BAGAS - PBL 3

A. Klarifikasi Istilah
1. Akral dingin
Suhu tubuh ekstremitas yang dibawah suhu normal (Guyton, 2006).
B. Batasan Masalah
1. Identitas asien
a. !enis kelamin " laki#laki
b. $sia " %& tahun
'. !enis asien " ru(ukan
2. )eluhan utama saat ini " anas tinggi, mual, muntah
*. )eluhan sebelumnya " lemas, tak na+su makan
,. -nset " 1 minggu
%. .aktor eringan " tidur dengan osisi setengah duduk (/osisi
.owler)
6. )eluhan lain " mual tana muntah, na+su makan berkurang
searuhnya, batuk tidak berdahak, demam (#),
terkadang sesak, keterbatasan akti0itas sehari#
hari
1. 2iwayat enyakit " diabetes mellitus (se(ak % tahun yang lalu,
rutin berobat), enyakit (antung 'oroner
&. /emeriksaan +isik
a. )eadaan umum " tamak lemah dan gelisah
b. 3enyut nadi " teraba lemah
'. 4kstremitas " akral teraba dingin
C. Analisis Masalah
1. /ato+isiologi demam
3emam berawal dari adanya irogen di dalam tubuh. /irogen
meruakan agen yang menyebabkan demam. /irogen daat berasal dari luar
tubuh atau disebut sebagai irogen eksogen misalnya toksin bakteri dan
mikroba lain, ada (uga yang berasal dari dalam tubuh atau disebut sebagai
irogen endogen misalnya mediator interleukin#1 (I5#1), I5#6, dan 67..
/irogen yang dileaskan di dalam sirkulasi darah menyebabkan sel endothel
di kailer hyothalamus meleaskan metabolit asam arakidonat (/rewitt,
200%).
Asam arakidonat akan dimetabolisme sebagai /rostaglandin 42
(/G42) yang daat melewati sawar darah otak dan menu(u ke area
termoregulasi di hyothalamus. 8al ini memi'u eningkatan thermal set point
men(adi titik suhu tubuh yang baru. 9aka akan ter(adi tiga +ase demam yaitu
(/rewitt, 200%)"
a. .ase inisiasi
6ubuh berusaha men'aai thermal set point yang baru dengan 'ara
0asokonstriksi, kontraksi otot olos m. ere'tor ylorus, dan menggigil
yang bertu(uan men(aga anas tubuh tidak keluar dan memroduksi anas
tubuh (/rewitt, 200%).
b. .ase plateau
6ubuh berhasil men'aai suhu tubuh yang baru sehingga roses
menggigil berhenti (/rewitt, 200%).
'. .ase devervescence
6ubuh membuang anas tubuh dengan 'ara 0asodilatasi sehingga kulit
terlihat kemerahan (flushing), eningkatan sekresi keringat (diaphoresis),
dan merasa hangat (/rewitt, 200%).
2. /ato+isiologi batuk
6erdaat dua resetor yaitu yang sensiti+ terhada benda asing ('arina
dan laring) serta yang sensiti+ terhada iritan dan korosi+ (bronkiolus
terminalis dan al0eolus). )eduanya akan mengirimkan imuls ner0us a++erent
(mayoritas ner0us 0agus) menu(u medulla oblongata dan dilan(utkan melalui
sirkuit sara+. )emudian akan dikirimkan melalui ner0us e++erent menu(u
organ e+ektor dan menghasilkan urutan e+ek seerti berikut (Guyton, 2006)"
a. insirasi udara 2,% 5 se'ara 'eat
b. enutuan eiglottis dan li'a 0o'alis untuk men(ebak udara dalam ulmo
'. kontraksi mus'ulus abdominalis untuk mendorong dia+ragma ke atas yang
dibantu kontraksi m. inter'ostalis internus yang menyebabkan tekanan
intraulmoner meningkat hingga &60 mm8g
d. se'ara tiba#tiba li'a 0o'alis dan eiglottis membuka dengan lebar
e. udara keluar dari ulmo se'ara 'eat dengan ke'eatan 1%#100 mil:(am
+. gerakan udara yang 'eat akan membawa ;at asing dan iritan keluar
sehingga tu(uan re+leks batuk ter'aai.
DAFTAR PUSTAKA
Guyton A<, 8all !4. 2006. Textbook of Medical Pysiology 11
th
Edition. /hiladelhia"
4lse0ier Saunders.
/rewitt 49. 200%. .e0er" .a'ts, .i'tion, /hysiology. Crit Care Nurse Sul" &#10,
12, 1,.
Approach Considerations
Cardiogenic shock is an emergency requiring immediate resuscitative therapy before shock
irreversibly damages vital organs. The key to a good outcome in patients with cardiogenic
shock is an organized approach, with rapid diagnosis and prompt initiation of pharmacologic
therapy to maintain blood pressure and cardiac output.
All patients require admission to an intensive care setting, which may involve emergent
transfer to the cardiac catheterization suite, critical care transport to a tertiary care center, or
internal transfer to the intensive care unit (C!".
#arly and definitive restoration of coronary blood flow is the most important intervention for
achieving an improved survival rate. At present, it represents standard therapy for patients
with cardiogenic shock due to myocardial ischemia.
Correction of electrolyte and acid$base abnormalities, such as hypokalemia,
hypomagnesemia, and acidosis, is essential in cardiogenic shock.
Cardiogenic shock may be prevented with early revascularization in patients with myocardial
infarction (%" and with required intervention in patients with structural heart disease.
Procedures
&lacement of a central line may facilitate volume resuscitation, provide vascular access for
multiple infusions, and allow invasive monitoring of central venous pressure. Central venous
pressure may also be used to guide fluid resuscitation.
Although not necessary for the diagnosis of cardiogenic shock, invasive monitoring with a
pulmonary artery catheter may be helpful in guiding fluid resuscitation in situations in which
left ventricular preload is difficult to determine.
&ulmonary artery catheter pressure measurements may also be useful in prognosis.
'etrospective evaluation of these measurements from the ()*C+ trial demonstrated that
stroke volume inde, ((-" and stroke work inde, ((." vary inversely with mortality.
/012
An arterial line may be placed to provide continuous blood pressure monitoring. This is
particularly useful if the patient requires inotropic medications.
An intra$aortic balloon pump may be placed in the emergency department as a bridge to
percutaneous coronary intervention (&C" or coronary artery bypass graft (CA34", to
decrease myocardial workload and to improve end$organ perfusion.
PCI and coronary artery bypass
Clinicians should be alert to the fact that the ()*C+ trial demonstrated that either &C or
coronary artery bypass is the treatment of choice for cardiogenic shock and that each has
been shown to markedly decrease mortality rates at 0 year. &C should be initiated within 51
minutes of presentation6 however, it remains helpful, as an acute intervention, within 07 hours
of presentation.
f such a facility is not immediately available, thrombolytics should be considered. )owever,
this treatment is second best. An increased mortality is seen in situations in which
thrombolytics are used instead of &C. This is due to the relative ineffectiveness of the
thrombolytic medications to lyse clots in low$blood pressure situations.
/00, 02
Consultations
Consult a cardiologist at the earliest opportunity because his or her insight and e,pertise may
be invaluable for facilitating echocardiographic support, placement of an intra$aortic balloon
pump (A3&", and transfer to more definitive care (eg, cardiac catheterization suite, C!,
operating room". n severe cases, also consider discussing the case with a cardiothoracic
surgeon.
Deterrence and prevention
Although cardiogenic shock is not entirely preventable, measures can be taken to minimize
the risk of occurrence, recognize it at earlier stages, and begin corrective therapy more
e,peditiously. 8eterrence and prevention require a high degree of suspicion and heightened
awareness.
Care is required in treating patients with acute coronary syndromes who are not yet in
cardiogenic shock. Careful use of beta blockers and AC# inhibitors in these patients is
essential to avoid hypotension leading to cardiogenic shock.
/02
Prehospital Care
&rehospital care is aimed at minimizing any further ischemia and shock. All patients require
intravenous access, high$flow o,ygen administered by mask, and cardiac monitoring.
Twelve$lead electrocardiography performed in the field by appropriately trained paramedics
may be useful in decreasing door$to$&C times and9or time to the administration of
thrombolytics because acute (T$segment elevation myocardial infarctions ((T#%s" can be
identified earlier. The emergency department (#8" can thus be alerted and may mobilize the
appropriate resources.
notropic medications should be considered in systems with appropriately trained
paramedical personnel.
.hen clinically necessary, positive pressure ventilation and endotracheal intubation should
be performed. Continuous positive airway pressure (C&A&" or bilevel positive airway
pressure (3i&A&" support can be considered in appropriately equipped systems.
Resuscitation, Ventilation, and Pharmacologic Intervention
nitial management includes fluid resuscitation to correct hypovolemia and hypotension,
unless pulmonary edema is present. Central venous and arterial lines are often required.
(wan$4anz catheterization and continuous percutaneous o,imetry are routine.
*,ygenation and airway protection are critical6 intubation and mechanical ventilation are
commonly required. )owever, although positive pressure ventilation may improve
o,ygenation, it may also compromise venous return, preload, to the heart. n any event, the
patient should be treated with high$flow o,ygen. (tudies in patients with acute cardiogenic
pulmonary edema have shown noninvasive ventilation to improve hemodynamics and reduce
the intubation rate. %ortality is, however, unaffected.
A study by (hin et al suggested that patients who receive e,tracorporeal cardiopulmonary
resuscitation (C&'" versus conventional C&' for longer than 01 minutes following in$hospital
arrest have a greater chance of survival.
/072
All patients with cardiogenic shock require close hemodynamic monitoring, volume support to
ensure adequate sufficient preload, and ventilatory support.
Pharmacologic therapy
&atients with myocardial infarction (%" or acute coronary syndrome are given aspirin and
heparin. 3oth of these medications have been shown to be effective in reducing mortality in
separate studies. 3efore initiating therapy, however, care should be taken to ensure that the
patient does not have a myocardial wall rupture that is amenable to surgery.
There is no need to start clopidogrel until after angiography, since angiography may
demonstrate that there is a need for urgent coronary bypass.
/02
The glycoprotein b9a inhibitors improve the outcome of patients with non:(T$segment
elevation acute coronary syndrome (;(TAC(". They have been found to reduce recurrent %
following percutaneous coronary intervention (&C" and in cardiogenic shock.
Hemodynamic Support
8opamine, norepinephrine, and epinephrine are vasoconstricting drugs that help to maintain
adequate blood pressure during life$threatening hypotension and help to preserve perfusion
pressure for optimizing flow in various organs. The mean blood pressure required for
adequate splanchnic and renal perfusion (mean arterial pressure /%A&2 of <1 or <= mm )g"
is based on clinical indices of organ function.
n patients with inadequate tissue perfusion and adequate intravascular volume, initiation of
inotropic and9or vasopressor drug therapy may be necessary. 8opamine increases
myocardial contractility and supports the blood pressure6 however, it may increase
myocardial o,ygen demand. 8obutamine may be preferable if the systolic blood pressure is
higher than >1 mm )g6 it has the advantage of not affecting myocardial o,ygen demand as
much as dopamine does. )owever, the resulting tachycardia may preclude the use of this
inotropic agent in some patients.
8opamine is usually initiated at a rate of =$01 mcg9kg9min intravenously, and the infusion rate
is ad?usted according to the blood pressure and other hemodynamic parameters. *ften,
patients may require high doses of dopamine (as much as 71 mcg9kg9min".
f the patient remains hypotensive despite moderate doses of dopamine, a direct
vasoconstrictor (eg, norepinephrine" should be started at a dose of 1.= mcg9kg9min and
titrated to maintain an %A& of <1 mm )g. The potent vasoconstrictors (eg, norepinephrine"
have traditionally been avoided because of their adverse effects on cardiac output and renal
perfusion.
Vasopressor supportive therapy
The following is a brief review of the mechanism of action and indications for drugs used for
hemodynamic support of cardiogenic shock.
/0@, 0A2
Dopamine
8opamine is a precursor of norepinephrine and epinephrine and has varying effects
according to the doses infused. A dose of less than = mcg9kg9min causes vasodilation of
renal, mesenteric, and coronary beds. At a dose of =$01 mcg9kg9min, beta0$adrenergic
effects induce an increase in cardiac contractility and heart rate.
At doses of appro,imately 01 mcg9kg9min, alpha$adrenergic effects lead to arterial
vasoconstriction and an elevation in blood pressure. The blood pressure increases primarily
as a result of the inotropic effect. The undesirable effects are tachycardia and increased
pulmonary shunting, as well as the potential for decreased splanchnic perfusion and
increased pulmonary arterial wedge pressure.
Norepinephrine
;orepinephrine is a potent alpha$adrenergic agonist with minimal beta$adrenergic agonist
effects. ;orepinephrine can increase blood pressure successfully in patients who remain
hypotensive following dopamine. The dose of norepinephrine may vary from 1.7$0.=
mcg9kg9min, and large doses, as high as @.@ mcg9kg9min, have been used because of the
alpha$receptor down$regulation in persons with sepsis.
Epinephrine
#pinephrine can increase the %A& by increasing the cardiac inde, and stroke volume, as
well as systemic vascular resistance ((-'" and heart rate. #pinephrine decreases the
splanchnic blood flow and may increase o,ygen delivery and consumption.
Administration of this agent is associated with an increase in systemic and regional lactate
concentrations. The use of epinephrine is recommended only in patients who are
unresponsive to traditional agents. The undesirable effects are an increase in lactate
concentration, a potential to produce myocardial ischemia, the development of arrhythmias,
and a reduction in splanchnic flow.
Levosimendan
Bevosimendan, though not approved for use in the !nited (tates, can be considered for use
in con?unction with vasopressors. t should be used with caution, however, as it can cause
hypotension. !sed with vasopressors, levosimendan may improve hemodynamics and
improve coronary blood flow.
/0=, 0<2
Inotropic supportive therapy
Dobutamine
8obutamine (sympathomimetic agent" is a beta0$receptor agonist, although it has some
beta7$receptor and minimal alpha$receptor activity. ntravenous dobutamine induces
significant positive inotropic effects, with mild chronotropic effects. t also induces mild
peripheral vasodilation (decrease in afterload". The combined effect of increased inotropy
and decreased afterload induces a significant increase in cardiac output.
n the setting of acute myocardial infarction (%", dobutamine use could increase the size of
the infarct because of the increase in myocardial o,ygen consumption that may ensue. n
general, avoid dobutamine in patients with moderate or severe hypotension (eg, systolic
blood pressure C >1 mm )g" because of the peripheral vasodilation.
Phosphodiesterase inhibitors
&hosphodiesterase inhibitors (&8s", which include inamrinone (formerly amrinone" and
milrinone, are inotropic agents with vasodilating properties and long half$lives. The
hemodynamic properties of &8s are (0" a positive inotropic effect on the myocardium and
peripheral vasodilation (decreased afterload" and (7" a reduction in pulmonary vascular
resistance (decreased preload".
&8s are beneficial in persons with cardiac pump failure, but they may require concomitant
vasopressor administration. !nlike catecholamine inotropes, these drugs are not dependent
on adrenoreceptor activity6 therefore, patients are less likely to develop tolerance to these
medications.
&8s are less likely than catecholamines to cause adverse effects known to be associated
with adrenoreceptor activity (eg, increased myocardial o,ygen demand, myocardial
ischemia". They are also associated with less tachycardia and myocardial o,ygen
consumption. )owever, the incidence of tachyarrhythmias is greater with &8s than with
dobutamine.
Thrombolytic Therapy
Although thrombolytic therapy (TT" reduces mortality rates in patients with acute myocardial
infarction (%", its benefits for patients with cardiogenic shock secondary to % are
disappointing. .hen used early in the course of %, TT reduces the likelihood of subsequent
development of cardiogenic shock after the initial event.
n the 4ruppo taliano &er lo (tudio 8ella (treptokinase ;ellDnfarto %iocardio trial, @1$day
mortality rates were <5.5E in patients with cardiogenic shock who received streptokinase,
compared to F1.0E in patients who received a placebo.
(imilarly, other studies employing a tissue plasminogen activator did not show reductions in
mortality rates from cardiogenic shock. Bower rates of reperfusion of the infarct$related artery
in patients with cardiogenic shock may help to e,plain the disappointing results from TT.
*ther reasons for the decreased efficacy of TT are the e,istence of hemodynamic,
mechanical, and metabolic causes of cardiogenic shock that are unaffected by TT.
Thrombolytic therapy plus IAP
A prospective cohort study demonstrated the potential survival benefit of combining TT with
A3& counterpulsation in patients with % complicated by cardiogenic shock.
/0F2
*ut of 0051 patients enrolled, the treatments were (0" no TT and no A3& counterpulsation
(@@E, n G 7>=", (7" A3& counterpulsation only (@@E, n G 7F5", (@" TT only (0=E, n G 0@7",
and (A" TT and A3& counterpulsation (05E, n G 0<1".
&atients in cardiogenic shock who were treated with TT had lower in$hospital mortality rates
than did those who did not receive TT (=AE vs <AE", and patients selected for A3&
counterpulsation had lower in$hospital mortality rates than did those who did not receive A3&
counterpulsation (=1E vs F7E".
Hurthermore, a significant difference was noted in inhospital mortality rates among the A
treatment groups6 ie, TT plus A3& counterpulsation (AFE", A3& counterpulsation only
(=7E", TT only (<@E", no TT and no A3& counterpulsation (FFE".
'evascularization influenced in$hospital mortality rates significantly (@5E with
revascularization vs F>E without revascularization".
&atients who are unsuitable for invasive therapy should be treated with a thrombolytic agent
in the absence of contraindications. This is a class recommendation by American College of
Cardiology (ACC"9American )eart Association (A)A" guidelines.
Intra!Aortic alloon Pump
The use of the A3& reduces systolic left ventricular afterload and augments diastolic
coronary perfusion pressure, thereby increasing cardiac output and improving coronary artery
blood flow. The A3& is effective for the initial stabilization of patients with cardiogenic shock.
)owever, an A3& is not definitive therapy6 the A3& stabilizes patients so that definitive
diagnostic and therapeutic interventions can be performed.
/0>, 052
The A3& also may be a useful ad?unct to thrombolysis for initial stabilization and transfer of
patients to a tertiary care facility. (ome studies have shown lower mortality rates in patients
with myocardial infarction (%" and cardiogenic shock treated with an A3& and subsequent
revascularization, as previously mentioned.
Complications may be documented in up to @1E of patients who undergo A3& therapy6
these relate primarily to local vascular problems, embolism, infection, and hemolysis.
The impact of treatment with an A3& on long$term survival is controversial and depends on
the patientIs hemodynamic status and the etiology of the cardiogenic shock. &atient selection
is the key issue6 inserting the A3& early, rather than waiting until full$blown cardiogenic
shock has developed, may result in clinical benefit.
'amanathan et al found that rapid and complete reversal of systemic hypoperfusion with
A3& counterpulsation in the ()*C+ trial and ()*C+ registry was independently associated
with improved inhospital, @1$day, and 0$year survival, regardless of early revascularization.
This suggests that complete reversal of systemic hypoperfusion with A3& counterpulsation is
an important early prognostic feature.
/712
n the A3&$()*C+ study, <11 patients with cardiogenic shock complicating acute
myocardial infarction were randomized to intraaortic balloon counterpulsation or no intraaortic
balloon counterpulsation. All patients were e,pected to undergo early revascularization. !se
of intraaortic balloon counterpulsation did not significantly reduce @1$day mortality in these
patients.
/702
Ventricular Assist Devices
n recent years, left ventricular assist devices (B-A8s" capable of providing complete short$
term hemodynamic support have been developed. The application of B-A8 during
reperfusion, after acute coronary occlusion, causes reduction of the left ventricular preload,
increases regional myocardial blood flow and lactate e,traction, and improves general
cardiac function. The B-A8 makes it possible to maintain the collateral blood flow as a result
of maintaining the cardiac output and aortic pressure, keeping wall tension low and reducing
the e,tent of microvascular reperfusion in?ury.
/0>, 05, 772
A pooled analysis from 0F studies showed that the mean age of this group of patients with
B-A8s was =5.= J A.= years and that mean support duration was 0A<.7 J <1.7 hours. n
F>.=E of patients (range, =@.>$011E", ad?unctive reperfusion therapy, mainly percutaneous
transluminal coronary angioplasty (&TCA", was used. %ean weaning and survival rates were
=>.=E (range, A<$F=E" and A1E (range, 75$=>E", respectively.
/0>2
n any case, comparing studies is difficult because important data are usually missing, mean
age of patients were different, and time to treatment is not standardized. )emodynamic
presentation seems to be worse compared with data reported in the ()*C+ trial, with lower
cardiac inde,, lower systolic aortic pressure, and higher serum lactates. Taking these
considerations into account, B-A8 support seems to give no survival improvement in patients
with cardiogenic shock complicating acute myocardial infarction (%", compared with early
reperfusion alone or in combination with A3&.
n a randomized, controlled trial in which 075 patients with end$stage heart failure who were
ineligible for cardiac transplantation were assigned either to receive an B-A8 (<> patients" or
to undergo optimal medical management, survival rates were higher in the B-A8 group. The
rates of survival at 0 year were =7E in the device group and 7=E in the medical therapy
group, while the rates at 7 years were 7@E and >E, respectively. n addition, the quality of
life was significantly improved at 0 year in the device group.
/7@2
mplantable B-A8s are being used as a bridge to heart transplantation for patients with acute
% and cardiogenic shock.
/7A2
According to the )eart%ate 8ata 'egistry
/7=2
, from 05><$055>, A0
patients (=E of the total number of )eart%ate & patients" were supported with this
implantable pneumatic device for acute %, and 7= (<0E" were successfully bridged to heart
transplantation.
)owever, B-A8s as a bridging option for patients with cardiogenic shock must be considered
cautiously and must be avoided in patients who are unlikely to survive or are not likely to be
transplant candidates. Hurther investigations are required to better define indications, support
modalities, and outcomes.
The indications for insertion of a ventricular assist device are controversial. (uch an
aggressive approach to support the circulatory system in cardiogenic shock is appropriate (0"
after the failure of medical treatment and an A3&, (7" when the cause of cardiogenic shock is
potentially reversible, or (@" if the device can be used as a bridging option.
Percutaneous Transluminal Coronary Angioplasty
The retrospective and prospective data favor aggressive mechanical revascularization in
patients with cardiogenic shock secondary to myocardial infarction (%".
'eestablishing blood flow in the infarct$related artery may improve left ventricular function
and survival following %. n acute %, studies show that percutaneous transluminal coronary
angioplasty (&TCA" can achieve adequate flow in >1$51E of patients, compared with =1$<1E
of patients after thrombolytic therapy (TT".
(everal retrospective clinical trials have shown that patients with cardiogenic shock due to
myocardial ischemia benefitted (reduction in @1d mortality rates" when treated with
angioplasty. A study of direct (primary" &TCA in patients with cardiogenic shock reported
lower mortality rates in patients treated with angioplasty combined with the use of stents than
in patients treat with medical therapy.
A study by Antoniucci et al found that mortality rates increase in relation to the length of time
to treatment in patients with acute % who are not considered to be at low risk. To study the
relationship of time to treatment and mortality in patients with acute %, a series of 0@@<
patients who underwent successful primary &TCA were stratified into low$risk and not low
risk patient groups. The <$month mortality rate was 5.@E for not:low risk patients and 0.@E
for the low$risk patients. An increase in the mortality rate from A.>E to 07.5E with increasing
time to reperfusion was observed in the not low:risk group. A delay from symptom onset to
treatment resulted in higher mortality rates for the not low:risk patients.
/7<2
Coronary Artery ypass "ra#ting
Critical left main artery disease and @$vessel coronary artery disease are common findings in
patients who develop cardiogenic shock. The potential contribution of ischemia in the
noninfarcted zone contributes to the deterioration of already compromised myocardial
function.
Coronary artery bypass grafting (CA34" in the setting of cardiogenic shock is generally
associated with high surgical morbidity and mortality rates. 3ecause the results of
percutaneous interventions can be favorable, routine bypass surgery is often discouraged for
these patients.
A 711A task force of the ACC and the A)A gave a class recommendation to the
performance of primary &C or emergent CA34 in patients younger than F= years who have
(T#% who develop shock within @< hours of myocardial infarction (%" and can be treated
within 0> hours of shock onset. &erformance of primary &C or emergent CA34 was
considered reasonable in patients older than F= years (class a recommendation".
Revasculari$ation in the SH%C& Trial
'esults from the ()*C+ trial supported the superiority of a strategy that combines early
revascularization with medical management in patients with cardiogenic shock. n the study,
patients were assigned to receive either optimal medical management, including an A3& and
TT, or cardiac catheterization followed by revascularization using &TCA or CA34.
/7F, 00, 7>2
The mortality rates at @1 days were A<.FE in the early intervention group and =<E in patients
treated with optimal medical management. Although these @1$day results did not reach
statistical significance, the mortality rate at < months was significantly lower in the early
intervention group (=1.@E vs <@.0E".
/7F2
The 0$year survival rates were also reported from the ()*C+ trial.
/002
The survival rate at 0$
year was A<.FE for patients in the early revascularization group and @@.<E in the
conservative management group. The treatment benefit was apparent only for patients
younger than F= years (=0.<E survival rate in early revascularization group vs @@.@E in
patients treated with optimal medical management".
3ased on the outcome of this study, the recommendation is that patients with acute
myocardial infarction (%" complicated by cardiogenic shock, particularly those younger than
F= years, should be rapidly transferred to a center with personnel capable of performing early
angiography and revascularization procedures.
Patient Trans#er
mmediately transfer a patient who develops cardiogenic shock to an institution at which
invasive monitoring, coronary revascularization, and skilled personnel are available to provide
e,pert care.
&atients with cardiogenic shock who are admitted to a hospital without facilities for
revascularization should be immediately transferred to a tertiary care center with such
facilities. f time to &C is more than 0 hour and onset of symptoms has been within @ hours,
rapid administration of TT is recommended.
t should be kept in mind, however, that attempts to transfer a patient with cardiogenic shock
must be made only when everything possible has been done to stabilize his or her condition
and when the level of care during the transfer will not significantly decrease.
'edication Summary
-asopressors augment the coronary and cerebral blood flow during the low$flow state
associated with shock. (ympathomimetic amines with both alpha$ and beta$adrenergic
effects are indicated for persons with cardiogenic shock. 8opamine and dobutamine are the
drugs of choice to improve cardiac contractility, with dopamine the preferred agent in patients
with hypotension.
-asodilators rela, vascular smooth muscle and reduce the (-', allowing for improved
forward flow, which improves cardiac output.
8iuretics are used to decrease plasma volume and peripheral edema. The reduction in
e,tracellular fluid and plasma volume associated with diuresis may initially decrease cardiac
output and, consequently, blood pressure, with a compensatory increase in peripheral
vascular resistance. .ith continuing diuretic therapy, the plasma volume and peripheral
vascular resistance usually return to pretreatment values.
Inotropic Agents
Class Summary
These agents augment coronary and cerebral blood flow during the low$flow state associated
with cardiogenic shock. They also improve cardiac output in refractory hypotension and
shock.
-iew full drug information
Dopamine

8opamine stimulates adrenergic and dopaminergic receptors. ts hemodynamic effect
depends on the dose. Bower doses primarily stimulate dopaminergic receptors that produce
renal and mesenteric vasodilation. )igher doses produce cardiac stimulation and
vasoconstriction.
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Dobutamine

8obutamine is a sympathomimetic amine with stronger beta effects than alpha effects. t
produces systemic vasodilation and increases the inotropic state. )igher doses may cause
an increase in heart rate, e,acerbating myocardial ischemia.
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(orepinephrine )*evophed+

;orepinephrine is a naturally occurring catecholamine with potent alpha$receptor and mild
beta$receptor activity. t stimulates beta0$ and alpha$adrenergic receptors, resulting in
increased cardiac muscle contractility, heart rate, and vasoconstriction. ;orepinephrine
increases blood pressure and afterload. ncreased afterload may result in decreased cardiac
output, increased myocardial o,ygen demand, and cardiac ischemia.
;orepinephrine is generally reserved for use in patients with severe hypotension (eg, systolic
blood pressure C F1 mm )g" or hypotension unresponsive to other medication.
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'ilrinone

%ilrinone is a selective phosphodiesterase inhibitor in cardiac and vascular tissue with
positive inotropic and vasodilator effects6 it has little chronotropic activity. This agentDs mode
of action differs from that of either digitalis glycosides or catecholamines.
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Inamrinone

Hormerly known as amrinone, inamrinone is a phosphodiesterase inhibitor with positive
inotropic and vasodilator activity. t produces vasodilation and increases the inotropic state.
namrinone is more likely to cause tachycardia than is dobutamine, and it may e,acerbate
myocardial ischemia.
Vasodilators
Class Summary
-asodilators decrease preload and9or afterload.
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(itroglycerin IV

This agent causes rela,ation of vascular smooth muscle by stimulating intracellular cyclic
guanosine monophosphate production. The result is a decrease in preload and blood
pressure (ie, afterload".
Antiplatelet Agents, Cardiovascular
Class Summary
Agents that irreversibly inhibit platelet aggregation may improve morbidity.
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Aspirin )Anacin, Ascriptin Regular Strength, ayer Aspirin Regimen Regular,
u##erin, ,cotrin+

Aspirin is an odorless, white, powdery substance available in >0 mg, @7= mg, and =11 mg, for
oral use. .hen e,posed to moisture, aspirin hydrolyzes into salicylic acid and acetic acids. t
is a stronger inhibitor of prostaglandin synthesis and platelet aggregation than are other
salicylic acid derivatives. The acetyl group is responsible for inactivation of cyclo$o,ygenase
via acetylation. Aspirin is hydrolyzed rapidly in plasma, and elimination follows zero order
pharmacokinetics.
Aspirin irreversibly inhibits platelet aggregation by inhibiting platelet cyclo$o,ygenase. This, in
turn, inhibits the conversion of arachidonic acid to prostaglandin 07 (a potent vasodilator and
inhibitor of platelet activation" and thrombo,ane A7 (a potent vasoconstrictor and platelet
aggregate". &latelet$inhibition lasts for the life of the cell (appro,imately 01 d".
Aspirin may be used at a low dose to inhibit platelet aggregation and improve complications
of venous stases and thrombosis. t reduces the likelihood of myocardial infarction (%" and is
also very effective in reducing the risk of stroke. #arly administration of aspirin in patients with
acute % may reduce cardiac mortality in the first month.
%pioid Analgesics
Class Summary
Analgesics reduce pain, which decreases sympathetic stress and provides some preload
reduction.
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'orphine sul#ate )Duramorph, Astramorph, 'S Contin, &adian, %ramorph SR+

%orphine sulfate is the drug of choice for narcotic analgesia due to its reliable and predictable
effects, safety profile, and ease of reversibility with nalo,one. -arious intravenous doses are
used6 the drug is commonly titrated until the desired effect is achieved.
Diuretics, *oop
Class Summary
These drugs cause diuresis to decrease plasma volume and edema and thereby decrease
cardiac output and, consequently, blood pressure. The initial decrease in cardiac output
causes a compensatory increase in peripheral vascular resistance. .ith continuing diuretic
therapy, e,tracellular fluid and plasma volumes return almost to pretreatment levels.
&eripheral vascular resistance decreases below that of the pretreatment baseline.
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-urosemide )*asi.+

Hurosemide increases the e,cretion of water by interfering with the chloride$binding
cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending
loop of )enle and the distal renal tubule.
ndividualize the dose to the patient. 8epending on the response, administer furosemide at
increments of 71$A1mg no sooner than <$> hours after the previous dose, until the desired
diuresis occurs. .hen treating infants, titrate the drug in increments of 0mg9kg9dose until a
satisfactory effect is achieved.
Cardiovascular, %ther
Class Summary
These drugs cause arterial and venous dilation by binding to the cyclic guanosine
monophosphate (4%&" receptors on vascular smooth muscle, causing smooth muscle
rela,ation. ;atriuretic peptides produce dose$dependent decreases in pulmonary capillary
wedge pressure and systemic arterial pressure.
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(esiritide )(atrecor+

;esiritide is a recombinant deo,yribonucleic acid (8;A" form of human 3$type natriuretic
peptide (h3;&", which dilates veins and arteries.
)uman 3;& binds to the particulate guanylate cyclase receptor of vascular smooth muscle
and endothelial cells. 3inding to the receptor causes an increase in cyclic 4%&, which serves
as a second messenger to dilate veins and arteries. &ulmonary capillary wedge pressure is
reduced and dyspnea is improved in patients with acutely decompensated congestive heart
failure.
;esiritide may be considered in the treatment of patients with cardiogenic shock. Although
nesiritide has been shown to increase mortality and renal dysfunction, it continues to be
studied as a treatment for acute congestive heart failure and currently retains !( Hood and
8rug Administration (H8A" approval. )owever, it should be used with caution in the setting of
cardiogenic shock because it has been shown to cause hypotension.