CLINICIAN’S POCKET REFERENCE - PART 6 doc

Anxiety, exertion, pain, fever, hypoxia, hypotension, increased sympathetic tone secondary to drugs with adrenergic effects [eg, epinephrine], ergic effect eg, atropine, PE, COPD, AMI, C

PFTs, remember that some patients may have combined restrictive and obstructive diseasessuch as emphysema and asbestosis.

OXYGEN AND HUMIDITY SUPPLEMENTS

Table 18–2 describes various methods of oxygen and humidity supplementation

18

TABLE 18–1

Differential Diagnosis of Pulmonary Function Tests

Restrictive Obstructive Test Disease Disease

OBSTRUCTIVE AIRWAYS DISEASE (COPD)

Test Normal Mild Moderate Severe

RV (% of

RESTRICTIVE LUNG DISEASE

Test Normal Mild–Moderate Severe

Humidity Therapy

Humidity generators are divided into humidifiers and nebulizers Patients with intact upperairways do not need as high a percentage of relative humidity (% RH) as do patients with ar-tificial airways (endotracheal tubes or tracheostomy tubes) Artificial airways require higherhumidity to prevent secretions from obstructing the tubes To bring the % RH of the inspiredgas up to room humidity (30–40% RH) when using the nasal cannula, simple oxygen mask,partial rebreathing mask, or nonrebreathing mask, the bubble-diffuser humidifier is the de-vice of choice

To provide medium to high levels of % RH, aerosol devices such as the face tent,aerosol mask, aerosol T piece, and aerosol collar are the devices of choice The humiditygenerator for these devices is the aerosol-jet nebulizer, which can provide cool or heatedmist The gas that powers the nebulizer may be blended to any desired inspired oxygen con-centration (FiO2)

BRONCHOPULMONARY HYGIENE

The following is a listing of the modalities available through the respiratory care or nursingservices of most hospitals All are designed to help patients with their bronchopulmonaryhygiene, more commonly referred to as “pulmonary toilet.” Bronchopulmonary hygiene is

needs

an exact Fi02

Abbreviation: COPD = chronic obstructive pulmonary disease.

• Treatment of COPD, acute asthma, cystic fibrosis, and bronchiectasis

• Help in inducing sputum for diagnostic tests

Goals

• Relief of bronchospasm

• Help in decreasing the viscosity and in clearing of secretions

To Order: Specify the following:

• Frequency

• Heated or cool mist

• Medications: In sterile water or NS

2 TC&DB: Ordered on a timed schedule or as needed

• Example P&PD qid of RUL and RML 5 min/lobe or TC&DB q4h.

Specify the following:

• Frequency (such as 10 min q1–2h while awake)

• Device (if you have a preference)

Example Incentive spirometry 10 min every hour with blow bottle.

TOPICAL MEDICATIONS

The following agents can be added to aerosol therapy to prevent or treat pulmonary cations caused by bronchoconstriction, mucosal congestion, or inspissated secretions Re-member, even though these are primarily topical agents, some systemic absorption can oftenoccur

compli-Acetylcysteine (Mucomyst): A mucolytic agent useful for treating retained mucoidsecretions; inspissated secretions; and impacted mucoid plugs seen in diseases such asCOPD, cystic fibrosis, and pneumonia A bronchodilator should be given along with Mu-comyst

Usual Adult Dosage 1–3 mL of 20% acetylcysteine in 0.5 mL (2–10 mg) of Bronkosol

Albuterol (Ventolin, Proventil): A short-acting selective bronchodilator with pally beta-2 activity; can cause tachycardia Onset 15 min Peak effect at 0.5–1 h, duration3–5 h

princi-Usual Dosage 2.5 mg in 3 mL NS q4h

Metaproterenol (Alupent, Metaprel): A short-acting bronchodilator with both

beta-1 and beta-2 activity; can cause tachycardia Peak effect at 0.5–beta-1 h, duration 3–5 h

Usual Dosage 0.3 mL (10–15 mg) of a 5% solution in 2.5 mL NS bid–qid

Racemic Epinephrine: Contains both d and l forms of epinephrine Useful becausethe alpha effects result in mucosal vasoconstriction that reduces mucosal engorgement andthe bronchodilation lessens the risk of hypoxemia Most useful for laryngotracheobronchitisand immediately after extubation in children

Usual Dosage 0.125–0.5 mL (3–10 mg) in 2.5 mL NS

Ipratropium Bromide (Atrovent): A parasympatholytic bronchodilating agent thatcauses bronchodilation and a decrease in secretions with “drying” of the respiratory mu-cosa This is minimally absorbed and rarely results in tachycardia Onset 45 min, duration4–6 h

Usual Dosage 0.5 mg in 3 mL NS qid

Atropine: A parasympatholytic agent that causes bronchodilation and a decrease in cretions with “drying” of the respiratory mucosa This is readily absorbed and, therefore hascardiac effects (tachycardia)

se-18

18

The formal procedure for obtaining a readable ECG is given in Chapter 13, page 266 Everyelectrocardiogram should be approached in a systematic, stepwise fashion Many automatedECG machines can give a preliminary interpretation of a tracing; however, all automated in-terpretations require analysis and sign-off by a physician Determine each of the following:

• Standardization With the ECG machine set on 1 mV, a 10-mm standardization

mark (0.1 mV/mm) is evident (Figure 19–1)

• Axis If the QRS is upright (more positive than negative) in leads I and aVF, the axis

is normal The normal axis range is –30 degrees to +105 degrees

• Intervals Determine the PR, QRS, and QT intervals (Figure 19–2) Intervals are

measured in the limb leads The PR should be 0.12–0.20 s, and the QRS, <0.12 s.The QT interval increases with decreasing heart rate, usually <0.44 s The QT inter-val usually does not exceed one half of the RR interval (the distance between two

R waves)

• Rate Count the number of QRS cycles in a 6-s strip and multiply it by 10 to roughly

estimate the rate If the rhythm is regular you can be more exact in determining therate by dividing 300 by the number of 0.20-s intervals (usually depicted by darkershading) and then extrapolating for any fraction of a 0.20-s segment

• Rhythm Determine whether each QRS is preceded by a P wave, look for variation

in the PR interval and RR interval (the duration between two QRS cycles), and lookfor ectopic beats

• Hypertrophy One way to determine LVH is to calculate the sum of the S wave in

V1or V2plus the R wave in V5or V6 A sum >35 indicates LVH Some other criteriafor LVH are R >11 mm in aVL or R in I + S in aVF >25 mm

• Infarction or Ischemia Check for the presence of ST-segment elevation or

depres-sion, Q waves, inverted T waves, and poor R-wave progression in the precordialleads

A more detailed discussion of each of these categories is presented in the following sections

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BASIC INFORMATION

Equipment

Bipolar Leads

• Lead I: Left arm to right arm

• Lead II: Left leg to right arm

• Lead III: Left leg to left arm

Precordial Leads: V1to V6across the chest, as shown in the section on grams in Chapter 13 (see Figure 13–9, page 267)

electrocardio-ECG Paper: With the ECG machine set at 25 mm/s, each small box represents 0.04 sand each large box 0.2 s (see Figure 19–1, above) Most ECG machines automatically print

a standardization mark

Normal ECG Complex

Note: A small amplitude in the Q, R, or S wave is represented by a lowercase letter; a large

amplitude by an uppercase letter The pattern shown in Figure 19–2 could also be noted asqRs

• P Wave Caused by depolarization of the atria With normal sinus rhythm, the P

19

0.04 s 0.20 s

FIGURE 19–1 Examples of a 10-mm standardization mark and time marks and

standard electrocardiogram paper running at 25 mm/s

• QRS Complex Represents ventricular depolarization

• Q Wave The first negative deflection of the QRS complex (not always present and,

if present, may be pathologic)

• R Wave The first positive deflection (R) is the positive deflection that sometimes

occurs after the S wave)

• S Wave The negative deflection following the R wave

• T Wave Caused by repolarization of the ventricles and follows the QRS complex.

Normally upright in leads I, II, V3, V4, V5, and V6and inverted in aVR

AXIS DEVIATION

The term axis, which represents the sum of the vectors of the electrical depolarization of the

ventricles, gives some idea of the electrical orientation of the heart in the body In a healthy

19

0.04 s Time (s)

FIGURE 19–2 Diagram of the electrocardiographic complexes, intervals, and

seg-ments The U wave is normally not well seen (Reprinted, with permission, from:

Goldman MJ [ed]: Principles of Clinical Electrocardiography, 12th ed Lange

Med-ical Publications, Los Altos CA, 1986.)

The QRS axis is midway between two leads that have QRS complexes of equal tude, or the axis is 90 degrees to the lead in which the QRS is isoelectric, that is, the ampli-tude of the R wave equals the amplitude of the S wave.

ampli-• Normal Axis QRS positive in I and aVF (0–90 degrees) Normal axis is actually

–30 to 105 degrees

• LAD QRS positive in I and negative in aVF, –30 to –90 degrees

• RAD QRS negative in I and positive in aVF, +105 to +180 degrees

• Extreme Right Axis Deviation QRS negative in I and negative in aVF, +180 to

+270 or –90 to –180 degrees

Clinical Correlations

• RAD Seen with RVH, RBBB, COPD, and acute PE (a sudden change in axis toward

the right), as well as in healthy individuals (occasionally)

• LAD Seen with LVH, LAHB (–45 to –90 degrees), LBBB, and in some healthy

ExtremeRAD

Normal

FIGURE 19–3 Graphic representation of the “axis deviation.”

Electrocardio-graphic representations of each type of axis are shown in each quadrant The largearrow is the normal axis

× 10.

• Method 2 (for regular rhythms) Count the number of large squares (0.2-s boxes)

between two successive cycles The rate is equal to 300 divided by the number ofsquares Extrapolate if the QRS complex does not fall exactly on the 0.2-s marks (eg,

if each QRS complex is separated by 2.4 0.20-s segments, the rate is 120 bpm Therate between two 0.20-s segments is 150 bpm, and between three 0.20-s segments is

Clinical Correlations Anxiety, exertion, pain, fever, hypoxia, hypotension, increased

sympathetic tone (secondary to drugs with adrenergic effects [eg, epinephrine]), ergic effect (eg, atropine), PE, COPD, AMI, CHF, hyperthyroidism, and others

anticholin-Sinus Bradycardia: Normal sinus rhythm with a heart rate <60 bpm (Figure 19–7)

Clinical Correlations Well-trained athlete, normal variant, secondary to medications

(eg, beta-blockers, digitalis, clonidine), hypothyroidism, hypothermia, sick sinus syndrome(tachy–brady syndrome), and others

19FIGURE 19–4 Sample strip for rapid rate determination (see text for procedure).

Estimating the rate by counting the number of beats (eight) in the two 3-s intervals.The rate is 8 × 10, or 80 bpm (method 1) Using method 2, each beat is separatedfrom another beat by four 0.20-s intervals, so you divide 300 by 4, and the rate is

75 bpm Because the beats are separated by exactly four beats, you do not need toextrapolate

• If asymptomatic (good urine output, adequate BP, and normal sensorium), no apy needed

ther-• If hypotensive or disoriented: See Chapter 21, page 460

Sinus Arrhythmia: Normal sinus rhythm with a somewhat irregular heart rate tion causes a slight increase in rate; expiration decreases the rate Normal variation betweeninspiration and expiration is 10% or less

Inspira-Atrial Arrhythmias

PAC: Ectopic atrial focus firing prematurely followed by a normal QRS (Figure 19–8).The compensatory pause following the PAC is partial; the RR interval between beats 4 and 6

is less than between beats 1 and 3 or 6 and 8

Clinical Correlations Usually not of clinical significance; can be caused by stress,

caf-feine, and myocardial disease

PAT: A run of three or more consecutive PACs The heart rate is usually between 140 and

250 bpm The P wave may not be visible, but the RR interval is very regular (Figure 19–9)

Clinical Correlations Can be seen in healthy individuals but also occurs with a variety

of heart diseases Symptoms include palpitations, light-headedness, and syncope

Treatment

• Increase Vagal Tone Valsalva maneuver or carotid massage

19

FIGURE 19–5 Normal sinus rhythm.

FIGURE 19–6 Sinus tachycardia The rate is 120–130 bpm.

• Medical Treatment Can include adenosine, verapamil, digoxin, edrophonium, or

beta-blockers (propranolol, metoprolol, and esmolol) Verapamil and beta-blockersshould be used cautiously at the same time because asystole can occur

• Cardioversion with Synchronized DC Shock Particularly in the hemodynamically

unstable patient (see Chapter 21, page 467)

MAT: An atrial arrhythmia that originates from ectopic atrial foci It is characterized byvarying P-wave morphology and PR interval and is irregular (Figure 19–10)

Clinical Correlations Most commonly associated with COPD, also seen in elderly

pa-tients, CHF, diabetes, or use of theophylline Antiarrhythmics are often ineffective Treat theunderlying disease

AFib: Irregularly irregular rhythm with no discernible P waves The ventricular rate ally varies between 100 and 180 bpm (Figure 19–11) The ventricular response is slowerwith digoxin, verapamil, or beta-blocker therapy and with AV nodal disease

usu-Clinical Correlations Seen in some healthy individuals but commonly associated with

organic heart disease (CAD, hypertensive heart disease, or rheumatic mitral valve disease),thyrotoxicosis, alcohol abuse, pericarditis, PE, and postoperatively

Treatment

• Pharmacologic Therapy Intravenous adenosine, verapamil, digoxin, and

beta-blockers (propranolol, metoprolol, and esmolol) can be used to slow down theventricular response, and quinidine, procainamide, propafenone, ibutilide, and

19FIGURE 19–7 Sinus bradycardia The rate is approximately 38 bpm.

FIGURE 19–8 Premature atrial contraction (PAC) The fifth beat is a PAC.

amiodarone can be used to maintain or convert to sinus rhythm (see individualagents in Chapter 21)

• DC-Synchronized Cardioversion Indicated if associated with increased

myocar-dial ischemia, hypotension, or pulmonary edema (see Chapter 21, page 467)

Atrial Flutter: Characterized by sawtooth flutter waves with an atrial rate between 250and 350 bpm; the rate may be regular or irregular depending on whether the atrial impulsesare conducted through the AV node at a regular interval or at a variable interval (Fig-ure 19–12)

Example: One ventricular contraction (QRS) for every two flutter waves = 2:1 flutter Clinical Correlations Seen with valvular heart disease, pericarditis, ischemic heart dis-

ease, pulmonary disease including PE, and alcohol abuse

Treatment Do NOT use quinidine or procainamide (atrial conduction may decrease to

the point where 1:1 atrial:ventricular conduction can occur and the ventricular rate will crease and hemodynamic compromise can occur), otherwise, similar to treatment of atrialfibrillation Ibutilide (a new Class III antiarrhythmic) is very effective

FIGURE 19–9 Paroxysmal atrial tachycardia.

FIGURE 19–10 Multifocal atrial tachycardia.

ure 19–13) Three or more premature junctional beats in a row constitute a junctional cardia, which has the same clinical significance as PAT.

tachy-Ventricular Arrhythmias

PVC: As implied by the name, a premature beat arising in the ventricle P waves may bepresent but have no relation to the QRS of the PVC The QRS is usually >0.12 s with a leftbundle branch pattern A compensatory pause follows a PVC that is usually longer than after

a PAC (Figure 19–14) The RR interval between beats 1 and 3 is equal to that between beats

3 and 5 Thus, the pause following the PVC (the fourth beat) is fully compensatory The lowing patterns are recognized:

fol-• Bigeminy One normal sinus beat followed by one PVC in an alternating fashion

(Figure 19–15)

• Trigeminy Sequence of two normal beats followed by one PVC

• Unifocal PVCs Arise from one site in the ventricle Each has the same

configura-tion in a single lead (See Figure 19–14.)

• Multifocal PVCs Arise from different sites; therefore, have different shapes (Figure

19–16)

Clinical Correlations PVCs occur in healthy persons and with excessive caffeine ingestion,

anemia, anxiety, organic heart disease (ischemic, valvular, or hypertensive), secondary tomedications (epinephrine and isoproterenol; from toxic level of digitalis and theophylline),

19FIGURE 19–11 Atrial fibrillation.

FIGURE 19–12 Atrial flutter with atrioventricular (AV) block (3:1 to 5:1

conduc-tion)

or predisposing metabolic abnormalities (hypoxia, hypokalemia, acidosis, alkalosis, or pomagnesemia)

hy-Criteria for Treatment In the setting of an AMI:

• >5 PVCs in 1 min (many clinicians would treat any PVC associated with an MI orinjury pattern on ECG)

• PVCs in couplets (two in a row)

• Numerous multifocal PVCs

• PVC that falls on the preceding T wave (R on T)

Treatment See also Chapter 21, page 459.

• Lidocaine Most commonly used; other antiarrhythmics include procainamide, and

Clinical Correlations See the section on PVCs Patients with ventricular aneurysm are

more susceptible to developing ventricular arrhythmias

Treatment See Chapter 21, page 459.

Ventricular Fibrillation: Erratic electrical activity from the ventricles, which fibrillate

or twitch asynchronously No cardiac output occurs with this rhythm (Figure 19–18)

Clinical Correlations One of two patterns seen with cardiac arrest (the other would be

asystole or flat line)

Treatment See Chapter 21, page 252.

Heart Blocks

First-Degree Block: PR interval >0.2 s (or five small boxes) Usually not clinicallysignificant (Figure 19–19) Drugs such as beta-blockers, digitalis, and calcium channelblockers (especially verapamil) can cause first-degree block

Second-Degree Block

Mobitz Type I (Wenckebach) Progressive prolongation of the PR interval until the P

wave is blocked and not followed by a QRS complex (Figure 19–20) May occur as a 2:1,3:2, or 4:3 block The ratio of the atrial:ventricular beats can vary With a 4:3 block, everyfourth P wave is not followed by a QRS

19FIGURE 19–15 Ventricular bigeminy.

FIGURE 19–16 Multifocal PVCs The second, sixth, seventh, and ninth beats are

PVCs Only the second and sixth PVCs have the same morphology

Clinical Correlations Seen with acute myocardial ischemia such as inferior MI, ASDs,

valvular heart disease, rheumatic fever, or digitalis or propranolol toxicity Can be transient.May progress to bradycardia (rare)

Treatment Usually expectant; if bradycardia occurs: atropine, isoproterenol, or a

pace-maker

Mobitz Type II A series of P waves with conducted QRS complexes followed by a

nonconducted P wave The PR interval for the conducted beats remains constant May occur

as a 2:1, 3:2, or 4:3 block The ratio of the atrial:ventricular beats can vary With a 4:3 block,

every fourth P wave is not followed by a QRS (Note: AV block that is 2:1 can be either

Mobitz type I or type II and may be difficult to differentiate In general, Mobitz I has a longed PR with a narrow QRS; Mobitz II has a normal PR interval with a bundle branch pat-tern [wide QRS])

pro-Clinical Correlations Implies severe conduction system disease that can progress into

complete heart block May be seen in acute anterior MI and cardiomyopathy

Treatment Use of a temporary cardiac pacemaker, particularly when associated with an

acute anterior MI

Third-Degree Block: Complete AV block with independent atrial and ventricular rates.The ventricular rate is usually 20–40 bpm (Figure 19–21)

Clinical Correlations May occur as the result of degenerative changes in the

conduc-tion system in the elderly, from digitalis toxicity, transiently with an acute inferior MI (due

19

FIGURE 19–17 Ventricular tachycardia.

FIGURE 19–18 Ventricular fibrillation.

to temporary ischemia of the AV junction), and after acute anterior MI (much higher bility of mortality than after inferior MI); can result in syncope or CHF

proba-Treatment Usually requires placement of a temporary or permanent pacemaker

BBB: Complete BBB is present when the QRS complex is >0.12 s (or three small boxes

on the ECG strip) Look at leads I, V1, and V6 Degenerative changes and ischemic heart ease are the most common causes

dis-RBBB: The RSR′ pattern seen in V1and or V2 Also a wide S in leads I and V6(Figure19–22)

Clinical Correlations May be seen in healthy persons but usually associated with

dis-eases affecting the right side of the heart (pulmonary hypertension, ASD, or ischemia); den onset is associated with pulmonary embolism or acute exacerbation of COPD

sud-LBBB: The RR′ in leads I and/or V6 The QRS complex may actually be more slurredthan double-peaked as in the RBBB A wide S wave is seen in V1(Figure 19–23)

Clinical Correlations Associated with organic heart disease (hypertensive, valvular,

and ischemic) as well as severe aortic stenosis Development of a new LBBB after an AMImay be an indication for inserting a temporary cardiac pacemaker

19FIGURE 19–19 First-degree AV block The PR interval is 0.26 s.

FIGURE 19–20 Second-degree AV block, Mobitz type I (Wenckebach), with 4:3

conduction

Clinical Correlations Seen with chronic diffuse pulmonary disease, pulmonary

hyper-tension, and congenital heart disease (ASD)

LAE: Notched P wave (“P mitral pattern”) seen in leads I and II A wide (0.11 s orgreater), slurred biphasic P in V1with a wider terminal than initial component (negative de-flection) (Figure 19–25)

Clinical Correlations Seen with mitral stenosis or mitral regurgitation or secondary to

LVH with hypertensive cardiovascular disease

19

FIGURE 19–21 Third-degree AV block (complete heart block) The atrial rate is

100 bpm; the ventricular rate is 47 bpm

FIGURE 19–22 Leads I, V1, and V6demonstrate the right bundle branch block(RBBB) pattern

pro-Clinical Correlations Associated with mitral stenosis, chronic diffuse pulmonary

dis-ease, chronic recurrent PE, congenital heart disease (eg, tetralogy of Fallot), and lar hypertrophy (VH and RVH, with LVH findings often predominating)

biventricu-LVH: Voltage criteria (patients >age 35): S in V1or V2plus an R in V5or V6>35 mm, or

R wave in aVL >11 mm, or R wave in I plus S wave in III >25 mm, or an R in V5or V6>26

mm The QRS complex may be >0.10 s wide in V5or V6 ST-segment depression and T-wave inversion in the anterolateral leads (I, aVL, V5, and V6) suggest LVH with strain(Figure 19–27)

FIGURE 19–27 Left ventricular hypertrophy, leads V1, V2, V5, and V6 The S wave

in the V2+ R wave in V5is 55 mm Note the ST changes and T-wave inversion in V5

and V6, suggesting “strain.”

FIGURE 19–28 ST-segment depression in leads II, III, and aVF in a patient with

acute inferior subendocardial ischemia/infarction

Clinical Correlations Hypertension, aortic stenosis or insufficiency, long-standing

CAD, and some forms of congenital heart disease

MYOCARDIAL INFARCTION

(See also Chapter 21, page 459.)

Myocardial Ischemia: Inadequate oxygen supply to the myocardium because ofblockage or spasm of the coronary arteries The ECG can show ST-segment depression(subendocardial ischemia) (Figure 19–28), ST elevation (transmural ischemia) (Figure19–29), or symmetrically inverted (“flipped”) T waves (Figure 19–30) in the area of is-chemia (eg, inferior ischemia in II, III, and F; anterior ischemia in V1to V6; lateral ischemia

in I, aVL; anterolateral ischemia in I, aVL, V5, and V6; anteroseptal ischemia in V1, V2, V3,and V4

MI: Refers to myocardial necrosis caused by severe ischemia Can be transmural (ST evation early, T-wave inversion, and Q waves late) or subendocardial (ST depression and T-wave inversion without evidence of Q waves) Table 19–1 outlines the localization of MIs

el-• Acute Injury Phase Hyperacute T waves, then ST-segment elevation Hyperacute T

waves return to normal in minutes to hours ST elevation usually regresses afterhours to days Persistent ST elevation suggests a left ventricular aneurysm

• Evolving Phase Occurs hours to days after an MI Deep T-wave inversion occurs

and then replaces ST-segment elevation, and the T wave may return to normal

• Q Waves Occur hours to days after a transmural MI A Q wave is the initial negative

deflection of the QRS complex A “significant” Q wave is 0.04 s in duration and

>25% the height of the R wave (Figure 19–31) May regress to normal after years

ELECTROLYTE AND DRUG EFFECTS

Electrolytes

Hyperkalemia: Narrow, symmetrical, diffuse, peaked T waves With severe kalemia, PR prolongation occurs, the P wave flattens and is lost, and the QRS widens andcan progress to ventricular fibrillation (Figure 19–32)

hyper-Hypokalemia: ST-segment depression with the appearance of U waves (a positive flection after the T wave) (Figure 19–33)

de-19

FIGURE 19–31 Q waves in leads V1, V2, and V3in a patient with an acute teroseptal transmural myocardial infarction Note the ST elevation in helping to de-termine the acute nature of the infarction

an-TABLE 19–1

Localization of Transmural Myocardial Infarction on ECG

Location Presence of Q Wave or Reciprocal ST

of MI ST-Segment Elevation Depression

Anterior V1to V6(also poor R-waveII, III, aVF

progression in leads V1to V6)*

an-terior leadsPosterior Abnormally tall R and T waves in V1to V3

V1to V3Subendocardial No abnormal Q wave ST-segment

elevation in the anterior, lateral, orinferior leads

*Normally in V1to V6, the R-wave amplitude gradually increases and the S wave creases with a “biphasic” QRS (R = S) in V3or V4 With an anterior MI, there will be aloss of R-wave voltage and the biphasic QRS will appear more laterally in V4to V6, hence

de-the term poor R-wave progression.

Hypercalcemia: Short QT interval

Hypocalcemia: Prolonged QT interval

Drugs

Digitalis Effect: Downsloping ST segment

Digitalis Toxicity

• Arrhythmias PVCs, bigeminy, trigeminy, ventricular tachycardia, ventricular

fibril-lation, PAT, nodal rhythms, and sinus bradycardia

• Conduction Abnormalities First-degree, second-degree, and third-degree heart

MISCELLANEOUS ECG CHANGES

Pericarditis: Diffuse ST elevation concave upward and/or diffuse PR depression and/ordiffuse T-wave inversion (Figure 19–34)

Clinical Correlations Idiopathic, viral infections, as well as other infections, including

bacterial, fungal, and TB, AMI, collagen–vascular diseases, uremia, cancer, Dressler’s drome, and postpericardiotomy syndrome

43

FIGURE 19–34 Acute pericarditis.

FIGURE 19–35 Sinus bradycardia, J-point elevation with ST-segment elevation

and prolonged QT interval (0.56 s) in a patient with hypothermia

Hypothermia: Sinus bradycardia, AV junctional rhythm, or ventricular fibrillation mon Classically, J point (the end of the QRS complex and the beginning of the ST segment)elevated and an intraventricular conduction delay and a prolonged QT interval possible (Fig-ure 19–35)

com-WPW Syndrome: A preexcitation syndrome caused by conduction from the SA node

to the ventricle through an accessory pathway that bypasses the AV node Classically, ashort PR interval occurs along with a delta wave (a delay in the initial deflection of the QRScomplex) Clinically, these patients commonly have tachyarrhythmias, such as atrial fibrilla-tion (Figure 19–36)

19

FIGURE 19–36 Short PR interval and delta waves in leads II, aVF, and V3in a tient with Wolff–Parkinson–White syndrome

pa-TREATMENT OF THE CRITICALLY ILL PATIENT

Patients in the ICU setting typically have multisystem disease or injuries The interactionsbetween different dysfunctional organ systems is complicated and often overwhelming forthe student or junior house officer

This chapter describes a system-by-system approach to dealing with the critically ill tient This approach forces the clinician to focus sequentially on each major organ systemand to evaluate each system’s function and interaction with other organ systems This ap-proach also allows the physician to integrate abnormalities within each system into a strat-egy for treating the patient as a whole A complete but concise daily progress note willdocument this critical evaluation and integration process

pa-ICU PROGRESS NOTE

The ICU progress note is a concise, well-organized means of documenting the events of thepast 24 h The organization of a daily progress note is outlined here The most importantparts of this note are the assessment and the plan Although the collected data can be foundelsewhere in the chart, the physician’s written assessment and interpretation of these dataand events communicate the medical decision-making process to all who read the chart

A simple organizational approach to the daily ICU progress note:

A Outline the patient’s problem list and/or injury summary.

1 Include all active problems, major inactive problems, significant past medical

his-tory

B Outline events and procedures of the past 24 h.

C List current medications.

D Flow sheet data

Central Venous Pressure

Pulmonary Artery Catheters

Determinations of Cardiac Output

Shock States

Clinical Pulmonary Physiology

Mechanical Ventilators Specific Problems in Critically IllPatients

Quick Reference to Critical CareFormulas/ICU FormulasGuidelines for Adult Critical Care DrugInfusions

Copyright 2002 The McGraw-Hill Companies, Inc Click Here for Terms of Use

Sample ICU Progress Note

PROBLEM LIST:

• S/P MVA

• Left pulmonary concussion

• Left hemopneumothorax S/P left chest tube

• Grade 4 splenic injury S/P splenectomy

• Acute renal failure

• ARDS

• Complex past medical history:

Hypertension

Gout

• Allergic: Morphine sulfate

EVENTS OF PAST 24 HOURS:

• Increasing FiO 2and PEEP

8 Infectious disease status

9 Prophylaxis (ie, DVT, ETOH, stress ulcer, etc)

With each of the areas listed in item 9, try to anticipate and avoid complications

G.Outline therapeutic plan for the day.

The following is an example of an ICU progress note that uses this approach It is writtenfor a trauma patient but can easily be modified for any clinical setting

20

(continued)

• HEENT pupil equal and reactive EOM intact

• Neck immobilized

• Cardiovascular: RRR, no increased JVD, 2+ capillary refill, toes warm

• Pulmonary: Coarse BS bilat., decreased on left Chest tube in place

• Gastrointestinal: Midline incision healing well, soft, nondistended, no

guarding, + bowel sounds

• Extremities: Warm well perfused

ASSESSMENT:

• Neurologic: Stable, continue sedation while on ventilator.

• Cardiovascular: Continues to require intermittent fluid challenge to

main-tain BP, this may be the cause of acute renal failure Will continue fluids

and may add dopamine to improve CO

• Pulmonary: Worsening FiO 2and PEEP requirements overnight, likely ARDScomplicated by pulmonary contusion Will obtain CXR this AMand wean

FiO 2and increase PEEP as tolerated by BP and CO

• Gastrointestinal: S/P splenectomy, ileus continues, will place feeding tube

today

• Renal: Acute renal failure continues Will proceed with renal ultrasound to

R/O postrenal cause

• Hematologic: S/P splenectomy HCT stable, will give postsplenectomy

Under-Inspection

Inspection of the cardiovascular system is divided into three main areas:

Jugular Venous Distention

• Daily examination of the patient in the ICU should include examination of neckveins to look for JVD A patient sitting at a 45-degree angle who has distended neck

• Bruising of the anterior chest wall is commonly associated with blunt trauma from asteering wheel Such an injury pattern should alert the physician to the possibility of

a myocardial contusion Treatment of this condition consists of continuous ECGmonitoring and vigorous correction of arrhythmias

Extremity Perfusion

• Check all four extremities for distal perfusion, including pulses, color, temperature,and capillary refill

• Pay special attention to the following areas:

Sites distal to long bone fractures or dislocations

Sites distal to indwelling arterial catheters

Blood Pressure

Blood pressure over the short term is considered adequate if renal perfusion is maintained

In a young, previously healthy individual, an adequate BP usually corresponds to a MAP ofgreater than 70 mm Hg

Technical Tip: If the cuff is too small an obese arm will give a systolic BP 10–15 mm Hg

higher than the actual pressure

Systolic Hypertension: A systolic blood pressure >140 mm Hg with a normal diastolicpressure In the acute care setting, systolic hypertension is thought to be secondary to in-creased cardiac output

Systolic hypertension is seen in the following situations:

• Generalized response to stress

• Pain

• Thyrotoxicosis

• Anemia

Diastolic Hypertension: A diastolic pressure >90 mm Hg

Isolated diastolic hypertension is associated with three general disease categories:

• Renal disease

• Endocrine disorders

• Neurologic disorders

Treatment of Hypertension: Hypertension is of concern in the ICU when confronting

a new MI or a vascular anastomosis and especially following carotid artery surgery Ideally,the systolic blood pressure in this instance is maintained above 130 and below 160 A sys-tolic pressure >180 mm Hg usually requires immediate treatment Several drugs are com-monly used to treat acute hypertension in the ICU setting These include nitroprusside(Nipride), hydralazine (Apresoline), labetalol (Normodyne), a beta-blocker, or nitroglycerin.Beta-blockade should be used with Nipride in treating hypertension associated with an

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• Thyrotoxicosis

• Arterial venous fistula

• Aortic insufficiency

Narrow Pulse Pressure: A pulse pressure <25 mm Hg

A narrow pulse pressure is associated with:

Mean Arterial Blood Pressure

MAP is calculated by taking the diastolic pressure plus one third of the pulse pressure MAP

is used to calculate several other hemodynamic variables

Paradoxical Pulse: Paradoxical pulse is a function of the change in intrathoracic sures during inspiration and expiration Normally, systolic blood pressure falls between

pres-6 and 10 mm Hg with inspiration This fall is reflected by a systolic blood pressure thatvaries with respiration If this variation occurs over a range >10 mm Hg, the patient is said

to have a paradoxical pulse (Figure 20–1) For the technique to measure the paradoxicalpulse, see Chapter 13, page 298

Conditions associated with a paradoxical pulse:

de-Systolic Murmurs: Abrupt onset caused by conditions that have clinical significancefor the acutely ill patient:

1 Papillary muscle injury Papillary muscle dysfunction following AMI is characterized

by an apical systolic murmur The injury to the papillary muscle may cause a murmur

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of grade I–II/VI After rupture of the papillary muscle, a sudden pansystolic murmur ofgrade II–IV/VI may appear The diagnosis of papillary muscle rupture can be made ei-ther at cardiac catheterization or by echocardiography.

2 Intraventricular septum rupture May be indicated by the appearance of a loud

sys-tolic murmur of abrupt onset A catastrophic event that may follow MI Usually panied by massive pulmonary edema This situation is an indication for emergencycardiac catheterization

accom-Diastolic Murmurs: The major concern is the appearance of a diastolic murmur in theacutely injured patient is bacterial endocarditis, an entity that is becoming more common inpatients who are treated in ICUs for long periods Foreign bodies, such as central venouslines, hyperalimentation lines, and pulmonary artery catheters, all contribute to the increas-ing incidence of bacterial endocarditis

1 Gallop Defined as three sequential heart sounds in which the first two beats of the

triplet are closer together than the third The result is a sound that resembles the gallop

2 Pericardial friction rub Classically described as the sound of two pieces of leather

rubbing together Frequently high pitched and may be intermittent Common following openheart surgery (in this setting, does not necessarily indicate pathologic changes)

view of cardiovascular physiology may be helpful.

Determinants of Cardiac Output

Cardiac output is determined by heart rate and stroke volume Stroke volume depends on thefollowing:

ven-Starling’s Law: When the myocardial muscle cell is stretched, the developed tension

in-creases to a maximum and then declines as the stretch becomes more extreme (Figure20–2)

Afterload: Defined as the resistance to ventricular ejection Measured clinically by thecalculation of SVR

Contractility: The ability of the heart to alter its contractile force and velocity dent of fiber length In simple terms, it represents the intrinsic strength of the individual

indepen-muscle fiber cells Contractility can be increased by stimulation of beta-receptors in theheart (see below)

Brief Review of the Adrenergic, or Sympathetic

Nervous System

Cardiac output and its determinants (preload, afterload, and contractility) are all influenced

by the adrenergic nervous system The adrenergic system releases catecholamines rine and norepinephrine), which bind to end-organ receptors These adrenergic receptors aredivided into two classes, designated alpha (α) and beta (β), and their actions are summa-rized in Table 20–1

(epineph-20

Alpha-1 Receptors: Adrenergic receptors found primarily in the peripheral arterial tem When stimulated, these receptors cause vasoconstriction and increase BP, SVR, andafterload.

sys-Beta-1 Receptors: Found primarily on the SA node of the heart When activated, thesereceptors stimulate the SA node to increase the heart rate and increase contractility This in-creases CO and BP

Beta-2 Receptors: Found in the peripheral vascular tree as well as in the bronchial wallsmooth muscle Activation causes vasodilation of the peripheral vasculature and bronchodi-latation Hemodynamically, this decreases SVR, BP, and afterload

These adrenergic receptors are important because many of the cardiovascular drugsused in the ICU act through their sympathomimetic properties These drugs usually havespecific receptor affinity (ie, β versus α) and consequently differ in their effects Drugs thatact on alpha-1 receptors, for example, are called “vasopressors” because they cause vaso-constriction Drugs that act on beta-1 receptors are conversely called “inotropes” becausethey increase contractility and heart rate Commonly used sympathomimetics are listed inTable 20–2 A guide to administration of these agents appears in Table 20–10

CENTRAL VENOUS PRESSURE

The CVP catheter is one of two major devices used in cardiovascular instrumentation Theother major device, the pulmonary artery catheter (often called the Swan–Ganz catheter), isconsidered in the next section

The CVP reading reflects the right ventricular filling pressure This filling pressure fines the ability of the right side of the heart to accept and pump blood

de-Method

A 14-gauge intravenous catheter is inserted into the internal jugular or subclavian vein (seeChapter 13) A pressure transducer connected to the monitor provides the recordings Achest x-ray is required to confirm the position of the catheter in the superior vena cava Thezero point for the manometer is usually 5 cm below the sternal notch, in the midaxillary

More important than the actual isolated measurements of CVP are the relative changes thattake place as a patient’s fluid or cardiac status changes Therefore, serial readings are made.The implications of CVP readings are given in Table 20–3

CVP Limitations

• CVP does not reflect total blood volume or left ventricular function

• CVP will be altered by changes in pulmonary artery resistance and compliance ofthe right ventricle

• Use may be limited by changes in intrathoracic pressure, such as those that occurduring positive pressure ventilation or pneumothorax or in the presence of tumors

• CVP may be normal in the face of sepsis or hypovolemia accompanied by mised myocardial function

pulmonale, COPD, sion pneumothorax,cardiac tamponade

ten-Abbreviations: CVP = central venous pressure; CHF = congestive heart failure; COPD =

chronic obstructive pulmonary disease