EKG: SECTION FOUR

F. Ventricular dysrhythmias

Ventricular dysrhythmias are frequently unstable and unpredictable. These dysrhythmias are also potentially lethal, because the heart does not provide a synchronous or coordinated contraction so SV and coronary flow are compromised.

1. Premature Ventricular Complexes

• Most common arrhythmia seen in a healthy adult. PVCs (or VPBs) are seen in 50-63% of healthy individuals and in 72-93% of post MI patients.

PVCs are a normal finding in adults of all ages. The frequency can be during stress, with ingestion of caffeine, and with sympathomimetic drugs such as some over-the-counter cold remedies.

The frequency is also in patients with a tendency to develop ventricular tachycardia.

PVCs are also a/w drugs like lidocaine, procainamide, quinidine, and propranolol; and a/w disease states like MI, cardiomyopathy, CVA, CHF, hypokalemia, mitral valve prolapse, infectious disease, ischemia, and electrolyte imbalance.

The carboxy-Hb of 4-6% that is seen in cigarette smokers is a/w numbers of PVCs in CV patients during exercise. Atmospheric pollution produces similar dysrhythmias.

• Originates in the ventricle and interrupts normal regularity.

A wide QRS complex that occurs earlier than would be expected from the sinus rate, and that almost always has an abnormal morphology.

• Fails to conduct retrograde through the AV node in half of patients, in which case it results in a compensatory pause. That is, the next P wave occurs at the same time as would be expected had the PVC not occurred.

• When it does conduct through the AV node, the following P wave may occur either sooner or later than would be expected.

• PVCs may be early or late — a late PVC is only slightly premature and is a/w a non-related P wave (the timing is similar to fusion beats).

• PVCs may be single or multiformed (formerly called single or multifocal).

• The HR depends on the number of PVCs.

• Patients are often unaware that they are having PVCs, but they may have palpitations, skipped beats, dizziness, SOB, chest discomfort, angina, or hypotension.

• PVCs are not preceded or initiated by a P wave.

If a PVC is preceded by a P wave, it is not a premature P — it is a nonconducted P.

• A PVC is initiated in the ventricle; therefore, there is no PR interval.

• The QRS is always wide and bizarre, and has a longer duration than normal because depolarization originates in the ventricle and follows an abnormal pathway.

• The T wave is in the opposite direction from the R.

• There may be couplets, salvos, bigeminy, trigeminy, or a compensatory pause.

A couplet is 2 consecutive PVCs and a salvo is a short run of 3 or 4 PVCs.

A couplet can be a normal finding, but is more suggestive of electrical heart disease than are single PVCs.

Bigeminy (group of 2) refers to pairs of complexes and signifies a normal sinus beat followed by a PVC.

Trigeminy (group of 3) refers to a PVC with 2 consecutive sinus beats or vice versa.

• PVCs may be treated if they occur more than 6/min. The tx. consists of the administration of medications like lidocaine (bolus then drip), Pronestyl, bretylium, or Inderal.

The cause (electrolyte imbalance, etc.) also should be corrected.

Compensatory Pause: A PVC wipes out the expected sinus related QRS and there is a compensatory pause before next normal cycle.

The pause occurs because the AV node is refractory and does not allow retrograde conduction so the next sinus impulse comes when it is supposed to.

The duration is what you would expect from 2 normal beats.

The PVC hides the normal SA impulse — similar to the QRS hiding atrial repolarization on a normal ECG.

• R on T Phenomenon: If an R falls on a T wave, it may cause VT or V-fib.

• Fusion Beats

Fusion beats are usually a combination of a SA impulse and a PVC, or a SA impulse and an artificial pacemaker impulse.

Fusion or capture complexes confirm the coexistence of supraventricular and ventricular foci. The same chamber of the heart is depolarized by 2 simultaneous impulses leading to blending or fusion of the two.

The two impulses are both trying to control the heart at same time; the complex has characteristics of the supraventricular and the ventricular beat.

The first part of the complex looks normal because of the sinus influence, but the last half is abnormal.

The fusion complex is usually more narrow than the PVC.

You need to look at both the normal and the PVC beats and then look at the fusion beat to differentiate this dysrhythmia.

Pacemakers produce ventricle foci so a fusion beat is expected in patients with pacemakers.

Fusion beats are seen with ventricular ectopy so their presence can be used to help differentiate SVT with aberrancy from VT.

Fusion beats are treated as PVCs. If the overall rate is OK; it is usually not necessary to report fusion beats unless there are more than 5/min.

Differentiating PVCs from Aberrant PACs — Precordial Concordance (see page 6) confirms ventricular ectopy. Normally the QRSs in precordial leads change from downward in V₁ to upward in V₆. When the depolarizing current is directed toward base of the heart from a ventricular focus, this progression is altered and all of the precordial leads are upright or downward.

PVCs tend to be mono- or biphasic in V₁ and V₆.

V₆ is usually predominantly negative in the presence of a L ventricular PVC .

V₁ is predominantly negative in the presence of a R ventricular PVC.

2. Idioventricular Escape Rhythms

• Originates in the His-Purkinje system.

• The first beat of an escape rhythm occurs later in the cycle than expected (after a beat is missed).

• Usually regular with a rate of 20-40 (inherent ventricular rate).

The slow rate Æ Ø cardiac output and also permits the emergence of lethal dysrhythmias.

• Usually there is no P or PR interval (if present, they bear no relation to the QRS).

• The QRS is wide and bizarre, because it originated in the ventricle and was not conducted normally.

• Diagnosed when only ventricular escape complexes are present, and they occur at 20 to 40 beats per minute.

• This rhythm is barely consistent with life.

• If you see this, you should start CPR immediately, and should move the patient to an ICU as soon as possible.

• DO NOT give lidocaine or any other antiarrhythmic medication for this rhythm. You could cause asystole and death by inhibiting the only spontaneous rhythm the patient's heart is able to generate.

• Management: The ventricular rate needs to be accelerated. The rhythm is enhanced with drugs, pacing, or calcium.

3. Ventricular Escape Complexes

• A wide QRS occurring later than would be expected from the sinus rate.

• Like all escape complexes, it can occur only when the normal cardiac pacemaker does not function, as in sinus arrest.

4. Accelerated Ventricular Rhythm

• Diagnosed when only ventricular escape complexes are present, and they occur at 60 to 100 beats per minute.

• Usually seen in the setting of acute MI.

• If the patient is in sinus rhythm, the rate of this rhythm tends to be about the same as the rate of the sinus rhythm. In this case, the two rhythms will speed up and slow down so that they alternately capture the ventricle, with characteristic periods of fusion QRS complexes during the Ds in rate.

• This rhythm is usually benign. Because it occurs in the setting of acute MI, patients who exhibit it are already in an ICU where any malignant sequelae can be treated readily.

5. Ventricular Tachycardia (VT)

• VT is usually initiated by PVCs, but carried on by re-entry mechanisms.

• A single focus VT looks like a series of PVCs.

• It is usually regular or slightly irregular with a rate of 150-250 bpm.

• The beats are not preceded by P waves (the P wave is lost in the QRS); however, a dissociated P may be occasionally seen.

• There is no PR interval.

• The QRS is wide and bizarre and its duration is increased.

• If it is seen, the T wave is in the opposite direction of the QRS.

• The atria and ventricles beat independently so the cardiac output is decreased.

Often there is no palpable pulse.

• VT often changes to V-fib (and carries a high risk of sudden death).

• Etiology

VT is normal in rare individuals.

It is seen 2° to electrolyte (hyper- or hypokalemia, hyper or hypocalcemia) and metabolic disorders (hypoxemia, acidosis), drug effects (digitalis toxicity), after an MI, or in association with cardiomyopathy and mitral valve prolapse.

It may be caused by the R on T phenomena.

• Diagnosed when three or more PVCs occur in a row at a rate of 100-120 beats per minute or faster.

• The major clinical distinctions are between hemodynamically unstable versus stable VT and between sustained versus unsustained VT.

Hemodynamically unstable ventricular tachycardia is a life threatening emergency for which the ACLS protocol should be initiated immediately. Synchronized cardioversion is usually the tx. of choice. Awake patients should be sedated heavily before cardioversion if at all possible.

• Sustained ventricular tachycardia is defined as having a duration of 30 seconds or more, or being hemodynamically unstable.

The immediate treatment is specified by the ACLS protocol.

For long-term treatment, it is important to realize that these patients have a 20% to 40% sudden death mortality, when untreated, over the 12 months following initial presentation.

Empiric treatment with antiarrhythmic drugs does not reduce this mortality.

Effective treatment with drugs and/or an implantable cardioverter defibrillator reduces the sudden death mortality over the next 12 months to 0-2%. Therefore, consultation with a cardiac electrophysiologist is recommended during the initial hospital stay to ensure adequate evaluation and tx. before discharge from the hospital.

• Management — If the patient is stable lidocaine is the treatment of choice — bolus then drip.

Other treatments include procainamide and quinidine, which prolong the refractory period and breakthe cycle; potassium chloride; or b-blockers.

Counter shock is used if the patient is unstable.

If the patient is receiving digitalis, the digitalis should be D.C.'d.

Vagal stimulation will not stop VT; the ectopic focus must be depressed.

Calcium-channel blockers are also ineffective.

6. Polymorphic Ventricular Tachycardia or Torsades de Pointes (twisting of points)

• Special form of VT characterized by changing QRS morphology, sometimes accompanied by slight changes in the rate. • A particularly malignant form of VT that is thought to be intermediate between ordinary monomorphic VT and ventricular fibrillation.

• For etiology, think of proarrhythmia, as from type IA antiarrhythmic medications, hypokalemia, hypomagnesemia, profound bradycardia, and idiopathic prolonged QT syndrome.

7. Ventricular Fibrillation

• A lethal rhythm characterized by absence of both organized electrical and organized mechanical activity. There are rapid, irregular ineffective ventricle contractions.

• Equivalent to cardiac death. There is no cardiac output with V-fib. Initiate CPR immediately.

• There is no P, QRS, or T wave.

• V-fib is multifocal.

• Coarse V-fib is thought to be recent onset V-fib and thus easier to revert with unsynchronized countershock than fine V-fib.

Epinephrine may convert fine fib into coarse fib (one reason we use it in CPR).

VENTRICULAR FIBRILLATION (V-FIB)

• Signs and symptoms of V-fib include loss of conscious within seconds, seizures, no pulse, and dilated pupils.

• Etiology — R on T, VT, MI, digitalis or quinidine toxicity, electrolyte disturbances, CAD, dying heart.

• Management of V-fib — includes the use of drugs like lidocaine and procainamide, or unsynchronized countershock (stops the heart by depolarizing all of the cells at once so SA can take over).

V-fib rarely spontaneously terminates.

8. Parasystole

• Results from intermittent capture of the ventricle by a ventricular focus that has an entrance block.

(It is not depolarized when the remainder of the ventricle is activated.)

• Characterized by PVCs with variable coupling intervals (intervals from the preceding normal QRS complex to the premature complex) and with constant intervals between the premature complexes. Detection of the latter constancy usually requires finding the least common denominator of the intervals between premature complexes, because of the intermittency of ventricular capture by the focus.

• Rare.

• Usually considered benign, although any premature ventricular activation can induce malignant ventricular rhythms in the ischemic myocardium.

9. Asystole Rhythm (Ventricular Standstill)

• A terminal, lethal phenomenon.

• P waves may or may not be present — atrial electrical activity stops at same time or shortly after the cessation of ventricular activity.

• Initiate CPR immediately. This is an agonal rhythm that is not consistent with life.

• Diagnosed when only ventricular escape complexes are present, and they occur very slowly.

10. Pulseless Electrical Activity (PEA) — formerly called electromechanical dissociation or EMD.

• Complexes appear on the monitor but there is no pulse or BP, because the electrical conduction is not coupled to the mechanical contraction.

• When giving CPR to these patients, you check effectiveness with the femoral or carotid pulse.

• PEA is seen with tamponade, severe hypovolemia, tension pneumothorax, massive pulmonary emboli, massive MIs, ruptured papillary muscles, CHF, etc.

PART V: Differential Diagnosis of Wide QRS tachycardias

PART VI: ST Segment Monitoring

PART VII: ELECTRICAL INTERVENTION

Pacemaker Electrocardiography and Trouble-Shooting

Pacemakers

All pacemakers deliver current to the heart. There are unipolar and bipolar pacemakers. An unipolar system has a single negative electrode in the chamber of the heart being paced. A bipolar system has both poles in the chamber of the heart being paced. The ECG pacing spike is larger in the unipolar system. Patients with pacemakers should carry a pacemaker I.D.

Pacemaker codes:

• 1st letter: chamber paced

Ventricle, atrium, dual chamber, or single chamber

• 2nd letter: chamber sensed

Ventricle, atrium, dual chamber, or single chamber

• 3rd letter: mode of response

Inhibits pacing, triggered, dual (both I and T), or none (0)

• 4th letter: programmable functions

Programmable, multiprogrammable, communicating, or rate modulating

• 5th letter: tachyarrhythmia function (antitachycardia pacing)

Meaning of selected individual letters

• V = ventricle

• A = atrium

• D = double (with mode of response this means atrial triggered and ventricular inhibited)

• 0 = none

• T = triggered

• I = inhibited

• R = reverse

• P = programmable (rate and/or output)

• M = multi-programmable

The more common models include fixed rate (asynchronous — VOO, AOO, DOO), ventricular demand (VVI, VVT), atrial demand (AAI, AAT), atrial synchronized (VAT), and AV sequential (DVI). If the patient expects to do any activity, he needs a rate adjusting pacemaker. This type of pacemaker stores the previous R-R and generates the next beat based on it.

Problems with pacemakers include loss of capture (the electrical stimuli fails to produce a QRS complex, the pacing electrode is displaced, or the milliamperage is too low); non-sensing (the pacemaker fails to recognize spontaneous heartbeats — this results in competition), and loss of pacing artifact (the pacing stimulus does not produce a spike on the ECG — this is the result of battery failure, pulse generator breakage, or wire disconnections or breakage).

Pacemaker cells have been harvested and reproduced in test tubes and replaced, but there is no way to "reglue" them yet.

Pacemaker Terms

• Rate — the heart rate at which the pulse generator will pace.

• Standby rate — the lowest rate at which the pulse generator will pace.

• Electrical output or milliamperes (mA) — amount of current needed to trigger myocardial depolarization (0.1-20 mA).

• Sensitivity or millivolts (mV) — the voltage needed to respond to the heart's electrical activity (0.5-20 mV).

• Mode — represented by an abbreviation based on the pacemaker code; indicates the pacemaker's capabilities.

• Atrioventricular (AV) interval (also called the AV delay) in dual-chamber pacemakers — time between an atrial event (either sensed or paced) and a paced ventricular event. The pacemaker tries to sense an R wave during this interval. Expressed in milliseconds (msec). 250 msec is a commonly programmed AV interval. If the pacemaker senses an intrinsic R wave, ventricular pacing doesn't occur. If an R wave is not sensed, ventricular pacing occurs at the end of the AV interval. The pacemaker's AV delay may be longer or shorter than the patient's intrinsic PR interval.

• Ventriculoatrial (VA) interval in dual-chamber pacemakers — time between a ventricular event (either sensed or paced) and a paced atrial event. The pacemaker tries to sense atrial activity during this time. Also measured in msec (e.g., 700 msec).

• Pulse interval in dual-chamber pacemakers — the total of the AV and VA intervals in msec.

Represents an entire cycle.

• Programmed standby rate — number of pulses per minute.

• Hysteresesis — a prolonged pulse interval intended to give the heart an opportunity to beat spontaneously. For example, if a pacemaker is set at 70 pulses/minute, the intrinsic rate will be allowed to fall to 60 pulses/minutes before the pacemaker delivers a stimulus. If hysteresis ends and natural depolarization doesn't occur, the pacemaker returns to its faster rate.

• Special antitachycardia functions — the response of the pacemaker to tachycardia such as by burst pacing.

AUTOMATIC IMPLANTABLE CARDIOVERTER DEFIBRILLATORS

A lead system and pulse generator are implanted. This system is capable of sensing either ventricular tachycardia or fibrillation and cardioverting or defibrillating the patient automatically. The AICD will not shock the patient unless the actual HR is greater than the set rate. The device can recharge in 10-30 sec (x 4).

The device helps treat ventricular tachycardia and ventricular fibrillation by monitoring heart activity and delivering countershocks when dysrhythmias arise. The AICD is approved for patients who have survived at least one episode of cardiac arrest not a/w an acute MI and patients with recurrent tachydysrhythmias who haven't had a cardiac arrest.

Within 10-35 seconds after the problem is sensed, the AICD typically delivers its first shock at 25 joules.

If the first shock fails to convert the rhythm, the AICD delivers a 2nd shock at 30 joules and, if necessary, a 3rd and 4th shock at 30 joules. After the 4th shock, a normal ECG must be sensed for at least 35 seconds before a new four-shock sequence can occur.

The AICD decreases mortality in patients with sudden cardiac death unassociated with MI from 40% to 2% within 2 years after the initial sudden death event.

Fourth generation AICD transvenous systems are now available. A pacing and defibrillating electrode are placed in the right ventricle. The device is programmed to deliver bradycardia, anti-tachycardia, low energy cardioversion, and high energy defibrillation. The newer devices ignore the gradually increasing HR in an exercising heart, but respond to sudden increases in HR by delivering a shock. These newer devices also monitor the response to the shock and step up the voltage if the heart does not respond.

COUNTERSHOCK

Countershock is the delivery of a high intensity charge to heart. This charge causes complete depolarization of the heart and interrupts the dysrhythmia, allowing the SA node to regain control. There are two types: synchronous cardioversion and defibrillation (asynchronous).

Synchronous cardioversion delivers a charge of 25-50 watt/sec (up to 400 if necessary) when the patient's QRS is sensed. The charge is delivered during the QRS to prevent the R on T phenomena. The charge is synchronized to fall someplace other than on a T wave. Synchronized cardioversion is used to manage fast dysrhythmias that have definite QRS complexes, for example, atrial fib with fast ventricular response or V tach. The patient should be NPO 8 hours before if possible; digitalis should be withheld for 24 hours. The patient should be sedated. The procedure may create a paradoxical reaction; additionally, the patient may become irritable, confused, and hyperactive. Check the BP, rhythm, and respiration before, during, and after the procedure and observe for the s/s of emboli. This procedure should not be used in patients who have digitalis toxicity.

Defibrillation or asynchronous cardioversion uses a nonsynchronized mode to treat fast dysrhythmias without QRS complexes (V fib). This procedure is also useful for patients who have pulseless VT. Direct current is applied to the chest wall to interrupt or convert dysrhythmias to normal sinus rhythm. The charge should be delivered as soon as possible. The procedure is unsuccessful if the cardiac muscle is anoxic. The required energy levels vary with body size — less than 50 kg, use 3.5-6.0 watt sec-1 kg-1; greater than 50 kg, use full out. The average charge is 200-400 watt/sec. Saline pads with electrode paste prevent bridging. The paddles should be placed on the right upper sternum under the clavicle and left of the apex of the heart under the arm. After the shock there is always a period of electrical instability so if possible before shock, fix hypokalemia, hypoxia, digitalis toxicity, acid/base imbalance.

Cough — A cough increases arterial and cardiac pressure and can be as effective as CPR. It gains time to get the crash cart.

APPENDIX A: CONDUCTION SYSTEM

APPENDIX B: CORONARY CIRCULATION

Location of Arteries and Structures Nourished By Them

APPENDIX C: Comparison of Q-Wave and Non-Q-Wave Myocardial Infarctions

___________Q Wave_________________________________________________________Non-QWave_______________________

Pathology Larger area of infarction ______________________________________________Smaller area of infarction

Enzyme elevation

1. CK ___Greater elevation _____________________________________________________Less elevation

2. SGOT Greater elevation ______________________________________________________Less elevation

ECG____ Pathologic Q waves present_____________________________________________Absent pathologic Q waves

_______ST-segment elevation __________________________________________________ST-segment depression (in acute phase) (in acute phase)

Imaging

1. Technetium-99M

________Helpful in diagnosis__________________________________________________ Not helpful in majority of cases pyrophosphate

2. Echocardiogram

_______Shows larger regional wall_________________________________________Shows smaller area of wall motion motion abnormality abnormality

3. PET scan

__________Reveals homogenous defects___________________________________________ Nonhomogeneous defects

Angiographic findings

______Total coronary occlusion commonly seen in infarct related artery soon after Q-Wave_____Total occlusion is infrequently observed in early hrs ______________________________________________________________________________in infarct-related artery; mod. increase next days

Reinfarction Can occur___________________________________________________________Higher incidence

Postinfarct angina Can occur ______________________________________________________Higher incidence

Calcium channel blockers Early and late beneficial effects not_________________________Diltiazem specifically reduces incidence

_______________________equivocally proven______________________________________ of early reinfarction and severe angina

_________________________________________________________________________Nifedipine reduces postinfarct angina and unstable angina

Beta-adrenergic blockers Improve long-term survival_________________________________Not effective

Mortality

1. Early ___________Higher in-hospital mortality rate ________________________________Lower in-hospital mortality rate

2. Late ——— ________________________________________________________________Similar or even higher than Q-wave infarction

APPENDIX D: TESTS USED IN DIAGNOSIS OF ACUTE MI

Myocardial cells that are irreversibly injured release a number of enzymes into the circulation where they can be measured.

Increased CK, LDH, AST (SGOT) with increased CK-MB and LDH-1 isoenzymes; temporal pattern of release is of diagnostic importance.

Isoenzymes may help rule out noncardiac causes that may elevate the routine enzymes.

Creatine Phosphokinase (CK)

• Onset of elevation starts 4-8 h after MI, peaks at 24 h, and returns to normal in 72-96 h except in the case of large infarctions when CK clearance is delayed. Coronary reperfusion causes an earlier peak (within 12 h).

• Sensitivity > 90%.

• Specificity — CK is elevated in other conditions.

Two- to threefold increase of total CK may follow IM injection.

Other causes of increased total CK — muscular dystrophy, myopathies, direct current (DC) cardioversion, cardiac catheterization, hypothermia, stroke, trauma, surgery, convulsions, prolonged immobilization, COPD associated with LV CHF, pulmonary embolism, shock, myxedema, extensive 3rd degree burns, strenuous exercise, diabetic ketoacidosis, acute alcohol intoxication (rhabdomyolysis), and small bowel infarction• Amount of CK increase may be correlated with severity of infarction

CK-MB Isoenzyme — more specific for myocardial necrosis than CK alone. Not present in significant concentrations in extracardiac tissue; particularly useful when skeletal muscle and brain damage are suspected.

• Onset of elevation occurs by 4-6 h, peaks within 18-24 h, and returns to normal within 48-72 h.

• Most specific and sensitive enzyme clinically available for diagnosis of MI.

• CK-MB present in substantial amounts only in myocardium and rarely in skeletal muscle of patients with muscular dystrophy of Duchenne type. Its presence in normal skeletal muscle is debatable.

• Can also be elevated in myocardial contusion, myocarditis, cardiopulmonary resuscitation, hypothyroidism, after DC cardioversion, and cardiac surgery.

• Not elevated following IM injection, noncardiac surgery, exercise, uncomplicated cardiac catheterization, or pneumonia.

• Reperfusion (by angioplasty, thrombolysis, or spontaneously) of myocardium causes an early peaking of CK-MB (8-12 h).

Aspartate Aminotransferase (AST; previously SGOT)

• Activity increased in 8-12 h. Peaks at 18-36 h and returns to normal within 3-5 days.

• Very sensitive.

• Specificity is poor due to its elevation in other conditions — liver disorders, hepatic congestion, biliary tract diseases, shock, skeletal muscle trauma, oral contraceptives, pericarditis, pulmonary emboli, myocarditis, cardiac catheterization, cardiac surgery.

Lactic Dehydrogenase (LDH)

• Onset of elevation occurs in 24-48 h; peaks at 3-6 days, and remains elevated for as long as 7-14 days. Last of three standard enzymes to become elevated.

• Very sensitive.

• Specificity is poor due to elevation in hemolysis, leukemia, lymphoma, liver disorders, renal disorders, burns, heart failure and hepatic congestion, DC cardioversion, myxedema, skeletal muscle trauma, and pulmonary emboli.

LDH₁ Isoenzyme — elevation may suggest cardiac disease or hemolysis.

• 5 LDH isoenzymes but LDH₁ predominates in heart.

• Rises before total LDH (within 8-24 h) and may rise when there is no rise in total LDH.

• Following acute MI, the ratio of LDH₁ to LDH₂ becomes > 1.

• Sensitivity > 95%; generally done only when the initial CK and CK-MB might have missed MI (after 48 h). LDH₁ isoenzyme is of diagnostic value in patients with acute MI who present after significant delay after onset of symptomatology.

• Levels may be elevated in minimal hemolysis.

Other Enzymes Used for Diagnosing MI

• Myoglobin.

• New radioimmunoassay against troponin I may be a more specific marker for myocardial injury.

• CK isoenzyme-(3). CKMM subtype.

• Myosin light chains.

• Tropomyosin.

Nonspecific Lab. Findings

• Elevated WBC and neutrophil counts (appear in few hours and persist for 3-7 days).

• Elevated erythrocyte sedimentation rate.

• Alanine aminotransferase (ALT; previously SGPT) — time course of elevation is intermediate between CK and LDH; lacks tissue specificity.

Chest X-Ray

• May be normal in acute MI or cardiomegaly may be present.

• If pulmonary capillary wedge pressure is > 18-25 mm Hg, signs of CHF may occur — pulmonary vascular redistribution to the apices, interstitial pulmonary edema (blurring of pulmonary vasculature, perihilar haze, Kerley B lines, lattice pattern), and pleural effusion.

Imaging Techniques: Infarct Avid Imaging (^99mTc Pyrophosphate)

• Usually positive between 1 day and 1 week of MI.

• Peak uptake occurs 2-3 days post-MI.

• Returns to normal between 1 and 2 weeks.

1. False positive

a. Previous MI, unstable angina, calcified aneurysm, pericarditis, myocardial contusion, calcified aortic or mitral valve, cardioversion, penetrating wounds, cardiomyopathy, malignancy, amyloidosis, calcified cartilage, rib fractures, breast tissue.

b. Sensitivity and specificity are high for transmural (Q-wave) infarcts (~ 90%), but are lower for non-Q-wave infarcts.

2. Uses

a. To diagnose MI when clinical history is not clear.

b. To diagnose MI when delay in hospitalization occurs and enzyme peaks are missed.

c. To detect MI in patients when their cardiac enzymes are altered after cardiac surgery.

d. To detect RV infarcts.

e. To diagnose MI when ECG is difficult to interpret (in presence of LBBB pacemaker rhythm).

f. To detect infarct extension.

g. To locate and size an MI.

h. Infarct avid imaging should be used in conjunction with clinical history, ECG, and tests for enzyme levels. Other promising new techniques include MRI and PET. Monoclonal antibodies may also prove useful in the future.

Imaging Techniques to Assess LV Function and Complications in Acute MI

1. Echocardiography and Doppler

a. Limited role in diagnosis of acute MI.

b. Useful in assessing regional wall motion abnormality and global LV dysfunction.

c. Useful for diagnosing complications of acute MI, e.g., mitral regurgitation due to ruptured papillary muscle or papillary muscle dysfunction, ventricular septal defect, infarct expansion, cardiac rupture, LV aneurysm, pseudoaneurysm, LV thrombus, pericardial effusion.

d. May play a useful role in prognostication of acute MI.

e. May have potential role in assessing reperfusion after thrombolytic therapy.

2. Radionuclide ventriculography: Uses.

a. To determine ejection fraction (EF).

b. To detect regional wall motion abnormality.

c. To help differentiate true LV aneurysm from false aneurysm.

d. Separation of RV and LV dysfunction.

e. Detection of pericardial effusion.

APPENDIX E: ANTIARRHYTHMIC AGENTS

ANTIARRTHYMICS

Meds Quinidine (IA) Beta-blockers — Bretylium Nifedipine

Procainamide (IA) "olol" drugs Amiodarone Verapamil

Lidocaine (IB) Propranolol Other calcium

Phenytoin (IB) Acebutolol channel

Mexiletine (IB) Esmolol blockers

Encainide (IC) Atenolol

Flecainide (IC)

Propafenone (IC)

Actions Blocks Na⁺, Block b₁ receptors, Slows repolarization, Blocks Ca⁺⁺movement

Slows conduction, Blocks SNS effects, Blocks K⁺ channels

Marked inhibition through AV, and on heart at AV node

ECG Characteristics of Class IA Antiarrhythmics — Quinidine, procainamide, disopyramide, moricizine

• ? slight widening of QRS complex; increased widening of QRS = early sign of toxicity.

• Prolonged QT interval.

• Quinidine and procainamide may also produce U waves and flattened or inverted T waves.

ECG Characteristics of Class IB Antiarrhythmics— Lidocaine, mexiletine, tocainide

• ? shortened QT interval.

• Phenytoin may slightly shorten the PR interval.

• Mexiletine apparently doesn't change the ECG.

ECG Characteristics of Class IC Antiarrhythmics — Flecainide, encainide, propafenone, indecainide, lorcainide, aprindine

• ? lengthened PR interval.

• Widened QRS complex.

• Prolonged QT interval.

ECG Characteristics of Class II Antiarrhythmics — b-adrenergic blockers, propafenone

• ? slight lengthening PR interval.

• ? shorten QT interval slightly.

• Decrease heart rate.

ECG Characteristics of Class III Antiarrhythmics — Bretylium, amiodarone, N-acetylprocainide (acecainide), sotalol

• ? widening of QRS complex.

• ? Prolongation of QT interval.

• Decrease heart rate.

ECG Characteristics of Class IV Antiarrhythmics — Ca⁺⁺-channel blockers

• ? lengthening of PR interval.

• Decrease heart rate.

Beta Blockers Available In United States

Medication

Acebutolol 3-4 400 mg/d

Sectral ®

Atenolol 6-9 50 mg/d

Tenormin ®

Betaxolol 14-22 10 mg/d

Kerlone ®

Bisoprolol 9-12 5 mg/d

Zebeta ®

Carteolol 5-6 2.5 mg/d

Cartrol ®

Esmolol 0.15 50 mg/kg/min

Brevibloc ®

Labetalol 6-8 200 mg bid

Normodyne ®, Trandate ®

Metoprolol 3-7 100 mg/d

Lopressor ®

Nadolol 20-24 40 mg/d

Corgard ®

Penbutolol 5 20 mg/d

Levatol ®

Pindolol 3-4 10 mg bid

Visken ®

Propranolol 4 60 mg bid

Inderal ®

Sotalol 80 mg bid

Betapace ®

Timolol 4-5 10 mg bid

Blocadren ®

Beta-Adrenergic Blockers (class II drugs)

• Given to reduce the HR, contractility, and ventricular wall tension; decreases oxygen demand and prolongs diastolic filling, thus increasing coronary filling.

• Beta blockers are also antiarrhythmic.

• Contraindicated in CHF, pulmonary edema, asthma, COPD, heart block, and hypotension.

• Chronic routine use for 2 years decreases total mortality, sudden death, and reinfarction rate.

• IV metoprolol (Lopressor ®) 5 mg given q 5-10 min to 15 mg followed by 50-100 mg PO BID if no contraindications (hypersensitivity, overt CHF, 2° or 3° AV block, cardiogenic shock) or complications; later atenolol 50-100 mg daily.

Ca⁺⁺ Antagonists

• Potential value as anti-injury agents in the setting of reperfusion, as antiplatelet agents, and as coronary vasodilators; may thus minimize platelet activation in the vicinity of lysed thrombi by decreasing shearing forces.

• Diltiazem, at least, apparently adversely affects prognosis in patients with CHF or impaired LV function.

Unique Adverse Reactions of Calcium Channel Blockers

Medication Initial Dosage

Diltiazem 30 mg QID

Sustained-release 60-120 mg BID

Nicardipine 20 mg TID

Nifedipine 10 mg TID

Sustained-release 30 mg QD

Verapamil 80 mg TID

Sustained-release 240 mg QD

Digitalis

• Increases automaticity in cardiac muscle cells, but decreases AV conduction by increasing parasympathetic tone.

Lidocaine (Class I)

• Suppress reperfusion arrhythmias. Lidocaine is the agent of choice for ventricular tachycardia and ventricular fibrillation.

• Lidocaine decreases automaticity in the ventricles.

• Slows the impulse movement through the AV junction and His bundle by blocking Na⁺ movement (it decreases the rate of phase zero depolarization).

• Lidocaine has no anticholinergic effects.

• Lidocaine's production of a negative inotropic action, neurologic side effects, and an increased incidence of asystole preclude its prophylactic use.

Magnesium

• Appears to have favorable effects on cardiac arrhythmias, coronary blood flow, platelet aggregation, and myocardial metabolism.

• Administration of MgSO₄ is controversial (no change in mortality compared to placebos in 1995 trials).

• MgSO₄ IV — 2-6 gm IV over 15 min followed by infusion of 3-20 mg/min for 5-48 h.

Quinidine (Class I)

• Suppresses automaticity, especially in ectopic cells.

• Has an indirect atropine-like effect so it increases conduction.

APPENDIX F: THROMBOLYTICS

Reperfusion — PTCA or IV thrombolytic therapy with plasminogen activators.

Recent studies — 160-325 mg aspirin plus 5000 units of IV heparin should be given with institution of thrombolytic therapy; then 325 mg aspirin daily and a continuous infusion of heparin for 2-5 days.

Every minute counts — ideally within 1-3 h after onset of symptoms; beneficial if given within 6 h; some benefit appears possible up to 12 h.

Clinical factors that favor proceeding with thrombolytic therapy include anterior wall injury, hemodynamically complicated infarction, and widespread ECG evidence of myocardial jeopardy.

tPA (tissue plasminogen activator) — more effective at restoring flow than streptokinase or APSAC.

Recommended total dose = 100 mg; begin with 5-10 mg bolus followed by 60 mg IV over first hour and

20 mg each in 2nd and 3rd hours. New data suggests that it may be beneficial beyond 6 hours.

Streptokinase — 1.5 million units IV over 1 h.

APSAC (anisoylated plasminogen streptokinase activator complex) — single dose of 30 mg over 2-5 min.

Both streptokinase and APSAC are antigenic; once one has been used repeat administration with either agent should be avoided.

Allergic reactions to streptokinase and APSAC — approximately 2%.

Contraindications for Thrombolytics — history of CVA, trauma or invasive or surgical procedure within 2 weeks (or prolonged CPR), marked hypertension (systolic > 180 mm Hg and/or diastolic > 100 mm Hg), active peptic ulcer disease, bleeding diathesis, suspected aortic dissection, hemorrhagic retinopathy, intracranial neoplasm; hepatic failure = relative contraindication.

Complications — hemorrhagic stroke most serious and occurs in approximately 0.4% of cases; rate increases with advancing age; vascular access sites.

If thrombolytic agents are given in combination with aspirin, the post MI mortality decreases by 23-42% (with no increase in cerebral hemorrhage). Thrombolysis can paradoxically initiate platelet aggregation and activate the clotting cascade. There is a slight risk of stroke in patients who are over 75 y. o. tPA was given by paramedics in the Washington "MITI" study.

Aspirin inhibits platelet function and causes vasoconstriction. The current recommendation is that men over 50 with risk factors take 325 mg every other day (the study has not been completed for women or men over 50 who do not have risk factors).

Heparin is used to prevent reocclusion (the IV form of heparin is given with tPA). The desired aPTT with heparin therapy is usually 60-85 seconds. Adjust heparin to keep PTT at 1.5-2 times normal.

Hirudin, which is derived from leeches, is currently being used as a substitute for heparin in some studies; currently investigational; powerful antithrombin somewhat similar to heparin..

PTCA may be performed when thrombolytic agents cannot be used or if the patient develops cardiogenic shock. The latest research (JAMA, July 1996) recommends a CABG over PTCA as therapy. PTCA as primary intervention — generally reserved for those with contraindications to pharmacologic thrombolysis — advanced age (> 70 years) cardiogenic shock (systolic BP <100 mm Hg); infarction resulting from occlusion of previous CABG.

APPENDIX G: MISCELLANEOUS DRUGS USED AFTER MYOCARDIAL INFARCTION

ACE Inhibitors:

• Facilitate the formation of prostaglandin vasodilators, nitrous oxide, and free-radical scavengers.; also appear to have some antiarrhythmic properties.

• Patients with significant LV dysfunction have increased circulating natriuretic peptide; treatment with ACE inhibitors improves their survival.

• ACE inhibitors improve mortality and prevent CHF and recurrent MI in patients with ejection fraction of _ 40%.

• These drugs appear to modulate heart remodeling post MI, result in less hypertrophy; prognosis is worse with cardiac dilation, because dilation increases stress. LV end systolic volume is a good predictor of survival post MI.

• ACE is present in all vascular beds and many tissues (kidney, heart, brain, adrenal, testes).

Tissue angiotensin has a local effect on the function of the heart and vessels.

• Tissue specific ACE inhibitors have fewer side effects.

Captopril is least tissue specific of the ACE inhibitors currently on the marker; captopril target dose 50 mg TID or pharmacologically equivalent doses of other ACE inhibitors.

• Many patients must stop taking the inhibitors because a major side effect is a chronic cough — the cough is due to bradycardic enhancement.

Analgesics — judicious use of narcotics; inhibits further release of catecholamines and subsequent predisposition to arrhythmias and increased myocardial oxygen consumption (MVO₂).

Sublingual NTG — up to three 0.4 mg doses at 5 min. intervals if hypotension does not occur; idiosyncratic reactions can cause marked hypotension and bradycardia.

Morphine — opiates depress sympathetic nervous system as well as central nervous system resulting in mild arteriolar dilation and venodilation and thus decreased afterload and decreased preload; 2-4 mg IV every 5 min with relative impunity until pain is relieved or toxicity is manifested by hypotension, vomiting, or respiratory depression. 2-3 mg/kg may be needed.

Has vagotonic effect which may cause bradycardia or advanced degrees of heart block/Morphine-induced hypotension (decreases sympathetically mediated arteriolar and venous constriction resulting in venous pooling a subsequent decrease in cardiac output and BP) — minimize with supine position, elevation of legs, IV fluids and atropine (if HR is not increased) and patient does not have overt or incipient pulmonary edema. Fairly rare although nausea and vomiting are common side effects.

Demerol — a vagolytic agent; therefore the drug of choice if the patient is hypotensive or bradycardic.

Nitrous Oxide — effective; also decreases afterload; generally well tolerated for as long as 24-48 h when used intermittently.

Intravenous Beta-Blockers — decrease ischemia by lowering MVO₂.

NSAIDs and Glucocorticoids (except aspirin) — AVOID; can impair healing, produce larger infarct scar, and increase risk of myocardial rupture.

Research has shown (NEJM, October/1994) that the combination of thrombolytic agents, ASA, and beta-blockers improve survival. No improvements were seen with prophylactic use of lidocaine or calcium blockers. (Internists and family practitioners were less aware of these treatments than cardiologists.)

Measures should also be taken to decrease O₂ demand:

The patient should be on bed rest followed by limited physical activity

Beta-adrenergic blockers to decrease heart rate

Arterial vasodilators such as nifedipine, nitrates (IV NTG) or angiotensin-converting enzyme (ACE) inhibitors to decrease afterload

Diuretics to decrease preload;

Oxygen to avoid hypoxemia.

Gastrointestinal Agents — Measures should also be undertaken to prevent nausea and vomiting and stool softeners are needed to decrease straining; straining can precipitate bradycardia and be followed by increased venous return to heart.

Hypolipidemic Agents are important for secondary prevention of death and morbidity post MI.

Nitrates

• May decrease excessive coronary reactivity and hence ischemia; used to manage acute ischemic syndromes.

• Some nitrates cause venous and arterial dilation, thus decreasing both preload and afterload.

• Alleviate coronary artery spasm and increase collateral flow.

• May attenuate platelet adhesion and aggregation, although this is not proven.

• Usually given by continuous IV for 24-36 h, then intermittently by an oral route (with a 10 h free period). It is important to avoid rebound tachycardia and hypotension when titrating IV nitrates.

NITRATES

Antianginal

Medication _

Erythrityl tetranitrate Sublingual/ 5 mg

Cardilate ® Transmucosal 5 mg

Chewable 10 mg

Isorbide dinitrate Sublingual 2.5-10 mg

Oral 20-60 mg

Oral (S-R) 40 mg

Aerosol spray 0.4 mg

Sublingual 0.3-0.8 mg

Transmucosal 1-3 mg

Oral (S-R) 6.5-19.5 mg

Topical ointment, 2% 1.2-5.0 cm

Transdermal disc 10-30 mg/24h

or patch

APPENDIX H: ISCHEMIA/Infarction

EVALUATION OF MI: The diagnosis is based on ECG changes, enzymes, physical examination and possibly radio-nucleotide imaging.

Four Hemodynamic Categories of MI

• No pulmonary congestion or hypo-perfusion (low mortality, less than 5%).

• Pulmonary capillary wedge > 18 mm Hg and cardiac index > 2.2 (pulmonary congestion with normal cardiac output and mortality of less than 10%).

• Pulmonary capillary wedge < 18 mm Hg and CI < 2.2 (no pulmonary congestion but hypo-perfusion and mortality less than 25%).

• Pulmonary capillary wedge > 18 mm Hg and CI < 2.2 (pulmonary congestion with hypo-perfusion and mortality less than 50%).

Hemodynamic Parameters of 4 Categories of MI

• Normal CO and wedge • High to normal CO and wedge (need diuresis, inotropics, afterload reduction)

• Low CO and wedge (hypovolemic — need fluids) • Low CO and high wedge (need inotropics, afterload reduction, intra-aortic pump)

MANAGEMENT POST MI: The patient's rhythm and enzyme changes should be monitored. A change in compliance post-MI can produce acute pulmonary edema when you attempt to improve preload by volume loading, so the wedge pressure must be monitored when attempting a volume challenge.

MYOCARDIAL INFARCTION COMPLICATIONS

• Aneurysm Formation

Aneurysms form in 15% of MI patients. Can occur weeks to month after infarct.

May lead to CHF, systemic embolization of mural thrombi, and dysrhythmias.

May present as worsening dyspnea due to heart failure, symptoms of arrhythmias, or symptoms of arterial emboli, or may be asymptomatic.

Signs include abnormal precordial bulge, double apical impulse, dyskinetic impulse, S₄, S₃; signs of CHF may be associated with MR or VSD.

ECG — shows persistent ST elevation.

Chest x-ray — may be within normal limits or show cardiomegaly; abnormal bulge or angulation in area of aneurysm; left atrial enlargement; calcium in ventricular wall.

• Arterial Embolism From Site of Infarct (usually within first 3 weeks)

May be directly related to both the site and size of the infarct.

Can result in symptoms of stroke, or in renal or mesenteric infarction, or in cold, painful extremity.

• Cardiac Tamponade

Heart is surrounded by fluid held in the pericardial sac resulting in constriction of the heart with a resulting decrease in cardiac filling and a decrease in heart sounds.

Other signs and symptoms include a paradoxical pulse, decreased ECG voltage, neck vein distention, increased heart size, an enlarged liver and spleen, rales, wheezes, extreme anxiety, and decreased urinary output (the patient may go into shock).

There is usually a sudden decrease in BP and cardiac output and an increase in CVP, PAP, and HR.

Also seen with cardiac surgery, acute pericarditis, ventricle rupture, or aortic dissection.

Evidence of tamponade may be seen on x-ray, scan, echo, or pericardiocentesis.

Management of tamponade includes the administration of steroids and diuretics and a pericardiocentesis or pericardiectomy.

• Cardiogenic Shock — "power failure".

Cumulative loss of _ 40% of LV muscle mass usually results in cardiogenic shock.

BP inadequate to perfuse kidneys and other organs adequately.

Symptoms — restlessness, decreased mentation, shortness of breath.

Signs included obtundation, confusion; tachycardia; cool, moist skin;.

Characterized by systolic BP of < 80-90 mm Hg, cardiac index < 1.8 L/min/m², and PWP > 18 mm Hg;

urinary output < 20-30 cc/h; associated signs of CHF; metabolic acidosis.

Diagnosis not based on hypotension alone.

Mortality directly related to decreased stroke volume; mortality rate > 70%.

Risk factors include advanced age, decreased LV ejection fraction on admission, large infarct, history of diabetes mellitus, and previous MI.

Relatively small infarct superimposed on a previously compromised heart may precipitate hemodynamic disaster.

Treatment — attempt to maintain coronary perfusion pressure by increasing BP with vasopressors, intra-aortic balloon pump, and manipulation of blood volume to a level that ensures optimal LV filling pressure (PWP approximately 20 mm Hg)

Cardiogenic shock is seen in 15% of MI patients — vicious cycle of progressively irreversible hemodynamic changes resulting in decreased peripheral and coronary perfusion (circulatory failure) and increased pulmonary congestion. Hypotension, acidosis, hypoxemia and myocardial depressant factor also depress myocardial function.

Mortality = 80-90% mortality.

If the wedge is increased, the patient needs venous dilation; if it is decreased, the patient needs fluid.

Both vasopressor and vasodilator therapy are used in shock.

Inotropic agents increase stroke volume and decrease heart rate, wedge pressure, and systemic vascular resistance. Therefore the BP should increase.

• CVA Secondary to Thromboemboli: Necrosis of the endothelium roughens the surface, predisposing to thrombus formation.

• Congestive Heart Failure — some degree of CHF in approximately 40-50% of patients with acute MI; acute LV failure signifies that > 25% of LV is dysfunctional or ischemic.

Clinical signs = rales, S₃ and S₄ gallops; CXR changes.

Characterized by increased PWP and PAP but these may result from decreased diastolic ventricular compliance (diastolic failure) or decreased stroke volume with secondary cardiac dilatation (systolic failure).

Anterior wall infarcts are associated with more severe CHF than are inferior infarcts.

"Stunned myocardium" — acute ischemic episode may cause myocardial injury that is reversible if the myocardium is reperfused; temporarily unable to contract.

Treatment — preload reduction (furosemide and NTG) to decrease pulmonary congestion and decrease MVO₂; digoxin is of little value.

Furosemide's initial effect is venodilation; this effect is achieved within 5 min of IV administration; avoid hypovolemia from excessive diuresis.

Pulmonary congestion, decreased contractility and abnormal wall motion often occur.

• Dressler's Postinfarction Syndrome — delayed form of acute pericarditis; can occur 1 week to several months after acute myocardial infarction.

Poorly understood; possibly antigen-antibody response (autoimmune disorder) to necrotic myocardium.

Pericardial pain, fever, friction rub, pleural effusion, pleuritis, tachycardia, and arthralgias may accompany this syndrome.

Treatment — aspirin; occasionally glucocorticoids if NSAIDs fail but steroids could alter healing.

• Dysrhythmias — most common complication; affect > 90% of acute MI patients; ischemic myocardium electrically unstable.

Both sinus tachycardia and atrial fibrillation are associated with increased mortality and are seen most often with anterior infarctions.

Causes — ischemia, hypoxemia, autonomic nervous system imbalances, lactic acidosis, electrolyte abnormalities, alteration of impulse conduction pathways or conduction defects, drug toxicity, or hemodynamic abnormalities.

Treatment — correct any electrolyte imbalances, provide adequate oxygenation, reduce sympathetic nervous system stimulation, and diminish MVO₂.

Hypokalemia = risk factor; maintain K⁺ at approximately 4.5 mmol/L.

_ Ventricular Dysrhythmias

Risk for ventricular fibrillation is highest during the first 4 hours after infarction.

b-blockers — effective in abolishing PVCs in MI patients and in preventing ventricular fibrillation.

Use routinely if no contraindications.

Treat (lidocaine, bretylium, amiodarone, electrocardioversion, defibrillation) sustained or symptomatic ventricular arrhythmias; carefully watch frequent PVCs (> 5/min), R-on-T, multiformed PVCs, ventricular bigeminy and PVCs occurring in couplets.

Prophylactic administration of lidocaine controversial; cardiodepressant and proarrhythmic; may predispose pt. to bradycardia and asystole, CNS depression, and seizures.

Torsades de pointes — polymorphic ventricular tachycardia; change in amplitude and cycle length cause appearance of oscillation around baseline; associated with preceding QT prolongation (often > 0.60 sec).

Etiology includes hypoxemia, hypokalemia, hypomagnesemia, intracranial events such as SAH, 3° AV block, toxicity due to quinidine, dig., phenothiazines, or tricyclics.

Treatment — overdrive pacing, magnesium sulfate.

Accelerated idioventricular rhythm (slow VT) — rate 60-100 bpm:

Common with inferoposterior infarct where it is usually associated with sinus bradycardia.

Often occurs transiently during thrombolytic therapy at time of reperfusion.

Usually benign and doesn't precede classic ventricular tachycardia.

_ Supraventricular Dysrhythmias

Bradycardia from parasympathetic nervous system overactivity may be treated with atropine or transvenous pacing if patient is symptomatic; elevating legs also helpful.

Especially common with inferior infarcts.

AV blocks and intraventricular conduction disturbances:

Mortality associated with AV block and anterior infarcts markedly greater than that associated with inferior infarcts.

Anterior infarcts — usually associated with trifascicular blocks of extensive necrosis.

Inferior infarcts — usually associated with AV nodal ischemia.

Sinus tachycardia — usually secondary to anxiety, pain, excessive sympathetic stimulation resulting in adrenal tone, pericardial inflammation, hypoxemia from pulmonary congestion, venous congestion, CHF or other remediable factors.

Atrial fibrillation/flutter — may be indicative of failure or atrial infarction.

• Myocardial Infarct Expansion

Disproportionate thinning and stretching of the infarct within first 5-10 days post-MI.

Associated with LV rupture, papillary rupture, VSD.

Symptoms of increased CHF and chest pain without ECG or enzyme evidence of further infarction.

• Myocardial Infarct Extension

Increased ischemic pain.

Reappearance of increased CK-MB 48 h after initial symptoms.

ECG evidence of further infarction.

• Organic Brain Syndrome may occur post MI, if blood flow to brain is decreased; decreased cerebral perfusion; thromboemboli may cause TIA or CVA.

• Papillary Muscle (or Chordae Tendineae) Dysfunction or Rupture (1st-2nd week)

Permits systolic regurgitant flow from LV to LA.

Contributing factors — thinning of wall, poor collateral flow, shearing effect of contraction against stiffened necrotic area, marked necrosis at terminal end of blood supply, and aging of myocardium with laceration of myocardial microstructure. 80% of time, it occurs in inferior or posterior MI.

Posterior papillary muscle more commonly affected as its only blood if from post. descending branch of RCA or dominant LCA.

Anterior papillary muscle normally has a dual blood supply from tributaries of diagonal branch of LAD and marginal branch of LCxA

Dysfunction may be transient; symptoms may be mild or catastrophic.

Symptoms — often sudden onset of _ SOB; symptoms of Ø output (Ø mentation, lethargy).

Complete or partial rupture Æ acute mitral insufficiency Æ sudden _ LAP and _ PAP, Ø CO, and acute pulmonary edema. Systolic apical murmur; usually occurs after S₁ and radiates to axilla.

S₁ and S₂ widely split.

May see large v waves in PWP tracing.

LA v wave amplitude may reach levels of 50-70 mm Hg.

Suspect when shock, acute pulmonary edema, apical thrill, and high-pitched holosystolic murmur at apex develop in AMI pt.

Differential diagnosis — septal rupture; use bedside Doppler.

Complete papillary muscle rupture = absolute surgical emergency; rapid dx. and surgical intervention is imperative.

Medical management of ruptured papillary muscle to support pt. preoperatively — decrease preload (results in improved alignment of papillary muscles and decreased size of regurgitant valve orifice) and Ø afterload (Ø resistance Æ Ø backflow ) with IABP, dopamine, nitroprusside or NTG infusion; ? diuretics and/or digitalis.

MR may also be result of alteration in size of shape of ventricle due to impaired contractility or aneurysm formation

• Pericarditis

Sharp, positional pain; worse when recumbent; pain _ with inspiration; pain Ø when pt. sits up and leans forward.

Pericardial friction rub 1-3 days after acute MI. Rub may be evanescent. Tachycardia.

Treatment — ASA. NSAIDs may ? delay infarct healing.

Pericarditis may be due to a transmural infarction that produces a rough epicardial layer and irritation of pericardial surface resulting in inflammation. It is usually seen 2-4 days post MI.

• Postinfarction Angina (within 1st 10 days)

Suggests viable myocardium still subject to ischemia.

Angina pectoris; S₄; hypertension; hypotension in severe cases; pale, clammy skin; ECG evidence of ischemia.

• Pulmonary Embolus (anytime)

Esp. common with CHF and prolonged bedrest.

Symptoms — dyspnea, pleuritic chest pain (with pulmonary infarction), diaphoresis, anxiety, hemoptysis; calf pain with thrombophlebitis of extremity.

Signs — tachypnea, tachycardia, fever, pleural rub (with pulmonary infarction), hypotension if embolus massive; loud P₂, ± distended neck veins; hypoxia.

• Rupture of Heart Structures: The papillary muscles, chordae tendineae or ventricular wall may rupture and produce pulmonary edema and shock. These structures usually rupture after day 3.

Ventricular septal rupture is seen with anterior or inferior MIs and causes shunting of blood, decreased CO, increased right heart work, and pulmonary congestion. The septum usually ruptures 10-11 days after the MI. The s/s include a palpable thrill, a loud systolic murmur, CHF, increased PAP, and decreased BP and cardiac output.

More common in women and previously hypertensive patients.

_ Myocardial Rupture — ruptured LV causes massive hemorrhage into the pericardial cavity (hemopericardium).

Causes death by impairment of cardiac filling (cardiac tamponade).

Sudden disappearance of pulse, BP, and consciousness while ECG shows sinus rhythm.

Higher incidence with 1st infarct, hx. of hypertension, no hx. of angina, and relatively large Q-wave infarcts.

_ Rupture of the Ventricular Wall is rare and when it does occur it causes tamponade and death within a few minutes. It is seen more in women than men, especially if they have HTN. It is most likely to occur 5-21 days after the MI.

_ Septal Rupture — rupture of a septal infarct ; rarely; Æ acquired VSD. (within 1st 2 weeks)

Present with severe CHF (_ dyspnea, Ø mentation, lethargy) a/w sudden appearance of holosystolic murmur at apex or left mid- or lower sternal border; often acc. by a parasternal thrill. ?

pulseless electrical activity.

Differential diagnosis — papillary muscle rupture; use bedside Doppler.

Preoperative treatment — Ø afterload (Ø resistance Æ Ø backflow ) with IABP, nitroprusside or NTG infusion.

• RV Infarction — ~ 1/3 of patients with inferoposterior infarcts demonstrate at least a minor degree of RV necrosis; some also have extensive RV infarct.

Presentation — JVD, Kussmaul's sign (paradoxical pulse — BP Ø exceeds 10 mm Hg on inspiration while venous pressure remains steady or _), and hepatomegaly with or without ST elevation in right precordial leads, esp. V₄R

Volume expansion often improves CO and hypotension.

• Sudden Death — risk factors = age > 65 years, previous angina pectoris, hypotension or cardiogenic shock, acute systolic hypertension at time of admission, DM, dysrhythmias or conduction defects, previous MI.

• Thromboembolism — often clinically silent; found in 45% of patients at autopsy.

Thrombi may form on the endocardial surface of myocardial infarcts or ventricular aneurysms + DVT.

• Ventricular Aneurysm — = dyskinesis; local expansile paradoxical wall motion during systole.

Infarct heals as thin fibrous scar which fails to move with rest of the ventricular myocardium.

Most common at the apex; occur months to years after AMI.

Don't predispose to nor a/w cardiac rupture.

May be complicated by ejection fraction, SV, CHF, arterial embolism, and ventricular tachyarrhythmias.

Physical finding of greatest value = double, diffuse, or displaced apical impulse.

APPENDIX I: DIAGNOSTIC AND THERAPEUTIC PROCEDURES

IN CORONARY ARTERY DISEASE

• Cardiac Catheterization:

Involves the insertion of a radiopaque catheter into an artery (left side) or vein (right).

Used with stress test/pacing to assess the functional impact of CAD.

Used to evaluate pressures, cardiac output, O₂ levels, coronary circulation, ventricular function, heart dz., and hemodynamic function.

Catheterization is also used to perform angiography. Dye is used to visualize ventricle motion and coronary blood flow.

Histamines and steroids are given prior to the procedure to the possibility of a reaction to the radiopaque iodine dye.

NTG and calcium blockers are used during the procedure to spasm.

Dye is an osmotic diuretic so the patient must be well hydrated.

Smokers have an risk of complications as nicotine produces aggravation of coronary spasm after vessel manipulation.

• Coronary Artery Bypass Graft (CABG):

Performed for revascularization.

Veins used for the procedure take on arterial characteristics (get thicker walls) within one month.

30% of the grafts thrombose in first year. Platelet derived growth (PDGF) factor has been implicated in the thrombosis process — clinical studies are currently being conducted with Ab to PDGF.

• Chest X-ray:

Used to assess heart size and position, chamber size, pulmonary blood flow, and line placement.

• Directional Atherectomy (DVI):

A rotating blade cuts away lesions, leaving scalloped edges and a vacuum sucks the lesion out after it is cut.

This tool actually creates a potent stimulus for hyperplasia and rescarring.

• ECG Stress Test:

ECG of a heart at rest can be normal even in the presence of CAD.

Stress test is used to document ischemia and necrosis.

Patient walks on a moving treadmill during the test. A continuous ECG is recorded during the procedure.

Speed and grade of the treadmill q 3 min. until the patient's HR reaches a target HR (220-age) x (0.85) or the patient fatigues — unless symptoms develop. (Patients taking b- blockers are unable to their HR.)

S & S that necessitate stopping the test include pallor, ataxia, hypotension, ST changes, tachycardia, block, bradycardia, and chest pain.

Patient is monitored for an additional 5-10 minutes after test.

False + exercise test may occur if any of the following are present: hyperventilation, abnormal electrolytes, vasomotor instability, and certain drugs — Valium; antihistamines; digitalis [Ds the ST]; and lithium [Ds ST, T, and HR].

Contraindications — severe LV dysfunction, an acute MI within 10 days, unstable angina, and uncompensated aortic stenosis or cardiomyopathy.

All post MI patients need a stress test or catheter test to uncover residual ischemia.

ST depression during the test (post MI) is predictive of mortality.

• Echocardiography:

Non-invasive method of recording cardiac structures and motion using the echo (reflection) of high frequency ultrasound.

Transesophageal echo recording is the invasive form of this test.

Tells about the thickness of the septum and walls and about the diameter of the LV cavity, the motion of heart, the heart size and shape, and valve structure.

Fibrotic, calcified, and scarred structures reflect more sound waves; therefore, appear more dense.

Smokers are poor candidates for echo due to interference by carbon monoxide.

Two modes of echocardiography — M and two dimensional.

M mode uses a single ultrasound beam and information is displayed on a strip chart along with an ECG for reference.

Two dimensional mode is more advanced and rotates throughout the chest wall; information is recorded on a printout and videotape.

Used to dx mitral/aortic valve dz., pericardial effusion, LV size and function, tumors, idiopathic hypertrophic subaortic stenosis, shunts, and hypokinesis.

Echo combined with dobutamine gives a better picture of the heart damage. (Drug is infused during the echo and wall motion is monitored.)

• Electrophysiology:

Clinical indications include refractory or incapacitating supraventricular tachydysrhythmias, sustained ventricular tachycardia unrelated to an acute MI, sudden cardiac death unrelated to a myocardial infarction, unexplained syncope in patients with CV disease, recurrent wide QRS complex tachycardia, and nonsustained ventricular tachycardia in patients with cardiovascular dz.

Procedure involves the percutaneous introduction of 1-6 catheters. Rapid pacing is then done to stress the heart and conduction system and study the origin of the dysrhythmia and the electrophysiologic properties of accessory bypass tracts.

Drug therapy may be used during the test to evaluate the effectiveness of various cardiac drugs on the dysrhythmia.

Procedure takes 4-6 hours. During this time, a His-bundle electrogram is recorded to locate the site of conduction abnormalities.

Recordings are made from the RA, the RV, and the His bundle.

The electro- or histogram divides the PR interval into 3 components — the PA time (intra-atrial conduction, 37 msec), the A-H time (AV nodal conduction, 77 msec), and H-V time (conduction through the His-Purkinje system, 40 msec).

PA and H-V times are mostly unaffected by the ANS.

A-H time varies with vagal and sympathetic stimulation and with HR.

Sinus node recovery time, refractory periods, and action potential duration can be evaluated with this technique.

Techniques allow for the precise localization and catheter ablation of an accessory bypass tract. With cryoablation, the cells are frozen; with thermal ablation, the catheter tip heats the area and destroys the cells, with radiofrequency ablation, current is used to destroy the cells.

• Heart Transplant:

Indications for transplant include L ventricular failure, congenital disorders, and cardiomyopathy. An immunosuppressive protocol (cyclosporine, steroids, azathioprine, OKT3) is used. Bacterial and viral infections are seen in over 60% of the patients. Cyclosporine is nephrotoxic so most patients need a kidney transplant after the heart transplant. CAD in the transplanted organ does not cause the usual symptoms.

< 10% of these patients have chest pain and < 50% have ECG changes. The CAD is often misdiagnosed and the patient is treated for rejection instead. In 1989, the one yr. survival was 80% (5 yr., 60%). (Liver: 1/2 patients die on waiting list; kidney: one y. survival is 85-95%; 10 yr. is 75-85%).

• Holter Monitor:

A Holter monitor is a small portable monitor that is worn for 12-48 hours. One or two lead ECG recordings are usually obtained via 3-5 electrodes. Monitors are available now that can do 4 lead ECGs. The additional leads provide clearer information regarding atrial activity and screen out artifact abnormalities that appear only on one channel. The recordings can identify supraventricular dysrhythmias with aberrancy and document ST segment abnormalities. Usually modifications of leads V₁ and V₅ are used. The patient records activities and symptoms in a diary which are later correlated with the strip.

• Intervascular Stents:

Stents are coils that are left in vessels to support the wall and push back dissections. Complications included thrombosis and clotting, with restenosis in 41% of the cases, spasm, collapse, and dislodgement. They now use a balloon to open the stent even more. Gianturco-Roubin is one of the more common stents. Newer stents are biodegradable.

• Lasers:

There are several types of lasers available. Lasers are used in CV surgery to unclog vessels. The laser vaporizes plaque and produces a smoother wall than PCTA. Light is converted to thermal energy and protein is coagulated while water is vaporized. A relativity smooth wall results and PLTs do not adhere so there is a minimum inflammatory response. Lasers are also used to reseal tears due to angioplasty but may create tears themselves. Lasers produce either thermal or mechanical perforations in 20% of the CAD treatments. Mechanical perforations occur because the fiber optics are relatively inflexible. Laser therapy is useful for total occlusions that PCTA cannot fix or to enlarge a stenosis so that PCTA can be performed. Laser therapy is not an improvement over PCTA therapy and it is more time consuming. 45% of the vessels restenose in 6 months.

• Magnetic Resonance Imaging (MRI):

With MRI, the nuclei of certain isotopes (for example, hydrogen atoms in water and fat) are lined up in an external magnetic field. The nucleus of each atom behaves like a tiny bar magnet when patient is surrounded by a large magnet. A short radio frequency is used to apply a second external magnetic field that changes the orientation of the nuclear magnets; the nuclei then tilt. As they realign themselves they emit a radio frequency that has a spatial form and this energy is used to form the MRI image. Normally the nuclei of hydrogen atoms in the body are randomly oriented. By varying the timing, orientation and strength of the magnetic fields, it is possible to obtain a wide range of image contrasts. Other types of MRI are used to obtain images of such things as blood, capillary permeability, and turbulence. Fast MRI allows imaging of the heart in a fraction of a second. Echo-planar MRI acquires images in 30 ms, while turbo-FLASH obtains images in 300 ms — both techniques produce peripheral nerve stimulation as a side effects.; therefore, there may be a potential to trigger a dysrhythmia. Contraindications for MRI studies include pacemakers, ferromagnetic cerebral aneurysm clips, cochlear implants or metal fragments in the eye. Sternal wires, clips used in bypass surgery and prosthetic valves are now considered safe.

• Percutaneous Transluminal Coronary Angioplasty (PTCA):

Another variant of dye contrast cardiac catheterization and is an alternative to bypass surgery. PTCA improves coronary flow by enlarging the lumen of the artery. The lesion is compressed with a pressurized balloon. The stretch produced by the balloon leads to an inflammatory/injury response with resulting fibrosis. Lesions in older patients may be calcified and non-compressible. Usually cardiac patients have thrombosis and stenosis, so they often need both PTCA and fibrinolytic drug therapy. The PTCA should not be done for at least 24 hours after administration of the drug. Post PTCA care involves monitoring the ECG and providing care similar to that following catheterization. The arterial sheaths are removed 3-5 hours after the procedure; they are not removed right away because of the danger of bleeding from the heparin given during the procedure. If heparin therapy is continued after the procedure, the sheaths are left in overnight. Patients must stay on their backs while the sheaths are in place and they should not lift their heads up off the pillow. They can bend the leg without the sheath to get relief from back strain. Pressure is applied on the groin site for 15-30 minutes after sheath removal. Pressure is applied over the area if the patient coughs or sneezes. Bleeding is a serious risk so we apply a pressure bandage and sandbag after sheath removal. The circulation should be checked (pulse, color, temperature, sensation) looking for emboli, thrombi s/s, especially the first 4 hours after the procedure. The patient is placed on bedrest for 6-8 hours after sheath removal. The patient is NPO the first hour, then given fluids 2nd hour; solids are reintroduced after 2 hours. Fluids are forced to help eliminate the dye. Coagulation, cardiac enzymes, and electrolytes are evaluated. Complications include angina due to occlusion of catheter, coronary artery dissection (intimal tear), spasm, MI, bradycardia, ventricular tachycardia and fib, CVAs, emboli, infection, allergic reaction, systemic hypotension, bronchospasm, death, HA, hot flashes due to vasodilation, and N/V as side effects of the dye, and at the catheter site (thrombosis, bleeding, pseudo-aneurysms, A-V fistulas, laceration of the vessel). One half of the patients have angina during balloon inflation. Those patients who have no ST deviation after the procedure have no coronary events; those with ST elevation are at higher risk than those with ST depression. Trended data should be used (patient's baseline with changes overlaid) to monitor the ST. If there is more than a 2 mm change, the MD should be notified. (Alcohol, exercise, stress, eating, and pregnancy can also change the ST segment.) PTCA is good for relieving angina, improving exercise performance and reducing the need for anti-angina medications. As compared with just medications, it does not reduce the incidence of MI, or increase survival or ventricle performance (NEJM 11/94). As compared to CABG, MIs and deaths were similar, but PTCA was associated with persistent angina and the need for continued medication, while the CABG patient was more likely to have a procedure-related Q wave MI (NEJM 7/96). Thirty percent of the PTCA patients restenose in 6 months and may develop aneurysms or intimal splitting. The initial cost of PTCA is 1/3 to 1/2 of the cost of a CABG but with restenosis, the costs are the same over time. PLT derived grow factor Ab has been used to prevent reocclusion after PTCA in animals; clinical trials with humans started this year. Restenosis lesions harbor human cytomegalovirus (HCMV) and high levels of tumor suppressor protein (p53). HCMV causes a symptomless infection in healthy individuals — it has been suggested that injury associated with PTCA activates latent HCMV. HCMV inactivates p53 in smooth muscle cells, predisposing them to increased growth.

• Pharmacologic Stress Test:

This method is used if the patient cannot exercise, has an aortic aneurysm or ventricular pacemaker, or is taking calcium or beta blockers and is contraindicated in COPD patients. In the past, we gave dipyridamole (t_1/2 is 2 minute), which inhibits adenosine uptake by the RBCs and thus produces coronary vasodilation. We are using adenosine (t_1/2 is 2 sec) in some hospitals now. Patients are more likely to have chest pain, SOB, flushing, and AV block with adenosine, but the side effects are short lived. The side effects with dipyridamole last longer than adenosine, but require no therapy. The 201tl is injected after the dipyridamole or adenosine.

• Phonocardiography:

Phonocardiography uses sound recording to evaluate the timing of the cardiac cycle and the characteristics of murmurs. Audible vibrations produced by the heart, great vessels and valves are recorded by 3 microphones and converted to electrical signals then recorded on paper. The microphones are placed over the base and apex of the heart. There are no risks to this procedure. An ECG and the carotid pulse are recorded also for reference points.

• Pull-Back Atherectomy:

This tool leaves a round lumen and is used to cut calcified lesions.

• Radioisotopes:

Low dose radiation is used to measure ventricle function or myocardial perfusion, looking at living versus dead cells. This tool tells about ischemia versus death.

• Roto-Borer:

The roto-borer is a high speed rotational coronary angioplasty that is used to grind plaque on calcified lesions. Scar tissue recloses the hole made by the tool.

• Technetium Pyrophosphate (Teboroxime) (99Tc):

A technetium scan is used to evaluate gated cardiac function. The ECG provides a "gate" (physiological marker) for end-diastole and end-systole. The R-R interval is divided into segments by the computer and a gamma counter records radioactivity from each segment. Technetium is used to identify a MI that is 12 hours to 6 days old. Technetium employs hot spot imaging — the damaged cells pick up the isotope because of their high calcium concentration and the infarct becomes radioactive. Bone also picks up the isotope. False positive readings occur with breast tumors, old age, aneurysms, and cardiomyopathies. The scan is performed 2-3 hours after injection of the isotope. The operator takes several 5 minute scans from different angles. The patient must lie quiet. This test can be used to tag RBCs; to evaluate wall motion, ventricle performance, and ejection fraction; and to see pre- and post-fibrolytic agent reperfusion changes.

• Thallium 201 (201tl) Scan

A thallium scan is a cold spot scan. The isotope is picked up by living heart cells. The infarct on the scintigram is a dark spot and is called cold spot. The patient must be NPO 2-4 hours before the test so digestion does not divert the radioactivity. This scan is used to assess perfusion after exercise. Areas with decreased perfusion are not able to take up isotope during exercise, but will 4 hours later so we do 2 scans. The isotope is injected via a heplock 1 min. before the patient stops exercising and a scan is performed immediately after the exercise and again 4 hours later. Areas that reperfuse in 4 hours suggest reversible ischemia (CAD). This tool will show whether the heart can increase its ejection fraction with exercise.

APPENDIX J: DEFINITIONS

Block — an abnormal delay or failure of conduction; must be differentiated from normal physiologic delays (e.g., atrial flutter with 2:1 conduction or sinus node suppression following atrial ectopy.)

Cycle — one complete systole and diastole sequence; may be measured from P-P or R-R or T-T intervals.

Ectopic — arises from outside the normal pacemaker of the heart; can arise from the atria, AV junction, or ventricles; can be premature beats, escape beats, or a continuous rhythm.

Escape — occurs late or ends a cycle longer than the dominant cycle (passive).

Paradoxical Pulse: a diagnostic sign. There is an abnormal drop in systolic BP when the patient inspires. With inspiration the vessels of the lung increase in size secondary to the increased negative pressure and the blood pools causing a decrease in SV and pulse strength. This sign is seen with positive pressure ventilation, right ventricular infarct, hypovolemia, and in 1/3 of tamponade patients.

Premature — occurs early or ends a cycle shorter than the dominant cycle (active).

Pulse Pressure: affected by stroke volume and compliance. The greater the CO, the greater the pressure increase during systole and the fall during diastole; therefore, the greater the pulse pressure. The greater the compliance, the smaller the pressure rise (arteriosclerosis decreases compliance, as does some HTN.)

Pulsus Alternans: a diagnostic sign. There are alternating strong and weak beats due to a change in L ventricular contractile force. This sign is seen on the ECG as alternating tall and short QRSs. Pulsus alternans are seen with tamponade, L ventricular failure, digitalis toxicity, paroxysmal SVT, AV block, falling BP, and aortic insufficiency. It is common among patients at increased risk for ventricular dysrhythmias.

Ventricular Contractile Asynergy:

• Hypokinesis: generalized reduction in myocardial contraction

• Asyneresis: localized or discrete area of reduced wall motion

• Akinesis: total absence of wall motion in a discrete area

• Dyskinesis: paradoxical systolic expansion of a portion of the L ventricular wall

• Asynchrony: a disturbance in the temporal sequence of L ventricular wall contraction

APPENDIX K: MISCELLANEOUS

Sex after a MI

The patient's sexual habits prior to the cardiac event should be assessed and used as a guide for teaching. Eighty percent of the post MI patients return to daily activities including sex in 4-6 weeks. Sexual activity can be resumed when the patient can climb two flights of stairs without chest pain, SOB, or extreme fatigue. The heart is usually stressed only 4-6 min. of a 10-16 min. sexual experience. An orgasm will generally increase the HR above 150 bpm and the BP to 160/90 mm Hg for 15-20 seconds similar to climbing two flights of stairs. Angina and palpitations may occur post-orgasm. The patient should be instructed to call the MD if the s/s last longer than 15 min. Masturbation, manual and oral stimulation are OK; anal intercourse may produce dysrhythmias. Patients should avoid sex if they are cold or too hot, immediately after a shower, or after a heavy meal or moderate or heavy consumption of alcohol. They should wait 2 hours after food/drink.

THE AGING CV SYSTEM

The peak maturity of all systems is at age 19-23. We do not notice our losses, because we have massive reserves (there is a net loss of cells but we have 5x the number that we need). Humans notice a loss of immediate recall in the mid to late 40s.

Exercise in a 20 y. o. produces a 20 fold _ in cardiac output, but it only produces a 3-4 fold _ in a 70 y. o. The maximal HR at age 65 Ø 40% from age 40 due to _ parasympathetic dominance; the SV reaches its limits at time of peak HR. _ oxygen demand and ineffective metabolism prevent additional HR _ beyond that level.

Orthostatic hypotension may develop because the baroreceptors are not as effective and elderly patients may faint with severe stress. The blood vessels lose their elasticity with age and there is expansion of the vessels when cardiac output increases. The vessel Ds also Æ in auto-regulatory control of flow to the brain, coronaries, and kidney.

With aging there is a decrease in the ability to regulate temperature andin the recognition of referred pain. The decrease in pain recognition may lead to silent MIs, blunting angina, and perception of L arm pain.

The elderly experience decreased digitalis tolerance and decreased tolerance to other drug,.i.e. nitrates.

INFECTIVE ENDOCARDITIS

The endocardium lines the heart chambers, covers the valves, and is continuous with the endothelial lining of the blood vessels adjacent to heart. It provides a smooth surface and prevents friction between the blood and the heart.

Endocarditis is an inflammation of the endocardium, especially the valves. Non-bacterial endocarditis is associated with blood stasis, MI, trauma, aging, collagen diseases, and artificial valves. Bacterial endocarditis is associated with bacteria, viruses, fungus, rickettsiae, and parasites — strep. and staph. are the most common organisms. The organisms enter the blood stream via dental cleaning, bladder catheterization, URI, skin infections, etc.

Risk factors include mitral valve prolapse, prosthetic valves, ventricular septal defect, previous attack of bacterial endocarditis, male gender, IV drug abuse, long term central vessel catheterization, and recent cardiac surgery.

Pathophysiology: A valve is usually damaged, leading to an inflammatory reaction. The damage exposes the basement membrane allowing the release of chemicals that are chemotaxic for PLTs. PLT activation and thrombus formation then create nonbacterial thrombotic endocarditis or infective carditis if micro-organisms are present in the blood.

Not all micro-organisms are capable of colonizing — the organisms must be able to survive interactions with complement, Ab, PLTs, etc. and they must also adhere to the damaged surface where they then proliferate and propagate the vegetation. Within 3-6 hours after the initiation of the infection, bacterial colonies form within aggregates of fibrin and PLTs and increase in size by 24 hours. The bacteria may activate the clotting cascade and promote the production of fibrin. As they multiply deep in the fibrin network, the bacteria become less susceptible to body defense mechanisms.

Clinical manifestations: acute, subacute, and chronic. The patient may have murmurs (75%), fever, petechiae on knees, elbows, ankles, eyes, and lips (25-50%), splenomegaly (50%), CHF (50-80%), immune complex deposition in various organs, anorexia, weight loss, night sweats, positive serum C&S, and back pain (25%). Osler nodes are pea sized tender reddish lesions on the fingers and toes. Right sided lesions are seen in drug addicts and in patients with congenital defects. ECGs, C&S, and scans of organs that emboli may have lodged in are used for evaluation. Management includes antimicrobial therapy for 4-6 weeks (IV then PO), prophylactic antibiotics, and rest.

REFERENCES

Drew, B. J. (1997). University of California, San Francisco course syllabus, Nursing 222, Cardiac Rhythm Theory and Analysis.

Evans, T. (1996). ECG Interpretation Cribsheets. 3rd ed. San Francisco, CA: Ring Mountain Press.

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