The Cardiac Patient

Each year in the United States, over a million patients are admitted for unstable angina (USA) and almost the same number for myocardial infarction (MI). Rapid recognition and therapy given in the first few hours can significantly reduce mortality and halt the progression of the disease process. Clinical differentiation of acute (MI) (aka AMI) and USA relies heavily on the presence or absence of electrocardiogram (ECG) findings. The ECG is of value only if used and interpreted in the context of the patient’s history, detailed physical examination, and appropriate laboratory and radiographic studies in order to determine the probability of coronary artery disease (CHD) and potential for myocardial injury and infarction.

PATIENT PRESENTATION

The chief complaint of chest pain should be considered cardiac in origin until proven otherwise. To the clinician “chest pain” refers to those terms commonly used by the patient to describe a discomfort, heaviness, tightness, or squeezing band surrounding or within one’s chest. Angina pectoris, commonly known as angina, severe chest pain due to ischemia and injury to the myocardium. The term derives from the Greek ankhon (“strangling”) and the Latin pectus (“chest”), and in fact many patients in cardiac crisis describe chest pain as a strangling in the chest.

The degree of severity of the chest pain as described by the patient may or may not represent the degree of severity of the cardiac event. In other words, there can be severe pain with little or no risk of a cardiac event, but an infarction can occur without any warning or and perception of pain. Chest pain due to cardiac disease can occur in almost all age groups. Approximately 7.8 million Americans 20 years and older have survived myocardial infarction. Nearly 7 million Americans have chest pain or discomfort (angina pectoris) due to decreased myocardial blood supply (ischemia).

It is important to realize that as many woman as men suffer AMI. Woman’s symptoms often are less dramatic than men and have just as devastating effects. Despite publications supporting this premise, there is still a belief that woman are less prone to heart attach and sadly there is often a critical delay in recognition and implementation of appropriate aggressive interventions. Another misconception is the belief that only older woman are casualties of heart attack. It is negligent to pass over signs and symptoms in any patient, because of age or gender, who presents with signs and symptoms of a heart attack. There are many terms describing the onset and frequency of chest pain. Despite the terminology, any complaint of chest pain deserves urgent medical attention and should be treated as a heart attack until proven otherwise.

Angina Pectoris---Physiology and Signs and Symptoms

Angina pectoris is a syndrome characterized by episodic pain when the heart suffers oxygen deficiency. This deficiency can be caused by three types of cardiac stressors:

• A decreased flow of oxygenated blood to the myocardium (ischemia) as a result of atherosclerosis, thrombosis, embolism, or coronary artery vasospasm.
• A decreased capacity of the blood to carry oxygen, resulting from conditions such as severe anemia.
• An increase in cardiac workload, which causes an increases in the need for oxygen, resulting from conditions such as hypertension or aortic stenosis.

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Cocaine-Induced Chest Pain

Of the many complications that are associated with cocaine use the most frequent complaint is chest pain. The incidence among cocaine users who present to the hospital has been reported to be as high as 40 percent. Ischemia including acute coronary syndrome (ACS), is the most common cocaine-associated cardiac disorder.

Other cocaine-related cardiac complications include coronary artery spasm, acute myocardial infarction, atherosclerosis, myocarditis, endocarditis, cardiomyopathy, arrhythmias, and hypertension.

Of all patients presenting with cocaine-associated chest pain, approximately 6 percent are experiencing MI and 15 percent have ACS. The risk of MI is 24-fold higher in the first hour after cocaine use, but has been documented for up to 6 weeks following cocaine withdrawal. Demographic and historical factors are not reliable for predicting cocaine-associated MI, but most patients are young, male cigarette smokers without other risk factors for atherosclerosis. Young patients should be questioned about cocaine use if they present with chest pain, and anyone with potential cocaine toxicity should receive a complete evaluation.

The pathophysiology of cocaine-induced myocardial ischemia is multifactorial, and the extent to which the mechanisms may interact is unknown. Coronary thrombosis can develop in the presence of normal or diseased coronary arteries, possibly as a result of alterations in platelet and endothelial functions. Studies have proven that cocaine increases human platelet activation and aggregation. Additionally, vascular spasm my cause damage to the endothelium, creation a nidus for platelet aggregation and fibrin deposition and resulting in thrombus formation.

In some patients activation of the sympathetic nervous system causes the release of excessive amounts of norepinephrine, which causes platelets to aggregate and release thromboxane A. This vasoconstrictor causes coronary artery spasm. As anaerobic metabolism continues, production of adenosine triphosphate (ATP) decreases. This allows sodium to accumulate inside the cells and potassium to accumulate outside, impairing the heart’s sequence of depolarization and repolarization. Ischemia decreases compliance of the left ventricle, causing diastolic murmurs. Ischemia of the papillary muscles attached to the mitral valve causes systolic murmurs.

Increasing ischemia causes greater cell damage, which stimulates more pain nerve endings and changes the pattern of classic angina to unstable angina. This often precedes a myocardial infarction. Symptoms typically occur at rest, rather than on exertion (thus attacks usually occur at night). Many patients have concurrent atherosclerosis of a major coronary artery, but this is often mild or not in proportion the degree of symptoms (Prinzmetal’s angina). Ischemia and hypoxia damage the heart cells, white blood cells, and platelets, which then release potassium, histamine, and serotonin. These substances stimulate pain nerve endings. At the same time, the metabolism switches from aerobic to anaerobic. This produces lactic acid which also stimulates pain nerve endings.

Sensory nerves for the heart stimulate nerves that synapse with sensory nerves for other parts of the body, at the thoracic level of the spinal cord. Pain is referred from the heart to areas of the body also supplied by these nerves. Pain and decreased cardiac function stimulate neural reflexes, which activate the sympathetic and parasympathetic branches of the autonomic nervous system.

Probable Signs and Symptoms

• Manifests as pain during stress (pain relieved by rest), during sleep, and after a heavy meal, after exposure to cold, tachycardia, and increased pulse strength and blood pressure.
• Manifests as retrosternal pain that is described as a feeling of tightness, pressure, heaviness, squeezing, or burning.
• Manifests as changes in the ST segment and T waves in reflecting leads with reciprocal changes.
• Listen for audible (third or fourth heart sounds or a high-pitched mid- to late-systolic) murmur over the apex.
• Manifests as increased frequency and severity of anginal attacks or new symptoms or new patterns of referred pain.

Approaching the Patient

In the majority of patient encounters, the simplest approach is “tell me what’s wrong.” The clinician should note that patients’ vocabularies differ according to cultural background, socioeconomic factors, and their response to pain and variable body sensations. It is dangerous to presume interpretation and understanding are accurate when little English is spoken between the examiner and the patient. Many facilities provide translators for various languages and for those who are hearing and speech impaired.

Listen as the patient speaks. Are the words clear and distinct, slurred, or muffled? Is the patient slow to respond? Maintain eye contact while listening to the patient. Do not be annoyed when the patient does not return eye contact; be aware of cultural norms in this regard.

The classic or textbook presentation of the patient’s chief complaint as “crushing, squeezing pressure in the midchest or beneath the sternum tat radiates to the neck and left shoulder and arm” may not be seen in the majority of cases. This classic scenario is least common in women and older individuals. Tolerance and affect play a role in the patient’s manner and presentation during an acute MI.

Other chief complaints suggestive of cardiac disease are syncope, dyspnea, palpitations, dizziness, altered mental status, malaise, and hypotension. The patient may present with a history of a fall injury. In this scenario question the patient for any feelings of dizziness and/or near-syncopal episodes that may be the cause of the fall. New-onset atrial fibrillation may be the only clue to the previously undetected heart problem. Many diabetics may present atypically when having a cardiac event. New-onset congestive heart failure and pulmonary edema are more common occurrences in, but not limited to older adults. Relevant to all of these patient presentations is determining the nature, onset, duration, intensity, previous similar episodes, associated symptoms, and frequency.

PATIENT HISTORY

History taking is an art because people are different not only in their body makeup but how they experience and express sensations so that gathering the appropriate information can be challenging. Greeting the patient, maintaining eye contact, and touching while respecting personal space are part of this art. Understanding patience, and word choices can help set a cooperative atmosphere and not take valuable time away from focusing on the patient’s problem. The clinician who is sensitive to the patient’s comfort and feelings can enhance communication skills. Documentation, although important, should not intrude upon the patient-caregiver relationship during this communication process. Lack of eye contact for a period with continued verbal questioning while taking notes may be interpreted as impersonal care.

Listening to family members, companions, and caregivers allows the family unit to participate. This is important when there is a language barrier, when the patient is unable to clearly respond, or when ethnicity or social mores indicate deference to a family member. Everything should be done to preserve the patient’s integrity. Remember that the patient is suffering, so simple, short questions are best. Do not use a loud, arrogant, or impatient tone. Although there may be a need to be assertive in a confusing situation, most patient scenarios do not call for aggressively exerting control.

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CHIEF COMPLAINT

The chief complaint and symptoms associated with cardiac disease most commonly include chest pain or discomfort. Often a severe degree of pain is termed “sharp”. The clinician will interpret this as the quality or character of the pain, whereas the patient equates “sharp” with intensity. Some say the pain feels like heartburn. This is a self-interpreted perception, and the clinician should ask when this sensation occurred and if and how it was resolved.

It may help to encourage the patient to describe or relate the symptoms to previous experiences. To ensure proper interpretation, acknowledge your understanding of the answer. Volunteering terms and phrases with an explanation may assist but should not be done as a rule. Premature interruption, or finishing the patient’s sentence, is inappropriate. First, it is rude and second, the patient often feels intimidated and agrees rather than argue the point. Often this occurs when the clinician feels a sense of urgency and may be impatient to continue with care. The sense of timing for interrupting the patient is an important and acquired skill. Also, many patients, when asked “Do you have chest pain?” will answer, “No, it’s a tightness” or, “it’s burning a hole through me” or, “it won’t let me breathe” or, “it feels like a heavy weight” or, “it makes me feel like I can’t breathe.” Women may say, “My bra suddenly feels so tight.”

OPQRST OF CHEST PAIN

In asking about the chief complaint, keep in mind the mnemonic OPQRST:

O = Onset/origin: “When did this start?” is the simplest approach. Time is critical and contributes to decisions for reperfusion. Precipitating factors and determining what the patient was doing when it started are key clues. Sudden temperature change or pain at rest or awakening from sleep carries a graver prognosis. Asking focused questions to find out the exact time may be critical in deciding which therapy to initiate. Ask whether onset occurred relative to a meal, a TV show, a friend’s visit, or a telephone call. These associations may clarify the time of onset.

P = Provocation: “What happened?” “What started this?” “What were you doing at the time?” are easy questions. If the pain is a recurrence, is it the same or different? If different, in what way? Is it exertional or not? Is it related to deep breathing, on inspiration or exhalation? Chest pain may occur with emotional stress as well as physical exertion.

P also applies to palliation. What has the patient done to relieve the pain? Was it effective? Was it effective in the past, but not now? Chest pain may be relieved by rest without medication, and it may “just go away.” This type may last less than 15 minutes. However, persistent, intense symptoms that last more than 15 minutes are of concern.

Q = Quality: “Tell me what it feels like.” The patient should be encouraged to describe the pain in his or her own words like tearing, pressure, heaviness, pushing, urging, sharp.

R = Region/radiation: “Point to where it hurts.” “Point to where it moves.” “Does the pain travel anywhere?” “Does it seem to come from or go to anywhere?”
Pain may go to the jaw, to the neck, to one or both shoulders and down one or both arms. Discomfort may also occur in the back, straight through from back to front, or feel like a constricting band that inhibits breathing and the patient is short-of-breath or cannot take a deep breath.

S = Severity: Ask “How bad is it?” A simple technique is to ask the patient to use a number scale from 1 to 10, 10 = severe or the worst and 1 = the least to describe the pain. Obtain a baseline severity score and repeat each time an intervention is performed. This technique is especially useful when asking the patient questions about any change in the level of pain after a medication and/or a treatment.

T= Timing: “How long did the pain last?” “Is it constant?” “Does it come and go?” For example, when, after what activity, or after which medication? Again, persistent, intense symptoms that last more than 15 minutes should signal a sense of urgency.

Aggravating or alleviating factors are helpful in developing the differential diagnosis. Actions such as moving one’s arms or bending over that precipitate the pain can be meaningful. These pains are frequently described as sharp, knifelike, or stabbing. Pain brought on by breathing may be related to a musculoskeletal or pleuritic, lung-related problem. Difficulty in breathing (dyspnea), or a sensation of inability to catch one’s breath or inability to take a deep breath, is seen as a rapid, almost gasping shallow breathing accompanying the pain.

Positional history may be helpful. The patient may prefer sitting and leaning forward with hands supported on the knees or on either side of the thighs in order to “breathe easier” while experiencing chest pain. This is called tripod positioning. Central chest pain/pressure that is worse when supine and improves when sitting up and leaning forward is suggestive of pain that is myocardial in origin. The clinician may ask the stable patient to perform the action that brings on or aggravates the pain. Knowing the factors that alleviate pain is important as well. For example, some mild hiatal hernia problems seem to improve when the patient is sitting upright.

Patients with chest pain may also have gastrointestinal symptoms. Associated signs and symptoms include belching, nausea, emesis (vomiting), or a feeling of “agida low in the belly.” Diaphoresis, pale, cold, and clammy skin are also grave signs. Vagal stimulation resulting from the pain of AMI can cause emesis and marked diaphoresis.

Palpitations and signs of ectopy with or without chest pain may be presenting symptom of cardiac disease. Palpitations are often described as a fluttering sensation, irregular beating, skipping, or “my heart is beating fast in my neck.” The patient may also complain of “skipped beats” or a feeling that his or her heart “turns over.” No matter the nature or origin of the ectopy, the associated or primary symptoms of palpitations should be of concern and warrant further investigation.

Questioning about past medical and medication history provides additional information, such as other illnesses, allergies, recent trauma, and surgeries. Asking about previous medical problems—specifically occurrence of congestive heart failure, heart attack, angina, hypertension, or chronic lung disease—is important.

For example, hypercholesterolemia is a significant risk factor. Because of neurologic and vascular changes caused by the disease, diabetics may voice very minor complaints, if any, when experiencing a cardiac event. They may not perceive, feel, or describe chest pain in the classic sense. They may also associate diaphoresis as a sign of their “sugar imbalance” or “too much insulin this morning.” Associated symptoms and signs may be the only clues. Recall, diabetes is an important risk factor for cardiac disease.

Inquiring about patient allergies may provide indirect information about not-yet-revealed medical conditions or problems. The patient may not consider it important enough to volunteer this information and the over-the-counter (OTC) medication taken for that allergy.

MEDICATION HISTORY

Medication use—particularly nitroglycerin (NTG), Isordil, beta-blockers, digitalis, diuretics, angiotensin reversing blockers, ACE inhibitors, antihypertensives, antiarrhythmics, and calcium channel blockers—should be of particular interest to the clinician. Ask for a list of medications, or if the patient has brought them along. First responders often collect medications and bring them with the patient on admission. Patients may not know the true category of their medications. Ask why the patient is taking a medication. For example, ask simple, straight-forward questions such as, “Are you taking this for your blood pressure?” “Are you taking this for water retention?” Examples of medications that may flag a concern for the clinician are nitrates, beta-blockers, digitalis preparations, diuretics, antihypertensives, and antiarrythmics. Ask about regularity of use in a nonthreatening manner, because additions or omissions may precipitate a cardiac event. Ask if there has been a recent change in dosage or a recent stopping of medication. All of this is relevant and should be documented. Again, ask in a nonthreatening and nonjudgmental manner that will elicit a straightforward response.

Another area of concern involves asking if the patient recently saw a physician and received medication in the office or was recently discharged from the hospital and was given unfamiliar medications. Some cardiac medications have a long-lasting effect that may alter ECG measurements--for instance, amiodarone and tricyclic antidepressants prolong the QT interval. Asking the patient “Did you or your doctor recently stop or change the dosage of a medication?” may provide essential clues to the immediate problem. Knowing the half-life of a medication will help with the ECG analysis. For instance, the elimination half-life average for amiodarone is 58 days and ranges from 25 to 100 days. The use of oral contraceptives or replacement hormone therapy often is often not reported by the patient as a medication.

Ask, too, for a list of medication from all physicians caring for the patient. This list should include dermatologists, allergists, and other specialists who may have prescribed medications.

Another consideration is the use of sexual enhancement drugs that cause a drop in systemic blood pressure in many patients. This is caused by a dilation of general blood vessels, as well as the vessels that foster erection of the penis. A history of cyanopsia (blue vision) is another sign that the patient may have taken these drugs for some time. It is not unusual for a female partner to take the same medication as she may believe that if works for him it could work for her. The same side effects will occur. Before considering the use of nitroglycerin for chest pain it is imperative to as if anyone in the home is taking these drugs, prescribed or herbal or over-the-counter.

Some patients may deny having heart problems because they do not perceive a relationship between high blood pressure or diabetes and heart disease. Use of cholesterol-lowering drugs may be the only clue that the patient has a problem. Too often, patients feel that if they are on medication, they no longer have the disease or problem. For instance, a patient denies having high blood pressure—but medication history reveals antihypertensive medications. When questioned, the patient responds, “That’s why I don’t have high blood pressure.” Abrupt discontinuation of medications because of the side effects is another problem. For instance, stopping medications such as the beta-blockers may trigger cardiac events.

In addition, over-the-counter medications may precipitate a cardiac event. Often patients do not see these as worthy of mentioning, so clinicians must ask the questions. Herbal homeopathic preparations can be cardiotoxic. Borrowing medications from family members or friends with “similar” problems is very common. In addition, recreational drugs such as cocaine can be cardiotoxic. Use of recreational drugs even in the relatively distant past can be a risk factor. To a recovering addict, 3 months of being “clean” is a “long time” of being drug-free. Therapy for concurrent illness and knowledge of the specifics of medication are important. Not only can this knowledge contribute to the diagnosis but it may also help determine the type of intervention. Certain medications or recent procedures may negate the use of a thrombolytic of fibriolytic intervention.

Social history gives clues to risk factors for cardiac disease. Recognized risk factors include smoking, diet including carbohydrate intolerance, sedentary living, obesity, personality type, and active psychosocial tensions. Alcohol abuse is another contributory factor to cardiomyopathy. Family members may report changes in personality or behavior. The patient recently became argumentative, or one who is usually outgoing becomes suddenly passive, or sleeps all the time, or has a poor attention span.

Genetics is a critical component of the cardiac assessment. Inquire about family history for stroke, heart disease, diabetes, and hypertension and the age of parents and siblings at death and the cause of death. Body weight, type 2 diabetes, smoking habits eating patterns, alcohol consumption, physical exercise or lack of, known lipid levels, vascular diseases, and unexplained sudden death are all considerations that contribute significantly to the patient history and can affect how quickly a diagnosis can be made.

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THE PHYSICAL EXAMINATION

Examination of the patient involves all the clinician’s senses; that is, the eyes, ears, sense of smell, and sense of touch—despite being a gloved activity. This can be done rapidly and effectively to gather needed pairing of history with the state of the body. Explaining what you are going to do before touching the patient, especially when removing clothing, will ensure a quick physical examination. Explaining what you are going to do with various equipment is also important, because clinicians tend to take for granted that everyone knows the tools. It is also important to let the patient know when it will or will not hurt. Apprehension is usually easy to see; addressing a patient’s fears may help minimize uneasiness about the procedure.

The ongoing physical assessment begins while observing the total patient. Start with looking for dyspnea and tripod positioning, while observing the patient’s expression. Is the patient fearful, agitated, angry, or frustrated? Are the eyes clear, bright, dull, or unseeing? Note the skin color, temperature, and hydration; assessing for diaphoresis. Assess carefully for jugular venous distention and peripheral edema.

Additional clues are surgical scars, especially on the chest, that indicate previous heart surgery or the presence of a pacemaker. Often only the pacemaker prominence is seen on the chest. Look for a nitroglycerin patch on the chest, arms, inner thighs, or lower abdomen. Look for signs of obesity, questioning actual or estimated weight as necessary.

Differentiation of the cause of chest pain and/or discomfort includes considering illnesses or insults that can occur in various organ systems. These include gastrointestinal, pulmonary, cardiac (including the great vessels), and the chest wall, which includes ribs, muscles, and the costrochondral junction.

DETAILED ASSESSMENT

It is vital to know the patient’s history and current status to determine whether the findings are appropriate for that patient. Then, change in future assessments will indicate a deviation from normal. Observe general appearance, gross deformities, apparent nutritional status, posture, gait, cooperation, speech patterns, and ability to speak in full sentences with or without difficulty, facial expression, and facial grimace during examination.

Overall Inspection

• Skin: Observe and record moisture, temperature, texture, turgor, thickness/thinness, edema, lesions, and changes in superficial vascularity.
• Nails: Observe and record color, size, shape, and clubbing.
• Pulses: Assess carotid, brachial, radial, popliteal, posterior tibial, and pedal. (Femoral is felt later, during palpation.) Assess for presence and equality.
• Neck: Assess carotid pulses, as above. Assess jugular venous neck distention; ideally the patient should be positioned at a 45-degree angle.
• Chest: Assess symmetry, precordial pulsations, and apical pulse for rate, rhythm, character, and intensity. Observe and record heaves, thrusts, thrills, vibrations, and pulsations.
• Abdomen: Observe and record pulsations, edema, size, and symmetry. Assess the five f’s of abdominal assessment: fluid (ascites), flatus, feces, fetus, and fatal tumor.
• Back: Assess for presacral edema, especially in patients who have been confined to bed or a recliner.
• Extremities: Assess the skin and distal circulation. Note posterior of the legs for varicosities. Assess for tenderness, erythema tibial, and/or pedal edema. Assess fingers for nicotine stains.

Auscultation

Auscultation should be done before palpation. This examination is performed with a bell/diaphragm stethoscope and, whenever possible, stethoscope-to-skin. When assessing breath sounds, use the diaphragm listening from base to apex, side-to-side comparing the sounds. Auscultation should be done anterior as well as posterior, and include the right and left midaxillary areas. Any adventitious sounds should be documented and whether they are unilateral or bilateral.

High-frequency heart sounds are best heard with the diphragm; low-frequency sounds are best heard with the bell of the stethoscope. Areas to auscultate include the anterolateral neck, abdomen, and femoral area for the presence of pulsation, bruits, and equality of sounds.

Palpation

Assess for presence or absence of rubs, thrills, or tenderness.

• Anterior precordium over the xyphoid area (right ventricle):
• Apical area: Assess the point of maximum impulse (PMI). If there is and increase this may indicate left ventricular hypertrophy(LVH). If shifted, this may indicate COPD.
• Pulmonic area: A thrill palpated here may indicate pulmonary stenosis, anemia, fever, or pregnancy.
• Aortic area: A thrill palpated here may indicate aortic dilation.
• Epigastric area: Pulsations felt here may indicate aneurysm.

Percussion

Use the flat of the fingers of the hand in contact with the part to be palpated. Tapping is done with the third finger of the other hand against the terminal joint of the third finger of the palpating hand. Abnormal findings ma occur when the examiner has arthritis or a bony defect of the hand or fingers. Note that bone is dense and air is not Therefore, percussion over a solid surface (i.e., bone) is duller than over air-filled surfaces such as the lungs.

Terminology of Percussion

• Resonance: decreased density usually heard over lung tissue
• Impaired resonance: slightly more dense; may be caused by fluid filling otherwise erated spaces
• Hyperresonance: lowest in density, heard over air-filled areas
• Dullness: a dense sound usually heard over dense tissue
• Tympany: very low density, over air-filled areas

Vital Signs

Alterations of blood pressure, heart rate, core temperature, blood glucose levels, and ventilatory status, including pulse oximetry, are determining factors in a cardiac event.

The carotid and radial pulses are palpated to determine rate and perfusion. Irregular rhythms can affect perfusion; for example, atrial fibrillation and atrial flutter as well as any ectopy. With and irregular rhythm, listen to the apical pulse while palpating the radial to determine the extent of any deficit. Absence of a palpable cartid pulse with an ectopic beat is not a differential tool between ventricular and ectopic beats.

Before palpating the carotid, inspect the neck for abnormal pulsations. Auscultate with the stethoscope to determine presence of a bruit. This murmur like sound may imply a vascular rather than a cardiac problem. Decreased pulsations may be caused by decreased stroke volume but also my be due to atherosclerotic narrowing or occlusion. A tortuous and kinked carotid artery produces a unilateral pulsing bulge. During palpation it is possible to detect a thrill.

A carotid bruit with or without a thrill in a middle-aged or older patient suggests, but does not prove, arterial narrowing. A murmur that is aortic in origin may radiate up the carotid and simulate a bruit. A carotid bruit and an aortic murmur can both be present.

Blood Pressure

Remember the basics: A proper-size blood pressure (BP) cuff is critical and should be place 2 to 3 centimeters (cm) above the antecubital area. Measure the blood pressure manually in patients with irregular rhythms such as atrial fibrillation or those with frequent ectopy as an automated measurement may be inaccurate.

Pitfalls in Taking Blood Pressure Readings

False High Readings

• Cuff is too short, too narrow, or too loose.
• Patient arm is elevated above the heart level.
• Anxiety and anger can cause a high blood pressure.

Rapid Deflation

• Can underestimate systolic pressure reading.
• Can overestimate diastolic pressure reading.

With Ovesity

• Place the cuff on the forearm and listen over the radial artery.
• For leg pressures, use a wide, long cuff on the lower one-third of the thigh. Center the bag over the posterior surface and wrap snugly. Listen for sounds over the popliteal area.

Causes or Weak and/or Soft BP Sounds

• Incorrect placement of the stethoscope.
• Incorrect placement of the stethoscope and poor perfusion, and arrhythmias.
• Venous engorgement from incomplete deflation and repeated inflation.

SUMMARY

The organized assessment of any cardiac patient is critical in determining the pathways of care. Associated diseases and therapies may conflict with many therapeutic modalities available to the clinician. This chapter provides one method, a baseline tool, for the organized approach to assessing patient presentation obtaining focused history, and performing a detailed physical examination.

There is a mantra of sorts that should come to mind when assessing any patient and planning interventions. This includes assessing ABCs, signs and symptoms of hypotension and hypoperfusion, chief complaint, history of present illness medication and medical history, vital signs including O 2 saturation levels (SPO2) and blood glucose monitoring (BGM), and questioning all elements of the patient’s chest pain. For the sake of brevity this directive will not be repeated when discussing interventions with arrhythmias and conditions in the following chapter.

This chapter is not meant to be all-inclusive in the techniques and approach to patient assessment. It is the responsibility of the clinician to maintain commitment to the current knowledge and techniques asked on the patient care standards in a specific work environment.

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