Welcome to CP 101, a brief overview of the assessment and treatment of chest pain. Chest pain patients present some of the most critical and challenging calls that providers face. Here I will forego details or long explanations, and present just the barebones that you can flesh out with further study and experience.
Chest pain patients can be divided into two categories: non-life threatening and life threatening. Those with non-life threatening (benign) disease can result from esophageal spasms, muscle strain, etc. Those with life threatening causes may include heart attack (myocardial infarction), aortic dissection, and pulmonary embolus, among others.
Telling the difference between non-life threatening and life-threatening cases is not always easy. However, considering the implications of the latter, we will concentrate here on life-threatening diseases that can cause chest pain.
Cardiac chest pain
Our focus here is on the patient that presents with chest pain/pressure/discomfort/ache that we suspect is coming from the heart. The classic presentation is crushing substernal chest pain or pressure radiating to the neck or arms with sweating (diaphoresis) and difficulty breathing (dyspnea).
However, providers don’t always get that typical presentation. The cardiac patient might present with substernal chest discomfort alone, or present with atypical chest pain, such as pleuritic chest pain or sharp chest pain. Or the patient may present with no chest pain at all, but with recent onset of dyspnea or fatigue.
For the classic presentation, it’s no problem, we treat. For the atypical presentation with some of the cardiac risk factors listed below, we treat. Even when unsure, we still tend to treat.
Cardiac risk factors
- Male sex
- Family history of heart disease
- Older age
- Race (higher incidence in African Americans, American Indians, and Mexican Americans)
- Diabetes
- Tobacco use
- Drug use (sympathomimetics such as cocaine or methamphetamines)
- Obesity
- Uncontrolled hypertension
- Elevated cholesterol
So what actually produces cardiac chest pain?
The cause is inadequate delivery of oxygen to cells and/or increased oxygen demand by the cells. Insufficient cellular oxygen levels (tissue hypoxia) can result in pain regardless of location (heart, bowel, fingers, legs, etc).
Inadequate oxygen delivery is the result of one or both of the following:
- Inadequate oxygen transfer from lungs to the blood
- Inadequate delivery of oxygenated blood to the cells (ischemia) due to a low cardiac output (systolic BP less than 90-100 mmHg) and/or insufficient blood getting past a narrowed artery or arteries supplying a particular body part, thus producing ischemic heart disease, or ischemic bowel, or an ischemic extremity, etc.
Cardiac oxygen demand is determined by workload, which is determined by cardiac output, which is determined by the heart rate and stroke volume (CO = HR x SV) and by the back pressure against the aortic valve (diastolic blood pressure) — which the heart must push against to open the valve and deliver the blood.
Increased workload causes increased oxygen demand and the potential for inadequate oxygen delivery to the heart, which may result in damage or death of heart muscle cells.
- Increased HR = increased CO = increased workload = increased oxygen demand.
- Increased SV = increased CO = increased workload = increased oxygen demand.
- Increased SV = increase stretch of heart muscle which increases contractility or how hard the heart muscle contracts = increased workload = increased oxygen demand.
- Increased diastolic BP = increased workload to open the aortic valve = increased oxygen demand.
Mindful of the above, the treatment should follow logically:
- Increase oxygen supplied to the blood (supplemental oxygen)
- o Initially 4 LPM nasal cannula
o Maintain oxygen saturation over 90 percent
- Deliver oxygen enriched blood via an adequate perfusion pressure: systolic blood pressure greater than 90-100 mmHg. If less than 90-100 mmHg, think “Tank/Tank/Pump/Rate” to determine the cause(s) and subsequent treatment.
- o Tank too empty (hypovolemia)?
o Tank too big (vasodilation)?
o Pump not pumping (potentially reversible causes like pericardial tamponade or tension pneumothorax versus irreversible causes such as a massive myocardial infarct)?
o Rate too slow to deliver adequate cardiac output or too fast to allow adequate filling of the heart?
Once you have an adequate perfusion pressure with adequate oxygen saturation, proceed to the next level:
- Dilate coronary arteries to increase flow of the oxygen-enriched blood around any blockage to reach hypoxic cardiac muscle (nitroglycerine sublingual tablet or oral spray every 5 minutes, up to three doses if systolic BP remains greater than 90-100 mmHg systolic; follow local protocol)
- Decrease the workload of the heart to decrease myocardial oxygen demand, thus decreasing the amount of hypoxic tissue and heart damage
- o Decrease preload by dilating the large veins, which in turn decreases blood return to the atria and ventricles and thus decreases stroke volume, which decreases cardiac output and thus decreases cardiac workload (nitro as above/consider morphine if the pain is not relieved by the nitroglycerine)
o Decrease afterload by dilating the large arteries causing a decrease in diastolic BP, which decreases the amount of pressure the heart has to generate to open the aortic valve, which decreases cardiac workload (nitro/morphine see above)
o Decrease HR and contractility, which will decrease CO, which will decrease cardiac workload (consider beta blockers if systolic BP is 90 - 100 mmHg or higher; follow local protocol).
- Treat/prevent obstruction
- o Mechanical obstruction:
• Stop the clot
— Inhibit platelets with early administration of aspirin (ASA); then add other platelet inhibitors depending on diagnosis — Clopidogril (Plavix), Glycoprotein IIb, IIIa inhibitors
— Thin the blood: heparin
• Bust the clot
— Fibrinolytics (clot busters)
— Percutaneous coronary intervention (PCI): balloon, stentso Coronary artery spasm:
- • Sympathomimetic overdose (cocaine, methamphetamines)
— Benzodiazepines
— ASA
— Nitroglycerine
• Princemetal’s angina (spontaneous spasm)
— ASA
— Nitroglycerine
— Calcium channel blockers
- If available, obtain prehospital 12 lead ECG
Non-cardiac chest pain producers you should know
- Aortic dissection
o All chest pain patients should have blood pressures taken in both arms
o Right versus left arm systolic BP difference greater than 15 mmHg suggests a dissection
o Pain is described as sharp and sudden more often than the classical ripping or tearing pain - Pneumothorax
o Decreased breath sounds on one side
o Decrease oxygen saturation
o Watch for tension pneumothorax: increase HR, decrease BP - Pericarditis
o Patient typically leans forward to decrease the pain from the inflamed heart beating against adjacent structures
o Fever - Pulmonary embolus
o History is key to early diagnosis
o Oxygen saturation variable
o Clear breath sounds (air is moving in and out just fine but the blood flow is blocked by clot or fat or air or amniotic fluid)
Summary
There are many factors to consider when approaching the chest pain patient, especially when caused by life threatening conditions. In 2004, one out of every four deaths in the United States was caused by ailing coronary arteries (coronary heart disease). Many of these deaths occurred before the patient could or would seek medical care.
While not every patient with chest pain is having a heart attack, less frequent chest pain conditions — such as aortic dissection or pulmonary embolus – can also be deadly. In order to improve the final outcome of the critical patient who experiences chest pain, it is essential that we manage that first prehospital contact with a thoughtful approach to assessment and treatment.
References
1. American Heart Association. Heart Disease and Stroke Statistics – 2008 Update. Dallas, Texas: American Heart Association; 2008.
2. American Heart Association. Part 8. Stabilization of the Patient With Acute Coronary Syndromes. Circulation. 2005;112:IV-89-110.
3. American Heart Association. Part 7.4. Monitoring and Medications. Circulation. 2005;112:IV-78-IV-83.
