Haemodynamic Monitoring in the Management Of Cardiogenic Shock in Coronary Care Units

Die behandeling en versorging van pasiënte wat aan akute miokardinfarksie ly , het die afgelope dekade opvallend verbeter. Daar het nuwe opvattings i.v .m . die behandeling van kardiogeniese skok ontstaan. Die onafgebroke waarneming van harthemodinamika deur koronêre sorgverpleegsters het die grootskaalse vooruitgang t.o .v . geneeshere se huidige “ koronêre sorg” moontlik gem aak. Die gebruik van ’n Swan-Ganz-regterhartkateter met vloeibeheerde termoverdunning het hem odinam iese waarneming en meting van pulmonale arteriële druk en pulmonaal-kapillêre wigdruk, sowel as dié van kardiale uitwerp, moontlik gemaak.

The m anagem ent and nursing care o f patients suffering from acute m yocardial infarction has changed dram atically over the past decade.
W ith the establishm ent o f coronary care units offering facilities for cardiac monitoring and staffed with nurses hold ing a post-basic diplom a in intensive nursing, the prevention or effective treatm ent o f life-threatening arrhythm ias became feasible and many have survived as a result o f this intensive and skilled care.
A n o th e r m ajo r p ro b lem arises from the n u m erous haem odynam ic changes which occur with acute myocardial infarction which often progress to a state o f cardiogenic shock with pulmonary oedem a and a low cardiac output.
The three basic aims o f therapy for the patient with acute m yocardial infarction are: (1) to reduce the increased pulm onary-capillary or wedge pressure, which will lead to pulm onary oedem a and (2) to improve the cardiac output thus im proving peripheral perfusion.
(3) The third aim to avoid increasing the imbalance between m yocardial oxygen supply and dem and, w hile en deavouring to achieve the above two aims.There are four m ajor factors which are responsible for increasing myocardial oxygen dem ands, namely preload, i.e. wedge pressure or pulm onary-capillary pressure, after load i.e. peripheral vascular resistance or the degree of impedance to ejection by the heart, which is measured clini cally as arterial systolic pressure, con tractility o f the myocardium inotrophy and heart rate (chronotrophy).
Over the last few years new concepts o f the treatment o f cardiogenic shock have developed and these depend on the manipulation o f afterload and preload so that the cardiac output is m aintained without an increase in myocardial oxy gen dem ands.The blood flow to vital organs such as the heart, brain and kidneys may therefore be increased without damaging the m yocardium .The frequent, " round the clock" m onitoring o f cardiac haem odynam ics by " coronary care" nurses has m ade it possible for the great forward strides w hich are being made by physicians in their" " coronary care" today.
H aem odynam ic m onitoring, using a b allo o n -tip p ed , (Sw an-G anz) flow -directed, therm odilution, right heart catheter, has made it possible to measure pulm onary arterial and pulm onary-capillary or wedge pressures as well as the cardiac output.
The catheter may also be used to m easure right atrial pressure i.e. central venous pressure and allow s blood specim ens to be taken from either the right atrium or the pulm onary artery.
This quadruple-lum en catheter (Fig. 1) has one large lumen which term inates at the tip, through which heparinised 0.45% saline is run.It is through this lumen that the pressure tracings o f pulm onary arterial and pulm onary-capillary or wedge pressures are measured (No: 4 in Fig. 1) A second sm all lumen leads to the little balloon at the catheter tip and allows it to be inflated and deflated (No: 1 in Fig. 1).A third lumen term inates either 20 or 30 cm (depending on the catheter model) proximal to the catheter tip and so com m uni cates with the right atrium or superior vena cava (No: 3 in Fig 1).The fourth small lumen carries the electrical leads from the therm istor tem perature detector, which is positioned on the catheter surface 4 cm proximal to the tip (No: 2 in Fig. 1.).The body o f the catheter is radio-opaque and can be vis ualised by fluoroscopy.The catheter is introduced via a peripheral vein and the procedure can be carried out at the bedside w ithout the use o f fluoroscopy.On reaching the superior vena cava or right atrium, the little balloon is partially inflated with air which allows it to be swept along with the blood flow, hence the name flowdirected, right heart catheter.
The catheter is inserted under pressure monitoring control so that the tracing is seen on the m onitor screen.(Fig. 2) As the catheter passes through the right atrium , pressure tracings show a pressure of about 5 m m /H g in a normal subject.A swing from about 30 m m /Hg to zero is seen as the catheter passes through the right ventricle, while the tracing shows a swing between about 30 m m /Hg and 15 m m /Hg as the catheter enters the pulm onary artery.The balloon is now Cardiac Output Computer com pletely inflated, being filled with the exact volume of air indicated on the catheter, and is allowed to advance to a wedge position, where it becomes impacted in a vessel o f the same diam eter and occludes it.The pressure reading taken at this stage would reflect the pressure beyond the balloon as the lumen is located at the catheter tip.The pressure beyond the balloon would therefore be that of the pulmonary capillary bed and would thus reflect the pressure in the left atrium and in fact the left ventricular filling pressure.(See Fig. 3).
In a normal subject a wedge pressure o f 5 to 12 m m /Hg is found, following myocardial infarction, however the pres sure may need to be maintained at 14 to 18 m m /H g, as optim al ventricular filling and myocardial function occur at this level in the post-infarction heart.
A wedge pressure o f 18 to 20 mm/Hg indicates the onset o f pulmonary congestion; 20 to 25 m m /H g, shows moderate congestion; 25 to 30 m m /H g shows severe congestion while a wedge pressure o f more than 30 m m /H g, indicates the onset o f pulmonary oedem a.
It is obvious then that wedge pressure readings which are a reflection o f preload, would offer most valuable guidance to the physician who will base his therapy on these pressure readings.
Cardiac output is measured by injecting a known amount o f iced saline through the lumen which ends in the right atrium or superior vena cava.
The therm istor tem perature detector is located 4 cm from the tip o f the catheter, lying in the pulmonary artery.The iced saline flows out into the right atrium or superior vena cava and cools the blood, hence the name ''therm odilution cathe ter" .The resultant change in blood tem perature is detected by the therm istor on the surface of the catheter.
The detected change in temperature reaches the cardiac output com puter (Fig. 4) via electrical leads from the ther mistor.The rectal tem perature of the patient forms part of the computed data essential for the therm odilution procedure.
The cardiac output is inversely proportional to the integral temperature change.This allows the cardiac output to be measured as well as the cardiac index and stroke work index to be calculated.
If the stroke work index is less than 20 m l/m 2 it is an indication that the patient is suffering from cardiogenic shock, while an index of 10ml/m2 has been associated with a 90% m ortality, (normal stroke index 4 0 ± 7 m l/m 2) The cardiac output determ ined by this method is highly accurate and reproducible.CARD IO G EN IC SHOCK Cardiogenic shock is a state of acute, severe left ventricu lar failure accom panied by a low cardiac output and high left ventricular filling pressure.The causes are; 1) most com m only, myocardial infarction with massive left ventricular damage usually in excess of 35% of the functioning left ventricle; 2) the condition may follow cardiac surgery; 3) it may be precipitated by arrhythmias; 4) Failure in conduction o f the impulse; 5) extreme bradycardias; 6) tachycardias eg.paroxysm al atrial tachycardia; 7) it may occur in valvular disease where the cusp of a valve ruptures e.g. the aortic or mitral valve or 8) in rupture o f the heart; 9) it can present as a result o f m yocarditis or cardiac myopathies; 10) it occurs where traum a to the heart results in pericardial tamponade which com presses the heart; 11) W here there is im paired filling of the left atrium as a result of pulm onary em bolism associated with reflex ischaemia; 12) in tension pneum othorax, which com presses the great veins or the heart itself; 13) it may be seen in the late stages o f congestive cardiac failure.

THE CLIN ICA L PICTURE
The cardiac output falls so that the systolic blood pressure drops below 90 m m /H g; the baroreceptors are stimulated so that there is a raised peripheral resistance.
The .skin is co ld , clam m y, pale and often m ottled.
Cyanosis may be present.The level o f consciousness may be altered or there may be some mental im pairm ent.The urinary output is diminished.The pulse may be very slow or very rapid and thready.Pulmonary oedem a will develop due to back pressure on the lungs (increased pulmonary capillary pressure) as a result o f a failure in the forward flow from the heart (cardiac output).The pressure on the right side o f the heart may rise causing a rise in the central venous pressure, but cardiogenic shock with pulmonary oedem a can occur w ithout a rise in the central venous pressure.For this reason it is far safer to measure left atrial pressure using a Swan-Ganz flow-directed right heart catheter.

THE M ANAGEM ENT O F THE PATIENT W ITH C A R DIOGENIC SHOCK
The m anagement o f cardiogenic shock which follow s is a som ew hat detailed account o f the m anipulation o f the haemodynamic status o f the patient by adm inistering drugs according to Swan-Ganz pulmonary arterial wedge pressure readings and thus im proving the cardiac output, while at the same time protecting the myocardium.
With this therapy, the mortality in cardiogenic shock which was in excess o f 90% has been reduced to between 50%-60%.
Though some o f these patients who survive may be left with a damaged myocardium and are often in chronic heart failure, it is hoped that this may improve in the future.
The initial clinical diagnosis is usually not difficult but it requires confirmation by the measurem ent o f the pulm onary arterial wedge pressure with a Sw an-G anz catheter, as some 10-20% o f patients have a low wedge pressure and will respond simply to fluid adm inistration and cannot therefore be said to be in true cardiogenic shock.The prognosis o f this group is much better.
W hile the left ventricle is much better adapted than the right to coping with pressure, it is still nevertheless more efficient as a volume pump than as a pressure pump.Under circum stances, where the left ventricular m uscle mass is acutely dam aged, it is unable to cope with the systemic pressure without a significant reduction in stroke volume.The peripheral vascular resistance therefore tends to be high as the baroreceptors tend to maintain the system ic blood pressure at the expense o f the cardiac output.Therefore the left ventricle is pumping against an increased afterload.
The atterload is determined mainly by the mean arterial blood pressure which reflects peripheral vascular resistance, but is also dependent on the tension in the walls o f the ventricle.
The preload or wedge pressure, refers to the diastolic distension o f the left ventricle just prior to the onset o f systole.It depends on left ventricular volume and end dias tolic pressure, both o f which tend to go up with left ventricu lar failure.
The effect o f the increased preload is to increase left ventricular contraction by the Starling principle.*but the consequence ot raised end diastolic pressure is pulm onary congestion because this pressure is obviously transm itted back to the left atrium, and to the pulm onary veins.^Starling's law o f the heart states that the strength o f cardiac contraction is proportional to myocardial fibre length (or left ventricular volume) at the onset o f contraction.
The normal left ventricular end diastolic pressure is up to 12 m m /H g, and pulm onary congestion is usually not apparent until the left atrial pressure esceeds 18-20 m m /Hg.This pressure can be measured by the Swan-Ganz catheter.
If left ventricular diastolic pressure rises significantly higher than 20 m m /H g the left ventricular output may be further reduced by overstretching the myocardial fibres.
The cardiac output is determ ined by the preload and con tractile state of the m yocardium and the afterload.A dam aged myocardium is less com pliant and requires a greater filling pressure than the normal heart, therefore a moderate increase in preload i.e. 12 to 14 m m /H g and greater contrac tility will tend to increase the cardiac output, whereas a higher afterload will tend to decrease it.
The older forms o f treatm ent of cardiogenic shock concen trated on using drugs to increase the contractility o f the myocardium and many o f these such as nor-adrenaline also actually increased the afterload by increasing peripheral vas cular resistance.These effects tend to be deleterious, for by increasing m yocardial oxygen dem ands, they tend to in crease the size o f the infarction and are therefore selfdefeating.
Isoprenaline also markedly increases the myocardial oxy gen demands because o f its positive inotropic and chrono tropic effects.
The most im portant m eans o f treatm ent then, is to reduce the'afterload or peripheral vascular resistance by means of vaso-dilator drugs.
Sodium nitroprusside solution by intravenous infusion is almost the most useful as it has a very rapid onset and short duration o f action and can be easily controlled.It can how ever only be used in an intensive care unit where adequate monitoring facilities are present and can o f course be disas trous if used inappropriately.It is appropriate in patients with high left ventricular filling pressures and reduced cardiac output and with a high peripheral vascular resistance.
Under these circum stances, even if the systemic blood pressure is on the low side, it will not drop further and may even increase w ith the adm inistration of nitroprusside.The reason for this is that the load on the left ventricle is decreased as the peripheral resistance is reduced and the stroke volume tends to increase, therefore as the cardiac output rises the blood pressure is maintained.
Preload reduction is desirable in addition in many cases.Reducing preload will reduce pulm onary congestion and improve oxygenation and will also reduce myocardial stretch and improve sub-endocardial blood flow.
By the reduction o f end diastolic volume and diameter, afterload will at the same tim e be reduced and many o f the drugs used will additionally cause some peripheral arteriolar dilation.Therefore the concept o f preload on its own is a little artificial.N itroglycerin and its derivatives have been the most effective drugs in this regard.
Sublingual glyceral trinitrate, which is known as T .N .T .will drop preload, but only for a short time and somewhat uncontrollable.Intravenous nitro-glycerin has been very use ful but is used less now ow ing to problems of supply o f the drugs.
Oral isosorbide dinitrate (Isordil) has been useful as it is effective and has a duration o f action of at least four hours.
It should be noted that sodium nitroprusside does have the action o f reducing preload by dilating the venous capacitance vessels as do the T .N .T .preparations, but to a lesser extent.
O ther vasodilators may be used and may be given orally such as hydralazine and prazosin (minipress).These have the advantage o f being able to be given orally and it may be possible to wean a patient from intravenous nitroprusside to an oral vaso-dilator, sometimes with the addition o f isosor bide.
Diuretics are still important and furosemide (Lasix) is still necessary in almost all patients.
Furosemide reduces pulmonary capillary pressure within minutes of administration probably due to a change in the distribution of venous blood and a venous dilatation, thus reducing preload.A further drop in pulm onary-capillary pressure follows some hours later due to the diuretic effect of the drug.Even when renal shut-down has occurred, the drug is most beneficial for its effect on reducing pulmonary capil lary pressure, the blood being dispersed to the dilated venous capacitance vessels.
Digitalis is not usually used in the acute phase o f m yocar dial infarction as the increase in contractility may extend the area o f infarction, but it may be useful later on with a dilated, failing ventricle.If it helps to reduce ventricular cavity size, the net effect on myocardial oxygen demand may be benefi cial.
Dopamine hydrochloride (Intropin) is presently the most useful^atecholam ine derivative.It has less tendency to cause tachycardia than isoprenaline and at low dosage tends to dilate the renal vascular bed and improve renal blood flow.In higher dosage it increases total peripheral vascular resis tance.
Glucagon is still useful occasionally, as a virtually pure inotropic agent with little effect on heart rate.
Isoprenaline is now rarely if ever used for cardiogenic shock except in some patients with mitral valve disease and high pulmonary vascular resistance and those with pulm o nary embolism who are in shock.It tends to dilate the pulm onary vasculature and is therefore still sometimes used after cardiac surgery.
M orphia may be a very useful drug for both its pain-killing and anxiety-relieving properties and for the fact that it re duces preload by venous dilatation.It remains therefore a drug o f choice in acute left ventricular failure.
Ventilation is occasionally required for patients in severe pulmonary oedema where oxygenation is a problem.
The use of the Swan-Ganz catheter allows one to make the diagnosis o f cardiogenic shock with confidence as well as to m onitor therapy.An additional advantage is the ability to diagnose remedial mechanical defects, such as rupture o f the interventricular septum or severe mitral regurgitation.
It is important if any surgically remedial disorder is present that this should be treated if possible.For example a patient with a ruptured aortic valve with severe aortic regurgitation may present with cardiogenic shock and there would be no hope unless this was recognised and he was sent for urgent aortic valve replacem ent.To some extent the same may apply with aortic stenosis and mitral regurgitation.
The use o f intra-aortic balloon counterpulsation in car diogenic shock is generally restricted to those patients in whom surgery is contemplated or in post-operative cardiac patients.It has been disappointing in the treatment o f car diogenic shock related to a large loss of functioning left ventricle.The patient often improves dramatically while on counter-pulsation, but is usually not able to be weaned from the pump.
The use o f preload and afterload reduction has in fact, larg ely rep lac ed the need fo r c o u n te rp u lsa tio n .T he (concluded on p age 56) The patient in cardiogenic shock has suffered m ajor haem odynam ic changes which have resulted in increased pulm onary-capillary or wedge pressure and dim inished car diac output.He is critically ill and has slender chance o f survival in the absence o f haem odynam ic m onitoring and the m eticulous prescription by a cardiologist o f the appropriate m e d ic a tio n to m a n ip u la te and c o rre c t the d is tu rb e d haem odynam ics.
Fig. 1 SW AN-GANZ THERMODILUTION CATHETER WITH QUADRUPLE LUMEN (1) Lumen through which balloon is inflated and deflated (2) Electrical lead from the Thermistor Temperature Detector which plugs into the Cardiac Output Computer (3) Lumen terminating 20 or 30cm proximal to tip i.e. in right atrium through which iced saline is injected (4) Large lumen terminating at tip, beyond the balloon, through which the infusion is run and through which the pulmonary arterial and pulm onary-capillary w edge pressures are measured.