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CTO Manual of Medicine and Surgery, 4th Edition - Cardiology 2CK
CTO Manual of Medicine and Surgery, 4th Edition - Cardiology 2CK
Cardiology
Coordinators
Antonio Martín Conejero
Miguel Sáez Alegre
Authors
Toni Soriano Colomé
Rafael Salguero Bodes
Alfonso Jurado Román
Roberto Martín Asenjo
David Filgueiras Rama
Javier de Juan Bagudá
Gerard Loughlin Ramírez
Sem Briongos Figuero
Felipe Díez del Hoyo
1
Card i o l ogy 1
Physical
point of maximal impact displaces down and left. LV aneurysms may
cause another ectopic focus (localization of aneurysm).
Examination
Chapter 01 Sometimes this apex beat can be displaced. For example, in hy-
pertrophic obstructive cardiomyopathy, a systolic double point of
maximal impact may be felt. When a systolic retraction of the apex
Some cardiac diseases present characteristic features when observed instead of an apical impulse is detected, constrictive pericarditis or
(Table 1). hypertrophy and RV displacing behind the LV must be suspected.
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A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
dent area (aortic or pulmonary). In mesosystole a mitral valve by a notch or dicrotic notch (palpable at times) caused by the closure of
prolapse might be heard, generally associated with a meso-tele- the aortic valve. With aging and arterial sclerosis, the initial wave tends
systolic murmur. to be more abrupt reaching a higher peak.
• Diastolic sounds. The most typical one is the opening snap in the
mitral valve stenosis. Pericardical knock can be heard in protodia- Pulsus paradoxys consists in a decrease in systolic blood pressure >10
stole in some cases of constrictive pericarditis, or atrial myxoma mmHg during inspiration. This is an magnification of a physiological
‘plop’ in which the tumor hits or occupies the atrioventricular canal. mechanism. During inspiration, pressure decreases inside the thorax
Pericardial friction rub depends on the position of the patient (bet- and increases venous return to the right heart. When the RV is filled
ter heard when the patient is bending forward) and is heard both in in diastole, the septum is displaced against the LV. During systole, since
systole and diastole. the preload is lower, blood pressure cannot reach the same level as dur-
ing espiration.
Click-
murmur
Opening snap
M T A P Pericardical knock M T
Figure 1. Principal sounds in heart auscultation Normal pulse Hypokinetic pulse Parvus et tardus pulse
The wave of normal arterial pulse has a rapid climb (commonly called
Pulsus alternans
primary or percussion wave), with a detectable “anacrotic” notch (max-
imum aortic velocity) reaching a unique well defined rounded peak
(called ”pre-dicrotic” wave), followed by a slower decline, interrupted Figure 2. Abnormalities in arterial pulse
Hypokinetic Hypovolemia, LV failure (AMI, mitral stenosis) Amplitude-diminished heartbeat, possible tachycardia
Dicrotic pulse · Dilated cardiomyopathy in low cardiac output Two peaks: one, systolic and the other, protodiastolic
· Generally associated with alternating pulse
Parvus et tardus Decrease in cardiac output volume (aortic stenosis) · Flat (weak) and prolonged wave
· Reduced differential pressure
Bigeminus Ventricular premature contraction, digitalis intoxication Alternation of normal and extrasystole heartbeats
Paradoxic Cardiac tamponade, respiratory tract obstruction, poor blood More than 10 mmHg drop in systolic pressure during
return (sometimes, in constrictive pericarditis) inspiration
Table 2. Some abnormalities of arterial pulse
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Card i o l ogy 1
In normal resting patients, heart rate (HR) ranges from 60-100 bpm, but
1.4. Jugular Venous Pressure can be lower in athletic young individuals. HR below 60 bpm constitute
bradycardia, and above 100 bpm, tachycardia.
Jugular veins pressure (JVP) is equivalent to the pressure in the right It is necessary to differentiate “p” waves (atrial activation) from QRS
atrium (central venous pressure). Its equivalent in the left side is the complexes (ventricular activation).
pulmonary capilary wedge pressure, measured with the Swan Ganz
catheter. Pressure in the atrium during dyastole is the same as the pres- Specially in young people, a physiological respiratory sinus arrythmia can
sure in the ventricle. appear. It consists on an inspiratory HR increase and an expiratory decrease.
Sometimes, there is a ‘wandering atrial pacemaker’ where the start of the
Hepatojugular reflux (more correctly named abdominojugular reflux) is heart impulse is produced more caudal (closer to the AV node). This is rep-
tested by firmly pressing for 10-15 seconds over the center of the abdo- resented in the ECG with negative or flattened P waves in the inferior leads.
men of the patient breathing normally so that they do not perform a
Valsalva maneuver. In healthy subjects, there is no evident elevation or In normal ECG, the paper moves forward 25 mm/sec. This is why 1 mm
it is mild when compressing, whereas the test is considered to be posi- equals 40 ms. In Figure 4, normal intervals are shown.
tive if JVP visibly elevates during compression, sustained for 10-15 sec-
onds and falls more than 4 cm when pressure is released. This positivity
denotes hypofunction of the right ventricle.
1 mm = 40 ms
Electrocardiogram
Chapter 02
QT
V3
V4R The electrical axis of any wave in ECG relies on the concept of a vector
V3R
which describes the motion in the frontal plane (expressed in degrees)
III 120º V2
II 60º V1 of such depolarization wave. Normal P, QRS and T point towards the
aVF 90º
lower-right quadrant of the heart.
Figure 3. Surface ECG standard leads The normal QRS axis is between -30º and +150º. An axis beyond -30º is
a left -deviated axis (as in left anterior fascicular block [LAFB]), whereas
It is highly recommended to follow a systemic order when analyzing a right heart axis (beyond +150º) is deviated to the right (as in left pos-
electrocardiographic records. terior fascicular block [LPFB]).
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A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
2.1. Main ECG Anomalies QRS right axis deviation appears (> 90º). In precordial leads, the vector
points towards V1 and V2 leads and instead of having a QRS complex
dominantly negative, QRS is dominantly positive with a dominant R
• P wave (better recorded in DII and V1). In RA hypertrophy, P wave pro- wave taller than S wave depth, along with aberrant secondary repolari-
duces a tall, peaked P in its first part (P pulmonale) in DII, increasing its zation (T-wave inversion and ST depression).
first positive component in V1. LA hypertrophy produces changes in the This is the traditional right ventricular hypertrophy or type “A”
second part of the wave, with a wide and uneven P in II (P mitral) and bi- growth. There exists a right ventricular hypertrophy type “C”,
phasic, prevailing the 2.nd negative component in V1. P wave disappears in characteristic of cor pulmonale, in which hypertrophy of the
atrial fibrillation (f waves) or in atrial flutter (F waves or ‘sawtooth waves’). right ventricle outflow tract causes a nondiscernible axis (iso-
P wave can also be inside the QRS complex in intranodal tachycardia or in diphasic complexes in all frontal leads). Acute right ventricular
ventricular tachycardia, being difficult to identify. P wave frequency is not volume overload (i.e. in pulmonary embolism) may cause these
related with QRS in an AV dissociation. alterations and the characteristic “SIQIIITIII” pattern (S in I, Q and
• PR Interval. It is enlarged in AV blocks, being sustained in 1.st degree AV negative T in III).
blocks, with a progressive enlargement in type I 2.nd degree AV blocks LV hypertrophy might deviate the QRS axis more to the left.
(Wenckebach) and variable in AV dissociation (as in complete 3rd degree However, it will produce high voltages in QRS, with aberrancies
AV block). It shortens in ventricular pre-excitation syndromes (Wolff- in repolarization (inversion of T wave and ST depression -espe-
Parkinson-White). PR interval depression is very specific (although in- cially in I, aVL, V5-V6 leads-). There are several ECG criteria to
frequent) of acute pericarditis. determine the existence of LV hypertrophy, although the exis-
• QRS complex. A Broad QRS complex (QRS > 120 ms) shows an ting different measure indexes generally show low sensibility
aberrant ventricular depolarization in which impulses are not but better specificity (Sokolov-Lyons, Cornell). This is why, at
triggered simultaneously in the His-Purkinje system. This occurs present, echocardiography is the first-choice test to prove hy-
when a His bundle branch block is present, when ventricular pre- pertrophy (even though cardiac magnetic resonance may be
excitation is produced by an accessory pathway with anterograde more precise; Figure 6).
conduction, under the influence of type I anti-
arrhythmic drugs which slow down the conduc-
tion, in hyperkalemia or when the impulse has a
ventricular origin (ventricular extrasystole, ven-
tricular tachycardia, infra-Hisian rhythm in com-
plete atrioventricular block, AIVR or pacemaker-
induced ventricular rhythm).
A bundle branch block is considered to be com-
plete if QRS is longer than 120 ms, or incomplete
if its length is less than 120 ms. QRS specific mor-
phology patterns enable differentiation of right
bundle branch block (RBBB) (rSR’ in V1-V2, wide
“s” wave in I and V5-V6) from left bundle branch
block (LBBB) (QRS is mainly negative in V1 as are
rS or QS and RR’ in V5-V6). In bundle branch block
the repolarization sequence is also affected (Figu-
re 5). RBBB appears in nearly 2% of the population
without any underlying heart disease. LBBB is less
frequent as a normal variation (0,1-0,7%) and fur-
ther investigations are required. Occasionally, BBB
are rate-dependent, appearing when a determi-
nate rate is reached and disappearing if the HR is
lower.
Normal q wave, a small physiologic wave appre-
ciated in leads I, II, III, aVF, aVL and V5-V6 indi-
cates depolarization of interventricular septum.
When Q wave is wider than 40 ms and deeper
than 2 mV (or 25% of depth of QRS complex), it
is considered a pathologic Q, which usually indi-
cates transmural infarction located in the area
explored by the lead in which the pathologic Q
wave appears. Sometimes, pathologic Q waves
are appreciated without infarction in hypertro-
phic cardiomyopathy or in Wolff-Parkinson-Whi-
te syndrome.
RV hypertrophy moves the ventricular depolariza-
Figure 5. Left bundle branch block (top) and Right bundle branch block characteristics
tion vector right and front. As a consequence, a in precordial leads
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Card i o l ogy 1
in women and children (child pattern) and in III lead. Generally,
T wave is negative in aVR.
Occasionally, flat T waves are detected, defined as “unspecific
alteration of repolarization”, and they are usually a normal vari-
ant (especially frequent following cardiac surgery), though it is
recommended to rule out subjacent ischemia. Anxiety, physical
exercising (including ergometry), hyperventilation, sustained
tachycardia, postprandial period, orthostatism, acute pancreati-
tis (affecting DII, DIII and aVF), and acute CVA may flatten or even
invert T waves.
• QT Interval. Corrected QT interval shortens in hypercalcemia and,
occasionally, under digoxin treatment, as well as in congenital
short QT syndrome. It is enlarged in hypocalcemia, in hypokalemia
and other endocrine metabolic alterations, and in acute ischemia
because of the use of drugs prolonging QT interval (class IA and III
Figure 6. ECG obtained from a patient suffering biventricular dilated anti-arrhythmic drugs, macrolide and quinolone antibiotics, tricy-
cardiomiopathy. Hypertrophic changes are remarkable as RBBB and clic antidepressants) or in congenital long QT syndrome. Negative
repolarization abnormalities or inverted U wave may indicate underlying ischemia, although it
is not a frequent finding.
Alternating QRS amplitude, generally implies the existence of a sig-
nificant pericardial effusion. A low QRS voltage might also appear in
Arrhythmias
pericardial effusion as in obesity, emphysema, RV arrhythmogenic
dysplasia and in restrictive cardiomyopathy.
• ST segment. Elevated ST to values over 1 mm may indicate trans-
mural lesion current (upwards convex), ventricular aneurysm (if it Chapter 03
persists after acute myocardial infarction [AMI]), pericarditis (dif-
fuse upwards ST elevation), Brugada syndrome (elevation in V1-V3
with negative T and incomplete right bundle branch block) or often,
benign early repolarization (normal variant seen in young people 3.1. Bradycardia
with dominant vagal hypertonia, with slight convex ST elevation and
notching of the J-point. This anomaly has been considered of no Underlying mechanisms in bradyarrhythmias (<60 bpm) may be re-
clinical relevance for a long time, but recently, it has been more fre- lated to many underlying circunstances such as a disturbance in the
quently reported in patients with sudden cardiac death than in the impulse generation system (as in sick sinus syndrome, Figure 7), or to
general population). a disturbance in the impulse conduction system. This forces a pace-
ST depression may also appear during ischemia episodes in stable/ maker slower than sinus pacemakers to set the heart rhythm (the
unstable angina or subendocardial acute myocardial infarction. It more distal the block point the more severe it usually is (Figure 8). In
may also indicate ventricular overload (secondary to hypertrophy, Figure 9, the pacemaker speed of the different conduction systems is
generally in a descending slope), digoxin effect or appear in bundle represented.
branch block.
Figure 7. Lead aVF ECG revealing characteristic signs of sinus dysfunction with significant sinus bradycardia
7
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
60-100 bpm
stimulation in patients with resynchronization usually reaches a nar-
rower fusion QRS than patients’ basal QRS.
Sinoatrial node
15-30 bpm
LAF
Figure 9. Heart conduction system Figure 10. 12-lead ECG from a patient in sustained atrial fibrillation with
VVIR pacemaker implantation stimulating RV apex at 100 bpm
The most frequent reversible cause of bradycardia are drugs which slow
heart conduction. The most frequent irreversible cause is idiopathic de- Chronic right apical pacing is harmful to contractile function in patients
generative fibrosis of the conduction system. with systolic dysfunction. In these cases, biventricular stimulation must
be considered (resynchronization).
Medical treatment usefulness is limited in acute transient manage-
ment; permanent pacemaker implantation is the required solution in Some conduction abnormalties
nonreversible cases (Table 3).
Sinus Node Disfunction
SITUATION INDICATION The etiology of this arrythmia remains unknown in the majority of cases.
It is related with degenerative changes in the elders. Some specific causes
· Biphasic or triphasic block · Only in case of symptoms
are rarer like sinus node ischemia, myocardial infiltrative process, Chagas’
· Sinus dysfunction secondary to bradycardia
disease, systemic diseases (hypothyroidism, advanced liver diseases…) or
· First degree AV block (asthenia, syncope, or repetitive
· Second degree Type I AV block presyncope) some drugs like ß-blockers, calcium antagonists, digoxin… When symp-
· Occasionally, to treat patients toms appear, the most frequent ones are extreme bradycardia related
with “blocker” drugs syncope and, sometimes, exercise intolerance (due to chronotropic in-
competence). Sometimes, sinus node dysfunction is associated with
· Second degree Type II AV block ALWAYS
phases of atrial tachycardia (mostly AF), alternating with bradycardia
· “High degree” AV block
periods. This is known as the tachycardia-bradycardia syndrome (Figure
· Third degree AV block
· Alternating bundle branch 11). Asymptomatic sinus node dysfunction does not require treatment.
block Pacemaker implantation might be considered in symptomatic cases to
relief symptoms. Sometimes atropine can be useful in acute episodes.
Other situations · Carotid sinus hypersensitivity
· Pure cardioinhibitory neurally
mediated syncope
· Ventricular arrhythmias
because of bradycardia
· Cardiac resynchronization
therapy
Ventricular stimulation with pacemaker from the RV apex produces a Figure 11. Detail of the electrocardiographical monitoring of the ending
of an atrial flutter episode. Note the 3,7 seconds pause at the end of it,
QRS similar to that in left bundle branch block (Figure 10). Biventricular
and the start of a sinus node rhythm with atrial extrasystoles
8
Card i o l ogy 1
Atrial-ventricular Disturbances
Response to atropine + -
• High-degree AV block. Two or more P consecutive waves are not con-
ducted to the ventricle, but with a posterior normal conduction pattern. QRS Normal (< 0.12) Wide (> 0.12)
• 3rd degree AV block. It consists on the presence of an AV dissociation.
Prognosis Good Poor
P waves are not conducted to the ventricle and are present with a regu-
lar but independent rythm compared to the QRS (which is also regular). Table 4. Complete AV block
3.2. Tachycardia
Premature Beats
Figure 12. First-degree AV block See Table 6.
Second-degree Failure in the conduction of some impulses Pacemaker Anterior AMI His bundle
block (Mobitz II) (P not followed by QRS)
Third-degree block A-V Dissociation Pacemaker
Table 5. Characteristics and treatment of bradyarrhythmias
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A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
ATRIAL
PREMATURE BEATS
VENTRICULAR
PREMATURE BEATS
Atrial Fibrillation
ECG · Premature P wave · Premature QRS
Atrial fibrillation (AF) is the most common type of arrhythmia after pre-
alterations · Normal QRS · Wide QRS
mature beats and also the most frequent sustained chronic arrhyth-
Subsequent Noncompensatory Compensatory
mia. ECG reveals a disorganized atrial activity without P waves, which
pause (usually)
are replaced with irregular waves of the T-QRS complex (“f” waves, at
Prevalence Present in 60% of adults
350-600 bpm) showing variable and irregular ventricular conduction
Consequences Usually few · Few in the absence of heart (ventricular response; Figure 15).
disease
· Clinical importance,
especially in ischemic heart
disease, if they are frequent,
complex or with R-on-T
phenomenon (in which the
premature beat matches
with the T wave of the
previous QRS beat)
Treatment · Remove excitants · Remove excitants
· β-blockers if · β-blockers if discomfort
discomfort in patients with no heart
· Consider ablation disease
in special cases · Patients with underlying
Figure 15. Atrial fibrillation
heart disease and premature
ventricular beats should be
treated with ß-blockers AF is classified into first episode (first documented AF episode of the pa-
· In some special cases (like tient, regardless of duration), paroxysmal (with spontaneous cardiover-
tachycardiomyopathy induced sion during the first week, usually within first 24-48 hours), persistent (it
by frequent premature beats), does not cardiovert spontaneously within seven days, although it may
radiofrequency ablation can be attempted) or permanent (chronic, it does not cardiovert spontane-
be useful ously nor is it pursued). Just as any other arrhythmia, it is called recur-
Table 6. Types of premature beats rent when there is more than one episode and sustained when it lasts
for more than 30 seconds.
Sinus Tachycardia AF may appear both in people with structural heart disease and in
“healthy” people. Among its causes, the following are found: emotional
It consists on a sinus rhythm with a rate of over 100 bpm, with identical stress, post-surgery, acute alcohol intake, hypoxemia, fever, hypercap-
P waves to the sinus ones (Figure 14). This arrhythmia starts and finishes nia, metabolic or hemodynamic alterations, hyperthyroidism, valvulop-
gradually, and its frequency may be slowed temporarily with vagal ma- athies, hypertensive heart disease, almost any structural heart disease,
neuvers. chronic obstructive pulmonary disease, sleep apnea, constituting a part
of the bradycardia-tachycardia syndrome...
There are multiple causes, since in most cases it is the result of stress,
anxiety, fever, anemia, hypovolemia, hypotension, exercise, thyrotoxicosis, AF may range from asymptomatic to result in hemodynamic intolerance
hypoxemia, heart failure, pulmonary embolism, adrenergic stimulus. Rare with syncope or acute pulmonary edema. Arrhythmia management in-
inappropriate sinus tachycardia, common among female health workers. volves assuming that its presence indicates a steep increase in stroke
does not have a recognizable triggering factor, and may require the use of risks, especially (although not exclusively) caused by the formation of
β-blockers, calcium antagonists or ivabradine. clots in the left atrial appendages. It is thus necessary to assess in all
cases the need for anticoagulant treatment, which will be necessary for
almost every patient with heart disease or underlying prosthetic cardiac
valves, as well as when suggested according to the CHADS-VASc score of
calculated risk (Table 7).
Currently, there are two potential treatment strategies for atrial fibrillation:
• Rate control strategy. It does not aim to restore sinus rhythm but to miti-
gate potential complications which may result from a permanent AF.
• Rhythm control strategy. Aimed at restoring sinus rhythm and sus-
taining it for the longest possible time.
Various clinical trials have shown that neither strategy is better than the
other in terms of mortality, but recent studies have shown that rhythm
control might be beneficial in terms of survival and thromboembolic
Figure 14. 12-lead ECG of patient with sinus tachycardia and no risk reduction. Hence, The strategy will be selected based on patient
structural heart disease characteristics and arrhythmia tolerance.
10
Card i o l ogy 1
CHA2DS2-
ANNUAL
ADJUSTED
Atrial Flutter
FACTOR POINTS
VASC SCORE STROKE RISK
RATE (%) The common typical flutter in an atrial tachycardia caused by a macro-
C (congestive heart failure 1 0 0 reentry around the tricuspid annulus, which cycles at 250-350 bpm (in a
or ventricular dysfunction counter-clockwise direction in the common type, clockwise in the reverse
with EF < 40%) type) and from which atrial depolarization takes place, showing in the
H (hypertension) 1 1 1.3 ECG saw-toothed regular atrial activity (F waves, positive in V1 and nega-
A2 (age > 75) 2 2 2.2 tive in inferior leads) with little mechanical activity (Figures 17 and 18).
D (diabetes mellitus) 1 3 3.2
S2 (prior stroke or TIA or 2 4 4.0
Common flutter is very frequent among patients with COPD or sleep
thromboembolism) apnea. There are atypical flutter circuits around other obstacles, which
V (coronary, aortic or 1 5 6.7 are less frequent (foramen ovale, cava veins, post-surgery scars; Figure
peripheral vascular disease) 19). Ventricular rate is usually half of the atrial one, due to 2:1 conduc-
A (age 65-74) 1 6 9.8 tion (around 150 bpm).
Sc (female gender) 1 7 9.6
The most effective treatment is synchronized electrical cardioversion,
8 6.7 which usually requires low energy. Anti-arrhythmic drugs are very in-
9 15.2 effective, except dibutilide and dofetilide, which shows only moderate
Table 7. Stroke risk calculation in atrial fibrillation according to score efficacy.
system CHA2DS2-VASc • Although stroke risk seems somewhat lower, anticoagulation treat-
ment must be conducted as analogous to AF. AV node “slowers” are
Figure 16 shows general management of a patient with atrial fibrillation. less effective than in AF to control ventricular response.
Atrial fibrillation
Asymptomatic
Heart rate control strategy or minimum symptoms, Symptomatic episode or,
especially when over 65 in general, first episode
in young people
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A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Pulmonary veins
• For recurrence prevention, drugs are also very limited, thus with recur- Upper cava
ring common or reverse flutters, or in a poorly tolerated first episode,
the procedure of choice is radiofrequency ablation of the cavotricuspid
isthmus (part of the reentry circuit), with a success rate of over 90% in
common flutter. In atypical cases, ablation efficacy is lower.
Right
atrium Left
atrium
Mitral ring
Coronary sinus
Tricuspid ring
Lower cava
Common flutter
Common flutter
V1
aVF Figure 19. Common and atypical flutter circuits: atrial layout representing
the placement of atrial macroreentry in common flutter
and atypical flutter because of atriotomy scar
12
Card i o l ogy 1
Tachycardia starts and finishes abruptly, and
may cause palpitations, hypotension, syncope.
It is prevalent among middle-aged women.
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A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Treatment consists in improving the patient’s pulmonary condition (ox- The treatment of acute tachycardia episodes because of AV reentrant
ygenation) and removing, if possible, theophylline and beta-agonists. is similar to AVNRT.
Calcium antagonists or magnesium sulfate may be useful.
Pre-excited Atrial Fibrillation
Pre-excitation Syndromes
When an AF appears with WPW syndrome (or a flutter or other quick
This occurs when there is a congenital atrial tachycardia) and the pathway performs a fast anterograde con-
accessory conductive pathway for elec- duction it is a medical emergency, since an excessively fast conduction
tric communication between atria and through the accessory pathway may result in ventricular fibrillation (VF).
ventricles which, in sinus, causes early Treatment involves electrical cardioversion. If it is well tolerated, electri-
depolarization of ventricles (it pre-ex- cal cardioversion will be performed or anti-arrhythmic drugs from the
cites them), causing a shortened PR, a Ic group or procainamide will be applied. Intravenous administration
“slurred” upstroke to the QRS complex of digoxin, calcium antagonists (and probably amiodarone) is contra-
(the ‘delta wave’, showing the fragment indicated, since by slowing node conduction and/or causing vasodila-
of ventricles depolarized through the ac- tion with increased in sympathetic tone they may facilitate conduction
cessory conductive pathway, and a broad through the accessory pathway and VF.
QRS (Figure 24).
Definitive treatment of accessory pathways is percutaneous cath-
There may be evident pre-excitation (es- eter ablation of the accesory pathway, which is more effective than
pecially the right pathways close to the anti-arrhythmic drugs and has low risk, and is therefore the treatment
sinus node) or be “inapparent” in the of choice for patients with tachycardia episodes. In subjects with as-
ECG (especially in the left pathways fur- ymptomatic pre-excitation, clinical observation is advisable, except
ther from the sinus node). for hazardous-activity professionals (professional drivers, sport play-
ers, etc.) or according to the patient’s wishes, when ablation is recom-
Accessory pathways may be bidirectional, mended.
only retrograde (concealed pathways) or
Figure 24. ECG in Wolff-
only antegrade. Conduction velocity and Parkinson-White syndrome Nonparoxysmal Junctional Tachycardia
refraction vary with each pathway.
It is a very rare type of tachycardia, caused by an increase in automatism
The combination of pre-excitation and paroxysmal tachycardia is called or triggered activity in the AV node. QRS is the same as the patient’s
Wolff-Parkinson-White (WPW) syndrome. It may be related to Ebstein’s basal and there is frequently AV dissociation or VA conduction. It starts
disease (birth defect most frequently related to WPW) and, maybe, with and ends gradually and heart rate varies with maneuvers affecting the
mitral valve prolapse and hypertrophic cardiomyopathy. autonomic nervous system (increased with vagolytic drugs, exercise or
catecholamines and decreased with vagal maneuvers or β-blockers).
There are two types of paroxysmal tachycardia by AV reentry related to Carotid sinus massage may transiently stop tachycardia, but does not
WPW (Figure 25): make it disappear.
14
Card i o l ogy 1
It is characteristic of digitalis toxicity, catecholamines increase, acute Other diseases causing intramyocardial scars (dilated cardiomyopathy,
lower myocardial infarction or myocarditis. Treatment is aimed at the right ventricular dysplasia, Chagas disease, etc.) may likewise present
root cause; electrical cardioversion should not be attempted, especially monomorphic ventricular tachycardia during their clinical course.
if the cause is digitalis toxicity, since it is not effective as far as it is not
caused by reentrant.
Ventricular Tachycardia
Ventricular tachycardia (VT) involves the presence of three or more
consecutive beats originating in the ventricles at over 100 bpm. A
wide QRS tachycardia is shown in the ECG (≥ 0.12 seconds), with AV
dissociation (there can be some retrograde P waves). A wide QRS
tachycardia has a high probability of being a VT, representing 98% of
the tachycardias in patients with underlying heart disease (specially
MI) (Figure 26).
The most frequent etiology of monomorphic VT is reentry through vi- In the acute phase of the acute myocardial infarction, which does not
able tissue channels located inside or on the edges of a prior acute myo- yet have a scar, arrhythmias are the result of myocardial irritability due
cardial infarction scar (Figure 27). to ischemia, i.e., ventricular premature beats, ventricular fibrillation or
accelerated idioventricular rhythm associated with reperfusion.
In the acute phase of the acute myocardial infarction, which does not
yet have a scar, arrhythmias are the result of myocardial irritability due Other diseases causing intramyocardial scars (dilated cardiomyopathy,
to ischemia, i.e., ventricular premature beats, ventricular fibrillation or right ventricular dysplasia, Chagas disease, etc.) may likewise present
accelerated idioventricular rhythm associated with reperfusion. monomorphic ventricular tachycardia during their clinical course.
15
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Figure 29. Torsades de Pointes episode in patient with severe sinus bradycardia, secondary long QT and ventricular premature beat with probable
afterpotentials that start the episode (evolved into VF and required defibrillation)
16
Card i o l ogy 1
Congenital LQTS (less frequent) is a genetic disorder due to mutations 30% of patients present recognizable mutations. Nevertheless,
affecting ion channels, with two classic phenotypical expressions: Ro- up to eight different genes (including calcium and potassium
mano-Ward syndrome (autosomal dominant) and Jervell-Lange-Nielsen channels) have been known to be involved in some cases of this
syndrome (autosomal recessive linked to congenital deafness and due syndrome.
to a potassium channel defect).
These patients present a typical ECG with an incomplete right bun-
Up to 12 genetic types LQTS are reported according to the affected gene dle branch block, a J point above 2 mm and a descending ST seg-
(named from 1 through 12), the first three being the most frequent (Ta- ment (coved-type) with a negative T wave in V1-V3 (this is a diagno-
ble 10). sis ECG, denominated type I). A pharmacologic test can be carried
out on patients with uncertains ECGs, consisting in the intravenous
infusion of flecainide, ajmaline or other sodium inhibiting drugs to
SUBTYPE
MUTATION
T WAVE TRIGGER TREATMENT
force the type I pattern to manifest itself in actually affected pa-
EFFECT tients (Figure 30).
LQTS 1 ↓ Activity K · Exercise β-blocker ± ICD
channels · Stress
· Swimming
LQTS 2 ↓ Activity K · Waking up β-blocker ± ICD
channels · Noises K+ supplements?
17
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
episodes triggered by physical exercise or stress. The bidirectional Sudden Cardiac Death
VT is also common in this syndrome. β-blockers may be useful in
these cases, although they usually require the implantation of an This is defined as a cardiopulmonary arrest occurred within the first
ICD. hour following the onset of symptoms of the disease. It is most fre-
quently caused by an ischemic cardiomyopathy (70-80% of the cases).
Accelerated Idioventricular Rhythm Other important diseases that may cause a sudden death are the di-
lated and hypertrophic cardiomyopathies (this is deemed to be the
The accelerated idioventricular rhythm (AIVR) is a ventricular rhythm most frequent cause of sudden death among competition athletes,
resulting from myocardial irritability with ectopic automaticity. The fre- even though data has been collected in Europe suggesting that right
quency of which usually oscillates between 60 and 120 bpm. It usually ventricular dysplasia can be at least as important as the hypertrophic
occurs in the context of an AMI and is frequently a sign of reperfusion. cardiomyopathy, or more), arrhythmogenic right ventricular cardiomy-
It is usually transitory and only produces major symptoms or hemody- opathy, channelopathies, or WPW syndrome. Figure 32 shows the main
namic alterations under exceptional circumstances, therefore it gen- causes of sudden death.
erally requires no treatment. In cases with hemodynamic instability it
must be treated with atropine.
18
Card i o l ogy 1
The implanted cardioverted defibrillator (ICD) is a very useful tool to prevent is based on the idea that many patients are at risk of suffering symptom-
arrhythmic sudden death. The current indications are detailed in Table 11. atic heart failure which may be prevented or alleviated with adequate
cardiovascular prevention measures. There is also a stage classification
described in Table 12.
CLINICAL STATUS
Secondary Aborted sudden Documented VF or VT because of
prevention death irreversible causes High risk of heart failure. Unidentified structural or
STAGE A
functional anomaly without signs or symptoms
Sustained SMVT with hemodynamic
monomorphic compromise or in patients with Structural heart disease clearly developed as the result of
STAGE B
ventricular ventricular dysfunction (LVEF a heart failure, but without signs or symptoms
tachycardia (SMVT) < 40%) Symptomatic heart failure associated with an underlying
STAGE C
Primary Nonsustained NVT in patients with ischemic structural disease
prevention Ventricular ventricular dysfunction (LVEF Advanced structural heart disease and symptoms of heart
Tachycardia (NVT) < 40%) with induced SMVT or VF STAGE D failure at rest despite receiving the maximum allowed
in the electrophysiology study medical treatment
Systolic heart Consider ICD in patients with EF
Table 12. Stage classification by the American Heart Association/
failure < 35% and functional class II-III
American College of Cardiology
of the NYHA classification despite
an optimal medical treatment
The reference to the nature of the predominant functional disorder
Special Channelopathies · Symptoms (syncope or aborted enables researchers to differentiate between systolic HF and diastol-
cases sudden death) ic HF, even though the current trend is to replace “systolic HF” and
· Congenital long QT where the
“diastolic HF” with “HF with reduced LVEF” (HFrEF) and “HF with a
patient suffers a syncope despite
the use of β-blockers preserved LVEF” (HFpEF). In the last few years, patients who have a
LVEF between this two groups (40-49%) are now defined as HF with
Hypertrophic Several sudden death risk factors mid-range LVEF (HFmrEF). This difference is essential when it comes
cardiomyopathy (see the applicable chapter) to deciding on the appropriate treatment for each patient (Table 13).
Dilated Syncope, sustained VT or aborted
cardiomyopathy sudden death
Table 11. Indications for the implantation of an ICD HF WITH HF WITH
REDUCED LVEF PRESERVED LVEF
Prevalence Greater (descending) Lower (increasing,
especially in the
19
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
4.2. Pathophysiology and hepatic, splanchnic and lower extremities congestion in the right-
sided CHF. If both signs and symptoms appear, we call it biventricular
and Clinical Characteristics CHF (Table 14).
The pathophysiology underlying a heart failure is showed in Figure 33. LEFT-SIDED CHF RIGHT-SIDED CHF
Symptoms due to low cardiac output (anterograde)
Peripheral tissue hypoperfusion Lung hypoperfusion symptoms
Ischemic C., signs (with consequently lower are rare. Arterial hypotension
cardiomyopathies, oxygen and nutrients tissue
etc. supply): oliguria, asthenia,
Hypertrophy weakness, insomnia, memory
apoptosis loss… being able to reach
fibrosis
cardiogenic shock and multiple
Myocardial lesion
organ failure
Activation Symptoms due to tissue congestion (retrograde)
of neurohormonal Lung congestion: dyspnea, Fluid retention symptoms:
Lower O2 inflow systems and inflammation
Increased O2 to tissues paroxysmal nocturnal dyspnea, pitting peripheral edemas,
requirement (anterograde orthopnea, acute pulmonary painful hepatomegaly, ascites,
· Renin-angiotensin
symptoms) aldosterone edema pleural effusion, protein-losing
· Endothelin enteropathy, oliguria
· ADH
Physical exam
Increased · Sympathetic system
postload Lung crackles, wheezes (cardiac Jugular vein distention,
asthma), pink frothy sputum, hepatojugular reflux,
S3 gallop, S4, pulsus alternans, hepatomegaly, elevated central
Perfusion - Natriuretic
pressure Hydrosaline peptides elevated pulmonary capillary venous pressure
retention pressure
Table 14. Clinical features of HF
20
Card i o l ogy 1
4.3. Diagnosis gram, and enables estimation of masses, volumes and LVEF with the
outmost exactitude.
• Blood test. A dilutional hyponatremia is usually a late sign of a heart
HF diagnosis is made based on the presence of typical signs and symp- failure, and is therefore usually associated with a poor prognosis.
toms which will guide the supplementary tests: Anemia and iron deficiency are frequent in advanced stages of the
• ECG can reveal nonspecific alterations or alterations suggesting disease and are also associated with a poor functional capacity and
the etiology of the clinical condition (Q waves demonstrating pre- higher mortality. Increased troponin levels indicate cell necrosis
vious AMI, cavity enlargement, supraventricular arrhythmia such and, therefore, a worsened prognosis.
as atrial fibrillation, bundle branch blocks, ventricular arrhythmias,
etc.). Brain natriuretic peptide (BNP) can be used for diagnostic and prog-
• Chest x-ray (Rx) can show cardiomegaly and signs of pulmonary nostic purposes. Natriuretic peptides are released as the result of an
venous hypertension, such as vascular redistribution, signs of a increase in ventricular dyastolic pressure. These peptides increase so-
peribronchial, perivascular and alveolar edema, a pleural or inter- dium and water excretion (by inhibiting its reabsorption in the proximal
cisural effusion. In accute pulmonary edema, a butterfly-shaped tube), and also produce arteriolar and venous vasodilation (countering
diffuse perihiliar bilateral pattern of alveolar infiltrate appears the effects of angiotensin II, vasopressin and sympathetic stimulation),
(Figure 35). therefore lowering peripheral vascular resistance.
21
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Treatment of HF With Reduced LVEF rates in patients with HFrEF (preventing both sudden death and the
death resulting from the progression of the HF). Drugs on which
Therapeutic measures which have shown to have an impact in mortality conclusive data has been obtained are carvedilol, metoprolol, biso-
are ACE inhibitors and ARBs, beta-blockers, MRAs, sacubitril/valsartan, prolol and nebivolol.
hydralazine + nitrates, ivabradine, implantable defibrillator and RCT. • Treatment must be initiated with low doses which are to be in-
Treatment of HFrEF is summarized in Figure 36. creased slowly since, given that these are negative inotropic drugs,
they can initially worsen HF. Their use is admitted for all of the func-
Angiotensin-converting enzyme (ACE) inhibitors tional classes reported by the NYHA, provided the patient is eu-
volemic, which can usually be obtained by means of a concomitant
and angiotensin II receptor blockers (ARBs) treatment with diuretics. Patients who are admitted because of an
exacerbation who are chronically treated with beta-blockers should
They reduce mortality, improve functional class and reduce disease pro- not suspend their use except in life threatening situations (acute
gression in asymptomatic patients with LVEF disfunction. pulmonary edema and cardiogenic shock).
• ACE inhibitors are vasodilators, modify myocardial remodeling af- • They are contraindicated in asthma patients, patients with AV blocks
ter AMI and reduce myocardial hypertrophy and vessel fibrosis and and in Prinzmetal’s angina.
hipertrophy. They improve vessel distensibility and suppress coro-
nary vasoconstriction. In the kidney, they reduce efferent arteriole Mineralocorticoid receptor antagonists
vasoconstriction and mesangial proliferation, and improve renal
blood flow. Given that these are mixed vasodilators (arterial and ve- (spironolactone and eplerenone)
nous), they lower preload and afterload, and favor an increased out-
put of the heart. These drugs are contraindicated in bilateral kidney • Spironolactone is a potassium-sparing diuretic, acting in the
artery stenosis and during pregnancy. Their main adverse events distal convoluted and collecting tubules antagonizing the aldo-
are cough, kidney injury, angioedema, and hyperkalemia (specially sterone effect (it secretes sodium and absorbs potassium and
in diabetic patients and when combining with MRAs). protons). Their beneficial effects on patients with HF is not the
• ARBs have not shown to be superior to ACE inhibitors, so these are result of the diuretic effect, but the antagonism of the delete-
reserved to patients developing intolerance to ACE inhibitors (main- rious effects of high aldosterone levels: vascular fibrosis, sym-
ly cough or angioedema). The concomitant use of an ARB, an ACE pathetic tone activation, reduction in arterial distensibility, in-
inhibitor and an MRA is contraindicated. creased sodium in the body… Its use at low doses has shown to
increase survival rate.
Beta-blockers • They should not be prescribed if creatinine values are over 2.5 mg/
dL or potassium levels are above 5,5 mEq/L, due to the high risk of
• Several studies have shown beta-blockers improve LVEF and func- hyperkalemia. This is especially important when associating them
tional class, lower hospitalization rates, and increase the survival with ACE inhibitors and ARBs.
Symptomatic HF
with LVEF<40%
ACEi & BB
Symptomatic No
ICD in primary prevention (LVEF <35 despite OMT)
LVEF≤35%?
Diuretics whether congestion signs/symptoms
Yes
or secondary (symptomatic VT/VF)
MRAs
Symptomatic No
LVEF≤35%?
Yes
Symptomatic
Yes LVEF≤35%? No
HDLZ/NT, No more actions.
digoxine, VAD, HT Reduce diuretic?
Figure 36. Current guidelines HFrEF treatment summary (ACEi: angiotensin-converting enzyme inhibitors; BB: beta-blockers; MRAs: mineralocorticoid
receptor antagonists; ARBs: angiotensin II receptor blockers; CRT: cardiac resynchronization therapy; SR: sinus rhythm; HR: heart rate; OMT: optical medical
treatment; HDLZ/NT: hydralazine + nitrates; ICD: implantable cardioverter-defibrillator; VAD: ventricular assist device; HT: Heart transplant)
22
Card i o l ogy 1
• Eplerenone (a more selective inhibitor to aldosterone) has • In digital intoxication, the earliest symptoms are gastrointestinal,
been shown to increase survival rates in patients who have suf- visual (“xanthopsia” or vision of a yellow halo) and confusion. It
fered an AMI and present a LVEF≤40% and clinical signs of HF or can also induce heart arrhythmias; most frequent ones are ven-
diabetes. In patients with a NYHA functional class ≥II, eplere- tricular premature beats and sinus bradycardia or AV blocks.
none appears to be useful to lower the combined cardiovascular Non-paroxysmal auricular tachycardia with variable AV block, ac-
mortality endpoint or hospital admission as a result of HF exac- celerated nodal rhythm or bidirectional ventricular tachycardia
erbation. Its main advantage as compared to spironolactone is are really specific. ST segment depression is not a sign of digoxin
that it causes a lower gynecomastia rate, even though it is more intoxication.
expensive.
23
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
24
Card i o l ogy 1
Implantable cardioverter-defibrillator (ICD) Cardiac rehabilitation units
It has become a device widely used in patients at high risk of sudden Cardiac rehabilitation units have demonstrated to reduce HF hospital
death, especially for ischemic heart disease. ICD should be indicated admissions and mortality. Regular aerobic exercise improves functional
in: capacity, reduce symptoms and HF hospital admissions.
• Patients with HF who have been resuscitated from cardiac arrest
(secondary prevention) Verapamil and diltiazem are contraindicated in patients with HFrEF.
• Patients that present symptoms (usually syncope or pre-syncope)
related to ventricular arrhythmias (secondary prevention). Treatment of HF With Preserved LVEF
• Patients with LVEF ≤35% and NYHA class II-III despite of optimal
medical treatment (primary prevention). Despite HF with preserved LVEF treatment:
• Patients, regardless of NYHA class, with LVEF ≤30% despite of opti- • Until now, no treatment has demonstrated to reduce morbidity in HF-
mal medical treatment (primary prevention). pEF. Thus, treatment must be directed to reduce symptoms, controlling
BP (vasodialtors), myocardial ischemia, evading tachycardia (BB, digox-
Generally, they should be indicated to patients with a life expectancy >1 in, calcium channel blockers…), favoring sinus rhythm (atrial fibrillation
year (thus, it is not indicated in NYHA class IV). reduces auricular filling phase), and reducing congestion.
• In contrast with HFrEF, the use of verapamil and diltiazem is not con-
Cardiac resyncronization therapy (CRT) traindicated.
• Diuretics and vasodilators must be used carefully, because it is neces-
It aims to improve the mechanical asynchrony which appears in a sary to maintain an adequate preload in order not to reduce cardiac
high percentage of patients with advanced systolic dysfunction re- output.
sponsible for a substantial ventricular contraction inefficiency. This
therapy is based on the use of a pacemaker that stimulates both
ventricles simultaneously, in order to maintain a synergy in the con-
traction of the left ventricle walls, thus obtaining a more effective 4.5. Acute Heart Failure
pumping. This is accomplished by placing one stimulating lead in the
apex of the RV and lead in the lateral or posterolateral epicardium of Treatment
the LV, generally through the coronary venous system. It has shown
to increase survival rate, functional class, exercise tolerance and
quality of life in patients with (patient must accomplish the three Acute Cardiogenic Pulmonary Edema
statements):
• Severe ventricular dysfunction (LVEF below 35%). Cardiogenic pulmonary edema is a medical emergency that requires
• Symptomatic (NYHA class II-IV) despite an adequate medical treat- careful monitoring in order to maintain blood pressure, heart rate
ment. and urine output and, occasionally, the pressure of the pulmonary
• With confirmed asynchrony (QRS wider than 150 ms [especially in vessels by means of a Swan-Ganz catheter. Treatment is to be quickly
case of a left bundle branch block, LBBB]). commenced:
• High-flow oxygen. Noninvasive or invasive mechanical ventilation
Indications for ICD and CRT frequently overlap; therefore, the current could be performed if necessary.
trend is to implant an CRT-ICD (Figure 39). • The patient should be seated, if possible, legs dangling.
• Morphine sulfate improves the symptoms because of vasodilatory
and central sedative effects.
• Potent diuretics should be used, such as furosemide, which also has
a vasodilatory effect.
• Vasodilators should be used when blood pressure is higher than 90
mmHg. Intravenous nitroglicerin is the drug of choice.
• Arterial hypotension may be treated with an intravenous positive
inotropic agent, such as dopamine, dobutamine or levosimendan.
• An intra-aortic balloon pump may be useful in some cases, espe-
cially when blood pressure is low.
Note that the use of sympathetic agonist drugs tends to worsen the
situation if the underlying heart disease is a condition with pure dia-
stolic dysfunction, such as mitral stenosis or hypertrophic obstruc-
tive cardiomyopathy, whether the triggering agent of the acute pul-
monary edema is atrial fibrillation with rapid ventricular response
(a relatively frequent event). Nevertheless, beta blockers or calcium
channel blockers may be useful, as they prolong diastolic time by
slowing conduction through the AV node and have lusotropic ef-
fects. However, an urgent electrical cardioversion is usually indicat-
Figure 39. Cardiac resynchronization therapy device ed in this case.
25
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Severe Myocardial Failure Treatment With these devices, patients may be discharged in order to wait for their
heart transplant at home, or they may serve as therapy for patients not
Intra-aortic Balloon Pump eligible for transplantation. Nonetheless, their long-term use is associ-
ated with a significant risk of complications like bleeding, embolism and
It is an effective percutaneous assisted circulation technique that can be infection (Figure 41).
implanted in conscious patients. A catheter with a balloon is introduced
in the femoral artery and pushed towards the thoracic aorta, placing Another alternative mechanical support for patients with very severe
the balloon immediately distal to the left subclavian artery. cardiac insufficiency is extracorporeal membrane oxygenation (ECMO),
which involves the removal of nonoxygenated blood from the superior
The balloon is inflated during diastole and deflated during systole. vena cava, its oxygenation inside the device and its reinfusion to the
ECG signal and invasive pressure should be monitored in order to inferior vena cava (veno-venous ECMO, respiratory support only) or to
synchronize the inflation and deflation. Correct use of this procedure the arterial territory (veno-arterial ECMO, respiratory and circulatory
results in decreased systolic blood pressure and increased diastolic support).
blood pressure (thus raising mean blood pressure).
26
Card i o l ogy 1
Heart Transplantation There are different anatomopathological transplant rejection de-
grees:
This is a very effective therapy for the treatment of end-stage heart • Hyperacute. It is currently rare, and it consists in a severe endothe-
failure. Results are good, not only regarding survival but also regarding lial lesion due to the presence of preformed antibodies against MHC
lifequality. Most of the patients who undergo a heart transplant are pa- or AB0 systems.
tients with ischemic or idiopatic dilated cardiomyopathy. Most frequent • Acute. It usually occurs after the first week and before the first year,
indications are summarized in Table 16. consisting in a lymphocytic infiltration. The most common immuno-
suppression combination therapy used to prevent this to happen is
Ergospirometry is the best tool to asses functional class and to correlate tacrolimus, mycophenolate and corticosteroids.
prognosis. Guidelines assess a peak O2 value ≤14ml/kg/min as the cutoff
to indicate heart transplantation. Currently, it is preferred not to talk Graft vascular disease seems to be favored by repeated rejection epi-
about contraindications but comorbidities that increase morbimorbid- sodes, CMV infection and hyperlipidemia. Angina is exceptional (donor
ity after transplantation (Table 17). heart is denervated) and might appear as sudden death or as a silent
myocardial infarction.
FACTORS WHICH INCREASE MORBIMORBIDITY Most frequent cancer types are skin and lymphomas (mainly non-Hodg-
AFTER HEART TRANSPLANTATION kin B-type, extranodal, related with EB infection).
A relative age limit for heart transplantation has been stated in 70 years
old. The most used surgical technique is the bicaval one. Cardiomyopathies are a wide group of diseases characterized by a struc-
tural and functional myocardial alteration in the absence of hemody-
Mortality causes vary depending on the moment they occur. Primary namical overload or coronary artery disfunction to justify it. Therefore,
graft failure is the most frequent death cause in the first year after the myocardial affectation in patients with coronary artery disease, valvo-
procedure, particularly in the first month (after the first month infec- pathies or hypertension are not considered as patients with cardiomy-
tions are the main cause). After the first year, vascular graft disease is opathy. Table 18 summarizes the main types of cardiomyopathy and
the main death cause, followed by cancer. its etiology.
27
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
28
Card i o l ogy 1
At an ultrastructural level, in addition to hypertrophy, there is a variable Examination may be normal except for the presence of a fourth sound
degree of fibrosis and disorganization of myocardial histology adopting and, occasionally, a double, prominent apical impulse.
a disarrayed pattern, as well as changes into the intramural coronary
arteries that show wall thickening and facilitate the appearance of myo- In patients with left ventricular outflow tract obstruction a hard systolic
cardial ischemia. murmur is heard, located in the apex and left sternal border, which may
irradiate to the heart’s base but not to the carotids (unlike aortic valve
At macroscopic level, it is common to find significant asymmetric hypertro- murmur).
phy (> 15 mm), which is, in most of the cases, septal. However, there are
other hypertrophy patterns, such as apical hypertrophic cardiomyopathy Likewise, an initially intense, bisferiens pulse is usually present and, if
(Yamaguchi’s disease, frequent in Japan), with giant inverted T-waves in the the obstruction is severe, there is a double inverted splitting of the sec-
precordial lead (Figure 43) or cases of concentric hypertrophy. ond heart sound.
29
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Whatever decreases preload (Valsalva maneuver, sudden standing, ar- An echocardiogram is the most important study to be performed, since
rhythmias) and/or afterload (vasodilators, exercise) or increases con- it assesses the magnitude and distribution of ventricular hypertrophy
tractility (positive inotropes, physical exercise), increases the outflow (normal septum diastolic thickness in adults is lower than 12 mm), the
tract obstructive gradient and the murmur’s intensity. On the other presence of SAM (which enhaces dynamic obstruction), and enables
hand, the murmur’s intensity decreases with increased preload (squat- quantitation of basal outflow tract gradient and after Valsalva-type ma-
ting, raising lower limbs, and volemia expansion) and/or afterload (va- neuvers; a frosted appearance of the ventricular septum is a common
soconstrictors such as phenylephrine, squatting) (Figure 44). feature (Figure 46).
Increases murmur
A
↑ Ventricle contractility ↓ Preload (less volume to send ↓ Afterload RV
(contraction with more strength) with more strength) (less flow resistance) SEPTUM
· Exercise · Valsava
· Sudden standing · Arterial vasodilators
· Isoprenaline · Exercise
· Digital · Tachycardia
· Nitroglycerin
Decreases murmur
RA
Diagnosis
The ECG usually shows certain changes, such as variable degrees of left
ventricular hypertrophy and left atrial growth. Abnormal Q waves in the
left precordial lead are characteristic in the absence of previous myocar-
dial infarction. In apical form, inverted “giant” T waves may be noticed B
in the precordial leads (Figure 45).
SEPTUM
RV
LV
Figure 46. Echocardiographic image in parasternal long axis (A) and short
axis (B) of a patient with asymmetric septal hypertrophic cardiomyopathy,
showing excessive thickness of intraventricular septum (arrows)
30
Card i o l ogy 1
for this mutation. Family members in which that mutation is not found Effective alternatives (in case of contraindications or inefficacy) are di-
do not need further studies, but those in which the mutation is present sopyramide, verapamil or diltiazem. In refractory cases they may even
must undergo a periodic follow-up including an ECG, an echocardiogra- be combined.
phy and a Holter.
Diuretics should be used with caution to avoid excessive preload de-
Cases in which no mutation is found in the index patient should undergo crease which would worsen the obstructive gradient; they are useful for
a periodic follow-up, despite the phenotypical initial appearance. relieving pulmonary congestion.
Treatment general goals are to control symptoms and to prevent sud- and Arrhythmia Management
den death with the implant of an ICD in selected patients. The diagnosis
of this entity contraindicates intense exercise and competition sports. One of the most important assessments to make in these patients is
the risk of having a sudden death, and whether it is indicated or not
Treatment in patients to implant an ICD (only treatment proven to reduce the risk of sudden
death). There is a series of factors which enable to identify patients at
with left ventricle outflow tract obstruction risk (Table 20). Classically, the presence of one or various of these fac-
tors were enough indication to implant an ICD. Currently, scores like
Treatment of symptomatic patients is summarized in Figure 47. HCM-SCD score must be performed. This score takes into consideration
the classical factors, but including others like left atrium size, outflow
tract gradient, age, myocardial thickness, etc. It is considered to be at
high risk patients with a score > 6%, thus ICD implant might be consid-
Symptomatic obstructive ered in patients with a lower score.
hypertrophic cardiomyopathy
Patients that present recurrent ventricular arrhythmias or ICD shocks,
ß-blockers
Verapamil-
Disopyramide
Positive inotropic ß-blockers or amiodarone might be an option to reduce its frequency.
diltiazem agents are
contraindicated
(digoxin)
HIGH RISK FACTORS POTENTIAL RISK MODIFIERS
If still Surgical Alcohol
symptomatic myectomy septal ablation · Aborted sudden death · Obstructive gradient
Of choice If high surgical risk · Spontaneous sustained · Unfavorable genotypes
monomorphic VT (SMVT) · Delayed enhancement
· Premature sudden death event in gadolinium areas
Figure 47. Symptomatic obstructive hypertrophic cardiomyopathy first degree relatives in myocardium as a result
treatment algorithm · Recent syncope of unknown origin of fibrosis
· Septal thickness > 30 mm · Left ventricle apical aneurism
Beta blockers are the treatment of choice due to their capability to · Nonsustained Holter VT
decrease contractility and cause bradycardia (then lengthening dias- (especially among young people)
tole). However, it is not proven that β-blockers lower the risk of sud- · HBP during ergometry
den death, thus their use has not proven benefit in asymptomatic Table 20. Factors related to sudden death risk in hypertrophic
patients. cardiomyopathy
31
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
5.2. Dilated Cardiomyopathy Cardiac magnetic resonance reveals a pattern of predominantly subepi-
cardial fibrosis, unlike infarct, which usually dominates the subendocar-
dium (Figure 49).
Concept and Etiology
The prevalence of this disease is about 1/2,500 individuals. It is defined
by evidence of left ventricular dilation and dysfunction without hemo-
dinamical overload or coronary artery disease, sufficient to cause the
observed overall systolic worsening. Right ventricle deterioration is not
necessary for diagnosis, although this is common in late stages and is
associated with worse prognosis.
5.3. Restrictive
Cardiomyopathy
Epidemiology
Much less frequent than dilated and hypertrophic cardiomyopathy,
restrictive cardiomyopathy is characterized by the presence of a
restrictive physiology for ventricular filling (with small increases in
Figure 48. Apical Four Chamber Echocardiogram view of left ventricle volume there are large increases in intraventricular pressure, due to
dilation and loss of normal ventricular geometry in patient with dilated increased rigidity of ventricular walls) in the absence of significant
cardiomyopathy dilation or abnormal parietal thickening of the ventricles. Therefore,
32
Card i o l ogy 1
it is a disease which affects predominantly the dyastolic heart func- Treatment is for diastolic heart failure and anticoagulation, corticoste-
tion, and only in late stages of the disease sistolic function is com- roids and hydroxyurea or interferon may be added. Surgery may obtain
promised. good results in certain cases with established fibrosis.
It is similar to constrictive pericarditis, with exertion dyspnea, fatigue, When medical treatment of heart failure is unsatisfactory, and in ad-
and predominant systemic venous congestion (hepatomegaly, ascites). vanced cases, surgical resection of fibrous endocardium replacing af-
Atrial fibrillation is very frequent, and up to one-third of patients suffer fected valves is the alternative of choice.
stroke episodes.
Amyloidosis
Diagnosis
It is rare for secondary amyloidosis (systemic amyloidosis [AA]) to af-
Furthermore, physical examination is similar to what may be seen in fect the myocardium, while cardiomyopathy is the most frequent cause
constrictive pericarditis, with increased venous pressure, Kussmaul of death in primary amyloidosis. Here (primary amyloidosis [AL]), the
sign, decreased sound intensity and third or fourth extra sounds. A deep heart is involved in up to 90% of cases. Organs other than the heart are
and quick y descent wave predominates in the jugular venous pulse, an frequently affected. Transthyretin-related (TTR) amyloidosis may cause
increased a wave, of similar width to v, and an x descent wave that can familiar cases of heart amyloidosis.
also be quick, adopting a “W” morphology. Apical impulse is easily felt
in restrictive cardiomyopathy even if it is decreased, which does not oc- Amyloidosis may cause restrictive cardiomyopathy (most frequently),
cur in constrictive pericarditis. dilated cardiomyopathy in advanced stages, in some cases ventricular
hypertrophy (infrequent in other etiologies of restrictive cardiomy-
Echocardiography is key for diagnosis; it helps on assessing the diastolic opathy), atrial or ventricular arrhythmias, conduction disorders or or-
function and its compromise. Sometimes, a slight symmetrical ventricu- thostatic hypotension. Sudden death is not exceptional. This disorder
lar wall thickening can be seen. Systolic function is usually normal. Bi- shows a preference for right cavities, at least in early stages. Pericardial
auricular dilation is really specific, due to the ventricular filling impair- effusion is very frequent.
ment.
A characteristic echocardiographic feature is a shiny “speckled” appear-
Cardiac biopsy, CT and MRI are really useful techniques for the differen- ance of the myocardium with thickening of intraventricular septum.
tial diagnosis with constrictive pericarditis, and also permit the detailed
analysis of the pericardium and tissue characterization. Treatment for plasma cell dyscrasias may be effective on patients
during initial stages of the disease, although the general prognosis is
Treatment bleak.
33
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
region known as “triangle of dysplasia” (i.e., right ventricular outflow version and/or anti-arrthymic drugs if they are well tolerated or
tract, apex, and inflow tract), although it may extend to the rest of the recurrent. Beta blockers, sotalol and amiodarone are effective for
right ventricle and even to the left ventricle (50% of the cases). prevention.
The clinical effect is the formation of intramyocardial reentrant cir- Tachycardia reentrant circuit catheter ablation involves a limitation,
cuits in the fibrofatty replacement area which facilitates the devel- since the potential circuits are multiple and progressive, and therefore
opment of sustained monomorphic ventricular tachycardia, typically recurrence avoidance cannot be guaranteed. ICD is prescribed for sud-
during exertion, even before developing morphologic abnormalities den death survivors and high risk individuals (such as those showing
that may be detected. impaired left ventricle and those with ventricular tachycardia, especially
if it is recurrent in spite of anti-arrhythmic drug therapy and/or catheter
This makes cardiomyopathy the main cause of sudden death in ablation).
sportspersons of certain European regions. In advanced stages, right
ventricle impairment progress towards severe right-sided heart fail- Treatment of right-sided heart failure (diuretics, water deprivation) is
ure; when both ventricles are affected it may mimic a dilated cardio- applied in advanced cases.
myopathy.
Incipient cases frequently pose a challenge, even more when its clinical
debut is an episode of sudden death.
• Magnetic resonance is the most sensitive imaging study to de-
tect structural abnormalities (aneurysms, dyskinetic and akinetic
segments in the right ventricle wall and cavity dilation) and intra-
myocardial fibrosis (with late gadolinium-enhanced technique).
Echocardiography and ventriculography with contrast are also
useful.
• Endomyocardial biopsy, which is not usually necessary, confirms fi-
brofatty degeneration. However, the segmented nature of the dis-
ease may result in false negatives.
• An ECG is very useful even though it may be normal or near normal
during initial stages.
The most frequent anomaly is the presence of inverted T-waves in
right precordial leads (V1-V3) in people over 14 years of age (prior
to this, they may be normal) in the absence of right bundle branch
block.
The most specific abnormality is the presence of epsilon waves in
V1-V3 (signs of low voltage in the final part of QRS, which is usua-
lly slightly widened, a reflection of late activity of involved regions)
(Figure 50). Figure 50. 12-derivation ECG of a patient with right ventricle dysplasia,
• A documented ventricular tachycardia episode with left bundle where ε waves (epsilon) (arrows) and inverted t waves may be noted in
branch block morfology (since it starts in the right ventricle) and right precordials V1-V4
upper axis strongly supports its diagnosis.
• First-degree family confirmed history of disease, verified presence
of one of the mutations responsible or even a sudden death family Spongiform Cardiomyopathy
event attributable to this disease also strongly support this diag-
nosis.
(noncompacted myocardial)
Treatment is basically symptomatic. Sustained monomorphic ven- There is a developmental defect in the growth of left ventricle myocar-
tricular tachycardia episodes are treated with electrical cardio- dial wall sinusoids, which is therefore highly trabeculated and with large
34
Card i o l ogy 1
Coronary Artery
intertrabecular recesses, resulting in a ventricular wall with spongy ap-
pearance. Patients may progress towards dilated forms, and the first
episodes may be strokes or arrhythmia.
Chapter 06
Disease
Tako-tsubo Cardiomyopathy
(dyskinesia or transient apical 6.1. Concepts
“ballooning”)
Myocardial blood supply comes from two coronary arteries which
come from the aorta (Figure 52 shows a diagram of the coronary
Initially reported in Japan, it usually affects postmenopausal women fol- anatomy).
lowing an emotionally or physical stressful situation (death of a relative,
medical procedures), and causes chest pain and electrical changes (ST-
segment transient elevation followed by deep, diffuse T-wave inversion)
similar to an acute myocardial infarction but in the absence of coronary
disease, together with mid-ventricular systolic and/or apical dysfunc-
Aorta Left main coronary
tion, disproportionate to the slightly increased cardiac enzymes reflect- artery
ing myocardial injury and over a surface greater than a single blood ves- Circumflex artery
sel (Figure 51). Right coronary
artery
Although its origin is unknown, it has been related to surges in sympa- Left anterior
thetic activity (stress cardiomyopathy) and usually returns to normality descending
artery
within the first two months. Treatment is empiric and customized, usu-
ally administering the treatment for an acute coronary syndrome with
ventricular dysfunction (beta blockers, ACE inhibitors). Prognosis is usu-
ally favorable and recurrences are rare.
Sinoatrial node
55% 45%
AV Node
90% 10%
35
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
36
Card i o l ogy 1
ͳ Comorbidities. Certain diseases presence is associated with an
increased cardiovascular disease risk: chronic kidney injury, auto-
immune diseases, cancer (treated with chemotherapy or radio- LDL Endothelium
Oxidized LDL
therapy), OSAHS, periodontal diseases and erectile disfunction.
Macrophage
ͳ Metabolic syndrome. It is defined as an association of central Monocyte
obesity and two of these:
ͧ Triglycerides >150 mg/dl. Foam
cells
ͧ HDL <1 mmol/l in male or < 1.3 mmol/l in female.
ͧ SBP >130 mmHg or DBP >85 mmHg.
ͧ Blood glucose >100 mg/dl or previously diagnosed type 2 diabetes.
Smooth muscle
ͳ Peripheral arterial disease. Cytokines proliferation
ͳ Hypercoagulability syndromes (hyperfibrinogenemia, hyper-
homocysteinemia…).
ͳ Estrogens. Medium layer Migration of smooth
ͳ Alcohol. Alcohol intake has a “J” effect. Reduced consumption muscle cells
This generates the atheroma plaque, with a lipid core -formed by LDL
cholesterol esters- which is sometimes even crystalized, surrounded Generally, the risk of a plaque presenting a complication increases in
by inflammatory cells, smooth muscle and collagen in different pro- proportion to the size of the plaque, even though possible complica-
portions, with the presence of vulnerable plaques (high contents of tions also depend on other factors.
lipids and inflammatory cells) and stable plaques (high fiber contents;
Figure 53). Nevertheless, given that the number of small plaques is much greater
than the number of large plaques, the small but vulnerable plaques are
Ruptures in the vulnerable plaques exposes subendotelial material the ones that generally cause, in absolute terms, acute coronary syn-
to bloodstream and activates platelets, which attach and aggregate dromes (Figure 55).
themselves, and set in motion the coagulation cascade, thus pro-
ducing thrombosis of the atheroma plaque which triggers the acute As an approximation, when a plaque occludes 70% of the arterial lu-
coronary syndromes (ACS), so that, if the occlusion is complete, it pro- men, it produces an ischemia triggered by physical exertion, cold or
duces an ACS with a persistent ST segment elevation in the ECG (which emotional stress, but not at rest. When the stenosis exceeds a value
causes a transmural infarction), and if the occlusion is subocclusive, it of 80% to 90% (serious or “severe”), it can produce an ischemia at
originates an ACS without ST segment elevation (with different vari- rest. Generally, a stenosis is considered angiographically significant
ables ranging from the subendocardial infarction to the unstable an- whether it occludes >70% of the arterial lumen (>50% in the left
gina; Figure 54). main coronary artery).
37
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Figure 55. Plaque complication risks depending on the luminal stenosis Clinical History
caused by plaque growth
Angina is the clinical translation of a transitory myocardial ischemia,
most frequently caused by coronary atherosclerosis. The typical patient
Myocardial Function Alteration is a male over 50 years old, with cardiovascular risk factors present-
ing, following physical exertion of a given intensity or an episode of
First, the diastolic function of the heart is involved as it is more sen- emotional stress, a retrosternal oppression which commences gradu-
sible to ischemia; later on, heart contractility is affected (systolic func- ally and disappears progressively with rest or sublingual nitroglycerine.
tion). If ischemia affects the papillary muscles, mitral regurgitation Episodes generally last less than 10 minutes. When only two of these
might occur. three characteristics are present, the event is said to be an (probable)
atypical angina.
The effects of ischemia in the myocardial tissue are summarized in Figure
56, and depend on the duration and intensity of the ischemia, among This oppression or heavy feeling can be irradiated to other zones (upper
other factors (collateral circulation presence, etc.). limbs up to the fingers, precordium, jaws or teeth, torso, etc.) and be
accompanied by other symptoms such as dyspnea or a persistent veg-
etative state (cold sweats, anxiety, nausea, asthenia, imminent death
Perfusion sensation, etc.).
(with profusion) Nonrecoverable
The most characteristic element of the stable angina is that its clinical
signs always appear, in all patients, after a similarly intense effort. The
Healthy Stunned Hibernating
myocardium myocardium myocardium Necrosis classification created by the Canadian Cardiovascular Society (CCS) is
Exercise used to establish such effort levels (Table 24).
(dobutamine,
Acute ischemia Chronic ischemia
dipyridamole)
Sometimes, the angina follows a circadian pattern in which the effort
SPECT threshold is lower in the mornings, the postprandial period or with cold.
Gammagraphy
(Tc, TI) No defects Reversible defects Irreversible defects Women are more likely to present atypical symptoms.
Stress echo
Rest When a patient with stable angina shows symptoms at rest or for pro-
longed periods of time (up to 20 minutes), or more intense symptoms
with progressively lower efforts throughout a four-week period, the
angina is said to have “destabilized” and is known as an “unstable an-
Figure 56. Effects of myocardial ischemia gina”.
They are classified into: An angina which, having commenced recently (two months after the
• Non-viable myocardium. Necrosis. It is produced by a complete initial event) imposes a marked limitation on the patient’s habitual ac-
occlusion of enough duration and without collateral circulation flow. tivities is also deemed unstable (Table 25).
38
Card i o l ogy 1
The pain is sudden, persistent and Angina only ocurring during strenuous efforts. Does not limit
I
especially intense (transfixing, tear) from ordinary lifestyle
the very beginning. It migrates to the
AORTIC DISSECTION zones to which the dissection expands. Slight limitation of physical activity. Angina appears when
Asymmetric reduction of arterial beats. walking fast or climbing stairs or steep roads.
II
Aortic regurgitation murmur. Mediastinal Patients can walk more than one or two blocks or climb one
widening in chest x-rays flight of stairs
The nature and location of the pain may be Strong limitation of physical activity. Angina appears after
III
similar to that of the coronary, but this one walking one or two blocks or climbing one flight of stairs
is prolonged, usually pleuritic, and changes Inability to perform any activity without angina. This
with the patients’ posture (it is alleviated by IV
ACUTE PERICARDITIS symptom can appear while at rest
flexing the trunk). Pericardial rub. Concave
and diffuse elevation of the ST segment. It Table 24. Angina clinical severity. Classification by the Canadian
can be alleviated with anti-inflammatories Cardiovascular Society
and not with nitroglycerin
Exercise angina. Exercise syncope.
AORTIC STENOSIS Dyspnea. Aortic systolic murmur Angina starting at rest. It usually persists for a
ANGINA AT REST
irradiated to carotid prolonged period of time (> 20 minutes)
Usually atypical pain, with variable duration
ANGINA OF Recently commenced angina ( > 2 months)
and no clear triggering factors, which cannot
MITRAL PROLAPSE RECENT ONSET reaching at least Class III on the CCS classification
be alleviated with nitroglycerin. Auscultation of
a mid-systolic or end-systolic click
In the previous four weeks, increase in the
It is originated by a right ventricular
ACCELERATED number, intensity, duration or reduction of the
ischemia. It may be very similar to
PULMONARY ANGINA threshold of onset in a patient suffering from
an angina and is connected to acute
HYPERTENSION stable stress angina
pulmonary embolism or chronic
pulmonary hypertension events
POST-INFARCTION Angina manifesting itself in the first few days
Epigastric and retrosternal pain. Usually ANGINA following a myocardial infarction
connected with the intake of food, especially
ESOPHAGEAL SPASM when these are very hot or very cold. Like Table 25. Classification of unstable angina
angina, it can be alleviated with nitroglycerin.
It can cause dysphagia The general treatment of a patient with stable angina is shown in
Burning epigastric and retrosternal pain Figure 57.
GASTROESOPHAGEAL especially when lying down after meals.
REFLUX Presence of acidity in the mouth. Quickly
alleviated with alkaline substances
Epigastric pain. It is worsened by fasting and
Diagnosis
PEPTIC ULCER alleviated by ingesting foods and taking
antacids
The diagnosis of chest angina is based on the patient’s medical history,
with its logic and limited sensitivity, and is complemented with addi-
It is localized to the right hypochondrium,
tional tests, such as a baseline ECG and an ergometry.
although it can be irradiated to the
right hemithorax and epigastrium. It is a
BILIARY DISEASE With current treatment, the prognosis of patients with stable angina is
prolonged pain with colic characteristics
(it “comes and goes”), and responds to usually favorable. The historic annual mortality rate has been estimated
analgesics-antispasmodic medication to be 2% to 3%, even though recent studies show it to be lower (not
Intense epigastric pain irradiated towards the exceeding an annual 1%).
PANCREATITIS back as a belt. It decreases when the patient
bends forward There are two ways to detect ischemia; exercise stress testing (assessing
Pain in the surface of the thoracic wall repolarization alterations during physical exercise) and imaging tech-
OSTEOMUSCULAR
PAIN
reproduced with mechanical palpation and niques (stress echocardiography or nuclear cardiology).
exacerbated when moving or coughing
Dull and persistent precordial pain with Stress testing
acute pain crisis lasting a couple of
seconds. It is triggered by anxiety and It is the most accessible and widely used coronary ischemia detection
family, economic and self-esteem troubles. test. It produces myocardial ischemia, increasing oxygen demand (due
It is in no way connected to physical
to exercise), testing clinical (symptoms onset), blood pressure and ECG
PSYCHOGENIC PAIN exertion. It usually causes dyspnea,
hyperventilation, palpitations, sighs, changes.
paresthesia, and general weakness. It can
be alleviated by very different means: Ergometries are deemed electrocardiographically positive when the ST
rest, exercise, tranquilizers, analgesics or segment displaces at least 1 mm measured at 80 ms from the “J” point
placebo (end of the QRS complex). Extension, magnitude and duration of ECG
Table 23. Differential diagnosis of chest pain changes are related with prognosis (Figure 58).
39
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Suspected angina
Anamnesis
Physical exploration
ECG at rest
Unstable angina Alternative diagnosis
Lab tests
Chest XR, if applicable
ACS management Confirm and treat
Risk stratification:
· Echocardiography: LVEF,
segmental contractility
· Ischemia detection tests: ergometry,
imaging ischemia detection
Early positivity in the first stage or prolonged duration (more than five
to six minutes) of ST segment depression upon exercise completion
40
Card i o l ogy 1
Imaging Treatment
Imaging techniques to detect ischemia are indicated in these situa- Medical treatment
tions:
• Baseline ECG alterations which contraindicate stress test. Angina medical treatment includes (Table 28):
• Non conclusive stress test • Antiaggregant therapy. Aspirin, in 75-150mg daily doses has prov-
• Need to further assess location, myocardial viability… en to reduce the incidence of acute events in patients with stable
angina. Clopidogrel should be used in patients with aspirin intoler-
Ischemia induction can be performed both with physical exertion and ance.
with drugs. The most physiological way and the one providing the most • Statins. Reduce infarct risk and mortality, even in patients with nor-
information is physical exertion. If the patient cannot make enough ef- mal cholesterol blood levels, therefore statins should be prescribed
fort, pharmacological stress test might be performed with either dobu- to every patient at a high dose.
tamine, dipyridamole or adenosine. • ACE inhibitors. Should be prescribed in patient with stable an-
gina who also present diabetes, hypertension, HF, LVEF asymp-
After ischemia induction, stress echocardiography, nuclear imaging tomatic disfunction or in patients with family history of AMI.
techniques or MRI can be used to detect it. These tests are more sensi- Although not accomplishing all these statements some authors
tive and specific than conventional exercise stress testing. recommend its use in all patients with confirmed coronary artery
disease.
Coronary angiography • ß-blockers. Have shown to increase survival rate in patients with
angina and history of AMI or HF. In the absence on these two,
The objective of this test is to assess coronary arteries anatomy by in- they do not improve prognosis but prevent angina episodes, thus
troducing contrast through them. It is the gold standard when estimat- although contraindicated beta blockers are the antianginals of
ing anatomical severity degree in coronary artery disease, allowing to choice.
take therapeutic decisions. • Calcium channel blockers. Verapamil and diltiazem mainly have a
cardioinhibitory effect, so their use with betablockers should be re-
Although being an invasive procedure, complications’ risk is low. In- stricted. On the other hand, dihydropyridines produce vasodilation
dications are listed in Table 27 (briefly, every patient with limiting with nearly no effect on cardiac contractibility, and therefore can be
symptoms despite optimal medical therapy and patients with un- used combined with betablockers. Calcium channel blockers are the
favorable prognosis). A lesion is considered to be angiographically treatment of choice in Prinzmetal’s angina.
significant when the stenosis is >70% (or >50% in the left main coro- • Nitrates. These should be used only in the case of beta-blockers in-
nary artery). efficiency or associated to them to alleviate angina symptoms.
• Ivabradine. It has been approved for the symptomatic treatment
of stable angina in patients in sinus rhythm >70bpm, especially if HF
CORONARY ANGIOGRAPHY or LVEF disfunction or in patients with beta-blockers intolerance or
1. Stable angina with low exercise workload despite medical treatment contraindications. Despite beta-blockers and calcium channel block-
or poor prognosis data in diagnostic tests ers, ivabradine does not modify heart contractility or blood pres-
sure.
2. In the non ST-segment elevation ACS in medium or high risk cases,
• Ranolazine. Sodium channel blockers. Based on its antianginal
and, where positive results are obtained, in ischemia detection tests
in low risk cases effect and increasement in cardiac functional capacity, rano-
lazine is indicated as symptomatic treatment of stable angina
3. In the context of AMI when first line treatment fails or in patients with beta-blockers
- Primary PTCA intolerance.
- Failed thrombolysis
- Successful thrombolysis (first 24h)
Table 27. General guidelines for a coronarography Table 28. Treatment of stable angina
41
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Pre-PTCA
coronarography
Figure 60. Myocardial revascularization with internal mammary artery
graft and aortocoronary saphenous vein graft
Plaque
CORONARY ANATOMY PREFERRED TECHNIQUE
1 or 2 vessel disease non affecting PCI
Balloon catheter proximal LAD
2 vessel disease affecting proximal LAD PCI or surgery
Left main disease Surgery (or PCI*)
Diabetes with multivessel disease Surgery (or PCI*)
Guide
3 vessel disease Surgery (or PCI*)
Inflated
balloom Bypass stenosis PCI
* Selected patients
Stent
Prinzmetal Angina
and Cardiac Syndrome X
Post-PTCA
coronarography The pathophysiology of Prinzmetal -or variant angina is coronary
spasm. The episodes usually occur at rest and preferably at night, and
cause elevation of the ST segment. The recommended treatment is the
Figure 59. Percutaneous transluminal coronary angioplasty use of calcium antagonists and nitrates. The intracoronary infusion of
42
Card i o l ogy 1
acetylcholine or ergonovine enables physicians to induce spasms and The incidence of NSTE-ACS is somewhat greater than that of the
confirm the diagnosis. STE-ACS. The hospital mortality rates of this second case are higher
(7%) than those of NSTEACS (5%), but after a few months mortality
Cardiac syndrome X (demonstrable angina and ischemia in detect on tests rates become equal for both cases (around 12% after six months)
with normal epicardial coronary arteries) is usually the result of a dysfunct and even seem to be higher in the case of NSTE-ACS in the long term,
on of the microvascular endothelium in patients with multiple cardiovascu- probably because this condition usually affects older patients with
lar risk factors. higher comorbidity levels (diabetes, renal failure, among others) and
a longer history of coronary disease. Therefore, recurrent reinfarc-
tion and ischemia rates are higher in patients suffering NSTE-ACS.
The general steps in case of an NEST-ACS are shown in Figure 62.
Acute Coronary Current recommendations suggest that the risk should be assessed
(hospital and long-term mortality) using one of the available scales
Syndrome
Chapter 07 (GRACE, TIMI, PURSUIT, etc.), which collect clinical variables with
prognosis implications (age, heart rate, blood pressure, Killip class,
diabetes, and coronary history), electrocardiographic, biochemi-
cal and imaging findings (mentioned above). The prognosis fac-
tors shown in cases of stable angina are also useful in this con-
7.1. Acute Coronary Syndrome text. These enable the patient to be placed in the low, medium
or high risk groups, and the treatment to be adjusted accordingly
Without ST Segment Elevation (Table 30).
Most ACS presents a common pathophysiology, a rupture or erosion · At-rest or prolonged angina
phenomenon followed by thrombosis in an atheroma plaque, together · Hemodynamic alterations (heart
failure, mitral insufficiency, peripheral
with coronary spasms and distal embolization of thrombus fragments. CLINICAL
hypoperfusion)
· Old age (> 75 years)
The degree of occlusion of the vessel lumen determines whether · Diabetes mellitus
there will be an acute coronary syndrome with a persistent rise/el-
evation (> 20 min) of the ST segment (STE-ACS, usually a complete Changes in the ST segment or profound T
ELECTROCARDIOGRAPHIC
occlusion and evolving towards a transmural infarction) or an acute wave inversion in all precordial leads
coronary syndrome without a persistent rise/elevation of the ST seg- · Ventricular dysfunction
ECHOCARDIOGRAPHY
ment (NSTE-ACS, usually subtotal or intermittent total occlusion be- · Extended contraction abnormalities
cause of distal embolization of thrombus fragments rich in plaques,
· Assessment of markers:
including unstable angina). The distal embolization of small thrombus
- Necrosis (T or I troponins, CPK-MB)
fragments is suspected to determine the presence of isolated sites of - Inflammation (C-reactive protein)
necrosis surrounded by myocardial inflammation zones causing the LAB TESTS - Neurohumoral activation (NT-pro-
increase in troponins (Figure 61). BNP, BNP)
· Renal impaired renal function
· Previous bypass surgery
OTHERS · PTCA over the last months
· Post-infarction angina
Table 30. High-risk criteria in patients with unstable angina
43
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Suspected NSTE-ACS
· Anamnesis
· Physical exploration
STE-ACS Alternative diagnosis
· ECG at rest (< 10 min) include V3R, V4R, V7-V9
· Lab test: troponin, CPK-MB, hemoglobin, leukocytes, creatinine
If:
· ASA + clopidogrel or ticagrelor if moderate-high risk · Refractory angina
· Anticoagulation · Recurrent angina with generalized ST or T wave changes
· Statin (precocious) · Heart failure
· Antianginals: -blockers (of choice) + nitroglycerine, others · Hemodynamic instability
· ACE inhibitor/ARA (in most cases) · Serious arrhythmias
Medical treatment and...
· No recurrence
· No heart failure Coronarography Urgent
· No changes in the ECG < 24-48 h coronarography
· No increased troponins
Upon discharge:
_ · Changes in lifestyle
+
· Medical treatment
· CVRF control
44
Card i o l ogy 1
Sometimes, this pain is not present or is atypical (patients with diabe- tricle AMI (V3R and V4R) or posterior wall (V7, V8 and V9), mainly in
tes, the elderly or women). It is frequently accompanied by vegetative patients with inferior AMI associated with those two subtypes.
symptoms (cold sweating, nausea, vomiting, anxiety and a feeling of
imminent death). It also appears at rest (sometimes, during or after ex- Changes may affect the following:
ercising); it is more frequent early in the morning (due to sympathetic • T wave (myocardial ischemic image):
activation and changes in circadian coagulation and platelet activity). ͳ Positive-peaked or isoelectric T: subendocardial ischemia.
Prior angina frequently occurs. ͳ Negative T: subendocardial or transmural ischemia.
Other forms include dyspnea, weakness, arrhythmias, systemic em- • ST segment (myocardial injury current; Figure 64).
bolism, hypotension, or any of the AMI complications when the initial ͳ Descended ST: subendocardial injury.
episode has gone undetected. It must be mentioned that the highest ͳ Elevated ST: subendocardial injury.
myocardial infarction mortality occurs during the first two hours after
appearance of symptoms, and ventricular fibrillation is the most com-
mon etiology.
Killip classification (Table 31) on arrival refers to the degree of hemo- Subendocardial ischemia Transmural ischemia
dynamic compromise of a clinically defined patient. The Forrester clas-
sification (Figure 63) is related to invasive hemodynamic measures, Figure 64. Injury current in ECG
which require rectification actions (shown in the figure). Both classifica-
tions have a prognostic influence. • QRS complex. Pathologic Q waves indicate transmural myocardial
necrosis. There are infarctions with Q waves (which are generally
transmural, consequence of STE-ACS) and infarctions without Q
I No cardiac failure waves (generally limited to subendocardial or nontransmural, con-
sequence of NSTE-ACS). The new-onset left bundle branch block in
II Mild cardiac failure (crackling, S3, pulmonary congestion) the setting of an AMI usually indicates extensive involvement of the
conduction system, and is associated with bigger-sized infarctions
III Acute pulmonary edema and of worse-prognosis.
IV Cardiogenic shock
ECG progression of an AMI because of complete occlusion of an epicar-
Table 31. Killip classification dial coronary artery shows evolutionary alterations that follow a spe-
cific pattern (Figure 65).
Ischemia
1.º
To increase cardiac Diuretics
output with amines,
vasodilators and IABP IV Peaked T
(typical:
Reduce preload cardiogenic Symmetric negative T
with diuretics shock)
and vasolidators 2.º
Infarction or necrosis
III
Decrease O2 Convex ST
(typical consumption elevation
Increase preload of RV AMI) with β-blockers Q wave
with fluids
Injury 3.º
2,2 L/min/m2 Cardiac index
Q wave
and negative T
Figure 63. Basic treatment according to the degree ST elevation
in Forrester classification
ECG is not usually normal even during the first minutes of the AMI. It Figure 65. Electrocardiographic progress in MI and localization
is recommended to register additional leads to evaluate the right ven- of electric alterations
45
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
• While necrosis is completed, ST segment tends to return to the iso- Traditionally, the markers used in the diagnosis of AMI have been cre-
electric line. Simultaneously, Q waves (and loss of R wave) develop atine phosphokinase (CPK), its CPK-MB fraction, and GOT and LDH en-
in the leads in which ST segment occurs. zymes (these two are no longer recommended). At present, the first
• Inversion of T wave usually persists or normalizes after several choice marker is cardiac specific troponin T or I. The time pattern of the
weeks or months. Persistence of ST elevation in leads in which ne- markers has major diagnostic value (Figure 68).
crosis waves have developed may indicate ventricular aneurysm
or segments with dyskinetic movements (paradoxic). However, in
some exceptional cases, a complete ECG normalization may occur.
• T wave alterations generally take up more leads than ST’s, which, in turn, Enzymes
CPK GOT LDH
take up more leads than Q waves (the ischemia area is greater than the Myoglobin
injury current area, and this is greater than the electric necrosis area).
• In regions opposite to where AMI is localized, electrocardiographic
alterations reciprocal (opposite) to those appearing in the leads lo-
calizing the AMI are appreciated, although these changes may also Troponin
correspond to concomitant ischemia, in other regions, because of
other compromised coronary bundle branch (Figures 66 and 67).
· Ischemia
· Severe, acute or chronic cardiac insufficiency
· Myocarditis or myopericarditis, complicates endocarditis
· Myocardial damage by contusion, catheter ablation, endomyocardial
biopsy or electric cardioversion
· Myocardial infarction in aortic dissection, aortic valvulopathy, severe
arrhythmias, hypertension episodes or pulmonary hypertension,
(pulmonary embolism, idiopathic, etc.)
· Cardiomyopathy such as hypertrophic, tako-tsubo or infiltrating
· Severe episode of sepsis or shock
· Cardiotoxic chemotherapy (5-fluorouracil, anthracycline, herceptin)
OTHER CIRCUMSTANCES
Figure 66. Anterolateral MI in acute phase
· Renal function impairement (acute or chronic)
· Hypothyroidism
I · Ischemic or hemorrhagic acute stroke
· Large burns or rhabdomyolysis
· Some poisoning
II
Table 32. Causes of cardiac specific troponin elevation
III
The initial action recommended in STE-ACS is shown in Figure 69.
At present, PTCA is considered the first-choice treatment as long as it is Table 34. Long term treatment for MI
performed immediately (within two hours after consultation) by a spe-
cialized team. It has been demonstrated that PTCA provides better clinical Apart from the medical treatment, smoking cessation, a cardiac healthy
results than in-hospital thrombolysis (less reinfarctions, artery reclusions, diet and weight loss are recommended if BMI is greater than 30 and
and less residual ventricular dysfunction), and that it may even improve waist circumference is over 102 cm in men and over 88 cm in women. A
by using stent, since the risk of the vessel reintervention is reduced. strict control of risk factors, aerobic physical exercising at least five days
a week (including participation in cardiac rehabilitation programs), and
Door-to-balloon time (the period from hospital arrival to angioplasty) evaluation of arrhythmic risk are also recommended.
must not exceed 90 minutes; otherwise, it loses its advantage over fibri-
nolysis. If the patient presents cardiogenic shock or if fibrinolysis is con- An implanted cardiac defibrillator is indicated after 40 days, to prevent
traindicated, PTCA is the treatment of choice, regardless of the delay. arrhythmic sudden death, if the patient remains with LVEF < 30%. Opti-
mal medical treatment and revascularization must always be granted, if
Nowadays, in the acute phase, it is recommended to only act over the indicated, before the implant. The main risk determinants are LV ejec-
artery responsible for the infarction and to consider complete revascu- tion fraction and functional class, as well as nonsustained ventricular
larization, when indicated, by PTCA or surgery in a differed way, after tachycardia and inducement of sustained ventricular tachycardia in the
the patient has stabilized. electrophysiologic study. It is convenient to wait for the resolution of
stunned myocardium in order to estimate residual ejection fraction.
There follow some contraindications of thrombolytic medication (Table Table 35 shows current indications to implant a defibrillator after a
33) to be checked before their administration to patients. myocardial infarction.
47
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
PRIMARY PREVENTION
(always, at least, 40 days SECONDARY PREVENTION
Supraventricular Tachycardia
following the AMI)
Sinus tachycardia generally indicates a major infarction with ventricular
· LVEF < 40%, VT · VF-produced sudden death
dysfunction and cardiac insufficiency associated. It must not be treated
nonsustained and VT recovered outside the acute
sustained inducible in phase as such.
electrophysiologic study · Sustained VT with poor
· LVEF < 35% and II-III hemodynamic tolerance and Sinus bradycardia is common in the acute phase of inferior infarction
functional class of NYHA depressed LVEF due to vagal hypertonicity, or secondary to opiates, and it appears in
· LVEF < 30% and I-III · Sustained VT well tolerated with
25% of cases.
functional class of NYHA normal LVEF (or almost normal)
(indication IIa*) (indication IIa*)
* Indication shows that the benefit appears greater than the implantation risk, so it is
Atrial fibrillation occurs in 10% to 20% and is associated with major
advisable infarctions with important ventricular dysfunction mainly in the elderly.
Table 35. Indications for automatic defibrillator implant after an AMI Anticoagulation is indicated due to the embolic risk involved.
Conduction disturbances
7.3. Complications Almost 10% of STE-ACSs are found with AV block, and are more related
to mortality (due to the myocardial extension producing the block than
of myocardial infarction the block itself, since the block associated with the inferior infarction
has a good prognosis; Table 37).
Arrhythmias
AV BLOCKS POST AMI SUPRA-HISIAN INFRA-HISIAN
Tachyarrhythmias Heart rate 40-60 bpm (narrow) < 40 bpm (wide)
Mechanisms producing ventricular arrhythmias in the acute phase of AMI Location Inferior Anterior
an infarction (primary arrhythmias) differ from those appearing in the Atropine response Responds No response
chronic phase of the disease (in which there is an anatomic substrate Prognosis Good Poor
for the onset of anatomica re-entries in the scar). The main arrhythmias
are shown in Table 36. Table 37. Atrial ventricular blocks in AMI
48
Card i o l ogy 1
Almost 20% of infarctions develop transitory bundle branch block, Mechanical Complications
which persists in 5% of cases. New-onset bundle branch block, mainly
left-sided, is related to extensive infarctions with severe systolic dys- These are included in Table 38, and in Figures 71, 72, 73, 74 and 75.
function and a poor prognosis.
Inferior AMI
with hypotension Cardiac rupture
Figure 70. Causes and treatment of inferior infarction with arterial Figure 71. Free wall rupture
hypotension
49
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Apical IVC
Mural thrombus
Infarcted
segment
RV LV
Thrombus
RV LV
Pseudoaneurysm
Others
Figure 73. Mitral regurgitation correction by papillary muscle rupture Postinfarction ischemia requires immediate intervention and an early
coronarography.
50
Card i o l ogy 1
Dyslipidemia
Statins are classified according to the expected reduction of LDL-
cholesterol levels in high-, moderate- or low-intensity therapy (Table
40).
Chapter 08
HIGH-INTENSITY MODERATE-INTENSITY LOW-INTENSITY
STATIN THERAPY STATIN THERAPY STATIN THERAPY
Although a comprehensive study of dyslipidemia is included in the En-
docrinology chapter, some considerations must be mentioned. Daily dose lowers Daily dose lowers LDL- Daily dose lowers
LDL-cholesterol cholesterol on average, LDL-cholesterol
on average, by by approximately on average, by
LDL elevation is related to a greater risk of coronary heart disease, and
approximately > 50% 30% to 49% < 30%
it is similarly related to VLDL. Levels of HDL are inversely related to de-
velopment of premature arteriosclerosis. Factors leading to a rise in
· Atorvastatin · Atorvastatin 10-(20) mg · Simvastatin 10 mg
HDL levels are physical exercise, lipid-lowering diet and female sexual (40)-80 mg · Rosuvastatin (5)-10 mg · Pravastatin 10-
hormones, whereas factors lowering HDL levels are obesity, sedentary · Rosuvastatin · Simvastatin 20-40 mg 20 mg
and smoking. 20-(40) mg · Pravastatin 40-(80) mg · Lovastatin 20 mg
· Lovastatin 40 mg · Fluvastatin 20-
· Fluvastatin 40 mg bid 40 mg
Saturated fatty acids (common in animal fat) cause an increase LDL
· Pitavastatin 2-4 mg · Pitavastatin 1 mg
cholesterol, whereas monounsaturated and polyunsaturated acids
cause an increase HDL. There are many drugs to decrease LDL, such Table 40. High, moderate and Low-Statin Therapy.
as statins. Others are ezetimibe or resins, such as cholestyramine, ( ) indicates less evidence
though these are hardly used nowadays due to the adverse events
produced.
The use of other lipid-lowering agents such as niacin or ezetimib has not
There is a close relationship between abdominal obesity (abdominal been shown to reduce the risk of atherosclerotic cardiovascular disease
waist diameter over 102 cm in men and over 88 in women) and isch- (Table 41).
aemic heart disease; hypercholesterolemia, hypertriglyceridemia and
hypertension are also associated.
CALORIES RELEASED
ACTIVE CONTRIBUTION TO DIET (%)
Metabolic syndrome is defined as a group of cardiovascular risk factors ap- IN COMPLETE
SUBSTANCE OVER TOTAL CALORIES
OXIDATION
pearing more frequently than usual. Metabolic syndrome components are
hypertension, abdominal obesity, hypertriglyceridemia, lower HDL levels Carbohydrates 4.1 kcal/g 50% to 65%%
and altered baseline glycemia. The metabolic syndrome pathophysiologic
basis seems to be related to insulin-resistance due to abdominal obesity. Fat 9.3 kcal/g Saturated: < 10%
Nowadays, there is a debate over whether metabolic syndrome adds an- Polyunsaturated: < 10%
other risk to the existing cardiovascular risks, although preliminary data Monounsaturated: 10% to 15%
suggests so, at least, in some cases. Treatment includes adequate diet
and regular physical exercise. Cholesterol - < 300 mg/day
The lastest guidelines for the treatment of blood colesterol to reduce Proteins 4.3 kcal/g 10% to 20%
atherosclerotic cardiovascular disease recommends:
Table 41. Active substances proportion in normal diet
51
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Hypertension
Systolic isolated HTN, common among the elderly, is characterized
by values over 140 mmHg of systolic and below 90 mmHg of dia-
stolic pressure and is also correlated with morbidity and mortality.
Chapter 09 However, systolic isolated HTN among young people has not been
revealed to improve prognosis with treatment, data also suggests
that this entity does not progress to systolic/diastolic HTN in every
case.
9.1. Essential Hypertension
Malignant HTN is a hypertensive emergency with ischemic organic
High blood pressure or hypertension is highly prevalent (30% to 45% damage (retina, kidney, heart or brain), especially papilledema on oph-
in the general population) and has a steady incidence. Almost half talmoscopy. Although the most frequent cause is untreated essential
the people with hypertension are unaware of the condition and, in hypertension, secondary causes of HTN must be thoroughly analyzed.
spite of new therapeutic advances, optimum control is achieved in Prognosis without treatment is 50% mortality in the first year. For treat-
less than half of patients; it is therefore a first-order public health ment, intravenous drugs such as labetalol, nitrates, nitroprusside or ni-
issue. cardipine are used.
Elevations in systolic and diastolic blood pressure are related to this Accelerated hypertension refers to patients who do not have papillede-
cardiovascular disease –systolic blood pressure (SBP) being a stron- ma but who have other severe vascular damage signs, such as hemor-
ger sign of potential complications than diastolic blood pressure rhages or retinal exudates.
(DBP) after 50 years of age-, and pulse pressure (difference between
systolic and diastolic pressure) in elderly patients also adds predic- Hypertensive crisis are SBP elevations > 180 mmHg and/or DBP > 120
tive value. mmHg. There are two types: hypertensive emergency and hypertensive
urgency.
The most frequent form of HBP is essential (usually starting between
30 and 50 years of age, although starting to appear in younger people, Hypertensive emergency describes an elevation in blood pressure ac-
even teenagers). Among younger people, secondary causes such as companied by severe acute damage to target organs threatening the
aortic coarctation should be ruled out, and among elderly patients, it patient’s life (encephalopathy, acute coronary syndrome, acute heart
is convenient to rule out other etiologies such as renal artery athero- failure, aortic dissection, ischemic or hemorrhagic stroke, pheochro-
sclerosis. mocytoma crisis, drugs such as cocaine, amphetamines or MDMA,
eclampsia or perioperative hypertension). The magnitude and speed
By consensus, adult high blood pressure (HBP) is defined as the pres- for correction of pressure values will depend on the involvement of
ence of SBP over 140 mmHg (systolic HTN) and/or DBP over 90 mmHg the organ at issue. For instance, for a stroke, correction will be small
(diastolic HTN). However, these limits are arbitrary since there is a con- and slow, whereas in a case of acute pulmonary edema or aortic dis-
nection with cardiovascular risks at lower values, especially in patients section, the correction must be major and quick. However, in most
with high cardiovascular risk. Complete patient risk level should be de- cases it is sufficient with a 25% correction of the BP values during the
termined, not only the BP level, to apply the correct therapeutic action first hours and slowly thereafter, since a sudden and intense BP drop
(this is carried out using calculation tables of cardiovascular risk, such as could cause greater organic and ischemic damage. The i.v. drugs used
Framingham’s risk score or Euroscore). are similar to the ones used for malignant HTN. When a major BP el-
evation is not accompanied by severe, acute organic damage, there
The most common classification of BP values is shown in Table 42. How- is hypertensive emergency. It is usually managed by restoring or in-
ever, the lastest guidelines defines HTN by BP > 130/80 mmHg. creasing antihypertensive therapy (in many cases it is the result of a
break in use).
TYPE SBP (mmHg) DBP (mmHg) Resistant or refractory hypertension occurs when values cannot be
lowered to desired levels in spite of lifestyle changes and after at least
Optimum < 120 and < 80
three drugs (including a diuretic). It may comprise up to 15% of patients
Normal 120-129 and/or 80-84 and the main causes are inadequate compliance with nonpharmaco-
logic instructions, use of hypertensive substances (liquorice, NSAIDs,
Normal-high 130-139 and/or 85-89
corticosteroids, cocaine, etc.), sleep apnea, unsuspected secondary
HTN level 1 140-159 and/or 90-99 cause, irreversible injury to target organs or volume overload (sodium
ingestion, insufficient doses of diuretic, progressive kidney failure or
HTN level 2 160-179 and/or 100-109
hyperaldosteronism). In these cases it is convenient to rule out “white
HTN level 3 ≥ 180 and/or ≥ 110 coat” hypertension, pseudo hypertension or the use of a cuff of inad-
equate size.
Systolic isolated HTN ≥ 140 and ≤ 90
Table 42. Classification of BP values “White coat” HTN or isolated clinical hypertension defines patients
with normal BP values outside of medical consultation -determined
In pediatrics, there is hypertension with BP values over 95% percent, by ambulatory blood pressure measurement (ABPM), see below- and,
adjusted to age and sex; values ranging between 90% and 95% are con- however, with consistently high values during consultation. It affects
sidered prehypertension. 15% of the population. It involves lower risk of damage to target organs
52
Card i o l ogy 1
ADVISABLE FOR ALL PATIENTS
than the real hypertension, but apparently greater than people with
normal BP, therefore requiring close follow up and even consideration · Blood analysis: fasting glycemia, cholesterol and its fractions,
fasting triglycerides, potassium, uric acid, creatinine, hemoglobin
of application of treatment if vascular risk is high or there are signs of
and hematocrit. Assessment of creatinine clearance or glomerular
damage to target organs. filtration rate using appropriate formulas
· Urine analysis: microscopic analysis and microalbumin test (reagent strip)
Masked HTN or isolated ambulatory HTN is the contrary phenomenon · ECG: to assess the presence of arrhythmia and signs of left-sided
(normal values during consultation, but higher elsewhere). It is just as ventricular hypertrophy
prevalent as clinical isolated HTN and is frequently associated with dam- ADVISABLE FOR MANY PATIENTS
age to some target organ, therefore requiring similar management as · Echocardiograph (size of ventricular hypertrophy)
HTN. · Carotid ultrasound (intima media thickness)
· Chest X-ray
Exertion HTN is characterized by normal BP at rest, but with excessive · Ankle-brachial index
increase during exertion (there is no consensus, but most define it as · Ophthalmoscopy
· Quantitation of proteinuria if reagent strip was positive for microalbumin
SBP > 210 mmHg among men and > 190 mmHg among women). Its
· Glucose tolerance test if glycemia is over 100 mg/dL
usefulness for diagnosis and prognosis of patients with HTN is contro-
· ABPM and/or SMBP
versial. In the event of abnormal results, ABPM is advisable. · Pulse wave velocity calculation
Table 43. Complementary examination of hypertensive patients
Measurement
of Blood Pressure The main “target” organs with damage caused by hypertension are the cen-
tral nervous system (typically strokes), heart (hypertrophy, myocardial isch-
A correct measurement of blood pressure is based on the auscultatory emia or arrhythmia) see Figure 76. Also, kidneys (renal failure because of
method of Korotkoff sounds. Pseudo hypertension appearing with ath- nephroangiosclerosis) and the retina (hypertensive retinopathy), Table 44.
erosclerosis may be suspected by palpating the radial artery with the
inflated cuff (Osler’s sign).
Diagnosis of HTN requires several elevated values over several days, ex-
cept in extreme cases.
53
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
avoid anti-inflammatories) and monitor other cardiovascular risk with a combination of two drugs and later adjustment of doses or addi-
factors. tion of a third drug.
To decide when to start drug therapy for hypertension, systolic and dia- Table 46 shows the main cases for or against the use of each drug
stolic pressure values alone are not enough in every case. It is advis- group.
able to assess the presence of established clinical or subclinical damage
of target organs and determine the overall cardiovascular risk (which
includes analyzing the presence and state of other cardiovascular risk DRUG ADVISABLE NOT ADVISABLE
factors). First line drugs
The latest recommendations for hypertension treatment published Thiazides · Heart failure · Gout
by the Joint National Committee of United States are included in the · Elderly · Diabetes risk
· African American · Metabolic
table below; there are slight differences with other available guidelines
syndrome
(Table 45).
ACE inhibitors · Heart failure · Pregnancy
or angiotensin II · Systolic dysfunction · Renal artery
RECOMENDATIONS FOR HTN TREATMENT · Diabetes bilateral stenosis
· Proteinuria · Hyperkalemia
· Drug therapy is advised for adults over 60 years of age if · Chronic kidney failure
their systolic blood pressure (SBP) > 150 mmHg or diastolic · Renovascular HTN
(DBP) > 90 mmHg. If SBP values obtained are < 140 mmHg · Metabolic syndrome
and there are no adverse effects, treatment does not need · Ventricular hypertrophy
to be adjusted
Calcium · Angina · Dihydropyridine
· In patients under 60 years of age, drug therapy is advised to reduce antagonists · Elderly in monotherapy
DBP < 90 mmHg. With lower levels of scientific evidence, it is · African american for myocardial
advisable to start treatment to lower SBP < 140 mmHg · Intermittent claudication ischemia
· In patients with chronic nephropathy or diabetes over 18 years · Metabolic syndrome · Constipation
of age, drug therapy aims for blood pressure < 140/90 mmHg · Ventricular hypertrophy
· For the general population (including diabetic patients) treatment · Pregnancy (second line)
may start with thiazides, calcium antagonists, ACE inhibitors
or angiotensin II. For African American patients (including diabetics), Second line drugs
thiazides or calcium antagonists are advisable to commence α-blockers · Benign prostatic · Heart failure
therapy. In case of chronic nephropathy, ACE inhibitors or hypertrophy · Orthostatic
angiotensin II are recommended to start therapy · Pheochromocytoma hypotension
· If targets are not attained within a month, it is recommended to
β-blockers · Coronary disease · Asthma
increase doses of the drug of choice or add a new drug (assess this
· Tachyarrhythmia · Bradyarrhythmia
to start with if BP > 160/100 mmHg). If targets are not met with
· Heart failure · Severe claudication
three drugs referring the patient to a unit specialized
· Hyperthyroidism · Diabetes risk
in hypertension is recommended · Pregnancy (second line) · Metabolic
Table 45. Recommendations for HTN treatment of the JNC-8 (2014) syndrome
Table 46. Situations that encourage or discourage the use of various
The therapeutic objective of hypertension treatment is to lower morbi- drugs for hypertension
mortality of the patient; for this purpose an operational goal is followed
aimed at lowering blood pressure to values below 140/90 mmHg in
general, being lower in diabetic patients, and with more leniency with ACE inhibitors are the drugs of choice in the presence of diabetes mel-
regard to SBP in elderly patients. litus, renovascular hypertension, and diabetic nephropathy -or from
another source-, ventricular systolic dysfunction or severe heart valve
The benefit of treatment is more closely related to lowering BP itself than failure, myocardial infarction history or high risk of developing diabetes.
with a specific drug. For this reason, it is considered that all antihyper- In case of cough or angioedema caused by ACE inhibitors, the alterna-
tensive drugs are first line and all combinations are accepted, except for tive is angiotensin II, which is useful when there is major ventricular
ACE inhibitors with angiotensin II. However, the only drugs, compared hypertrophy.
against placebos, which have been statistically shown to decrease mor-
bimortality, are diuretics and beta blockers. Newer drugs have not rep- Beta blockers are preferred in coronary patients, with atrial fibril-
licated this since it is unethical to design new studies against placebo. lation or other tachyarrhythmias, hyperthyroidism, heart failure,
sometimes migraine or if there is essential tremor. They are not the
For patients with mild blood pressure elevation and low-moderate car- best option in case of high risk of developing diabetes (metabolic
diovascular risk, treatment usually starts with a single drug in mono- syndrome).
therapy and doses are subsequently adjusted or other drugs are com-
bined to keep blood pressure values under control. However, patients Calcium antagonists are preferred in cases of isolated systolic HTN in
with markedly elevated blood pressure and high-very high cardiovascu- the elderly, African Americans, angina with contraindication for beta
lar risk usually require starting with antihypertensive therapy directly, blockers, atrial fibrillation or, sometimes, for patients with migraine.
54
Card i o l ogy 1
In resistant HTN cases, the application of potassium-sparing diuretics volved, this tends to be progressive and more frequently requires
such as spironolactone/eplerenone and amiloride or alpha blockers angioplasty or surgery.
such as doxazosin should be considered. In case medical treatment fails,
invasive procedures, such as renal denervation and carotid barorecep-
tor stimulation may be considered.
9.3. Special Cases
9.2. Secondary Hypertension In African American patients, diuretics and calcium antagonists appear
to offer more protection than other drug groups.
The most frequent cause of secondary hypertension is renal (renovas- For isolated systolic hypertension in advanced age, the drugs of choice
cular or renal parenchymaytous). are calcium antagonists or thiazides. Nevertheless, other first-line
drugs may be used, avoiding abrupt BP falls and monitoring orthostat-
Kidneys are both involved as victims (they develop nephroangiosclerosis) ic hypotension with more lenient goals than with other hypertensive
and executioners (pathogenesis involvement) in essential hypertension. patients.
Many drugs (vasoconstrictors, hydrosaline retention facilitators such In left-sided ventricular hypertrophy and in metabolic syndrome, the
as anti-inflammatories, and so forth) and endocrine and metabolic drugs of choice are ACE inhibitors, ARB or calcium antagonists.
disorders (hyperaldosteronism, hyperthyroidism, Cushing’s syndrome,
among others) cause hypertension. Alpha blockers (alpha-adrenergic-antagonists) are advisable for pheo-
chromocytoma.
Figure 77 lists the main causes of secondary HTN.
For benign prostatic hypertrophy, alpha blockers are advisable (al-
though they may be less safe than other antihypertensives in mono-
Neurogenic therapy).
alterations
Drugs Patients with previous stoke may, in general, use any drugs. However,
Hyperthyroidism treatment should be avoided during the first week after a stroke, unless
Aortic coarctation there is very high blood pressure.
Atherosclerosis Aortic regurgitation Hospital admission is not required for hypertensive emergencies; ini-
tial treatment is applied with oral drugs such as captopril, furosemide
Arteriovenous
or amlodipine. Fast acting nifedipine should not be considered, since it
fistules Suprarenal may cause hypotension and trigger myocardial ischemia.
alterations
55
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Pericardial Disease
pain generated by other conditions, especially by acute myocardial in-
farction (Table 48).
Chapter 10
ACUTE MYOCARDIAL
ACUTE PERICARDITIS
INFARCTION
ECG
56
Card i o l ogy 1
A B
PE
P
PE
LV
RV
RV
PE RA LV
LA
RA LA PE
PE
Figure 78. Echocardiography image of severe pericardial effusion (PE) in apical (A) and subcostal (B) four-chamber view
Specific forms coids have been administered. A transmural infarction or cardiac trau-
ma can also lead to pericarditis with no autoimmune etiology, such as
of pericarditis epistenocardiac pericarditis, during the early days of the condition.
57
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
with subsequent loss of normal elasticity of the pericardial tissue and Catheterization is usually unnecessary although, in some cases, it is
impairing diastolic function. In the early phase of diastole, ventricular performed to distinguish it from restrictive cardiomyopathy. The x and
filling is normal, but it is abruptly disrupted when the maximum elastic- y descents are prominent and a wave is usually increased, resulting in
ity of the pericardium is attained. Stroke volume decreases while there an “M” shape. In jugular vein pressure, y descent is the most prominent
is equalization of diastolic pressure in all four heart chambers. wave, interrupted by a rapid rise in pressure (called h wave).
CCP can potentially occur as a result of any pericardial disease, but it In the ventricle, diastolic pressure acquires a square root or dip-plateau
rarely occurs after acute pericarditis. In most cases, the origin is un- shape, since pressure increases rapidly when the limit of pericardium
known, but among the most common known causes are cardiac sur- distensibility is reached and it remains on a plateau.
gery, mediastinal radiotherapy, tuberculous pericarditis, connective
tissue diseases, and recurrent uremic pericarditis. This pressure pattern is very similar to the one in restrictive cardiomy-
opathy and, on rare occasions, endomyocardial biopsy may be required
Systemic congestion signs such as increased jugular venous pressure, to differentiate them. Left filling pressure is higher than right filling pres-
hepatosplenomegaly and edema are predominant. Hepatosplenomegaly sure by more than 5 mmHg in restrictive cardiomyopathy (in constrictive
is often accompanied by ascites and liver dysfunction, so it can easily be pericarditis they are usually almost equal); this difference is magnified
confused with cirrhosis. Dyspnea is uncommon, although there may be by volume overload or Valsalva maneuver in restrictive cardiomyopathy.
weakness and signs of malnutrition (systemic congestion may produce BNP elevation may support the diagnosis of restrictive cardiomyopathy.
protein-losing enteropathy). Other signs that can be detected include de-
creased apical impulse and intensity of heart sounds. Sometimes a sound Pericardiectomy (pericardial stripping) is the only definitive treatment
appears immediately after the second sound, which corresponds to a for constrictive pericarditis. This procedure consists of performing a
pericardial knock and should not be confused with a third sound. The longitudinal incision on the pericardium, finding a dissection plane and
Kussmaul sign (raised jugular vein pressure on inspiration) is very com- removing it carefully to prevent myocardial tears or lesions of the coro-
mon. A rapid “y” descent (prominent diastolic collapse of JVP) is usually nary vessels. If there is serious calcareous infiltration of the epicardium,
noted followed by a rapid rise and subsequent plateau, with a greater “a” it is better to leave some portions than run the risk of a complete re-
wave and, sometimes, a prominent “x” descent. moval.
The ECG may reveal decreased QRS complex voltage, flattening and in- The success of the intervention depends on the clinical course of the
version of T waves, and atrial fibrillation in about one-third of patients. condition since, in very advanced cases, pericardial stripping is very
complex and the improvement obtained is limited. Therefore, surgery
In about 50% of the patients, chest x-ray shows calcification of the peri- should be carried out at a relatively early stage.
cardium, although this does not always causes constriction. An echocar-
diography generally shows thickening of the pericardium but, in case it Operative mortality is about 5% to 10%. Benefits obtained from com-
is normal, this diagnosis should not be ruled out. plete cardiac decortication are progressive, it is only after several
months that complete improvement can be observed and that jugular
Cardiac MRI and CT scans are more reliable for detection of pericar- venous pressure returns to normal. Long term benefits are often very
dial thickening than echocardiography. However, pericardial thickening satisfactory.
does not necessarily indicate constriction (Figure 79).
Medical therapy consists of sodium restriction, diuretics, digoxin and, in
some cases, repeated pericardiocentesis. Due to the fact a large number of
cases of constrictive pericarditis are of tuberculous origin, this must be treat-
ed before surgery if suspected or this etiology cannot be ruled out. In case of
atrial fibrillation, anti-coagulation is indicated.
58
Card i o l ogy 1
Pathophysiology
of cardiac tamponade
Restrictive filling
of the right cavities
Arterial pulse
↑ Pressure in heart chambers ↓ Cardiac output
Cardiac tamponade
Sympathetic activation (pericardial fluid prevents
Renin-angiotensin-aldosterone system ventricular relaxation; it exerts
pressure on the septum)
Over
The increase in pericardial pressure compresses cardiac chambers (first 10 mmHg
the right atrium and the right ventricle during diastole, the moment of Arterial pulse
lowest pressure) and produces collapse. This complicates the filling of
the right cavities and results in an increase in the pressure of the sys- Expiration - Inspiration - Expiration
temic venous territory (this is why in chronic pericardial effusion there
is systemic congestion) and a fall in cardiac output that may cause hypo- Figure 81. Interdependence of the chambers
tension and signs of low anterograde cardiac output. in pericardial tamponade
Since all chambers are surrounded by the pericardial sac, the increase
in volume results in higher pressure compensated by interdependence Clinical manifestations are related to the decrease in cardiac output and
of the chambers (Figure 81). systemic congestion: hypotension, tachycardia and oliguria, increased
central venous pressure, dyspnea with orthopnea, liver congestion,
During inspiration, the negative pressure in the chest allows more blood among other conditions Physical examination reveals:
to return to the right chambers. In order to hold a greater volume in • Increased jugular venous pressure with a prominent X descent and
“compressed” cavities, there is distention of the right ventricle at the a reduced or almost absent Y descent. Dullness on percussion of the
expense of “compression” of the left ventricle by the septum, which can anterior chest.
lead to paradoxic pulse. As a result of the tamponade, the whole dias- • There is often paradoxic pulse (inspiratory decline in systolic blood
tole process is compromised (unlike cases of constrictive pericarditis, in pressure of more than 10 mmHg). This sign is not pathognomonic
which the first stage is not affected). and can be observed in constrictive pericarditis (one-third of cases),
restrictive cardiomyopathy, hypovolemic shock, asthma or severe
The body adapts by activating compensation mechanisms analogous to lung disease, and in other conditions of right ventricular diastolic
those of heart failure: activation of the sympathetic and renin-angioten- involvement.
sin-aldosterone system aims at increasing cardiac output and maintain • Kussmaul’s sign is characteristic of constrictive pericarditis, but it
peripheral perfusion. In cases of acute tamponade (aortic dissection, car- can also be observed during cardiac tamponade, especially if there
diac rupture, etc.), intrapericardial pressure rises so fast that the possibili- is a component of pericardial constriction.
ties of compensation are limited. In case of slow onset effusion, tempo- • Pericardial rub is rare and, if present, it suggests the possibility of
rary compensation is possible, but additional minor pressure elevations constrictive pericarditis.
can trigger florid tamponade. The factors that determine the presence
or absence of signs of pericardial tamponade are directly related to the Complementary Studies
magnitude and speed of the onset of the effusion and the stiffness of the
parietal pericardium, and inversely related to myocardial thickness. • ECG. There is often reactive sinus tachycardia. Decreased amplitude
of the QRS complex can be observed, as well as electrical alternans
Any pericarditis is a potential cause of cardiac tamponade. The most of the waves if the effusion is considerable.
frequent are tumors, idiopathic pericarditis (it rarely produces tampon- • Chest x-ray. The cardiac silhouette may be normal or, if the effusion
ade, but since it is the most common cause of pericarditis, it has a high is large, it may be increased in size or acquire a “water bottle” shape
incidence in global tamponades), and pericarditis with uremic and iatro- most frequently, lung fields are “clear”, with minimal or no alveolar
genic etiology (in interventional procedures or cardiac surgery). infiltrate (Figure 82).
59
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Treatment
Expanding blood volume with serum or additional blood reduces col-
lapse of the cavities. Diuretics are contraindicated, since they reduce
blood flow volume and may increase collapse, which can induce shock.
Enlarged cardiac silhouette with "tent shape"
Treatment consists of evacuating pericardial fluid and, as a result, in-
trapericardial pressure is reduced. In extreme cases, pericardiocentesis
Figure 82. X-ray of a pericardial effusion should be performed as soon as possible. Drainage can be performed
using two techniques:
• Echocardiography. Diastolic collapse of the right cavities and strik- • Pericardiocentesis. Under local anesthesia, a long needle is inserted
ing changes in ventricular filling flow with respiration are echocar- between the xiphoid process and the left costal arch, guiding it to-
diographic signs of tamponade (Figure 83). ward the left shoulder. The puncture can be guided by ECG, echocar-
diography or fluoroscopy (Figure 84).
A
PE
PE
LV
RV
RA LA
D
Pericardial effusion
Pericardiocentesis needle
60
Card i o l ogy 1
Valvular Heart
According to the speed of onset, VHD may produce different clinical
events because of the different heart chambers, pulmonary vascular-
ization and compensation mechanisms. For left VHD:
Disease
Chapter 11 • Acute onset (acute myocardial infarction, endocarditis, aortic dis-
section, prosthetic valve thrombosis) is generally poorly tolerated,
leading to heart failure with low cardiac output and pulmonary
edema. Therapeutic action must be immediate (generally surgery).
• Progressive or chronic onset activates compensatory mechanisms,
11.1. Basic Concepts with little or no symptoms, even maintaining normal ventricular
function until advanced stages. For these reason is essential to
Cardiac valves may be affected by congenital heart disease or by ac- recognize them early, because the surgical treatment in advanced
quired heart disease (Figure 85). stages can be harmful.
Increased life expectancy and reduction of rheumatic fever incidence in Primary VHD (consequence of rheumatic fever, degenerative diseases)
industrialized countries have altered the prevalence and the predomi- frequently progress, and surgical intervention becomes necessary soon-
nant etiology of valvular heart disease (VHD); calcific aortic stenosis is the er or later. Functional (secondary) VHD (related to dilation or to valve
most common, nowadays. An important detail regarding the prevalence system failure because of another reason) may reduce after treating the
and incidence is that studies usually refer to severe VHD requiring medi- primary cause.
cal care, treatment or surgical intervention since mild VHD constitutes an
incidental finding in healthy individuals. For instance, up to one-third of Semilunar valves stenosis (pulmonary and aortic valves) produces an el-
the population presents mild or low mitral or tricuspid regurgitation with evated afterload compensated with concentric hypertrophy, maintaining a
no risk of progressive deterioration. Likewise, rigid valves, slightly degen- good systolic function until advanced stages (hypertrophy stimulates the
erated or sclerotic, are commonly detected in old patients, with mild or onset of coronary diseases). As a general rule, symptoms appear before
no functional alteration, whose progression risk is hard to estimate. ventricular systolic dysfunction, suggesting that surgery is to be performed.
Arterial cone
Anterior semilunar cusp
Pulmonary valve Right semilunar cusp Left fibrous trigone
Left semilunar cusp
Right (coronary)
semilunar cusp
Aortic Left (coronary)
valve semilunar cusp
Posterior (noncoronary)
semilunar cusp
Anterior cusp
Tricuspid
Septal cusp valve
Posterior cusp
Anterior cusp
Mitral valve
Posterior cusp Right fibrous ring
(of tricuspid valve)
Left fibrous ring
(of mitral valve) Right fibrous trigone
Heart in systole viewed from base with atria removed
Left atrium
Anterior valve
Posterior valve
Tendinous chords
61
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Valve regurgitation produces volume overload with eccentric hyper- Apart from studying the hemodynamic degree of the valve, it is rec-
trophy associated with progressive ventricular dilation, initially com- ommended to analyze its anatomy and subvalvular apparatus in an
pensatory, and then becoming degenerative. It is frequently prior to attempt to establish the etiology and healing possibilities. A study on
symptoms, for which close monitoring is required for asymptomatic pa- the impact over myocardial function (volumes and ejection fraction),
tients. Likewise, this volume overload increases ejection fraction, and on the pulmonary vessels (pulmonary hypertension data), on systemic
an apparently normal value may indicate incipient myocardial systolic veins (size and flow of inferior vena cava), and on potentially altered
dysfunction. structures associated with VHD (e.g. aortic regurgitation associated
with ascending aortic dilation or coarctation) must also be performed.
In atrio-ventricular stenosis (mitral and tricuspid) symptoms are caused
by the increase in atrial pressure and retrograde congestion of the vein Mild or moderate VHD does not itself significantly affect cardiac func-
system (pulmonary in mitral stenosis and systemic in tricuspid stenosis). tion and does not require surgical treatment, except for special cases.
However, ventricles are not affected since they are protected against However, severe left VHD frequently requires surgical intervention.
such pressure or volume, so, ventricular diastole, rather than systole,
is compromised. Although there are some peculiarities included in the relevant chapter,
surgery is indicated in two cases:
VHD symptoms may be anterograde (low cardiac output data such as • Where symptoms exist.
asthenia, tendency to tiredness) or retrograde. In left VHD, mitral or • In asymptomatic cases, where significant impact over the cardiac
aortic, high blood pressure flows back into the pulmonary veins (result- function exists. In mitral stenosis, impact data appear in the atrium
ing in dyspnea and pulmonary edema). These vessels become more (atrial arrhythmias) and in the pulmonary artery (pulmonary hyper-
resistant, which initially protects the lung from pulmonary edema, tension), since the left ventricle “only” suffers a chronic diastolic
but subsequently if the edema persists, it leads to irreversible organic deficit. Mitral regurgitation and aortic stenosis or regurgitation im-
changes in the pulmonary arteriole with the pulmonary hypertension plies chronic pressure overload (aortic stenosis) or volume overload
and secondary right-side heart failure. (regurgitation) of the left ventricle, which makes it fail (ejection frac-
tion decreases). Surgery is indicated.
VHD may manifest by the onset of complications (emboli, endocardi-
tis, arrhythmias or sudden death). Sometimes, ergometry is useful to Table 49 shows a summary including etiology, symptoms and treat-
determine “hidden” symptoms, especially in people with poor physical ment of left valve heart diseases.
activity level.
As a general rule, a presurgical coronary angiography or cardiac CT is
Upon clinical suspicion based on exploratory findings, the first-choice indicated when surgery is scheduled with the purpose of reducing peri-
diagnosis method for all VHD is the echocardiogram, and the VHD is operative morbimortality and assessing the need for myocardial revas-
classified as mild, moderate or severe according to its hemodynamic cularization associated with the valve surgery, in patients with coronary
severity. disease or risk of acquiring it (Table 50).
SUMMARY OF VHD
In MR and AR, if LVEF < 30%: transplantation
MS MR AS AR
Rheumatic fever (RF) RF (MS + MR) < 30 years: unicuspid Valvular:
Mitral valve prolapse 30-70 years: bicuspid · Acute: endocarditis
ETIOLOGY MI isolated >70 years: degenerative · Chronic: RF
Dilation of annulus:
· Acute: aorta dissection
· Chronic: Marfan syndrome
Dyspnea Dyspnea Angina Dyspnea
SYMPTOMS · Syncope
· Dyspnea (more frequent)
· Diuretics
· Digoxin
MEDICAL TREATMENT
Nonvasodilators ACE inhibitors Nonvasodilators ACE inhibitors/Dihydropyridine
calcium antagonists
Surgery upon symptoms
If PH although LVEF < 60% and/ · LVEF< 50% although LVEF < 50% or LVESD > 50 mm
asymptomatic or LVESD ≥ 40 mm asymptomatic or LVEDD > 65 mm although
although asymptomatic · Children: surgery always asymptomatic
SURGICAL TREATMENT Favorable anatomy: Repair attempt: if not PROSTHESIS PROSTHESIS
PMBC possible, prosthesis · Alternative: Ross procedure · Alternative: Ross procedure
Unfavorable anatomy: · Children: valvuloplasty · In some cases, repair
prosthesis · Upon high surgical risk,
consider TAVI
Table 49. VHD summary
62
Card i o l ogy 1
PRESURGICAL CORONAROGRAPHY. INDICATIONS It is appropriate to know the differences (shown in Table 51) between
· Known coronary disease mechanical and biological prosthesis well, although the choice of one
· Suspected unstudied myocardial ischemia type of prosthesis over the other must be individualized.
· LV systolic dysfunction
· Existence of any coronary risk factor
· Men over 40 years of age or postmenopausal women
MECHANICAL PROSTHESIS BIOLOGICAL PROSTHESIS
· Suspicion of ischemic severe mitral regurgitation
Table 50. Indications of presurgical coronarography in VHD · No contraindications to chronic · Difficulties in or
anticoagulation contraindications for correct
Some concepts about valve prosthesis should be known. · Patients with coagulation chronic anticoagulation (high
indications for another reason hemorrhagic risk, lifestyle
Some prosthesis are made of biological material and others are purely or with high embolic risk or occupation, compliance
mechanical, Figure 86. (atrial fibrillation, mechanical problems)
prosthesis in another valve, · Resurgery because of prosthetic
severe left systolic dysfunction, thrombosis with proven poor
emboli family background, anticoagulation control
hypercoagulability conditions) · > 70 years of age
· High risk of valvular · Young woman with pregnancy
deterioration desire
(hyperparathyroidism) · Express desire of informed
· < 60 years of age patient
· Patients with high reintervention
risk (left ventricular dysfunction,
prior bypass surgery, multiple
prosthesis)
Almost all prosthesis are slightly restrictive and produce a murmur simi-
lar to mild stenosis of the relevant valve.
The main cause of mitral stenosis is rheumatic fever, and mitral insuf-
ficiency is commonly associated (double mitral injury).
Biological prosthesis only requires anticoagulation (INR 2.5) in the first Atrial fibrillation associated with mitral stenosis is very common; this
three months until endothelialization of the prosthetic material. association represents an extreme embolic risk.
63
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
↑ LA-LV Gradient
Mitral focus
better auscultated
in apex
↑ LA Pressure ↓ LV Filling
MT MT
AP ChA
Pulmonary Dilation
↓ Cardiac output
congestion of LA
In Figure 90, general guidelines for mitral stenosis are shown. Normally,
Right HF
this disease progresses slowly over period of 10-20 years before pro-
ducing symptoms. However, when symptoms appear, they progress in a
Figure 88. Mitral stenosis pathophysiology few years, which constitute a significant increase in mortality if no mea-
sures are performed. This is why symptoms with ordinary activity are
The main exploratory findings are summarized in Figure 89. Remember the base of surgical indication. Likewise, in asymptomatic patients, per-
that the greater the severity, the more accelerated the opening snap cutaneous mitral balloon commissurotomy (PMBC) can be performed
and the more delayed the closing. In the same way, the murmur presys- in cases of atrial fibrillation, PCWP > 25 mmHg with exercise or in very
tolic accentuation is lost upon atrial fibrillation. severe stenosis.
Atrial Fibrillation
or area <1 cm2
MVR
64
Card i o l ogy 1
Medical treatment consists of bradycardia (upon an increased diastolic From a pathophysiologic view, symptoms of retrograde congestion
time, a greater LV preload occurs), diuretics and antithrombotic treat- (ejection of blood retrograde into the atria) and that of low anterograde
ment, especially in case of atrial fibrillation. output (“lack of blood” flowing onwards since it flows back into the left
ventricle) are also included.
PMBC (surgical commissurotomy is no longer used) can be performed
when the valvular anatomy is favorable and there are no contraindica- Chronic mitral regurgitation murmur is better auscultated in the apex
tions (left atrial thrombus or moderate-to-severe MR). If unfavorable or armpit; it is systolic and generally larger when regurgitation becomes
(generally when one of these three criteria is met), replacement of the more severe, Figure 91.
prosthetic valve is indicated.
Define etiology
Primary MR Secondary MR
Surgery
(attempt of repair Symptomatic severe Asymptomatic
if possible) EF 30% to ≤60% EF 30% to ≥ 60%
MR with persistent severe MR
or LVESD ≥40mm and LESD <40 mm
NYHA class III-IV or progressive MR
or new onset AF
symptoms
or PASP >50 mmHg
Periodic monitoring
Likelihood of succesful MV surgery
repair > 95% and expected (MV repair preferred)
mortality < 1%
65
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Mitral valve repair is preferred over mitral valve replacement when pos-
sible (more feasible in mitral valve prolapse and lesser in rheumatic mi-
tral regurgitation) (Figure 93).
S1
Concomitant mitral valve surgery (preferred repair) is reasonable in pa- S2
tients with chronic primary moderate MR when undergoing cardiac sur- C
gery for other indications or for patients with chronic severe secondary
MR who are undergoing coronary coronary artery bypass graft or aortic
valve replacement.
Usual treatment of mitral regurgitation because of annulus dilation is In significant organic mitral regurgitation, mitral prolapse relat-
that of advanced heart failure. ed to the murmur involves a deterioration risk, especially in men
(Figure 95).
RV
Ao
LV
LA
66
Card i o l ogy 1
Aortic valve sclerosis without stenosis is common in elderly patients
with hypertension and produces a low intensity and short murmur. Se-
vere aortic stenosis is usually accompanied by a decrease in intensity
and inverted closure in S2. It is also common to indentify a parvus et
tardus pulse.
Aortic stenosis is considered severe when the aortic valve area is < 1.0 cm2 Transcatheter aortic valve replacement is recommended in patients
(or indexed AVA ≤ 0.6 cm2/m2). If systolic function and cardiac output who meet an indication for aortic valve replacement, who have a
are normal, aortic stenosis is severe as long as the mean systolic trans- moderate or high risk for surgical replacement.
valvular gradient exceeds 40 mmHg.
Aortic valvular sclerosis without stenosis is common in the elderly with
Upon systolic dysfunction, the ventricle cannot open the valve com- hypertension and produces a murmur with similar characteristics (albe-
pletely. The aortic valve area may still be compatible with aortic steno- it short and with low intensity). In order to differentiate them, remem-
sis. Dobutamine stress echo is used to determine the gradient growth ber that severe aortic stenosis is usually accompanied by a decrease in
with poor increase of the valvular area in cases of true aortic stenosis. intensity and inverted splitting in S2, and, at times, by parvus et tardus
pulse.
Characteristic symptoms of severe aortic stenosis are triggered by ef-
fort (angina, syncope or dyspnea). Nowadays, the main predominat-
ing symptom is dyspnea. The risk of sudden death in aortic stenosis 11.5. Aortic Regurgitation
increases exponentially when symptoms appear. The latter indicates
the need for aortic valve replacement.
The most common cause of aortic regurgitation in developed
Aortic stenosis murmur is auscultated in the aortic focus, radiating to countries is that associated with bicuspid aortic valve and primary
carotids and supraclavicular area (occasionally the apex: Gallavardin diseases causing dilation of the ascending aorta or the sinuses of
phenomenon). It is systolic and rhomboidal after aortic opening (some- Valsalva.
times an opening click may be heard, mainly in bicuspid valves). As the
murmur lasts longer, its severity also increases (Figure 97). Considering etiologies of aortic regurgitation as a result of direct in-
volvement of aortic leaflets, we must mention rheumatic heart disease
(chronic) and infective endocarditis (acute).
Aortic focus
radiating to carotids Considering etiologies of aortic regurgitation because of ascending aor-
ta dilatation, we must mention Marfan Syndrome (chronic) and acute
thoracic aortic dissection (acute). LV volume overload (because of blood
regurgitation) usually causes dilation, and, in the long-term, it may de-
teriorate systolic function (ejection fraction).
67
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Severe AS
Vmax ≥4 m/s Vmax 3 m/s-3.9 m/s
∆Pmean ≥4 mmHg ∆Pmean 20-39 mmHg
Abdominal ETT
The presence of ascending aorta dilation along with severe aortic regur-
gitation implies concomitant operative intervention to repair the aortic
MT AP MT
sinuses or replace the ascending aorta in patients with:
• Bicuspid aortic valve if the diameter of the aortic sinuses or ascend-
ing aorta is greater than 4.5 cm.
• Marfan Syndrome when the aorta reached 4.5 cm.
• Patients with ascending aorta or aortic sinus diameter 4.5 cm or
Hyperflux murmur Austin-Flint murmur greater.
68
Card i o l ogy 1
Aortic Regurgitation
Severe AR Progresive AR
(stages C and D) (stage B)
Vena contracta > 0.6 cm Vena contracta ≤ 0.6 cm
Holodiastolic aortic RVol < 60 mL/beat
flow reversal RF < 50%
RVol ≥ 50% ERO < 0.3 cm2
ERO ≥ 0.3 cm2
LV dilation
Other cardiac surgery
Symptomatic Asymptomatic YES NO
(stage D) (stage C)
LVEF < 50% Other cardiac LVEF ≥ 50% LVEF ≥ 50% LVEF ≥ 50%
(stage C2) surgery LVESD > 50 mm LVEDD > 65 mm LVESD ≤ 50 mm
(stage C2) Low surgical risk LVEDD ≤ 65 mm
With regard to pulmonary valve disease, it should be noted that: 12.1. Aortic Aneurysm
• Pulmonary stenosis is most frequently congenital.
• The most common cause of respiratory failure is pulmonary hyper-
tension, usually secondary to left heart diseases. Infrarenal abdominal aortic aneurysm is the most common form, al-
• Pulmonary valve disease murmurs are increased during inspiration though they may occur in almost any artery (Figure 101).
(Rivero-Carvallo’s sign).
• Graham-Steele’s murmur is the murmur of pulmonary regurgitation. Infrarenal abdominal aortic aneurysm (IAAA) is most frequent among
• Treatment for severe pulmonary stenosis is usually by means of per- males. The most frequent etiology is atherosclerosis. The aneurysm is
cutaneous catheter-balloon valvuloplasty. often identified by chance during another addominal test. The main risk
• For severe respiratory failure, an annuloplasty is performed concur- factors for IAAA rupture are diameter, hypertension, active smoking, fe-
rently with surgery on the originating left heart valve disease. male sex and presence of symptoms (expanding aneurysm).
STENOSIS REGURGITATION
Most frequent cause Rheumatic · Functional: pulmonary hypertension
· Organic: endocarditis
Symptoms · Of associated left-sided valve disease · Of originating disease
· Systemic congestion · Systemic congestion
Jugular pulse Increased A wave · Increased V wave
· Decreased (reversed) x sinus
Auscultation · Diastolic murmur · Systolic murmur
· Increase during inspiration · Increase during inspiration
Severity Severe: T 1/2 ≥ 190 ms or valve area ≤ 1.0 cm2 Reversed systolic flow in suprahepatic veins
Medical treatment Low sodium diet, diuretics Low sodium diet and diuretics
Surgery instructions · Severe tricusipd stenosis (TS) at the time of · Recommended for patients with severe tricuspid regurgitation (TR)
operation for left-sided valve disease undergoing left-sided valve surgery
· Isolated, symptomatic severe TS · Mild, moderate, or greater functional TR at the time of left-sided valve surgery
with either tricuspid annular dilation or prior evidence of right heart failure
· Symptoms because of severe primary TR unresponsive to medical therapy
Technique · Bioprosthesis · Prosthetic
· Commissurotomy · De Vega annuloplasty
· Percutaneous valvuloplasty in some cases · Bioprosthesis
Table 52. Main features of tricuspid valve disease
69
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Growth
*Emergency Programmed If not Consider
feasible > 0.5 cm/year
surgery surgery graft stent
Takayasu *Preferrable
if there
disease
is no rupture
Syphilitic
aneurysm
Splenic
Mycotic aneurysm aneurysm 11,5 mm
Vasculitis 76,4 mm
Atherosclerotic with aneurysmal
aneurysm dilatation
20,3 mm
Figure 101. Types of vascular aneurysms
Examination of these patients is key for the associated coronary dis- Figure 103. Ascending aorta aneurysm
ease; the latter may affect the prognosis and surgical risk of the patient.
Ascending aorta thoracic aneurysm may appear because of cystic medi-
Current treatment for this kind of aneurysms is shown in Figure 102. al necrosis (typical with Marfan, Ehler-Danlos syndromes or associated
The presence of symptoms, growth velocity over 0.5 cm a year, or the with bicuspid aortic valve) or tertiary syphilis.
presence of aorta diameter over 5.5 cm (5 cm in patients with low surgi-
cal risk) is indicative for surgery. Treatment for thoracic aortic aneurysms is shown in Figure 104.
Surgical repair requires a midline transabdoiminal approach or an ex- A diameter of ascending aorta aneurysms ≥ 5.5 cm, the presence of
traperitoneal incision in the left flank to perform aneurysmectomy and symptoms, or a growth velocity ≥ 0.5 cm a year are indications for sur-
placement of a synthetic tubular graft with iliac extension (if the ter- gery. In case of association with bicuspid aortic valve, aortic dissection or
ritory is also affected). Endovascular repair clearly represents a major Marfan syndrome, the former criteria are applied with lower diameters
advance in patients who have severe cardiopulmonary disease or other (> 45mm in Marfan and > 50 mm in bicuspid) according to the presence
risk factors. of other associated rupture risk factors.
70
Card i o l ogy 1
Thoracic aortic aneurysm
· Semi-annual size
follow-up
Symptomatic Asymptomatic · Treat risk factors
· Avoid intense exercise
· Beta blockers
Figure 104. Procedure for action in the event of thoracic aortic aneurysm
For patients undergoing aortic valve surgery coexisting with ascending aspects of these three pictures are nearly the same. The main charac-
aorta dilation, aorta intervention is also recommended at lower diam- teristics of intramural hematoma and penetrating ulcer are shown in
eters (4.5 cm). Bentall procedure is used for ascending aorta aneurysms Table 53.
with associated aortic failure; it consists of implanting an aortic valve
graft with reimplantation of coronary arteries. Hypertension is the main condition associated with increased wall
stress and development of thoracic aortic dissection. The dissection
Hypertensive treatment of choice in Marfan patients consists of beta flap is commonly found in the ascending thoracic aortic, within its first
blockers and possibly ARB. 2-3 cm.
The most frequent type of peripheral aneurysm is popliteal. It is usually Acute aortic dissection must be considered in all patients presenting
bilateral and, if it becomes thrombotic, there is a high risk of losing the intense chest, back or abdominal pain, especially with migratory fea-
limb involved. Therefore, treatment requires surgical repair based on tures. Dissection may involve arterial branches and lead to ischemia
aneurysm exclusion and placement of femoral popliteal bypass. perfusion deficits in the area involved. Typical findings of aortic dis-
section are asymmetric decrease of upper limb pulses and a diastolic
murmur of aortic valve regurgitation.
12.2. Acute Aortic Syndrome Stanford’s classification (Table 54 and Figure 105) divides acute
aortic syndromes (and aortic dissection) into type A or proximal:
if the ascending aorta is involved (the most frequent, prognosis is
Traumatic aortic rupture usually occurs after car accidents or serious poor, and requires surgical repair) and type B or distal: if they do
falls and is often located distal to left subclavian artery. Acute aortic not involve the ascending aorta (less frequent, better prognosis,
syndrome comprises three entities: classic aortic dissection, intramural treatment is medical and it should be managed medically unless life-
aortic hematoma and penetrating aortic ulcer. Clinical and therapeutic threatening complications develop).
Etiopathogenesis · Adventitia bleeding towards the media · Intima disruption secondary to atherosclerotic damage
· More frequent in descending aorta · More frequent in descending aorta
Epidemiology Elderly patients with same risk factors as aortic dissection
Diagnosis CT angio, MR angio or TEE focus on thoracic aorta
Treatment Similar to aortic dissectionin the corresponding segment of the · Similar to type B dissection
aorta · Surgery if:
- Hemodynamically unstable
- Pseudo aneurysm
- Acute rupture
- Continuous pain
- Distal embolization
Table 53. Intramural hematoma and penetrating ulcer
71
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
DE BAKEY CLASSIFICATION Urgent and definitive imaging of the aorta using transesophageal echo-
I Ascending aorta rupture, extending to descending cardiogram, computed tomographic imaging, or magnetic resonance
aorta imaging is recommended to identify or exclude thoracic aortic dissec-
II Ascending aorta rupture (only) tion in patients at high risk for the disease. Figure 106 shows recom-
III Descending aorta rupture mendations for acute aortic syndrome management.
STANFORD CLASSIFICATION
A (proximal) Involving ascending aorta Blood pressure and heart rate should be controlled in all patients with
B (distal) Not involving ascending aorta acute aortic syndrome, usually with nitroprusside and intravenous beta
blockers or labetalol. Type A dissections require emergency surgical repair
Table 54. Aorta dissection classification
(Figure 107). Anticoagulants are formally contraindicated.
Intimal tear
Adventitia
True lumen
False
lumen Type B dissecton
(does not involve
ascending aorta)
Figure 105. Aortic dissection classification Figure 107. Surgical treatment of type-A dissection
Type A Type B
72
Card i o l ogy 1
12.3. Deep Vein Thrombosis RISK OF DEEP VEIN THROMBOSIS
Risk factors
(bedridden patients, surgery, obesity, among others)
Prophylaxis
· Early ambulation
· Compression (elastic stockings Swelling
or intermittent pneumatic Pain
Clinical
compression) Cyanosis
· Nonfractionated heparin Edema
· Low molecular weight heparin
· Fondaparinux
· Antithrombotic or oral
anti-activated
Factor X drugs MR angio
Doppler ultrasound Plethysmography
Alternatives
D-dimer Venography
CT angio
Search Contraindications
Pulmonary Resolution
for other diagnosis for anticoagulants
embolism recurrence
in spite of treatment
Chronic
Vena cava filter anticoagulation
Indefinite
anticoagulation
73
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Other Venous Disorders Posthrombotic syndrome leading to chronic venous insufficiency can be
treated using elastic compression stockings, appropriate management
Chronic venous insufficiency is usually the consequence of deep vein during the acute phase of deep vein thrombosis, phlebotonic drugs (dis-
thrombosis, since the healing process may cause a dysfunction of the vein crete efficacy) and avoiding prolonged standing.
valve system, which leads to blood reflux to the superficial venous system
through perforating veins (Figure 109). Superficial venous thrombosis, unlike the deep form, does not cause
pulmonary embolism or chronic venous insufficiency. Its treatment con-
sists of relative rest, elastic compression stockings and anti-inflammato-
ry drugs. It does not require oral anticoagulation.
The most common cause for superior vena cava obstruction is tumors,
especially microcytic lung tumors, which are not resectable. It may
cause a typical edema on the face and upper limbs (Figure 111).
Venous ulcers usually affect the internal malleolus and have a humid
base. They are less painful than arterial ulcers, Figure 110.
Chronic venous
Figure 111. Patient with edema on the face and upper limbs
insufficiency
Skin atrophy,
Edema no hair 12.4. Peripheral Artery Disease
Pallor
Erythema
or cyanosis
Peripheral artery disease, also known as chronic limb ischemia, is due
to atherosclerosis and mainly affects the lower limbs of elderly patients,
causing intermittent claudication symptoms.
74
Card i o l ogy 1
episodes) and, sometimes, drugs that improve walking distances until
claudication, especially cilostazol (or, less markedly, pentoxifylline).
Humeral (15%)
75
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
Long-term prognosis of the disease is shown in Figure 115. Acute peripheral occlusion
Acute
OBLITERATING OBLITERATING
ATHEROSCLEROSIS THROMBOANGIITIS
Age Usually, over Young, below
50 years of age 45 years of age
Blood pressure Usually, hypertension Often hypotension
Raynaud’s syndrome No Commonly present
and migrating
phlebitis
Cholesterolemia High Normal or low
ESR (erythrocyte Normal High
Figure 116. Anatomy of thoracic outlet of upper limb nerve bundle sedimentation rate)
X-rays, · Hard, calcified, · Straight and small-
arteriography deformed, tortuous, caliber arteries, with
Etiology should be differentiated since local thrombosis may cause the irregularly-sized no calcification
same symptoms. Table 57 shows data which enables making a differ- arteries · Nonatheromatous
ential diagnosis. · Atheromatous aorta aorta
Table 58. Differential diagnosis between atherosclerosis and obliterating
Acute arterial ischemia treatment is shown in Figure 117. thromboangiitis
76
Card i o l ogy 1
RAYNAUD’S DISEASE Idiopathic
Quitting tobacco usually stops the progression of the disease; there-
fore, it is the most important step. The appearance of new lesions is a · Scleroderma
sign that patient has not achieved cessation. · Systemic erythematosus lupus
CONNECTING TISSUE
· Rheumatoid arthritis
DISORDERS
· Diabetes mellitus
Administration of nicotine gum or patches may be sufficient to maintain
· Dermatomyositis
the disease active. In certain cases, deviation of large vessels and local
debridement of lesions may be performed. Anticoagulant therapy has Cryoglobulinemia, macroglobulinemia
BLOOD DYSCRASIA
not yielded the expected results and use of corticosteroids has not been of Waldenstrom, myeloproliferative disorders
useful either. In some cases, amputation is necessary, usually more lim- · Hammer syndrome
ited than with obliterating atherosclerosis. TRAUMA · Vibration lesions
· Electric shocks
In subclavian steal syndrome, the occlusion is in the subclavian artery · Ergotamine
before the exit of the vertebral artery and causes symptoms of verte- DRUGS · β-blockers
brobasilar insufficiency (Figure 118). · Bleomycin, vincristine, cisplatin
· Syringomyelia
Raynaud’s phenomenon consists of recurrent episodes of vasocon- NEUROLOGIC
· Carpal tunnel syndrome
ALTERATIONS
striction affecting fingers most commonly, caused by exposure to cold · Poliomyelitis
or intense emotions. It is important to differentiate Raynaud’s disease Table 59. Diseases where Raynaud’s phenomenon is involved
from Raynaud’s phenomenon. Raynaud’s disease is not the result of an
underlying associated medical condition (idiopathic); it comprises more
than half the cases, being predominant among young women and with
usually milder manifestations.
12.5. Lymphedema
Basilar artery The most common cause of lymphedema globally, and mostly in tropi-
External
carotid Internal carotid cal Africa, is filariasis, which causes lymphatic obstruction due to nema-
artery artery
todes and a corresponding inflammatory response, which leads to el-
Common
Vertebral artery ephantiasis.
carotid
artery
Frequent causes of lymphedema are tumors, both due to lymphatic
infiltration of malignant cells and treatment (surgery with lymph
node exeresis or fibrosis caused by radiation therapy to the lymph
Left subclavian
artery system).
The clinical aspects are very important for diagnosis of this disease,
since lymphography is rarely used. Lympho-gammagraphy may be used
Right subclavian Occlusion to detect the blocking point of lymphatic drainage, and it is a useful
artery technique in oncology to detect the “sentinel ganglion” where sick tis-
sue is drained and in order to plan the surgery.
On the contrary, Raynaud’s phenomenon may be secondary to an un- The main goals of lymphedema treatment are to control edema (super-
derlying disorder (Table 59), often some process causing organic le- ficial lymphatic massage, soft, and applied from a distal to proximal di-
sions of the arterial wall. rection, physiotherapy and other techniques; any element compressing
the limbs, venous punctures, intense exercise or trauma of the involved
Most patients with mild and infrequent episodes do not require spe- limb should be avoided, which should be as long as possible above the
cial treatment. They should be instructed to avoid cold environmental heart level), maintain a healthy and clean skin, and prevent complica-
temperatures by using thick gloves and socks, and to avoid mechanic tions such as cellulitis or erysipelas and lymphangitis. It is advisable to
microtrauma. Tobacco is contraindicated due to its potential vasocon- raise the feet while in bed, use compression stockings and bandages
stricting effect. In severe cases, vasodilator therapy with drugs may be after emptying the edema by means of manual drainage; or use se-
administered, calcium antagonists are advisable to this end, and if there quential pneumatic compression boots during the day. Especially with
is no response, surgical sympathectomy may be considered, although lymphedema after breast surgery, good results have been shown with
any benefits are usually temporary. low-level laser therapy.
77
A m e r i c a n Manua l o f Ex am i na ti o n i n Me di c ine (2CK)
The presence of redness, pain and edema usually involves cellulitis or epilepsy, intoxication, and narcolepsy, loss of consciousness with en-
bacterial lymphangitis (it is known as linear swelling throughout the docrine and metabolic origin (hypoglycemia, hypoxia or hypocapnia
length of the limb). Common etiologic organisms are positive-coagu- because of hyperventilation) or vertebrobasilar transient ischemic at-
lase staphylococcus or β-hemolytic streptococcus, which require strong tack are not syncope episodes either. In subclavian steal syndrome,
treatment, nearly always with intravenous antibiotics. Chronic lymph- syncope is exceptional without other associated focal vertebrobasilar
edemas may exceptionally progress to lymphangiosarcoma. symptoms, triggered by physical exercise of the ipsilateral arm with
obstruction.
Surgery is used in severe cases which do not respond to medical treat-
ment and it consists of removing hypertrophied tissue and applying True syncopes are classified into three groups, according to their patho-
lympho-venous anastomosis to rechannel the flow from an obstructed physiology (Table 60).
lymphatic vessel to the venous system.
Clinical history is the most profitable data for diagnosing the type of
syncope. It is essential to investigate the situation and triggering fac-
tors, symptoms before and after the episode, as well as the presence
Syncope
of heart disease or neuropathy by means of thorough physical exami-
nation. Episodes during exertion, associated palpitations, episodes
while lying down, or family history of sudden death are risk data.
Chapter 13
Among other complementary tests, electrocardiogram (ECG) (if normal,
it almost completely rules out cardiac origin of syncope), orthostatism
test or active standing (measurement of BP in supine position and af-
Syncope is a symptom which consists of transient loss of consciousness ter three minutes of standing, a drop of over 20 mmHg of systolic BP
(usually just a few seconds, sometimes for some minutes), associated or over 10 mmHg of symptomatic diastolic BP is considered positive),
with postural tone loss and falling, with spontaneous and complete re- carotid sinus massage (which is diagnostic if it reproduces the syncope
covery, because of transient global cerebral hypoperfusion. There may be with a pause over three seconds or with a BP drop over 50 mmHg), basic
warning signs (weakness, dizziness, ear ringing, cold sweat). Presyncope blood work and chest X-rays are key.
is the imminent feeling of syncope without actually losing consciousness.
There are some ECG alterations that indicate a high risk in case of syn-
cope (Table 61).
13.1. Differential Diagnosis If this initial assessment is enough to reach a diagnosis, patient treat-
ment follows. If not, it is known as syncope of unknown origin, and
other tests are necessary that should be considered only with certain
Since there is no transient loss of consciousness, casual falling, cata- suspected clinical origins, such as Holter, echocardiography, tilt test,
plexy (loss of muscle tone associated with emotions or “fits of laugh- electrophysiology study, stress test, cardiac catheterization. Events loop
ter”, frequently associated with narcolepsy), drop attacks (“blue recorder or implantable Holter are useful with syncope of unknown ori-
knees” disease in middle-aged women), psychogenic pseudosyncope gin with suspected arrhythmic origin, especially when the frequency of
or transient ischemic attack, are not true syncope episodes. Even with syncope is very low (since in this context it is rare for the conventional
transient loss of consciousness, cases of cranio-encephalic trauma, Holter to provide any data of interest).
· Vaso-vagal (neurocardiogenic) classic: induced by emotional stress, fear, blood-phobia, pain or orthostatic stress
REFLEX OR
· Situational syncope: tusigen, sneezing, gastrointestinal stimulation (deglutition, defecation, abdominal pain,
NEURALLY
glossopharyngeal neuralgia), postprandial, postexercise, playing wind instruments, laughter
MEDIATED
· Carotid sinus syncope
SYNCOPE
· Atypical forms
· Primary autonomic failure (Shy-Drager, Parkinson, Lewy bodies disease, etc.) or secondary (neuropathy, diabetes,
ORTHOSTATIC
amyloidosis, uremia, marrow damage, etc.)
HYPOTENSION
· Drugs (diuretics, vasodilators, neuroleptics, antidepressants) or alcohol
SYNCOPE
· Volume depletion (bleeding, Addison, dehydration, digestive loss)
· Of arrhythmic origin:
- Sinus diffusion
- AV blocks
- Pacemaker or defibrillator dysfunction
CARDIAC SYNCOPE - Supraventricular or ventricular tachyarrhythmia
- Pro-arrhythmic drugs
· Cardiopulmonary structural disease: heart valve disorders, myocardial ischemia, pulmonary embolism, hypertrophic
cardiomyopathy or other outflow tract obstructions, aortic dissection, pericardium tamponade, atrial myxoma, valve
prosthesis dysfunction, pulmonary hypertension
Table 60. Syncope pathophysiology types
78
· 2.nd or 3.rd degree AV block Vaso-vagal syncope is the most common type. It is triggered by seeing
RHYTHM
· Sustained or nonsustained ventricular blood, prolonged standing, hot or tight environments, or even by emo-
ALTERATIONS
tachycardia tional stress. It appears to be caused by a reflex alteration which usually
· Pre-excitation begins with a decrease in venous return and secondary release of cate-
· Branch block cholamines which cause strong ventricular contractions, with a relatively
QRS ALTERATIONS · Left-sided ventricular hypertrophy criteria empty ventricle, with associated vagal discharge, hypotension and brady-
· Pathologic Q waves cardia. It has an excellent prognosis with almost null mortality.
· Epsilon wave
· Right precordial negative T waves A tilt test or tilt table test (not required for diagnosis in most cases) en-
REPOLARIZATION · Ischemic changes ables differentiating cardioinhibitory (with predominant bradycardia),
ALTERATIONS · Brugada pattern vasodepressor (with predominant hypotension) or mixed forms. Treat-
· Long QT interval ment consists of explaining the benign quality of the clinical picture in
Table 61. ECG Alterations involving high risk in patients with syncope spite of recurrence risk, advising the avoidance of triggering factors
and, in patients with prodrome symptoms, isometric counter-pressure
Figure 119 shows the general risk stratification of a patient with syn- maneuvers (cross legs while standing). It may be useful to increase hy-
cope. drosaline intake, avoiding diuretics and vasodilators. In refractory cases,
drugs may be used, drugs may be used and midodrine is the drug of
choice (adrenergic receptor stimulants), since serotonin reuptake in-
hibitors, other adrenergic stimulants (etilefrine), and mineralocorticoid
1. Confirmation of Suspected Syncope drugs (useful with orthostatic syncope), are not usually effective and
No show common side effects. Beta blockers are currently considered con-
Was there loss of consciousness? Fall, tonal crisis, cataplexy
traindicated.
Yes
No
Was recovery spontaneous? Metabolic alteration, In very special cases of vaso-vagal syncope recurrent in patients over
intoxication, RPC
Yes 40 years of age, with no response to usual treatment and with a cardio-
No
Is it due to global brain hypoperfusion? Concussion, epileptic crisis, inhibitory form, the use of a pacemaker may be prescribed, the same
pseudosyncope, as with cardioinhibitory carotid syncope, although this does not always
Yes
TIA/vertebrobasilar migraine
decrease syncope episodes since it does not mitigate the vasodepres-
sant effect.
2. Risk Classification of Syncope
No
Suspected neuromediated Yes
Benign Syncope
or orthostatic syncope?
No
Syncope with Unknown Profile
Family History:
• Sudden death
Yes High Risk
• Family heart disease