failure which develops as a consequence o f impaired left ventricular function (Sonnenblick, LeJenkel 1993). To understand better how various treatments are used to support a failing heart, it is important for critical care nurses to examine pathological alterations associated with CHF. These alterations are categorised into cardiac compensatory dysfunction and excess neurohormonal stimulation. Knowing the two categories of pathological alteration can alert health care providers to those patients who are at risk of developing
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Loss of vasodilating factor
I
Vasoconstriction
I Enhanced by process of
I Mural neurohormonal amplification
I Such as
I
I
Activation of the sympathetic nervous system
I
Angiotensin
I
Enhances the release of two factors
I Increase release of renin
I Noradrenaline
l
I Vasopressin
Fig. 4 Responses to loss ofvasodilating factor. progressive
or decompensatory
and mobilise interventions more
h e a r t failure q u i c k l y to
alleviate o r lessen its o c c u r r e n c e . REFERENCES BenzJJ 1994 Heart failure. In: Hudak C M, Ballo B M, eds. Critical Care Nursing. J B Lippincott, Philadelphia Cupples L A, D'Aqostino R B 1987 Framingham Study Monograph. Section 34. An epidemiological investigation of cardiovascular disease. Some risk factors related to the annual incidence of cardiovascular disease and death using pool of repeated biennial measurements: 30-year follow-up. In: Kannel W B, WolfP A, Garrison R J, eds. NIH Publication, No. 87-2703, US Department of Commerce. National Technical Information Service, Springfield, VA.
Entman M L, Michael L H 1988 Molecular and cellular basis for myocardial failure. In: Parmley W W, Chatterjee R, eds. Cardiology. J B Lippincott, Philadelphia Forster C, Armstrong P W 1990 Pacing-induced heart failure in the dog: evaluation of peripheral vascular alpha-adrenoreceptor subtypes. Journal Cardiovascular Pharmacology 16:708-716 Ganong W F 1981 Review of medical physiology. Lange Medical, Los Altos, CA Gardner P E 1989 The pulmonary circulation and gas exchange. In: Underhill S G, Woods S L, Froelicher E S, Halpenny C J, ed. Cardiac nursing, 2nd ed. J B Lippincott, Philadelphia, pp. 80-85 Goldstein R E, Boccuzzi S J, Cmess D, Nattel S 199? The adverse experience committee and the multicenter diltiazem post-infarction research group. Diltiazem increases late-onset congestive heart failure in postinfarction patients with early reduction in ejection fraction. Circulation 88:52-60 Michaelson C R 1983 Pathophysiology of heart failure: a conceptual framework for understanding clinical indicators and therapeutic modalities. In: Michaelson CR, ed. Congestive heart failure. C V Mosby, St Louis, pp 44-84 Mims B C 1992 Imbalance of oxygen supply and demand. In: Huddlestrom V B, ed. Multisystem organ failure. Mosby Year Book, St Louis Packer M 1992 Pathophysiology of chronic heart failure. Lancet 340:88-92 Parmley W W 1989 Pathophysiology and current therapy of congestive heart failure. American College of Cardiology 13 (4): 771-785 Rutenberg H L, SpannJ F 1976 Alteration of cardiac sympathetic neurotransmitter activity in congestive heart failure. In: Mason D T, ed. Congestive heart failure mechanisms, evaluation and treatment. York Medical Book, New York Weeks L C 1986 Advanced cardiovascular nursing. Blackwell Scientific, Boston