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19 The Circulatory System: The Heart

ObjectivesIn this chapter we will study• tests commonly used in diagnosing cardiovascular disorders;• the general symptoms and treatment of cardiac arrhythmias;• cardiac inflammation (pericarditis, endocarditis, and rheumatic heart disease);• cardiomyopathy; and• myocardial infarction.

Diagnosing Cardiovascular DisordersThe diagnosis of cardiovascular diseases begins withthe patient history and physical examination. A patientwho complains of tightness in the chest, a burningpain worsened by coughing, difficulty breathing,weakness, lightheadedness, and fatigue may be at riskfor one of many cardiovascular diseases, especially ifhe or she also has a family history of heart disease.Various aspects of cardiovascular function areroutinely assessed in a physical examination. Thepulse rate, strength, and rhythm are examined bypalpation; the heart sounds are studied by auscultationwith a stethoscope; and the blood pressure ismeasured with a sphygmomanometer.

If a cardiovascular disorder is suspected, furthertesting is warranted. Such tests include noninvasiveand invasive techniques as well as blood analysis.

Noninvasive TestsReduced cardiac output affects the oxygen andglucose supply to all organs, and the central nervoussystem is among the most sensitive to suchdeficiencies. Therefore, one of the most obvious signsof cardiac dysfunction is the impairment ofpsychological and motor functions such as attention,consciousness, coherent thought and speech, pupillaryreflexes, and visual gaze and tracking movements.Poor cardiac output also causes the blood hemoglobinto become dark red or violet in color. This effect ismost easily seen in areas of the body that have a densecapillary network and thin epithelium. Thus, acardiovascular assessment includes noting the color ofthe gums and other mucous membranes, conjunctivae,and nail beds. Cyanosis, or blueness of themembranes, suggests reduced cardiac function,although it also has other causes. Cyanosis therefore

brings to mind several etiological hypotheses andrequires further tests to narrow down its cause.

Palpation of the pulse and auscultation of theheart sounds are vital to any cardiovascularexamination. More sophisticated techniques involvevarious forms of cardiography, the measurement andrecording of cardiac functions. The best-known ofthese techniques is electrocardiography, the recordingof an electrocardiogram (ECG). A phonocardiogram,or record of the heart sounds, is made by placing amicrophone on the precordium (the chest wall anteriorto the heart) and connecting it to an amplifying andrecording instrument. An echocardiogram is similarin principle to a fetal sonogram. Oil is spread on thechest, and a device is placed against it that generatesultrasonic vibration and detects the echoes that comeback from the heart and associated structures. Therecord obtained through the cardiac cycle givesinformation on cardiac anatomy and such functionalcharacteristics as stroke volume and cardiac output.

Other specific diagnostic tests include thefollowing:

• A pulse tracing is a record of the pulsationproduced by blood flowing through a vessel. It isproduced by placing a sensor over a blood vesselsuch as the common carotid artery and recordingfluctuations in blood pressure over the course ofthe cardiac cycle. This method is used inconjunction with the ECG and phonocardiographyto determine the timing of the various events in thecardiac cycle.

• A Doppler study is a technique for listening tothe sounds of blood flowing in the vessels forevidence of obstructions to flow or valvulardefects in the heart. The sounds are amplified by amicrophone hand-held over the blood vessel.

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• A stress test is a study of the ECG and bloodpressure during exercise. A patient typicallywalks a treadmill until the maximum heart rate forhis or her age and sex is reached or until he or shebegins to show signs of cardiac distress such aschest or leg pain, extreme fatigue, or extremedyspnea. The ECG and blood pressure are thenexamined in comparison to pre-exercise recordsfor indicators of cardiovascular disease.

• A chest X ray is a routine part of a cardiacexamination. It shows the size, contour, andposition of the heart relative to surroundingstructures. A sharper silhouette of the heart can beobtained if the patient first swallows a contrastmedium such as barium, which makes theesophagus appear as a bright white backgroundagainst which the image of the heart stands out.

Invasive TestsExcept for the barium swallow, the techniques justmentioned are considered noninvasive because nothingenters the body. Invasive methods entail more risk butcan provide an overriding benefit in some cases bygiving the diagnostician more detailed and specificinformation.

In cardiac catheterization, a catheter (a thin,flexible tube) is threaded into a blood vessel until itenters a heart chamber. The catheter may then be usedto determine pressure within a heart chamber, towithdraw blood for measurement of blood oxygenlevel, or to introduce a contrast medium that enhancesimages of heart chamber function, valvular function,or the coronary arteries. Visualization of the coronaryarteries is called coronary angiography(arteriography). A catheter is threaded from thefemoral artery into the left ventricle, and a contrastdye is injected to allow filming of ventricular functionfor a few cardiac cycles. Then the catheter is pushedto the openings of the coronary arteries, and dye isinjected into the arteries so that they can be visualized.This method is used primarily to evaluateatherosclerosis.

Other invasive methods include PET scans,injection of radioisotopes to localize myocardialinfarcts or ischemic areas, and electrocardiographyusing electrodes introduced into the heart by way of acatheter to record from the AV bundle.

Blood AnalysisBlood samples also provide information about cardiacfunction. When cardiac muscle tissue is destroyed (asin myocardial infarction), enzymes and othercytoplasmic components leak into the blood. Theenzymes of greatest interest to cardiac function areaspartate transaminase, creatine kinase (CK), andlactate dehydrogenase (LDH). All of these enzymesappear in the serum within hours of a myocardialinfarction, and each enzyme is elevated at differenttimes. Aspartate transaminase peaks in 12 to 24 hoursand returns to normal in 2 to 7 days. CK peaks within24 hours and returns to normal in 3 to 5 days. LDHrises in 12 to 24 hours, peaks within 72 hours, andreturns to normal in 8 to 12 days.

Additionally, circulating sodium and potassiumconcentrations serve as markers in a manner similar tothat observed in skeletal muscle. The ability of theheart to effectively pump blood is measured in part bythe various blood gas measurements. Normalmeasurements for serum enzymes, ion concentrations,and blood gases are found in the Appendix of NormalValues at the end of this manual.

Cardiac ArrhythmiaCardiac arrhythmia (dysrhythmia) is any disturbanceof the normal heart rhythm. The signs and symptomsof arrhythmias vary from patient to patient, but ingeneral they include palpitations (awareness of theheartbeat), dizziness and syncope (fainting), anddiagnostic alterations in the ECG. However, becausethe patient may not experience a bout of arrhythmiawhile in the clinic, the physician may have the patientwear a monitor to record heart activity over a 24-hourperiod or longer.

Arrhythmia is treated with several techniques,including anti-arrhythmic drugs or a pacemaker. Animportant aspect of treatment is to reassure the patientand reduce anxiety, especially in cases that producepalpitations but pose no health risk. Precipitatingfactors such as exercise, alcohol, or caffeine may beidentified and the patient encouraged to modify his orher behavior.

Anti-arrhythmic drugs are the most commontreatment. Four classes of anti-arrhythmic drugs areavailable, with the choice determined by the type ofarrhythmia and the side effects of the drug: Na+

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channel blockers (lidocaine, quinidine, encainidine), β-blockers (propranolol, atenolol), K+ channel blockers(sotalol, aminodarone), and Ca2+ channel blockers(verapamil, diltiazem). Pacemakers are small, battery-powered devices with electrodes that stimulate theatria or ventricles in response to events in the heart.Today’s pacemakers are programmable and can beused to regulate both tachycardia and bradycardia.

Inflammatory Heart DiseasesA wide variety of microorganisms can infect thetissues of the heart and trigger cardiac inflammation,or carditis. Three examples are explored here—pericarditis, endocarditis, and rheumatic heartdisease.

PericarditisConditions elsewhere in the body often lead todisorders of the pericardium. For example, infection,connective tissue diseases, and radiation therapycommonly trigger pericarditis, inflammation of thepericardium. Pericarditis produces sudden chest painthat is worsened by breathing, often making a personthink he or she is having a heart attack. Othersymptoms include irritability, restlessness, malaise,and difficulty swallowing. Signs found uponexamination include tachycardia, a low fever, and araspy, sandpaper-like sound called a friction rubheard at the apex and left sternal margin of the heart.The friction rub occurs when the inflamed, roughenedpericardial membranes rub against each other.Pericarditis is treated with rest, analgesics, andnonsteroidal anti-inflammatory drugs.

Pericarditis usually resolves by itself in time, butsome cases are complicated by pericardial effusion,the seepage of fluid into the pericardial cavity. If thefluid accumulates slowly, the pericardium can stretchto accommodate it, but if it accumulates rapidly, itcan cause cardiac tamponade, a compression of theheart that prevents it from filling completely and thusreduces the stroke volume. As little as 50 to 100 ml offluid may induce serious tamponade. Cardiactamponade can be detected from a condition calledpulsus paradoxus in which the arterial blood pressureis more than 10 mm higher when the patient exhalesthan when he or she inhales. Echocardiograms are themost sensitive way of confirming cardiac tamponade.If serious, pericardial effusion is treated bypericardiocentesis—puncturing the pericardium andwithdrawing the fluid.

EndocarditisEndocarditis is inflammation of the endocardium,especially the heart valves. It usually results frominfection with bacteria, viruses, fungi, or parasites—but most often, the streptococcus and staphylococcustypes of bacteria. It is often triggered by mitral valveprolapse, implantation of artificial heart valves, long-term use of cardiac catheters, I.V. drug abuse, andcardiac surgery. Males are affected twice as often asfemales.

Pathogenesis begins when a heart valve or otherarea of endocardium is “prepared” by endothelialdamage to support colonization by microbes. Plateletsadhere to the damaged region and produce a thrombusthat can then serve as a focus of bacterial adhesion.Microbes can invade the blood from such sources asupper respiratory or skin infections, bladdercatheterization, or even dental cleaning. They adhereto the thrombus and begin to proliferate, so that within24 hours, there develops a lesion of alternating layersof bacterial colonies and clotted blood.

Typical signs of endocarditis include fever, weightloss, night sweats, a heart murmur, and abnormalitiesin the erythrocytes, urine, and ECG. The diagnosis isconfirmed by culturing bacteria from the blood and byechocardiography. The disease is treated withantibiotics, but repetitive episodes of endocarditis maydamage the valves so extensively that they requiresurgical replacement. Prevention of endocarditis is thereason some people are given antibiotics prior toreceiving dental work.

Rheumatic Heart DiseaseRheumatic fever is an inflammatory disease caused bythe immune response to a certain class ofstreptococcal bacteria. If untreated, it can lead torheumatic heart disease, a scarring and deformity ofthe heart. Rheumatic fever arises most often inchildren from 5 to 15 years of age, developing solelyas a complication of a streptococcal throat infection.If the throat infection is treated within 9 days,rheumatic fever usually does not develop. But iftreatment is delayed, the infection progresses torheumatic fever in about 3% of cases. This diseasegets its name not only because it produces a fever butalso because bacterial antigens bind to receptors in thesynovial joints and trigger an autoimmune response,leading to widespread joint pain, among othersymptoms.

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About 10% of children with rheumatic fever go onto develop rheumatic heart disease. This syndromebegins with carditis in all three layers of the heartwall, but the endocarditis is the most serious. Beadlikeclumps of “vegetation” develop on the heart valvesand chordae tendineae. These structures becomescarred and constricted, valve cusps may adhere toeach other, and eventually a patient can die ofcardiomegaly (enlargement of the heart), defects inelectrical conduction in the heart, and left heartfailure.

The first priority in treating rheumatic heartdisease is to inhibit the inflammation. Aspirin(salicylate) is the treatment of choice, but casesunresponsive to aspirin are treated withcorticosteroids. Penicillin G or other antibiotics areused to prevent recurrence of the streptococcusinfection. Severely damaged heart valves may requiresurgical replacement.

CardiomyopathiesCardiomyopathies are structural or functionalabnormalities of the myocardium. Most cases areidiopathic, but some are triggered by infectiousdiseases, toxins, cancer chemotherapy, alcoholism,connective tissue disease, or nutritional deficiencies.The two most common cardiomyopathies are dilatedand hypertrophic.

Dilated cardiomyopathy is characterized bydilation of the ventricle and loss of contractility, sothat the end-diastolic volume becomes greater (moreblood remains behind in the heart with each beat) andthe stroke volume is severely reduced. Patientscommonly experience dyspnea, fatigue, palpitations,dysrhythmia, and dizziness. Dilated cardiomyopathyis treated with digitalis to stimulate the heart, diureticsto promote water excretion and lower the bloodpressure, and bed rest, sometimes for extendedperiods. The prognosis depends on the extent ofmyocardial damage. Deaths from dilatedcardiomyopathy usually occur within 5 years ofdiagnosis and most commonly result from left-ventricular failure.

Hypertrophic cardiomyopathy is marked bythickening of the interventricular septum. It seems tohave a genetic basis. The diseased heart may appearnormal in size, but thickening of the septum reducesthe capacity of the ventricles. The ventricles stiffenand exhibit reduced filling and output. Angina,dizziness, palpitation, and dysrhythmia are among the

signs and symptoms. Beta-blockers such aspropanolol sometimes reduce ventricular stiffness andimprove ventricular filling and ejection. Some casesare treated by surgically removing part of thehypertrophied myocardium. The chance of long-termsurvival is good with appropriate management.

Hope is now available for some patients withcardiomyopathies through heart transplants. Butbecause donor hearts are in short supply, transplantsare usually limited to patients under the age of 50years, and even then most patients selected fortransplant die before a donor heart becomes available.In the United States, it is estimated that only 10% to12% of all patients with cardiomyopathies receivehearts annually. Successful transplantation results ina 50% to 70% 5-year survival rate.

Myocardial Ischemia and InfarctionCoronary atherosclerosis may cause myocardialischemia—a prolonged deficiency of blood flow to thecardiac muscle—and lead to myocardial infarction(MI), or heart attack. Frequently, an MI occursbecause platelets aggregate on an atheroscleroticplaque in a coronary artery and form a thrombus(blood clot), which can build up rapidly and block theartery or break loose and block a smaller arterydownstream. If half or more of the artery lumenbecomes blocked, blood flow may be inadequate tomeet the metabolic needs of the myocardium,especially when cardiac workload increases.

The myocardium can tolerate about 20 minutes ofischemia before tissue death begins. Within 8 seconds,the myocardial oxygen reserves are depleted and themuscle shifts to anaerobic fermentation. Fermentationgenerates hydrogen ions and lactic acid, lowering thetissue pH and contributing in multiple ways to cellularinjury. The cells leak K+, Ca2+, and Mg2+; theircontractility declines; and the heart’s pumping abilityis compromised. MI triggers a strong inflammatoryresponse leading, if the patient survives, to tissuerepair by fibrosis. Thus, some people’s hearts exhibitscar tissue that indicates earlier infarctions of whichthey may have been unaware.

The first symptom of an acute MI is often severechest pain, commonly described as a heavy, crushingsensation, “like an elephant sitting on my chest.” Thepain often radiates to the neck, jaw, back, shoulder,and left arm. Yet, in some cases, pain is absent.Consequently, the MI may not be immediatelydiagnosed or a patient may even deny that he or she

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has a life-threatening condition requiring emergencycare. Patient denial is a major factor in the delay oftreatment for MI and thus a major factor in mortality;50% of deaths from acute MI occur in the first 3 to 4hours of onset.

Other signs and symptoms of MI includerestlessness, pallor, apprehension, sweating, andcyanosis. The pulse is unusually fine and difficult tofeel (“thready”). An ECG often reveals arrhythmiawith abnormal Q waves, changes in the S-T segment,and inverted T waves. Myocardial enzymes areelevated (see previous discussion), and within 12hours the WBC count rises.

Diagnosis is based on the signs and symptoms justmentioned, along with the findings of imagingtechniques. Patients are admitted to the hospital wherethe cardiac rhythm and serum enzymes can be

monitored. Treatment involves the promptadministration of aspirin to minimize blood clottingand thrombolytic drugs such as tissue plasminogenactivator (TPA) or streptokinase, which break upblood clots that already exist and restore myocardialperfusion in about 3 minutes. Pain relief is usuallyaccomplished by administering sublingualnitroglycerin, a coronary vasodilator. Acute coronarycare is followed by bed rest, dietary modification, anda gradual return to normal activity.

Long-term survival depends upon many factors—degree of left-ventricular ischemia and dysfunction,age, diet, and potential for ventricular dysrhythmias.About 8% to 10% of those who suffer an acute MI diewithin 1 year, and most of these within 3 to 4 months.The most common cause of death is ventricularfibrillation.

Case Study 19 The Hard-Working ExecutivePaul is 42 years old and the president of a smallcompany. He is just beginning his daily workout at thelocal gym when he notices a slight tightness in hischest. As he continues riding an exercise bike, the painbecomes more severe and radiates to his left arm,shoulder, and jaw. Paul decides he is “overdoing it”and heads for the showers, intending to go back towork for the rest of the day and see how he feelstomorrow. After returning to his office, he begins tosweat and mentions to his secretary that he has anupset stomach. He thinks he might be coming downwith the flu, but needs to get a few things done beforegoing home.

Approximately 10 minutes later, Paul’s secretaryfinds him unconscious on the floor of his office andcalls an ambulance. When the paramedics arrive, theyfind that Paul is not breathing and has no detectablepulse. His skin is pale, cool, and clammy. Theyinitiate cardiopulmonary resuscitation, reestablishbreathing and a regular heartbeat, administer the clot-dissolving agent TPA, and begin transporting Paul tothe hospital. On the way, Paul regains consciousness,and a paramedic gives him an aspirin to chew. Theydetermine the following vital signs:

Heart rate = 50 beats/min and irregular

Blood pressure = 74/48 mmHg

Respiratory rate = 16 breaths/min and shallow

At the hospital, Paul is promptly placed on acardiac monitor, blood is drawn for enzyme analysis,and I.V. propanolol is given. Once Paul is stabilized,he is transported to the cardiac care unit (CCU). He isgiven nitroglycerin for pain relief and nasal oxygen tomaintain an adequate blood O2 level; his ECG andblood pressure are closely monitored by the nursingstaff.

Among the blood test results are the following:

pH = 7.18

Lactate = 42 mEq/L

Creatine kinase (CK) = 82 IU/L

Lactate dehydrogenase (LDH) = 130 IU/L

These results, coupled with the ECG,preadmission symptoms, and patient history, confirmthat Paul has suffered a myocardial infarction. Paul iskept in the hospital for 7 days for monitoring andtreatment. His cardiologist and his primary carephysician call on Paul in the hospital. His primarycare physician is well aware of Paul’s history: He isdivorced and overweight, smokes up to three packs ofcigarettes per day, is under treatment foratherosclerosis, and has a family history ofhypertension. Paul is frightened by his hospitalizationand resolves to lose weight and quit smoking. Hisphysician reinforces these decisions, prescribes a mildtranquilizer to relieve Paul’s anxiety, and discusses

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Paul’s rehabilitation with him. After 3 days of bedrest, Paul is encouraged to get up, rest in a chair, read,and walk to the bathroom as needed. He is released atthe end of the week, but scheduled for frequent visitsto his cardiologist for the next 6 weeks and counseledon gradual resumption of normal physical activity andon the issues of smoking, weight loss, work habits,and diet.

Based on this case study and other informationin this chapter, answer the following questions.

1. What risk factors predispose Paul to a myocardialinfarction?

2. Explain the physiological basis of Paul’s elevatedserum lactate and lactate dehydrogenaseconcentrations.

3. Explain why Paul is given an aspirin to chew onthe way to the hospital.

4. If Paul’s MI results from occlusion of thecircumflex coronary artery only, where would youexpect to find the myocardial lesion in a PET scanof the heart?

5. Explain why Paul is given propanolol in thehospital. What type of drug is this? How would itimprove his condition?

6. Both nitroglycerin and streptokinase can restoreperfusion of the myocardium through anobstructed coronary artery, but they do so indifferent ways. Contrast the mechanisms of thesetwo drugs.

7. Why would you expect intravenous drug users tohave a high incidence of endocarditis?

8. Cardiac tamponade restricts the filling and strokevolume of the right side of the heart before theleft. Why do you think this is so?

9. Heart attack patients in a CCU are ideally kept ina private room and allowed few visitors for thefirst 2 or 3 days. The room should have a clock,calendar, and window to the outdoors, and thepatient may be provided with light reading if he orshe wishes, but it is better not to furnish a radio,television, or newspapers. Explain the reason forall of this.

10. At the age of 20, Oscar is diagnosed withinsufficiency of the bicuspid valve. Which of thefollowing could indicate a predisposition for thisdiagnosis?a. hypertrophic cardiomyopathyb. pericarditisc. a childhood history of rheumatic feverd. cardiac arrhythmiae. pericardial effusion

Selected Clinical Termscardiac catheterization Insertion of a narrow

flexible tube (catheter) into the heart for bloodsampling, pressure measurement, or dye injections.

cardiomyopathy Any structural or functionalabnormality of the myocardium.

coronary angiography A method in which a contrastmedium is injected into the coronary arteries and anX ray made to assess arterial occlusion or otherabnormalities.

echocardiogram An ultrasonic scan of the heart forthe purpose of assessing cardiac anatomy andfunction.

endocarditis Inflammation of the endocardium,usually as a result of bacterial or other infection.

friction rub A raspy sound heard near the apex andleft sternal margin of the heart when inflamedpericardial membranes rub across each other.

pericardial effusion Seepage of fluid into thepericardial cavity, presenting a risk of cardiactamponade.

pericarditis Inflammation of the pericardium usuallytriggered by pathologies elsewhere in the body.

pulse tracing A method of measuring pulsations inblood pressure in a particular blood vessel over thecardiac cycle.

rheumatic heart disease Scarring and deformity ofthe heart, especially the endocardium, as the resultof an autoimmune response to a streptococcusinfection.

stress test An evaluation of cardiovascular fitness byrecording the ECG and blood pressure during adefined strenuous exercise such as walking atreadmill.