In Pt 1, I reviewed anatomy, physiology, and the basic pathophysiology of shock. If you have not read that already, I recommend you do so first. With that, lets talk about a form of shock: Cardiogenic Shock.
In a nut shell, cardiogenic shock is an inability of the heart to pump enough blood to supply the tissues with oxygen. And is defined as insufficient forward cardiac output. Cardiogenic shock is usually the result of a significant bradycardia (heart rate that is too slow) or heart block, or a significant tachycardia (heart rate that is too fast) resulting in low cardiac output and hypoperfusion. Cardiogenic shock can also be caused by severe left ventricular failure secondary to acute myocardial infarction, congestive heart failure, chronic untreated hypertension, cardiomyopathy, or long term habitual use of stimulant drugs like cocaine.
The heart can be divided into two halves,. the left, and the right. The left side is responsible for receiving oxygenated blood from the lungs ( via the left atrium) and pumping it to the rest of the body (via the left ventricle). If the left sides ability to pump blood is compromised, then back pressure will build up in the system. Because the left ventricle is responsible for pumping blood to the systemic circulation, SVR, or systemic vesicular resistance plays a large part in the process. If the stroke volume and cardiac out put is not enough to overcome the SVR, (as in untreated hypertension) or the ventricle is weakened (as in a myocardial infarction or cardiomyopathy) then pressure will back up into the left ventricle. The hearts pumping ability can also be diminished by a cardiac tamponade, or a tension pneumo/hemothorax.
If the heart is not pumping blood into the systemic circulation effectively, then the body becomes hypoperfused. As the pressure builds in the left ventricle, the myocardium (heart muscle) will stretch to accommodate the larger volume of blood. The muscle can stretch, but only to a point before it weakens and fails, causing even less efficient contractions. The pressure will then spread to the left atrium. The left atrial pressure rises and is subsequently transmitted to the pulmonary veins and capillaries. When pulmonary capillary pressure is too high, it forces blood plasma across the alveoli-capillary membrane and to the lungs, causing pulmonary edema (fluid in the lungs).
The hypoperfusion is compounded by the fact that most cardiogenc shock due to left ventricular failure is accompanied by pulmonary edema, which dramatically reduces the ability of oxygen and carbon dioxide to diffuse across the alveoli-capillary membrane. Also, since left ventricular failure is often caused by an AMI (acute myocardial infarction) be awhere that your patient experiencing cardiogenic shock, may also be having an AMI.
Right ventricular failure by it self, will not likely result in hypoperfusen in the same way as left ventricular failure. But, right sided failure is interestingly often caused by left ventricular failure. Right sided failure can also be caused be chronic obstructive lung diseases like COPD. As the back pressure spreads to the right side of the heart, peripheral edema in the dependent parts of the body, and JVD (Jugular vein detention) often occur. These are both key signs to look for during your assessment.
The patient in cardiogenic shock may present tachycardic or bradycardic. Will likely be short of breath with possible chest pain. Possible JVD (right side failure). Lung sounds may be clear, diminished, wheezes, crackles, rales or absent depending on the severity of pulmonary edema. White or pink frothy sputum may be present. The patient will likely have fast labored respirations. Level of consciousness may be diminished due to hypoxia. Skins may be cyanotic and or diaphoretic. Spo2 reading will be low. Blood pressure will likely be normal or hypertensive (in exacerbated congestive heart failure) or low in decompensating shock.
Treatment is aimed at airway and cardiac support. The patient should be placed in a position of comfort. If pulmonary edema is present, the patient well likely prefer to be sitting upright in a high fowler’s position, with their legs hanging off the gurney. Although the patient may present in a state of shock, treatment should also consist of treating the underlying cause (AMI, CHF) which if managed effectively, can relieve the hypoperfusion.
When available, a 12 lead EKG should always be obtained. Support the airway and breathing with High flow O2 via non rebreather mask, you may need to assist ventilations via BVM (bag valve mask), CPAP, or intubation. Nitroglycerin (if blood pressure is acceptable) will reduce cardiac work load and oxygen demand through vasodilatation, and relieve pulmonary hypertension and edema. Morphine may also be useful. Furosemide 40-80mg IV will relieve pulmonary edema through diuresis. IV fluid administration should be minimal so as not to exacerbate the pulmonary edema.
Cardiac support with Dopamine at 2-10mcg/kg/minute, or Dobutamine at 2-20 mcd/kg/minute will increase the force of cardiac contractions, increasing systemic perfusion and reducing pulmonary hypertension. If the patient is bradycardic, than 0.5mg of Atropine IV, or trans-cutaneous pacing to increase the heart rate to a perfusing level is appropriate. Always be cautious of AMI in a badycardic patient, because bradycardia can be a protection response of an ischemic heart. Tachycardias (depending on the type, and severity) can be treated with 6-12mg of Adenosine, and other antiarrhythmics like Amiodarone and Lidocaine. Also Synchronized cardioversion if available, and in some systoms a Beta blocker may be indicated.
The patient may have additional cardiac compromise such as AMI which will require appropriate treatment, and transport destination.
*** Always treat your patients according to your local protocols and scope of practice. And use medical control as needed. ***
In part 3 we’ll leave medical, and deal with trauma, burns, and Hypovolemic Shock.
