treatment for the brady MI

[Ridryder 911]

Couple of things, Nitrates are NOT contraindicated in Right sided AMI, they should be closely monitored and it is discouraged to use, but technically it can be used, and does great on some patients. (No, I would not use on this particular patient)

Second, cardiogenic shock usually has either a tachydysrhythmia or high degree block, as well a low dose Dopamine may actually cause a reduction in blood pressure, but will increase renal perfusion and thus have potential diuretic effects. Dopamine at the alpha range (which produces > B/P) usually will damage the kidneys in the long run...

[FL_Medic]

Couple of things, Nitrates are NOT contraindicated in Right sided AMI, they should be closely monitored and it is discouraged to use, but technically it can be used, and does great on some patients. (No, I would not use on this particular patient)

Second, cardiogenic shock usually has either a tachydysrhythmia or high degree block, as well a low dose Dopamine may actually cause a reduction in blood pressure, but will increase renal perfusion and thus have potential diuretic effects. Dopamine at the alpha range (which produces > B/P) usually will damage the kidneys in the long run...

You're right I didn't mean to say contraindicated, my mistake. And I guess I wasn't explaining it good enough. I meant to just use the dopamine to try and manage the bp titrating accordingly, as soon as the lungs were clear I would switch to trendelenberg and fluids to manage the BP.

Hopefully with good management you wouldn't have to administer too much dopamine and the renal effects would be minimal, but at this point with that patient I really wouldn't be considering the renal effects to be honest, I'd be considering the pt. coding.

But you have alot more letters next to your name...

[Ace844]

You're right I didn't mean to say contraindicated, my mistake. And I guess I wasn't explaining it good enough. I meant to just use the dopamine to try and manage the bp titrating accordingly, as soon as the lungs were clear I would switch to trendelenberg and fluids to manage the BP.

Hopefully with good management you wouldn't have to administer too much dopamine and the renal effects would be minimal, but at this point with that patient I really wouldn't be considering the renal effects to be honest, I'd be considering the pt. coding.

But you have alot more letters next to your name...

You want the renal effects of the dopa for the reasons mentioned and also for the fact you don't want this patient to develop ATN 2nd to shock, and you don't want a similar set up with the liver...Backing off the dopa completely menas your just using it for a band aid and you'll be re-starting it shortly there after.

[FL_Medic]

You want the renal effects of the dopa for the reasons mentioned and also for the fact you don't want this patient to develop ATN 2nd to shock, and you don't want a similar set up with the liver...Backing off the dopa completely menas your just using it for a band aid and you'll be re-starting it shortly there after.

Every treatment we do is a bandaid, hopefully. I think if you get the lungs clear and pressure up you should be able to back off your aggressive treatments and use simple measures like fluids to manage your BP, given the pt. doesn't have rales anymore.

I meant renal damage. I have to learn to be carefull with the words I choose here, you guys are quick to jump on something.

[AZCEP]

The use of "renal-dose" Dopamine has never been proven to be terribly effective for increasing renal blood flow, or reducing systemic blood pressure. The interpatient variability is simply too great to suggest using it as a standard treatment without invasive monitoring capability. If you are allowed to float a Swan prehospital, you are too cool for most places.

The response to Dopamine will change dramatically depending on how sick a patient is. Some will respond favorably to 1-2 mcg/kg/min, while others won't consider a response until the dose is significantly higher. The best way to consistently increase renal blood flow with Dopamine is to get into the Beta range, and use the lowest dose to get the response you want.

[Ridryder 911]

Dopamine was never designed as a vasopressor or to raise pressure. It was just the side effects of overdosage that causes the alpha effects. True there is not much research, however be sure to carefully watch pressure when using lower to mid range Dopamine. Mesenteric dilatation and increasing renal perfusion, (even little) will cause a shift in fluid good or bad ... decrease afterload however can cause increased inotropic effects as well increases myocardial oxygen consumption.

Like all was discussed, a double edge sword effect. This patient needs a pacemaker, and if that does not cause enough ejection fraction, then placement of IABP until the mycocardium is healed, or decision for placement of possible intraventricular assist device (IVAD), or even a possible transplant candidate.

R/r 911

[ukcanuck]

NTG contraindicated for inferior wall MI?

Ok so I am new to forums like this - NTG is not CI for inf MI just a huge caution due to what it does to them in the vast majority of case

No NTG, but okay to use Morphine? They will both have similar actions on the RVI. Morphine is easier to titrate, so you will have fewer negative effects, but you still have to be careful.

quite agree to this - which is why it would be preferable then fire and forget NTG

Prehospital fibrinolysis isn't widely used in the States, but for those that are able, it might be a good consideration. Depending on how long it will take to get this patient to a PCI facility.

PCI is not that available over here esp for emergency cases. Most of the cases they do are pre planned and it takes some time (weeks) to get most pts in for an angiogram. It is pretty well nation wide that pre hospital thrombolysis is performed

Atropine would be a consideration, as mentioned previously, but I would shy away from it. The lower doses of Etomidate may very well reduce blood pressure, but if we can get the rate up with TCP, the situation resolves itself, right?

by using TCP would you actually increase the pressure as well as the rate or just the rate that dying and ineffective muscle is moving - not sure. i know that the rate will hopefully go up after capture but will this also bring the pressure up. In patients with functioning myocardium it should but will it in this case. The pt is already not pumping enough out due to dying/dead muscle will he have enough reserve to pump harder when we pace him? Another head scratcher :? Will this extend the MI to the point of no return if you have a distance to travel for thrombolytics or PCI

I like watching threads like this as it makes me think quite laterally as most of the people on here are based over that side and have a different take on the world. I used to operate over there and had top swap views rapidly when I came over here - very different helth care system

[Ace844]

For those who are interested here's alittle more information on 'Dopamine'

Dopamine is an endogenous catecholamine that is the precursor to norepinephrine in the catecholamine synthetic pathway. When administered therapeutically, dopamine is a complex agent. Dopamine, through its direct effects, is a weak partial beta-agonist. When initially administered, it releases norepinephrine through a tyramine-like effect.[135] It is a potent (relative to its receptor affinities) neuronal uptake inhibitor and by direct action acts as an agonist at dopamine D1 postsynaptic vasodilator receptors[136] and D2 presynaptic receptors on blood vessels and in the kidney.[137] The affinities for beta1 , beta2 , and alpha1B receptors are shown in Table 23-5 , where it can be seen that dopamine has extremely low affinity for all three adrenergic receptors.

At lower doses (≤2 µg/kg/min), dopamine causes a relatively selective dilation of splanchnic and renal arterial beds. This effect may be useful in promoting renal blood flow and maintaining GFR in selected patients who become refractory to diuretics, especially when caused by marginal renal perfusion. Dopamine also has direct renal tubular effects that promote natriuresis. At intermediate (2 to 10 µg/kg/min) infusion rates, dopamine, by virtue of its tyramine and neuronal uptake-inhibiting properties, enhances norepinephrine release from vascular and myocardial adrenergic neurons, thereby resulting in increased cardiac beta-adrenergic receptor activation and an increase in peripheral vascular resistance. In patients with advanced HF, who often have depleted intracardiac norepinephrine stores, dopamine is a less effective positive inotropic drug than are other "directly" acting inotropes. [128] [129] At higher infusion rates (5 to 20 µg/kg/min), peripheral vasoconstriction occurs as a result of direct alpha-adrenergic receptor stimulation. Increases in systemic vascular resistance are common even at intermediate infusion rates. On initial administration, tachycardia and arrhythmia tend to be more pronounced than with dobutamine[128] and are related to cardiac norepinephrine release.[135] [138]

In patients with advanced, decompensated HF, dopamine should not be used as a positive inotropic agent but rather should be used in low doses for renal perfusion and in intermediate to high doses to increase peripheral resistance. The latter property is often necessary for a variety of reasons, including sepsis, iatrogenic overvasodilation, and brain injury.

TABLE 23-5 -- Pharmacological Characteristics of Various Adrenergic Agonists Used to Treat Decompensated Heart Failure Agent Beta1 -Receptor Affinity (Kd , nM) Beta2 -Receptor Affinity (Kd , nM) Alpha1 -Receptor Affinity (Kd , nM) Uptake1 Affinity (nM) Intrinsic Activity * for Human Beta1 Receptors

Dobutamine 470 570 130 190,330 0.5

Dopamine 25,000 100,000 36,000 130,230 0.2

Epinephrine 20 20 160 1,400 1.0

Isoproterenol 20 20 >10,000 9,000 1.0

Norepinephrine 20 400 200 500,670 1.0

Phenylephrine >10,000 >10,000 1,000 >10,000 0

Median inhibitory concentration (IC50 ) data were converted to affinity constants using the Cheng-Prusoff equation.

Some data from Iverson LL (ed): The Uptake and Storage of Noradrenaline in Sympathetic Nerves. Cambridge, UK, Cambridge University Press, 1967.

*Relative to isoproterenol = 1.0 in nonfailing isolated human RV trabeculae. Affinity data are based on radioligand-cold ligand competition curves in (1) human ventricular myocardial membrane preparations (beta1 , beta2 , alpha1 in nonfailing hearts, norepinephrine, epinephrine, isoproterenol), (2) human recombinant beta2 receptors in COS cell membranes (isoproterenol, norepinephrine, and epinephrine), (3) DTT1 cell membranes (beta2 , dobutamine, and dopamine), and rat heart membranes (alpha1 , dobutamine). Additional alpha1 -agonist affinity data are derived from irreversible dibenamine antagonism in rabbit aorta, with

Management of Episodes of Acute Decompensation

As discussed earlier, acute manifestations of HF can either be in the context of new onset or be in subjects with established chronic HF. Treatment of acute episodes of HF are similar in these two scenarios, with the exception that a diagnostic work-up potentially leading to definitive therapy should be done in new cases. Since multiple-treatment modalities may be brought to bear on acute HF episodes, the discussion is

TABLE 24-4 -- Pharmacological Therapy for Acute, Decompensated Heart Failure Treatment Modality Specific Examples

Intravenous diuretics Furosemide, bumetatide, torsemide

Intravenous positive inotropic agents Dobutamine, milrinone, enoximone

Intravenous vasodilators Nitroprusside, nitroglycerine, nesiritide

Blood pressure, renal perfusion support Intravenous dopamine, intravenous vasopressin

divided into pharmacological and nonpharmacological forms of therapy.

PHARMACOLOGICAL THERAPY (see Chap. 23 ).

Table 24-4 gives the standard treatment modalities typically used to treat acute episodes of HF with advanced, Class IV symptoms. In general, treatment begins with intravenous diuretics, which in subjects with adequate organ perfusion often suffice to produce diuresis accompanied by a prompt drop in preload and relief of symptoms related to pulmonary edema. If peripheral perfusion is compromised or diuresis does not ensure, intravenous dobutamine, an inotropic beta/alpha-adrenergic agonist that produces an increase in cardiac output without substantially dropping preload or blood pressure, [129] or nesiritide (BNP)[130] (see Fig. 23-5 ), a vasodilator, can be added via a well-secured peripheral line. A PDEI such as milrinone[131] [132] or enoximone[133] [134] can also be used to treat decompensated HF but should not be administered without pulmonary artery pressure monitoring unless it is certain that left ventricular filling pressure is high (>15 mm Hg). The reason for this precaution is that PDEIs are such potent venodilators that in patients with normal or low filling pressure, they can drop preload to undesirably low levels. Finally, in decompensated subjects who are still receiving beta-blocking agents, a PDEI rather than a beta blocker is the treatment of choice because PDEIs retain full or even have enhanced activity in the presence of beta blockade.[135]

If the situation has not stabilized, additional inotropic support with or without supplemental afterload reduction is indicated and best delivered with the aid of pulmonary artery catheter monitoring. The combination of dobutamine and a PDEI is additive for effects on cardiac output and, via the PDEI, will produce a reduction in pulmonary artery and left ventricular filling pressure.[136] [137] The latter may provide welcome unloading of the right ventricle inasmuch as high pulmonary artery pressure can produce limiting right ventricular dysfunction in some patients.

Once optimal inotropic therapy is being delivered, pure vasodilators can be additionally administered to subjects with persistently high systemic or pulmonary vascular resistance. Vasodilators such as nitroprusside or nitroglycerin can also be used in lieu of a positive inotropic agent, particularly in patients with higher systemic vascular resistance. As a vasodilator, nesiritide has the unique property of preferentially increasing renal blood flow[138] [139] and theoretically may be of value in patients with compromised renal function; however, nesiritide may also precipitate renal failure and must be used cautiously in this setting.

Finally, in patients with blood pressure so low that renal perfusion is compromised, dopamine may be added to increase perfusion pressure and renal blood flow via this agent's alpha-adrenergic and dopaminergic properties. However, dopamine should not be considered an effective positive inotropic agent because the majority of its weak, partial beta-agonist effect is mediated by norepinephrine

TABLE 24-5 -- Nonpharmacological Therapy for Acute, Decompensated Heart Failure Treatment Modality Specific Examples

Oxygenation Supplemental oxygen, mechanical ventilation

Balloon counterpulsation Intraaortic balloon pump

VAD Pulsatile-flow LVAD

Pacing AV sequential pacemaker; biventricular pacing

Urgent cardiac catheterization PTCA, mitral valvuloplasty, pericardiocentesis

Urgent cardiac surgery CABG, AVR, MV repair or replacement, transplantation

AV = atrioventricular; AVR = aortic valve replacement; CABG = coronary artery bypass grafting; LVAD = left ventricular assist device; MV = mitral valve; PTCA = percutaneous transluminal coronary angioplasty; VAD = ventricular assist device.

release,[140] which results in tachyphylaxis within 12 hours of administration.

Adrenergic Agonists

Mechanism of Action

The most powerful way to increase contractility in the human heart is by the use of a beta-adrenergic receptor agonist. Beta-agonists operate through the mechanism that regulates contractility and heart rate on a beat-to-beat basis in the intact heart (see also Chap. 19 ).[110] As depicted in Figure 23-6 , this system is composed of two cell surface membrane receptors (beta1 and beta2 ); two G proteins (the stimulatory G protein, Gαs , and the inhibitory G protein, Gαi ); the adenylyl cyclase enzyme (which converts Mg-ATP to cAMP); cAMP-activated protein kinase (protein kinase A); compartmentalized phosphodiesterases, which modulate cAMP levels to produce selective signaling; and target structures whose phosphorylation leads to a positive inotropic effect by changes in Ca2+ handling (phospholamban, the ryanodine release channel, and slow inward current calcium channels). An important point in the function of beta-adrenergic pathways is that they are not all cAMP dependent[110] ; in Figure 23-6 the beta1 receptor is depicted with direct activation of voltage-sensitive Ca2+ channels as well as cAMP-dependent activation. The end result is a powerful positive inotropic as well as positive chronotropic effect.

In the failing human heart, beta-adrenergic pathways undergo desensitization, a pharmacological term encompassing the regulatory changes that occur in receptors, G proteins, and adenylyl cyclase.[111] [112] In advanced HF, the degree of beta-adrenergic receptor desensitization approaches 50 to 60 percent of the maximum capacity of signal transduction,[113] [114] and in severe HF, beta-agonists may no longer be able to support myocardial function.[115] However, the vast majority of patients with advanced HF still exhibit a substantial inotropic response to beta-agonists,[114] which is the basis for their usefulness as inotropic agents in the treatment of decompensated HF.

All beta-agonists are given intravenously for short-term support of decompensated HF. They are all arrhythmogenic to some extent through direct mechanisms as well as through increasing the skeletal muscle deposition of potassium[40] and important consideration in the heart, which has the most active uptake1 system of any organ and uses neuronal reuptake to terminate the majority of the action of released norepinephrine.

Although beta1 - and beta2 -adrenergic receptors are coupled to positive inotropic and chronotropic responses through cAMP-dependent and -independent mechanisms, these two receptors have important differences. For one thing, beta1 receptors are positioned inside or near the synaptic cleft area to mediate the effects of released norepinephrine, which also means that catecholamines that have high affinity for neuronal reuptake do not reach myocardial beta1 receptors unless neuronal reuptake is functionally decreased (as it is in myocardial failure) or absent (as it is in a recently [<2 years] transplanted heart). In addition, a growing body of evidence indicates that chronic beta1 receptor agonist occupancy or pathway activation, or both, is more deleterious than beta2 receptor activation.[110] [118] However, from an acute support standpoint, both receptors can be used in supporting cardiac function in decompensated patients.

NEURONAL REUPTAKE AFFINITIES FOR SYMPATHOMIMETIC AMINES.

Table 23-5 lists the adrenergic receptor and neuronal reuptake (uptake1 ) affinities for catecholamines that are used therapeutically to increase cardiac performance or increase systemic vascular resistance or blood pressure. Although the primary action of uptake1 is to terminate the action of norepinephrine, the functional status of uptake1 is also an important determinant of catecholamine therapeutic action when these agents are administered exogenously. For example, epinephrine, which has an affinity for uptake1 that is slightly lower than that of norepinephrine, is a much more potent therapeutic catecholamine when administered to denervated cardiac transplant hearts than to innervated hearts. [119] [120] When the heart is innervated, uptake1 removes much of the systemically administered epinephrine before it can reach myocardial beta1 -adrenergic receptors, which are preferentially located within the synaptic cleft area. In contrast, isoproterenol, which has essentially no affinity for uptake1 , is equally effective in innervated and denervated hearts.[121] [122]

The failing human heart has a functional impairment in uptake1 that essentially creates functional denervation, which in the case of catecholamines with higher affinity for uptake1 can offset some of the postsynaptic desensitization changes. Another way in which uptake1 can influence drug action is to compete with neurotransmitter norepinephrine for neuronal reuptake, which increases the amount of norepinephrine available in the synaptic cleft area. As can be observed in Table 23-5 , the substituted synthetic catecholamine, dobutamine, and the endogenous catecholamine, dopamine, have even higher affinity for uptake1 than does norepinephrine, and at least in the case of dopamine, this higher affinity contributes to its predominant inotropic action, which is to potentiate norepinephrine release.

BETA-ADRENOCEPTOR AGONISTS.

When left ventricular failure is severe, as manifested by marked reduction of cardiac index (<2 liters/min/m2 ), and pulmonary capillarywedge pressure is at optimal (18–24 mm Hg) or excessive (>24 mm Hg) levels despite therapy with diuretics, beta-adrenoceptor agonists are indicated. Although isoproterenol is a potent cardiac stimulant and improves ventricular performance, it should be avoided in STEMI patients. It also causes tachycardia and augments myocardial oxygen consumption and lactate production; in addition, it reduces coronary perfusion pressure by causing systemic vasodilation and in animal experiments it increases the extent of experimentally induced infarction. Norepinephrine also increases myocardial oxygen consumption because of its peripheral vasoconstrictor as well as positive inotropic actions.

Dopamine and dobutamine (see Chap. 23 ) can be particularly useful in patients with STEMI and reduced cardiac output, increased left ventricular filling pressure, pulmonary vascular congestion, and hypotension. Fortunately, the potentially deleterious alpha-adrenergic vasoconstrictor effects exerted by dopamine occur only at higher doses than those required to increase contractility. The vasodilating actions of dopamine on renal and splanchnic vessels and its positive inotropic effects generally improve hemodynamics and renal function. In patients with STEMI and severe left ventricular failure, this drug should be administered at a dose of 3 µg/kg/min while pulmonary capillary wedge and systemic arterial pressures as well as cardiac output are monitored. The dose can be increased stepwise to 20 µg/kg/min to reduce pulmonary capillary wedge pressure to approximately 20 mm Hg and elevate cardiac index to exceed 2 liters/min/m2 . It must be recognized, however, that doses exceeding 5 µg/kg/min activate peripheral alpha receptors and cause vasoconstriction.

Dobutamine has a positive inotropic action comparable to that of dopamine but a slightly less positive chronotropic effect and less vasoconstrictor activity. In patients with STEMI, dobutamine improves left ventricular performance without augmenting enzymatically estimated infarct size. It can be administered in a starting dose of 2.5 µg/kg/min and increased stepwise to a maximum of 30 µg/kg/min. Both dopamine and dobutamine must be given carefully and with constant monitoring of the electrocardiogram, systemic arterial pressure, and pulmonary artery or pulmonary artery occlusive pressure and, if possible, with frequent measurements of cardiac output. The dose must be reduced if the heart rate exceeds 100 to 110 beats/min, if supraventricular or ventricular tachyarrhythmias are precipitated, or if ST segment changes increase.

Nitroglycerin.

This drug has been shown in animal experiments to be less likely than nitroprusside to produce a "coronary steal"—that is, to divert blood flow from the ischemic to the nonischemic zone. Therefore, apart from consideration of its routine use in STEMI patients discussed earlier, it may be a particularly useful vasodilator in patients with STEMI complicated by left ventricular failure. Ten to 15 mg/min is infused and the dose is increased by 10 mg/min every 5 minutes until (1) the desired effect (improvement of hemodynamics or relief of ischemic chest pain) is achieved or (2) a decline in systolic arterial pressure to 90 mm Hg, or by more than 15 mm Hg, has occurred. Although both nitroglycerin and nitroprusside lower systemic arterial pressure, systemic vascular resistance, and the heart rate-systolic blood pressure product, the reduction of left ventricular filling pressure is more prominent with nitroglycerin because of its relatively greater effect than nitroprusside on venous capacitance vessels. Nevertheless, in patients with severe left ventricular failure, cardiac output often increases despite the reduction in left ventricular filling pressure produced by nitroglycerin.

Cardiogenic Shock

Cardiogenic shock is the most severe clinical expression of left ventricular failure and is associated with extensive damage to the left ventricular myocardium in more than 80 percent of STEMI patients in whom it occurs; the remainder have a mechanical defect such as ventricular septal or papillary muscle rupture or predominant right ventricular infarction.[27] In the past, cardiogenic shock has been reported to occur in up to 20 percent of patients with STEMI, but estimates from recent large randomized trials of fibrinolytic therapy and observational databases report an incidence rate in the range of 7 percent.[27] About 10 percent of patients with cardiogenic shock present with this condition at the time of admission, whereas 90 percent develop it during hospitalization. This low-output state is characterized by elevated ventricular filling pressures, low cardiac output, systemic hypotension, and evidence of vital organ hypoperfusion (e.g., clouded sensorium, cool extremities, oliguria, acidosis). Patients with cardiogenic shock due to STEMI are more likely to be older, to have a history of a prior myocardial infarction or congestive heart failure, and to have sustained an anterior infarction at the time of development of shock. Of note, although the incidence of cardiogenic shock in patients with STEMI has been relatively stable since the mid-1970s, the short-term mortality rate has decreased from 70 to 80 percent in the 1970s to 50 to 60 percent in the 1990s.[183] Cardiogenic shock is the cause of death in about 60 percent of patients dying after fibrinolysis for STEMI.

Medical Management

When the aforementioned mechanical complications are not present, cardiogenic shock is due to impairment of left ventricular function. Although dopamine or dobutamine usually improves the hemodynamics in these patients, unfortunately neither appears to improve hospital survival significantly. Similarly, vasodilators have been used in an effort to elevate cardiac output and to reduce left ventricular filling pressure. However, by lowering the already markedly reduced coronary perfusion pressure, myocardial perfusion can be compromised further, accelerating the vicious circle illustrated in Figure 46-10 . Vasodilators may nonetheless be used in conjunction with intraaortic balloon counterpulsation and inotropic agents in an effort to increase cardiac output while sustaining or elevating coronary perfusion pressure.

The systemic vascular resistance is usually elevated in patients with cardiogenic shock, but occasionally resistance is normal and in a few cases vasodilation actually predominates.[186] When systemic vascular resistance is not elevated (i.e., <1800 dynes/sec/cm5 ) in patients with cardiogenic shock, norepinephrine, which has both alpha- and beta-adrenoceptor agonist properties (in doses ranging from 2 to 10 µg/min), can be employed to increase diastolic arterial pressure, maintain coronary perfusion, and improve contractility. Norepinephrine should be used only when other means, including balloon counterpulsation, fail to maintain arterial diastolic pressure above 50 to 60 mm Hg in a previously normotensive patient. The use of alpha-adrenoceptor agents such as phenylephrine and methoxamine is contraindicated in patients with cardiogenic shock (unless systemic vascular resistance is inordinately low). Inspired by the observation that many patients with shock have a low systemic vascular resistance, Cotter and associates evaluated the benefit of the nitric oxide synthase inhibitor L-NMMA in patients in refractory shock.[187] The favorable impact of L-NMMA on the hemodynamics and clinical outcomes in this pilot study serves as the foundation for further investigation of nitric oxide synthase inhibition of cardiogenic shock.

[Spock]

Interesting comments on dopamine especially those regarding its misuse as a vasopressor even though in most ER's I've been in it seems to be used for that purpose often. One side effect of low dose dopamine that I have seen is increased heart rate which would be beneficial for this patient. I sometimes use low dose dopamine for open heart patients with a mild degree of renal insufficiency (creatinine >1.5). It almost always drives the heart rate up about 20 beats/minute.

Live long and prosper.

Spock

[Walker30613]

great read folks...... I guess will take the taoist philosophy with this one - less is better. Patients mentating well vitals are poor, but enough to perfuse the kidneys and brain, infarct on the right side? maybe bezold-jarish which responds to a small gentle bolus by fooling those darn baroreceptors in the pulmonary artery.

Otherwise

ASA

fi02 >.8

a smidgen Atropine if mentation is decreases

and an interventionalist if <60min away

otherwise TNK

and a [s:c3a4e19fcc]bit[/s:c3a4e19fcc] lots of luck.

nothing fancy.... this patient doesnt need an overly aggressive medic wasting time and myocytes, he needs pci/tnk.

thats my thoughts from the cheap seats!

jay