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Systolic blood pressure in cardiac decompensation and during compensation
I
T IS gwrrall~ assnmrtl that the systolic blood pressure falls in cardiac ilrcompensatioil ant1 that it rises as comprnsation becomes established. However, it has bee11 observed that patients with marked Sahli’ cardiac failure and severe cyanosis may show hypertension. first called attention to this increase in blood pressure and spoke of this phenomenon ‘as “~Ioclltlrllclistauull~.” 11~ nbsrrved this to be true llot only for valvular lesions, but for cardiac failure (111~ to twphysenia and arteriosclerosis, rxplainiirg this paradoxical iiicwaw as being tlur to stimulation of thcb \.asomotor ccllter. (ieisbock’ (‘onfirmed these observations, but rioted furtht>r that the blood pressure Lang alltl JIans\vetowa:~ fount1 an infell as the edema disapprarecl. crease in blood pressure to btt the rnlr it1 all mitral lesions and also in rmphysema with decolllperlsation. but reportctl it as occurring only in a small proportion of patieilts with aortic+ lrsions. I>urig and also E’reshe* have tlispntetl these observations. ‘1’11~ latter in a study of seven hundred cares of heart disease coldd only tint1 five with increase in blood pressure which he could attribl~te to tlrt~onlI~r~lsatio~~. IiOW~lkarewa” studied sixty patirtlts lrith cardiac tlcconll~eusation and observed a definit,e increase during drcoml,eiisation, and a fall in systolic pressure as compensation brcamr established. We have studied thirty-five patients with severe cardiac tlrcompensatioii. All showed signs, such as edema. ilyspnra, and varying degrees of cyanosis. \\‘r did not inclutle severt-l cases of auricular fibrillation in this group. Blood pressure readings (mrrcllry manometers) were taken on the day of admission ant1 therraftrr at varying intervals of from three to fivr days and on date of tlischarge. The treatment reThwe paceived was rest in bed, digitalis, and oItium whelp itldicatetl. tients 1VPre used as controls iITl(l rrcrivt~tl no medit~ation.
In sixteen (45.7 per cent) of thirty-five unselrcted cases with cardiac decompeusation, the s\-stolic blood pressure fell from 40 mm. as compensation became wtablished. Of these, fifteen improved and dischargctl ; death occurretl in only nne patient in the blood pressure fell.
severe 10 to were whom
Tn twelve pat,ients mained uncliarigecl. and three died.
(34.2 ~wr cent) the systolic blood pressure retllcw. Ilint, were improved ai~d discharged
()f
In five patients, Or l-I.2 as compensation occurred. two were improved.
prr cent, tile ant1 of thwe.
blootl
~)t*t’ssurc
\vas
i~l~~t~ilSt~t1
three tlietl ai~tl the renlailring
Jn two instances there was a definite fall ill blood pressure NS c’onipensation occurred, but, the blood prc~ssnre rose to thiit 011 atlniission before the patitwt left the hospital.
SO
('lI:\N(:F,
:: I
In fifteen patients with aortic regurgitation, there was a definite fall in t,he systolic blood pressure with return of compensation in five. The fall in blood pressure varied from 10 to 40 1n1l1. l’hwe patients were all improved and clischargetl from the hospital. rll four patients a rise in blood pressure of from 10 to 23 mm. occurrrtl, alit1 was pwscnt at the termination of the cases. Three of these (lied; the fourth was discharged as improved. In four other I);ttirnts tllere \vas 110 change in blood pressure, and of these OIII~ 011thdied, the others being discharged as improved. hi two patients the hlootl pressure fell from 10 to 25 mm., and then rose to that on adniissioll, although the patients were clinically improved. Tn six patients with chronic myocartlitis, emphywma, and cardiac dt~compensatiol1. the blootl pressllre fell front “0 to 40 lL1111. ill two instances with improvement ; in one patirllt, a fall of 14 mm., with death ; in three, no eliangr in blood ~nws~we. with tleath in t\vo ailL jn the final instance the patient was improved. Among four patients with mitral regurgita.tioll, :I fall ill blood pressure occurred in three. and in one there was 110 clri~~qy. .\ll of these were iniprovrd. Ill txv0 patients with Illitl’ill strllosis, tlichi*r \vas no change in blood pressure. 1\motlg sis I)atirnts with clironic~ Irephritis. a fall occurretl in three I)atitwts. a rise in on(’ patitalitj ~III~ no cli:\nge in two. All of thrse were cliscliarpecl as improved.
DISCUSSION , I
Our observations direct attention to the fall in blood pressure which occurs as cardiac compensation is established. The increase of systolic blood pressure at the time of decompensation was necessarily inferred because of the fall in pressure and the maintenance thereof as the patient improved. Among eight patients readmitted for recurring decompensation, we n-we able to note in five that the systolic blood pressure was from 20 to 10 mm. higher on the second and third admissions than on the first and second discharges. The explanation of an increase in blood pressure appears paradoxkal ~-hen this is riewrtl as a mechanical or dynamic problem, Reflex or incrrasrd tonns of the vasomoter center, as suggested by Sahli, offers a11 c>splanation. It is of interest t,o note that Cob&” has studied t~xperimcntally the relation of tlyspnra and cyanosis to blood pressure, ant1 finds the changes in blood pressure proportional to the C‘O, content of the blootl. C’yanosis. however. is not a frequent occurrence in aortic lesions, and it is
H
Fig.
3.
difficult to explain the rise in blood pressure on this basis. Lang and Manswetowa3 offer the accompanying diagram (Fig. 1) as a possible mechanical explanation : In Fig. 1 let H represent the heart,, and V, the arterial s;vstem. Under normal conditions, with no increased resistance, the blood pressure is represented on the manometer as 0. Assuming an increase in peripheral resistance by turnin g P, the blood pressure will rise to point M. This increase in peripheral resistance in cardiac clecompensation is a stasis in the arterial system. ,411owing then for this quant,ity of blood from H, t,he blood pressure will rise to ,V, which is still above the normal blood pressure. The possible r61e of passive congestion of the kidney, as a dctcrmining factor in the production of t,he hypertension, is also to be considered. Our studies have failed to prove this definitely, for the patients who did not show any changes in blood pressure readings showed the same evidence of passive congestion of the kiclney (as evidenced by urinary changes) as those that did manifest a rise and subsequent fall.
MEYER
AND
MIJLLES
:
(‘AHDTAC’
359
DE( ‘OXPETSATION
Geisbock’ inferred that, in decompensation with edema, a compression of the smaller arteries and capillaries occurred which produced an increased peripheral resistance and thus explained the increased pressure and also the fall as the edema disappeared. We were able to observe the fall in pressure with the general improvement of patients, but we do not accept Geisbock’s view, since it is well known that generalized edema may occur in many conditions without changes in blood pressure.
The systolic blood pressure fell in 45.7 per cent of unselected cases of cardiac failure as compensation became established. We observed this fall in cases of aortic regurgitation, mitral regurgitation, chronic mpocarditis, emphysema, and chronic nephritis. It is probable that a combination of mechanical factors and increased tonus of the rasomotor center are responsible for t,he initial rise in s;-stolic blootl pressure during dt~compcnsation. REFERENCES 1Snhli : Verlmndl. d. Kong. f. inn. Med., 1901, xix, 45. Geishock: Deutsch. Arcsh. f. klin. Med.. 190.5. lxxxiii. 3ti3. ::Lang and Mnnswetow:~ : Deutsch. Arch. f. klh. Med., 19n8, xiv, 4Quoted by C’obet (See 6). ~Loschkarewa : Deutsch. Axle. f. klin. Med., 1923-24, &iii, 36-l. ‘Told, R.: Deutsch. Arch. f. klin. Med., 1903-21, &iii, 053.
A.i.5.
T IS gwrrall~ assnmrtl that the systolic blood pressure falls in cardiac ilrcompensatioil ant1 that it rises as comprnsation becomes established. However, it has bee11 observed that patients with marked Sahli’ cardiac failure and severe cyanosis may show hypertension. first called attention to this increase in blood pressure and spoke of this phenomenon ‘as “~Ioclltlrllclistauull~.” 11~ nbsrrved this to be true llot only for valvular lesions, but for cardiac failure (111~ to twphysenia and arteriosclerosis, rxplainiirg this paradoxical iiicwaw as being tlur to stimulation of thcb \.asomotor ccllter. (ieisbock’ (‘onfirmed these observations, but rioted furtht>r that the blood pressure Lang alltl JIans\vetowa:~ fount1 an infell as the edema disapprarecl. crease in blood pressure to btt the rnlr it1 all mitral lesions and also in rmphysema with decolllperlsation. but reportctl it as occurring only in a small proportion of patieilts with aortic+ lrsions. I>urig and also E’reshe* have tlispntetl these observations. ‘1’11~ latter in a study of seven hundred cares of heart disease coldd only tint1 five with increase in blood pressure which he could attribl~te to tlrt~onlI~r~lsatio~~. IiOW~lkarewa” studied sixty patirtlts lrith cardiac tlcconll~eusation and observed a definit,e increase during drcoml,eiisation, and a fall in systolic pressure as compensation brcamr established. We have studied thirty-five patients with severe cardiac tlrcompensatioii. All showed signs, such as edema. ilyspnra, and varying degrees of cyanosis. \\‘r did not inclutle severt-l cases of auricular fibrillation in this group. Blood pressure readings (mrrcllry manometers) were taken on the day of admission ant1 therraftrr at varying intervals of from three to fivr days and on date of tlischarge. The treatment reThwe paceived was rest in bed, digitalis, and oItium whelp itldicatetl. tients 1VPre used as controls iITl(l rrcrivt~tl no medit~ation.
In sixteen (45.7 per cent) of thirty-five unselrcted cases with cardiac decompeusation, the s\-stolic blood pressure fell from 40 mm. as compensation became wtablished. Of these, fifteen improved and dischargctl ; death occurretl in only nne patient in the blood pressure fell.
severe 10 to were whom
Tn twelve pat,ients mained uncliarigecl. and three died.
(34.2 ~wr cent) the systolic blood pressure retllcw. Ilint, were improved ai~d discharged
()f
In five patients, Or l-I.2 as compensation occurred. two were improved.
prr cent, tile ant1 of thwe.
blootl
~)t*t’ssurc
\vas
i~l~~t~ilSt~t1
three tlietl ai~tl the renlailring
Jn two instances there was a definite fall ill blood pressure NS c’onipensation occurred, but, the blood prc~ssnre rose to thiit 011 atlniission before the patitwt left the hospital.
SO
('lI:\N(:F,
:: I
In fifteen patients with aortic regurgitation, there was a definite fall in t,he systolic blood pressure with return of compensation in five. The fall in blood pressure varied from 10 to 40 1n1l1. l’hwe patients were all improved and clischargetl from the hospital. rll four patients a rise in blood pressure of from 10 to 23 mm. occurrrtl, alit1 was pwscnt at the termination of the cases. Three of these (lied; the fourth was discharged as improved. In four other I);ttirnts tllere \vas 110 change in blood pressure, and of these OIII~ 011thdied, the others being discharged as improved. hi two patients the hlootl pressure fell from 10 to 25 mm., and then rose to that on adniissioll, although the patients were clinically improved. Tn six patients with chronic myocartlitis, emphywma, and cardiac dt~compensatiol1. the blootl pressllre fell front “0 to 40 lL1111. ill two instances with improvement ; in one patirllt, a fall of 14 mm., with death ; in three, no eliangr in blood ~nws~we. with tleath in t\vo ailL jn the final instance the patient was improved. Among four patients with mitral regurgita.tioll, :I fall ill blood pressure occurred in three. and in one there was 110 clri~~qy. .\ll of these were iniprovrd. Ill txv0 patients with Illitl’ill strllosis, tlichi*r \vas no change in blood pressure. 1\motlg sis I)atirnts with clironic~ Irephritis. a fall occurretl in three I)atitwts. a rise in on(’ patitalitj ~III~ no cli:\nge in two. All of thrse were cliscliarpecl as improved.
DISCUSSION , I
Our observations direct attention to the fall in blood pressure which occurs as cardiac compensation is established. The increase of systolic blood pressure at the time of decompensation was necessarily inferred because of the fall in pressure and the maintenance thereof as the patient improved. Among eight patients readmitted for recurring decompensation, we n-we able to note in five that the systolic blood pressure was from 20 to 10 mm. higher on the second and third admissions than on the first and second discharges. The explanation of an increase in blood pressure appears paradoxkal ~-hen this is riewrtl as a mechanical or dynamic problem, Reflex or incrrasrd tonns of the vasomoter center, as suggested by Sahli, offers a11 c>splanation. It is of interest t,o note that Cob&” has studied t~xperimcntally the relation of tlyspnra and cyanosis to blood pressure, ant1 finds the changes in blood pressure proportional to the C‘O, content of the blootl. C’yanosis. however. is not a frequent occurrence in aortic lesions, and it is
H
Fig.
3.
difficult to explain the rise in blood pressure on this basis. Lang and Manswetowa3 offer the accompanying diagram (Fig. 1) as a possible mechanical explanation : In Fig. 1 let H represent the heart,, and V, the arterial s;vstem. Under normal conditions, with no increased resistance, the blood pressure is represented on the manometer as 0. Assuming an increase in peripheral resistance by turnin g P, the blood pressure will rise to point M. This increase in peripheral resistance in cardiac clecompensation is a stasis in the arterial system. ,411owing then for this quant,ity of blood from H, t,he blood pressure will rise to ,V, which is still above the normal blood pressure. The possible r61e of passive congestion of the kidney, as a dctcrmining factor in the production of t,he hypertension, is also to be considered. Our studies have failed to prove this definitely, for the patients who did not show any changes in blood pressure readings showed the same evidence of passive congestion of the kiclney (as evidenced by urinary changes) as those that did manifest a rise and subsequent fall.
MEYER
AND
MIJLLES
:
(‘AHDTAC’
359
DE( ‘OXPETSATION
Geisbock’ inferred that, in decompensation with edema, a compression of the smaller arteries and capillaries occurred which produced an increased peripheral resistance and thus explained the increased pressure and also the fall as the edema disappeared. We were able to observe the fall in pressure with the general improvement of patients, but we do not accept Geisbock’s view, since it is well known that generalized edema may occur in many conditions without changes in blood pressure.
The systolic blood pressure fell in 45.7 per cent of unselected cases of cardiac failure as compensation became established. We observed this fall in cases of aortic regurgitation, mitral regurgitation, chronic mpocarditis, emphysema, and chronic nephritis. It is probable that a combination of mechanical factors and increased tonus of the rasomotor center are responsible for t,he initial rise in s;-stolic blootl pressure during dt~compcnsation. REFERENCES 1Snhli : Verlmndl. d. Kong. f. inn. Med., 1901, xix, 45. Geishock: Deutsch. Arcsh. f. klin. Med.. 190.5. lxxxiii. 3ti3. ::Lang and Mnnswetow:~ : Deutsch. Arch. f. klh. Med., 19n8, xiv, 4Quoted by C’obet (See 6). ~Loschkarewa : Deutsch. Axle. f. klin. Med., 1923-24, &iii, 36-l. ‘Told, R.: Deutsch. Arch. f. klin. Med., 1903-21, &iii, 053.
A.i.5.