Shock - Cardiogenic: Nursing

Cardiogenic shock is a life-threatening condition where the heart is unable to pump enough blood to the rest of the body due to cardiac dysfunction. This leads to acute hypoperfusion and hypoxia of the tissues and organs, despite the presence of an adequate intravascular volume in the cardiovascular system.

Alright, let’s go over the physiology of the cardiovascular system, which consists of the heart

and blood vessels. The heart pumps out blood to the body’s organs and tissues with each heartbeat, which consists of two phases: systole, which is when the heart contracts and pumps the blood out; and diastole, which is when the heart relaxes and fills with blood. The stroke volume, meaning the amount of blood pumped out by the heart in a single heartbeat, is influenced by the cardiac contractility, preload, and afterload. Contractility is how strongly the heart is contracting during systole. Preload is how much the heart’s smooth muscle is stretched at the end of diastole, and this is mainly dependent upon how much blood is filling the heart. The more they're stretched the more force they can generate during contraction, kind of like a rubber band. Afterload refers to the resistance that the heart must overcome to pump out blood during systole, and this is affected mainly by peripheral vascular resistance under non-pathological conditions. This is mainly determined by the vasodilation and vasoconstriction of blood vessels. If we multiply the stroke volume by the heart rate we’ll get the cardiac output, which is the amount of blood pumped out by the heart in one minute, and it’s the main measure of the heart’s function.

Okay, cardiogenic shock can be caused by any condition that prevents the heart from pumping enough oxygenated blood, thus affecting the cardiac output. The most common causes involve damage to the heart tissue. The most important is acute myocardial infarction where ischemia and necrosis of cardiac tissue impairs its ability to contract. Other disorders that damage the heart can also lead to cardiogenic shock, common ones include myocarditis, acute heart failure, and myocardial contusion from trauma. Next, arrhythmias including tachycardia, bradycardia, and heart block, can all decrease cardiac output. Finally, there are mechanical causes like aortic and mitral valve insufficiency. For example, with mitral valve insufficiency, the valve doesn’t close properly. So, during systole some of the blood goes from the left ventricle back into the left atrium instead of getting pumped out the aorta.

Risk factors for cardiogenic shock include advancing age, as well as having existing heart problems, such as chronic heart failure, a prior myocardial infarction, or multiple cardiovascular risk factors, such as long-standing high blood pressure, coronary heart disease, or diabetes mellitus. Also, taking medications that decrease cardiac contractility, like beta-blockers, or having electrolyte imbalances that can affect heart rhythm, like hyper- or hypokalemia, can be a risk factor for cardiogenic shock.

Now, the pathology of cardiogenic shock develops when the heart becomes unable to pump blood effectively. As a result, there’s a decrease in stroke volume, which in turn decreases cardiac output, causing blood pressure to drop, and ultimately causing hypoperfusion of organs and tissues. So, in order to increase cardiac output, the body releases vasoconstrictor molecules into the bloodstream. These include catecholamines like epinephrine and norepinephrine which cause vasoconstriction, increase heart rate, and contractility to maintain blood pressure and blood flow; as well as ADH which acts on the kidneys to increase fluid retention, and angiotensin II, which also constricts blood vessels and causes sodium retention in the kidneys, in turn, raising blood pressure. If the cause of shock is not managed in time, these compensatory mechanisms may begin to fail, leading to severe tissue hypoxia. Vital organs like the heart, brain, and kidneys may begin to shut down, leading to multiple organ failure. At the same time, since blood isn’t being pumped forward into the systemic circulation, it starts backing up into the pulmonary and systemic blood vessels. Eventually, fluid can be pushed out of the circulation and into the lungs and tissues, leading to complications like pulmonary and peripheral edema.

Usually, the initial clinical manifestations of cardiogenic shock are associated with tissue hypoperfusion, and include compensatory tachycardia, tachypnea, and hypotension.

During the initial stage, compensatory mechanisms such as increased heart rate and vascular constriction are sufficient to maintain cardiac output within the normal range. Cardiac output can best be seen by obtaining the mean arterial pressure, or the average pressure in one cardiac cycle, because it is a more accurate indicator of perfusion than a normal blood pressure. In this stage, the MAP is decreased by less than 10 mmHg from baseline. Clients may experience tachycardia, but compensatory mechanisms keep blood pressure at around the normal range, so it may be difficult to detect shock at this stage.

During the compensation stage, the compensatory mechanisms are fully active, but the MAP is decreased and is about 10-15 mmHg below baseline. The client’s skin can become cold and clammy, indicating that blood flow is being redirected to vital organs like the brain and heart. Other symptoms include pallor, severe hypotension and tachycardia, decreased peripheral pulses, and oliguria. As blood starts backing up in the body, clients may develop jugular venous distention, where the jugular vein that’s close to the heart becomes enlarged and distended; as well as pulmonary edema, which typically presents with dyspnea and crackles; and peripheral edema, causing the limbs to swell.

In the progressive stage, clients may develop organ failure because the compensatory mechanisms can no longer guarantee adequate blood flow to vital organs. The MAP is sustained at more than 20 mmHg below baseline. The client may experience anxiety, altered level of consciousness from decreased perfusion to the brain, cyanosis, increased respirations, decreased oxygen saturation from lung failure, profound hypotension, bradycardia, and irregular heart rhythm from heart failure, as well as anuria, which occurs due to kidney failure.

In the refractory stage, cell death occurs in the vital organs due to the lack of oxygen reaching the tissues. The MAP is still sustained at more than 20 mmHg from baseline. At this point, the damaged organs cannot respond to treatment, leading to multiple organ dysfunction. The client may experience a sudden loss of consciousness, shallow respirations, unmeasurable oxygen saturation, non-palpable pulses, or death.

Now, the diagnosis of cardiogenic shock starts with the client’s history and physical assessment. The client should be monitored closely to detect signs of hypoperfusion, such as a drop in oxygen saturation, low or declining blood pressure, or a decreased urinary output. This is usually followed by additional tests, including an ECG, an echocardiogram, and a chest X-ray to identify the precipitating cause of cardiogenic shock. Laboratory tests can reveal decreased oxygen levels, electrolyte abnormalities, and signs of end‐organ damage like elevated lactate levels.