The analysis of the effects of changes in peripheral resistance on cardiac output and Pv is intricate due to the shifting of both the cardiac and vascular function curves. When there is an increase in peripheral resistance (Fig. 19.11), the vascular function curve rotates counterclockwise but converges on the same Pv axis intercept as the control curve. It is important to note that vasoconstriction causes a counterclockwise rotation of the vascular function curve in Fig. 19.11, whereas in Fig. 19.5, the rotation is in a different direction because of the switching of axes for the vascular function curves. Additionally, the cardiac function curve in Fig. 19.11 shifts downward due to the heart's reduced ability to pump blood against the increased cardiac afterload resulting from the higher peripheral resistance. As both curves in Fig. 19.11 are displaced downward, the new equilibrium point (point B) falls below the control point (point A), indicating a decrease in cardiac output caused by an increase in peripheral resistance. The exact position of point B relative to point A depends on the magnitude of the shift in each curve. For instance, the increase in peripheral resistance caused by moderate or severe heart failure shifts the cardiac function curves downward and to the right (Fig. 19.10). Prior to changes in blood volume, cardiac output decreases and central venous pressure rises (from the control equilibrium point A to point B or point C). Following the increase in blood volume typically seen in heart failure, the vascular function curve is shifted to the right. Consequently, central venous pressure may be elevated without a reduction in cardiac output (point D) or, in severe heart failure, with some reduction in cardiac output (point E). Heart failure refers to conditions where the heart's pumping capability is impaired to the extent that body tissues are not adequately perfused. In heart failure, myocardial contractility is compromised, and it can be either acute or chronic. Therefore, on a graph of cardiac and vascular function curves, the cardiac function curve shifts downward and to the right as depicted in Fig. 19.10. Acute heart failure may be caused by toxic drug concentrations or certain pathological conditions such as coronary artery occlusion. In acute heart failure, there is no immediate change in blood volume. Consequently, the equilibrium point shifts from the intersection (point A) of the normal curves to the intersection (point B or point C) of the normal vascular function curve in Fig. 19.10. Chronic heart failure may occur in conditions like essential hypertension or ischemic heart disease. In chronic heart failure, both the cardiac function and vascular function curves shift. The shift in the vascular function curves is due to an increase in blood volume, partly caused by fluid retention by the kidneys. This fluid retention is related to the simultaneous reduction in glomerular filtration rate and decreased renal excretion of NaCl and water. The resultant hypervolemia is reflected by a rightward shift of the vascular function curve, as shown in Fig. 19.10. Therefore, in moderate degrees of heart failure, Pv is elevated, but cardiac output may be normal (point D). In more severe degrees of heart failure, Pv remains elevated, but cardiac output is abnormal (point E).
Analysis of the effects of changes in peripheral resistance on cardiac output and Pv is complex because both the cardiac and vascular function curves shift. When peripheral resistance increases (
Fig. 19.11 ), the vascular function curve is rotated counterclockwise, but it converges on the same Pv axis intercept as the control curve does. Note that vasoconstriction causes a counterclockwise rotation of the vascular function curve in
Fig. 19.11
Fig. 19.5 . The direction of rotation differs because the axes for the vascular function curves were switched in these two figures, as explained earlier. The cardiac function curve in
Fig. 19.11 is also shifted downward because at any given Pv, the heart is able to pump less blood against the greater cardiac afterload imposed by the increased peripheral resistance. Because both curves in
Fig. 19.11 are displaced downward, the new equilibrium point (point B) is below the control point (point A); that is, an increase in peripheral resistance diminishes cardiac output.
Whether point B falls directly below point A or lies slightly to the right or left of it depends on the magnitude of the shift in each curve. For example, if a given increase •Fig. 19.10 Moderateorsevereheartfailureshiftsthecardiacfunctioncurvesdownwardandtotheright.Beforechangesinbloodvolume,cardiacoutputdecreasesandcentralvenouspressurerises(fromcontrolequilibriumpointAtopointBorpointC).Aftertheincreaseinbloodvolumethatusuallyoccursinheartfailure,thevascularfunctioncurveisshiftedtotheright.Hence,centralvenouspressuremaybeelevatedwithnoreductionincardiacoutput(pointD)or,insevereheartfailure,withsomereductionincardiacoutput(pointE).
Heart failure isageneraltermthatappliestoconditionsinwhichthepumpingcapabilityoftheheartisimpairedtotheextentthatthetissuesofthebodyarenotadequatelyperfused.Inheartfailure,myocardialcontractilityisimpaired.Heartfailuremaybeacuteorchronic.Consequently,inagraphofcardiacandvascularfunctioncurves,thecardiacfunctioncurveisshifteddownwardandtotheright,asdepictedin
Fig.19.10
Acuteheartfailuremaybecausedbytoxicconcentrationsofdrugsorbycertainpathologicalconditionssuchascoronaryarteryocclusion.Inacuteheartfailure,bloodvolumedoesnotchangeimmediately.In
Fig.19.10 ,therefore,theequilibriumpointshiftsfromtheintersection(pointA)ofthenormalcurvestotheintersection(pointBorpointC)ofthenormalvascularfunctioncurve.
Chronicheartfailuremayoccurinconditionssuchasessentialhypertensionorischemicheartdisease.Inchronicheartfailure,boththecardiacfunctionandvascularfunctioncurvesshift.Thevascularfunctioncurveshiftsbecauseofanincreaseinbloodvolumecausedinpartbyfluidretentionbythekidneys.ThefluidretentionisrelatedtotheconcomitantreductioninglomerularfiltrationrateandthedecreasedrenalexcretionofNaClandwater(seealso ).Theresultanthypervolemiaisreflectedbyarightwardshiftofthevascularfunctioncurve,asshownin
Fig.19.10.
Hence,withmoderatedegreesofheartfailure,Pviselevated,butcardiacoutputmaybenormal(pointD).Withmoreseveredegreesofheartfailure,Pvisstillelevated,butcardiacoutputissubnormal(pointE).