CARDIOLOGY

REVIEW
DR. ARTA BAKSHANDEH
 PANCE REVIEW
■ Cardiomyopathy ■ Coronary Artery Disease
– Dilated – Acute Myocardial Infarction
■ Non-ST elevation
– Hypertrophic
■ ST- Elevation
– Restrictive
– Angina Pectoris
■ Congenital Heart Disease ■ Prinzmetal Variant
– Atrial Septal Defect ■ Stable
■ Unstable
– Coarctation of Aorta
– Patent Ductus Arteriosus ■ Heart Failure

– Tetralogy of Fallot ■ Traumatic, infectious, and inflammatory heart

conditions
– Ventricular Septal Defect
– Acute and subacute bacterial endocarditis
– Acute pericarditis
– Cardiac Tamponade
– Pericardial Effusion
CARDIOMYOPATHY
Dilated
Hypertrophic
Restrictive
Dilated Cardiomyopathy
Dilated cardiomyopathy (DCM) is a cardiomyopathy associated with left ventricular systolic dysfunction and chamber enlargement and may be due to
multiple causes including ischemic and nonischemic causes.

Description – left ventricular systolic dysfunction with chamber enlargement (dilation)

Types –
1. ischemic vs. nonischemic based on morphology ■ (CC) - patients may be asymptomatic or can present
2. primary (idiopathic) vs. secondary based on cause
with(
– symptoms of heart failure in severe cases
■ dyspnea
History and Physical ■ fatigue
■ decreased exercise tolerance
■ Clinical presentation ■ orthopnea
– Usually male ■ paroxysmal nocturnal dyspnea
■ edema (peripheral edema or ascites)
– mean age 56 years ■ rapid weight gain
– dyslipidemia in 17.5% ■ gastrointestinal symptoms, such as anorexia,
early satiety, weight loss, nausea, and
– mean ejection fraction 28.7% abdominal pain
– arrhythmia (cardiac arrest)
– hypertension in 50%
– syncope
– atrial fibrillation in 16.7% – chest pain (can suggest ischemia)
Dilated Cardiomyopathy
General physical - patients typically present with signs of heart failure
■ potential indicators of heart failure with reduced ejection fraction (systolic dysfunction)
– tachycardia (pulse > 90-100 beats/minute)
– systolic blood pressure < 90 mm Hg
– proportional pulse pressure < 33%
■ proportional pulse pressure = (systolic blood pressure - diastolic blood pressure/systolic blood pressure)
■ proportional pulse pressure < 25% may indicate reduced cardiac index
■ sinus tachycardia
■ cachexia common with disease progression
Skin
■ pigmentation of skin or scars may indicate hemochromatosis as cause
Neck
■ jugular venous distention +/ - hepatojugular reflux
Cardiac
■ assess gallop rhythm (S3) and murmur consistent with mitral regurgitation
Abdomen
■ hepatomegaly
■ ascites may appear with disease progression in children
Extremities
■ peripheral edema common with disease progression
Dilated Cardiomyopathy
Evaluation
■ Use echocardiography to assess left ventricular systolic function and chamber sizes.
■ Obtain an electrocardiogram (ECG) to evaluate for possible underlying ischemic heart disease.
■ Consider stress testing or coronary angiography to evaluate for possible ischemic heart disease.
Management
■ Use guideline-directed medical therapy for all patients with symptomatic heart failure with reduced
ejection fraction that includes:
– angiotensin-converting enzyme (ACE) inhibitors (or angiotensin receptor blockers [ARBs] if
intolerant to ACE inhibitors)
– beta blockers (such as carvedilol, metoprolol)
– Loop diuretics if signs of failure (furosemide, torsemide)
■ Treat the identified underlying causes of dilated cardiomyopathy (DCM) when possible.
■ Consider the placement of an implantable cardioverter defibrillator (ICD) in selected patients.
■ Offer cardiac resynchronization therapy (CRT) for selected patients with symptomatic heart failure, left
ventricular ejection fraction (LVEF) ≤ 35%, and a widened QRS (≥ 150 milliseconds), particularly
with a left bundle branch block configuration
■ In patients with DCM and refractory symptoms of heart failure despite optimal medical management,
consider mechanical circulatory support or selection for a cardiac transplantation
Hypertrophic Cardiomyopathy
Background History of present illness (HPI)
■ Hypertrophic cardiomyopathy (HCM) is a common inherited ■ disease course variable
cardiovascular disease characterized by hypertrophy of a nondilated ■ symptoms can present at any age
left ventricle in the absence of any other cardiac or systemic disease
(such as hypertension) that could account for observed hypertrophy. ■ heart failure symptoms (for example, exertional dyspnea) may occur at any age but more
frequently in middle-age adults
■ HCM is caused largely by mutations in genes encoding thick and
thin contractile myofilament proteins of the cardiac sarcomere. ■ end stage disease course variable and unpredictable, with some patients asymptomatic for many
years after systolic dysfunction arises
■ Phenotypically, HCM can be obstructive (70% of patients), with
presence of left ventricular outflow tract obstruction, or ■ women have more severe symptoms of heart failure (frequently associated with outflow
nonobstructive (30% of patients). obstruction), presenting later in life than men

■ Complications include syncope, heart failure, and sudden death. Family history (FH)
■ ask about family history of hypertrophic cardiomyopathy or sudden cardiac death
Physical Exam
(CC)
Neck
■ often asymptomatic
■ abnormal arterial pulse findings associated with hypertrophic cardiomyopathy may include
■ symptoms may include
– large amplitude
– chest pain (usually associated with exertional dyspnea), may be
anginal – rapidly rising pulse
– lightheadedness and syncope – pulsus bisferiens (biphasic pulse, may not be palpable)
– palpitations (due to atrial arrhythmia or ventricular arrhythmia) Cardiac
■ sudden death frequently the first clinical presentation ■ cardiovascular exam typically normal
■ patients with outflow obstruction may have
– arterial pulse with a rapid up and down stroke
– ejection systolic murmur at left sternal edge radiating to left upper sternal edge
– murmur intensified by movements that reduce ventricular preload or afterload, including
■ standing from a squatting positing
■ forced exhalation against a closed airway (Valsalva maneuver)
Hypertrophic Cardiomyopathy
Initial testing in patients suspected of having
HCM
■ Obtain a 12-lead electrocardiogram
(ECG) and transthoracic echocardiography (TTE)
■ Left ventricular hypertrophy in adults with HCM
is commonly defined as a maximal left
ventricular free wall thickness ≥ 15 mm, with 13-
14 mm considered borderline.
■ Use cardiac magnetic resonance imaging
(MRI) when TTE is inconclusive
■ Obtain a 24- to 48-hour ambulatory (Holter)
monitor to detect ventricular tachycardia and
identify candidates for implantable cardioverter The classic ECG finding in hypertrophic obstructive cardiomyopathy is large
dagger-like “septal Q waves” in the lateral — and sometimes inferior — leads due
defibrillators to the abnormally hypertrophied interventricular septum
 Hypertrophic
Cardiomyopathy
General symptom treatment
■ beta blockers recommended to treat angina or dyspnea in adults, with caution in patients
with sinus bradycardia or severe conduction disease
■ in patients who do not respond to beta blockers, have side effects, or
contraindications, verapamil (titrating from low doses up to 480 mg daily) recommended to
treat angina or dyspnea, using caution in patients with
– high outflow gradients
– heart failure
– sinus bradycardia
■ diltiazem may be considered for patients who do not tolerate verapamil or in whom
verapamil is contraindicated
■ in children or adolescents, consider beta blockers to treat angina or dyspnea but monitor for
side effects,
– depression
– fatigue
– impaired scholastic performance
■ in patients with history of sustained ventricular tachycardia or ventricular fibrillation,
amiodarone may be considered when implantation of implantable cardioverter defibrillator
not feasible or not preferred by patient 
Restrictive Cardiomyopathy
Restrictive cardiomyopathy (RCM) is disease of heart muscle characterized by impaired ventricular filling with typically preserved systolic function and
normal or mildly increased ventricular wall thickness.

Most restrictive cardiomyopathies are idiopathic (also called primary restrictive cardiomyopathy), and the most common identifiable causes
include cardiac amyloidosis , cardiac sarcoidosis, and hemosiderosis.
(CC) - typical presentation includes symptoms observed with heart failure and include
Most common secondary causes include
– dyspnea and exercise intolerance
• amyloidosis
• cardiac sarcoidosis – peripheral edema
• hemosiderosis due to hemochromatosis or transfusion siderosis
– fatigue
• Additional causes include
• noninfiltrative myocardial disorders, such as – orthopnea
• systemic sclerosis – paroxysmal nocturnal dyspnea
• pseudoxanthoma elasticum
• diabetic cardiomyopathy – night sweats
• infiltrative myocardial disorders, such as – weight loss
• Gaucher disease
• mucopolysaccharidosis type I (MPS I) – ascites
• fatty infiltration
• storage diseases, such as ■ sudden cardiac death may be initial presentation(3)
• glycogen storage disorders
■ dyspnea most common symptom of idiopathic restrictive cardiomyopathy
• Fabry disease
■ most patients with cardiac amyloidosis will display arrhythmia symptoms and extra-
cardiac symptoms, such as
– syncope
– dizziness
– easy bruising
– painful sensory neuropathy
Restrictive Cardiomyopathy
General physical Skin
■ assess for bradycardia and atrial fibrillation ■ skin rashes may suggest sarcoidosis as cause
■ orthostatic hypotension common in patients with – macules, papules, and plaques may occur as
cardiac amyloidosis isolated lesions or in groups
– lupus pernio (indurated, lumpy, violaceous
■ jugular venous distension in 52% lesions) is most characteristic skin lesion in
– systolic murmur in 49% sarcoidosis
– third heart sound in 27% – mucosal bleeding and echymosis may suggest
amyloidosis cause
– pulmonary rales in 18%
– ascites in 15% Neck
– edema in 15% ■ jugular vein distention
■ additional signs suggestive of restrictive cardiac ■ lymphadenopathy may suggest sarcoidosis cause
physiology may include Abdomen
– presence of Kussmaul's sign (increase in
■ look for ascites
jugular venous distention during inspiration)
– prominent apical impulse ■ splenomegaly may suggest sarcoidosis cause

– presence of S3 but rarely S4 Extremities

– regurgitant murmurs ■ look for edema
Restrictive Cardiomyopathy
Making the diagnosis Management overview
■ consider restrictive diagnosis in patient with signs and symptoms of ■ general treatment includes diuretics and aldosterone antagonists
heart failure but without cardiomegaly or systolic dysfunction ■ consider maintenance of sinus rhythm (with medications such as amiodarone)
■ echocardiography most important test to identify left ventricular and atrial fibrillation control as precipitated by diastolic dysfunction
dysfunction ■ AV block may be treated with permanent pacemaker
– extent of dysfunction may differ by cause ■ Treatment based on underlying cause; see
– findings may include – Amyloid light chain (AL) amyloidosis
■ elevated ventricular pressure ■ early treatment targeted at reversing amyloid deposition is crucial for maximizing
■ normal or reduced ventricular diastolic volume good prognosis
■ ■ diuretics are standard therapy in cardiac amyloidosis patients
normal or mildly increased wall thickness
■ additional treatment options include a combination of autologous stem cell
■ preserved systolic function
transplantation and melphalan and/or corticosteroids
■ biopsy is only definitive diagnosis for cardiac amyloidosis – Systemic sclerosis
■ hemodynamic features characteristic of restrictive cardiomyopathy – Cardiac sarcoidosis
assessed with cardiac catheterization ■ restriction caused by hemochromatosis may be treated with iron depletion
■ most restrictive cardiomyopathies are secondary to systemic disorder, therapy and repeated phlebotomy
which may be diagnosis based on medical history, physical exam, and Surgery and procedures
testing, including
■ implantable cardioverter defibrillator (ICD)
– blood tests – ICD recommended in patients with restrictive cardiomyopathy and
– electrocardiography (ECG) sustained ventricular arrhythmia causing hemodynamic instability to reduce
– echocardiography risk of sudden cardiac death (SCD) if expected survival > 1 year with good
functional status
■ additional imaging may include chest x-ray, computed tomography, – consider implantable cardioverter-defibrillator in patients with or at risk for
and magnetic resonance imaging clinically significant arrhythmia even if left ventricular ejection fraction >
35% 
CONGENITAL HEART
DISEASE
Atrial Septal Defect
Coarctation of Aorta
Patent Ductus Arteriosus
Tetralogy of Fallot
Ventricular Septal Defect
Congenital Heart Disease
■ O2 Saturation in shunts
– Left-sided to right sided heart shunts: increased SaO2 from 75% to about 80% in affected
chambers and vessels (Step up)
– Right-sided to left sided heart shunts: decreased SaO2 from 95% to about 80% in affected
chambers and vessels (Step down)
■ Left-sided to right sided heart shunts
– Volume overload in the right side of the heart; complications include:
■ Pulmonary HTN, RVH and LVH
– Examples include VSD, ASD and Patent Ductus Arteriosus
■ Right-sided to left sided heart shunts: Cyanotic congenital heart disease
– Complications include
■ Secondary Polycythemia, Increased incidence of septic emboli/metastatic abscess
– Examples include Tetralogy of Fallot and Coarctation of the Aorta
Ventricular Septal Defect
Defect in the membranous septum; associated with Cri du chat syndrome, Trisomy 13 and Trisomy 18

Most common congenital heart disease in CHILDREN

Most SPONTANEOUSLY CLODE

(CC)
■ 80%-90% of infants with small-to-moderate ventricular septal defect (VSD) present with only mild symptoms
– may have heart murmur in the newborn nursery
– may be asymptomatic
■ infants with moderate-to-large VSD not diagnosed in newborn nursery may develop symptoms, usually between several weeks to
several months of age, of pulmonary over circulation and/or heart failure including
– rapid shallow breathing
– difficulty breathing and/or sweating during feeding
– poor caloric intake and failure to thrive
– poor weight gain
■ in older child or adult with Eisenmenger syndrome
– dyspnea on exertion
– fainting
– hemoptysis
– cyanosis
Ventricular Septal Defect
General physical Diagnosis suspected in infants with clinical presentation including
■ assess general appearance, vital signs, and growth – characteristic heart murmur
Skin – tachypnea and hepatomegaly
■ cyanosis may appear in patients with Eisenmenger syndrome – dyspnea while feeding

Cardiac – poor caloric intake

■ characteristics of heart murmur on auscultation – failure to thrive

– murmurs typically pansystolic or holosystolic ■ echocardiography is necessary to confirm and clarify type of ventricular
– small ventricular septal defects (VSDs) may be loudest, are often very high- septal defect (VSD), as well as to evaluate for associated additional
pitched, and occasionally a thrill may also be noted congenital heart disease
– large VSDs may have murmurs with ■ prenatal diagnosis may also be made by fetal echocardiography
■ constant quality and little variation throughout cardiac cycle
■ diastolic rumble at apex due to increase in mitral inflow ■ initial diagnosis is rare in adults and can be confirmed with
■ associated thrill (less common)
echocardiography
– murmur may not be present in patients with large VSDs without shunt and
patients with Eisenmenger syndrome with right-to-left shunt
■ palpation of the precordium
– left ventricular volume overload with laterally displaced impulse and/or
increased pulmonary component in the second heart sound suggests larger VSD
– right ventricular heave and/or loud pulmonary component of second heart sound
suggest Eisenmenger syndrome
Extremities
■ clubbing may appear in patients with Eisenmenger syndrome
Eisenmenger’s syndrome
■ End-stage of congenital heart disease
with initial L>R shunt
■ Persistent increase in pulmomary
blood flow results in vasculopathy,
increased PVR and eventually R to L
shunt with hypoxia
■ Treatment is heart-lung transplant,
and palliative therapies (O2,
vasodilators,etc.)
■ Suspect this in 2nd-3rd decade of life
for VSD, 5th-6th decade for ASD
Atrial Septal Defect
■Patent foramen ovale (most common type); associated with fetal alcohol syndrome
■Most common congenital heart defect in ADULTS
■Common in children with Downs Syndrome (Trisomy 21)

(CC)
■ may be asymptomatic
■ With larger ASD shunts, exertional dyspnea or heart failure may develop,
– most commonly in the fourth decade of life or later in older child
■ RV lift; S2 widely split and fixed.
 Atrial Septal Defect
Evaluation Management
■ Asymptomatic infants and small children may have closure deferred until age 3-5 years,
■ Most patients with atrial septal defect (ASDs) are asymptomatic. Some patients will be even with a large atrial septal defect (ASD).
symptomatic. ■ Children with small defects with no evidence of volume overload on the right heart and
– Tachypnea, poor weight gain, and frequent pulmonary infections can be seen in with no other indications can be closely followed
infants. ■ Choice of procedure (surgical vs. transcatheter device closure)
– More commonly, presentation of exercise intolerance (dyspnea and fatigue) or – Perform surgical closure for sinus venosus, coronary sinus, and ostium primum defects
supraventricular arrhythmias eventually develop in older patients. – Consider either procedure in patients with secundum ASD depending on the anatomy of
the defect, patient preference, and if there will be concomitant surgical repair or
■ Initial diagnostic workup replacement of the tricuspid valve.
– The most common complication of device closure is development of arrhythmias, but
– Obtain cardiac imaging with or without saline contrast, using: more severe complications can occur including thrombosis arising from the device and
■ transthoracic echocardiography in children with good acoustic windows device erosion.
■ ASD closure in adults
■ more-sensitive transesophageal echocardiography for patients with poor
acoustic windows, including adults or obese patients – Perform surgical or percutaneous ASD closure in adults with:
■ right atrial or right ventricular enlargement with or without symptoms
– Additionally obtain a chest x-ray and an electrocardiogram to check for ■ ASD with right ventricular overload as measured by echocardiography or magnetic resonance
arrhythmias. imaging
– Assess resting oxygen saturation. – Additionally consider surgical or percutaneous closure in select adult patients.
■ Closure of secundum ASD by transcatheter device in children
■ Consider additional imaging for select patients, including: – Perform transcatheter device closure in children with hemodynamically significant
secundum ASD with suitable anatomic features
– cardiac catheterization, for determining pulmonary-to-systemic blood flow ratio
■ Management after closure
– coronary angiography, particularly in adults at high risk of coronary artery – Give prophylaxis against infective endocarditis for dental and other at-risk medical
disease procedures for the 6 months following device or surgical closure
– cardiac magnetic resonance imaging in patients with sinus venosus defects or in – Give palivizumab to infants ≤ 12 months old with hemodynamically significant ASDs,
patients with secundum or primum defects with uncertain defect location or including those receiving medication to control heart failure and requiring cardiac
associated hemodynamic burden surgery, or with moderate-to-severe pulmonary hypertension or cyanosis

– transesophageal echocardiography (if not performed for diagnosis), when

considering device closure

■ Diagnosis can be confirmed by typical findings on echocardiography including presence of

an ASD on two-dimensional ultrasound and evidence of left-to-right (or right-to-left)
shunting by color Doppler.
Patent Ductus Arteriosus
Ductus arteriosis remains open; associated with congenital Rubella

More common in females (2:1)

Evaluation Management
■ Patent ductus arteriosus (PDA) may be asymptomatic and without a heart ■ Patent ductus arteriosus (PDA) may decrease in size and spontaneously close without intervention,
murmur at birth with clinical signs becoming more evident and although > 60% of all preterm infants born < 28 weeks gestation will need medical or surgical
diagnostic after day 4 of life. treatment to prevent complications associated with persistent PDA.
■ Indomethacin or ibuprofen are the first-line interventions for the therapeutic or prophylactic
■ Clinically significant PDA may also occur without a heart murmur management of PDA.
('silent duct'), especially on days 1-3 of life.
– Ductal closure is induced using a 3-dose regimen of ibuprofen or indomethacin (typically
■ Symptomatic and hemodynamically significant PDA presents with a given in 3 bolus doses over a 36-hour period).
heart murmur, most often a systolic or systolic-diastolic "machine – If echocardiography is used after each dose to assess for closure, the number of doses
murmur" at the upper left sternal border along with additional clinical given may be able to be reduced or minimized
features including: ■ Additional nonsurgical management of PDA may include:
– bounding peripheral pulses – fluid restriction - maximum 130 mL/kg/day after the third day of life
– wide pulse pressure – close monitoring of feeds due to the increased risk for necrotizing enterocolitis (NEC)
– active precordium with increased precordial impulse ■ Surgical ligation of PDA may be indicated for preterm infants:
– an unexplained worsening of respiratory status without a murmur in – weighing < 800 g with a large left atrial aortic root on an echocardiogram
premature infants – aged > 4 weeks with persistent PDA
■ Echocardiography should be performed to confirm the diagnosis of PDA, – with persistent PDA on echocardiography despite 1 or more courses of cyclooxygenase
identify its hemodynamic significance, and provide an ongoing inhibitors
assessment for clinical resolution or progression. – in whom cyclooxygenase inhibitors are contraindicated
■ B-type natriuretic peptide may help detect PDA before symptoms ■ Surgical ligation of PDA may be associated with complications including:
develop and may indicate response to treatment. – chylothorax
– pneumothorax
– recurrent laryngeal nerve damage and/or vocal cord paralysis
– development of scoliosis
■ Avoiding preterm labor and delivery is the best primary prevention for preventing PDA.
 Coarctation of Aorta

Infantile coarctation: Narrowing of the aortic isthmus occurs between the subclavian artery and the ductus arteriosus; associated w/ Turner’s Syndrome

Adult coarctation: Constriction of the ligamentum arteriosum Physical Exam (Cont)

(CC) Skin
■ in children and adults - often incidental finding but symptoms may include
■ may be pale or cyanotic in infants
– headache (due to hypertension)
– symptoms of heart failure such as dyspnea, orthopnea, fatigue, edema Chest
– other possible symptoms ■ Rib notching noted in adults
■ exercise intolerance
■ tachypnea in infant
■ leg fatigue
■ cold feet Cardiac
■ claudication ■ Auscultation (an S4 usually noted)
■ in infants - may be asymptomatic until closure of ductus arteriosus, then – continuous or systolic murmur conducted to back (murmurs may be absent in up to half of
– poor feeding neonates)
– fast breathing
– harsh systolic ejection murmur over left sternal border and back
– pale, cool extremities and poor perfusion
– systolic ejection click over mid to lower left sternal border with associated bicuspid aortic valve
Physical Exam (General)
■ in infant - increasing distress at time of ductus arteriosus closure which may include signs ■ palpation
of – thrill at suprasternal notch (when associated with aortic stenosis)
– heart failure – increased left ventricular impulse, right ventricular heave
– cardiogenic shock with complete cardiovascular collapse
Abdomen
■ in older children and adults - usually well-appearing, may have well developed upper body
with underdeveloped legs ■ liver and spleen edges palpable below costal margin
■ blood pressure measurements Extremities
– upper limb hypertension occurs with coarctation of aorta, systolic blood pressure > 20
mm Hg higher in arm than leg
■ femoral, popliteal, and dorsalis pedis pulses
– often weak or absent (but can be normal if ductus or open or significant collateral blood
flow)
– femoral pulse may be decreased or delayed compared to brachial pulse
■ cool or cold feet or legs
 Coarctation of Aorta
Evaluation
■ The clinical presentation depends on the severity. Patients with severe or critical coarctation have signs and
symptoms early in life, while mild cases may not become evident until adulthood.
■ Suspect coarctation:
– in newborns within the first few days of life with distress at the time of closing of the ductus arteriosus
– in children or adults with unexplained hypertension, heart failure, exercise intolerance, or
underdeveloped lower extremities.
– when physical examination findings include a harsh systolic murmur (may be absent in newborn)
and/or a blood pressure and pulse pressure differential between the upper and lower extremities.
■ Transthoracic echocardiogram is the test of choice to confirm the diagnosis, with computed tomography and
magnetic resonance angiography playing an increasing role.
Management
■ Initial management in symptomatic newborns involves giving prostaglandin E1 to maintain or reopen the
ductus arteriosus, as well as resuscitative efforts to correct cardiogenic shock, including inotropic support,
ventilator support, and fluid resuscitation. If the ductus arteriosus has closed, urgent surgery or transcatheter
intervention may be needed.
■ In symptomatic children, give diuretics for heart failure. For hypertension, plan prompt surgical relief rather
than starting antihypertensive medications.
■ In adults with coarctation of aorta, initial management includes diuretics for heart failure and treatment of
hypertension.
■ For correction of coarctation, options include surgery or transcatheter treatment (balloon
angioplasty and/or stent placement).
Tetralogy of Fallot
PE: Skin
(CC) ■ cyanosis
– most neonates have mild-to-moderate cyanosis without respiratory distress
■ fetus with suspected cardiac defect or – neonates with severe outflow tract obstruction likely to have more
extracardiac anomaly based on significant cyanosis, especially as ductus arteriosus closes
routine prenatal ultrasound, or – infants with very mild outflow tract obstruction may not develop
noticeable cyanosis until obstruction worsens at age ≥ 2 months
chromosomal abnormality based on (uncommon)
prenatal genetic testing Cardiac
■ harsh systolic murmur at left upper sternal border
■ neonate or infant may have history of – caused by blood flow across obstructed right ventricular outflow tract
heart murmur or cyanosis – may be shorter, less audible with severe obstruction as pressure is relieved
by right to left shunting across the ventricular septal defect
■ infant or young child with ■ loud single second heart sound
hypercyanotic episodes ("tet spells") Extremities
in unoperated tetralogy of Fallot (ask ■ clubbing may be present if condition not surgically corrected
about onset, triggers, and frequency) Neuro

***Ask about maternal use of retinoic ■ neurodevelopmental delay may occur, especially with
– associated genetic disorder
acid during pregnancy
– neonatal cardiopulmonary bypass
– chronic cyanosis
Tetralogy of Fallot
Tetralogy of Fallot is a cyanotic congenital heart disease consisting of: Management
1. "malalignment" type ventricular septal defect (VSD)
2. aortic root that overrides ventricular septum ■ Preoperative prostaglandin E1 may be initiated in
3. right ventricular outflow and/or pulmonary valve obstruction neonates with severe pulmonary outflow tract
4. right ventricular hypertrophy obstruction to keep the ductus arteriosus patent and
allow adequate pulmonary blood flow.
Evaluation
■ Hypercyanotic episodes ("tet spells"), caused by periods
■ Diagnosis is suspected based on the presence of: of increased pulmonary vascular resistance, are
– heart murmur, cyanosis, or hypoxemia in a managed by placing the infant in the knee to chest
neonate or child position. Consider medications to increase systemic
vascular resistance and/or decrease pulmonary vascular
– cardiac or extracardiac anomaly on prenatal resistance to promote pulmonary blood flow,
ultrasound supplemental oxygen, IV hydration, or subcutaneous
– chromosomal abnormality on prenatal genetic morphine.
testing ■ Surgical closure of the ventricular septal defect
■ A chest x-ray classically shows a boot-shaped heart (VSD) with relief of the pulmonary outflow obstruction
and an electrocardiogram (ECG) shows right axis is the definitive treatment.
deviation and right ventricular hypertrophy. ■ Early repair and palliation followed by later repair have
similar mortality outcomes and the decision of when to
■ confirmed by either a fetal echocardiography or repair is primarily dependent on institutional preference.
a postnatal echocardiography
 CORONARY ARTERY
DISEASE
Angina Pectoris
Prinzmetal Variant
Stable
Unstable
Acute Myocardial Infarction
Non-ST elevation
ST- Elevation
 Click icon to add picture

Approach to patient
with CAD

Common risk factors for

CAD include dyslipidemia, tobacco
abuse, hypertension, family history
of CAD, diabetes mellitus, and
obesity.
Vasospastic Angina aka Prinzmetal Variant
■ A clinical entity characterized by Treatment
episodes of rest angina that promptly ■ Nitrates and calcium channel
respond to short-acting nitrates and blockers — Calcium channel blockers
are attributable to coronary artery (nifedipine, diltiazem, verapamil,
vasospasm and amlodipine) are the first-line therapy
for vasospastic angina.
■ Symptoms indistinguishable from
angina ■ For patients who do not have acceptable
improvement in symptoms on calcium
channel blocker therapy, we add a long-
acting nitrate
 Stable angina refers to chest pain or discomfort
Stable Angina caused by reduced blood flow to the heart muscle
that is usually caused by exertion and relieved
with rest.
Management
Lifestyle Symptoms of angina include sensations of
■ Encourage 30-60 minutes of moderate-intensity aerobic activity (for
example, brisk walking) at least 5 days (preferably 7 days) per week,
squeezing, pressure, heaviness, tightness, or pain
with an increase in daily lifestyle activities (for example, gardening,in the chest.
walking breaks at work) to improve cardiorespiratory fitness in all
patients
■ Encourage risk factor modification including weight control, blood
pressure control, smoking cessation, diabetes control, adherence to
healthy diet, and management of depression and stress
Medications
■ Use sublingual nitroglycerin or nitroglycerin spray for immediate relief
of angina:
– give sublingual tablets (0.3-0.6 mg) or lingual spray (1-2 sprays
[0.4-0.8 mg])
– repeat as needed every 5 minutes for up to 3 sublingual tablet
doses or 3 lingual sprays in a 15-minute period
■ Use beta blockers (examples include carvedilol, metoprolol succinate,
and bisoprolol) as initial therapy for relief of symptoms in patients with
stable ischemic heart disease
■ Use calcium channel blockers (examples include verapamil and
diltiazem) or long-acting nitrates for relief of symptoms if beta
blockers are clearly contraindicated or cause unacceptable adverse
events
■ Use calcium channel blockers or long-acting nitrates in combination
with beta blockers for relief of symptoms when beta blockers alone are
unsuccessful
Acute Myocardial Infarction
Normal EKG

Remember your leads

STEMI
■ ST segment elevation, unlike depression, will
localize to the ECG lead of the affected
myocardium. Note that 1 mm of ST elevation in 2
contiguous leads is required to diagnose STEMI,
however there are two major exceptions.
– Anterior STEMI requires 2 mm of ST
elevation in V2 and V3 in men > 40 years Inferior MI
old according to the ACC/AHA definition. A
total of 2.5 mm is required in men < 40
years old and only 1.5 mm required in
women.
– Posterior STEMI frequently has ST
depression in V1-V3 instead of elevation
since the vectors are completely reversed. If
a posterior ECG were obtained, ST
elevation will be seen in V7-V9, although
sometimes subtle. Since these posterior
changes occur from coronary thrombosis
and urgent treatment is needed, it is Anterior MI Pattern – Tombstoning
classified as a STEMI.
NSTEMI and UA
 Acute MI Management
Management
■ Initial management should be directed at reducing myocardial ischemia, starting anti-platelet therapy,
and identifying a reperfusion strategy that will restore blood flow to the culprit artery as quickly and as
safely as possible once the diagnosis of STEMI has been made, in order to minimize myocardial
injury.
■ Give aspirin 162-325 mg (chewed) as soon as STEMI is suspected.
■ Give oxygen if needed to prevent hypoxemia and maintain O2 saturation > 90%.
■ Give nitroglycerin 0.4 mg sublingually every 5 minutes (up to 3 doses) as needed for relief of
discomfort due to ischemia, or start intravenous nitroglycerin for control of ischemia.
■ Choose a reperfusion strategy:
– For patients that present < 12 hours from symptom onset
■ Perform primary percutaneous coronary intervention (PCI) if it can be done within 120 minutes or if
there is either
– a contraindication to fibrinolytic therapy
– acute severe heart failure or cardiogenic shock 
■ Administer fibrinolysis (in the absence of contraindications) if PCI cannot be done within 120 minutes
■ Perform urgent coronary artery bypass graft (CABG) if high-risk features and coronary anatomy are
not amenable to PCI
■ Give a P2Y12 inhibitor in addition to aspirin to all patients with STEMI (unless urgent CABG
planned) such as:
– clopidogrel (Plavix) 600 mg if having a primary percutaneous coronary intervention (PCI) or 300
mg if the patient is ≤ 75 years old and treated with fibrinolytic therapy
– alternatives to clopidogrel if having PCI include:
■ prasugrel (Effient) 60 mg, then 10 mg once daily
■ ticagrelor (Brilinta) 180 mg, then 90 mg twice daily
■ Give anticoagulant therapy as follows:
– if having primary PCI, use either IV unfractionated heparin or IV bivalirudin
– if treated with fibrinolytics, use IV unfractionated heparin, or fondaparinux
HEART FAILURE
Heart Failure
Decreased ventricular contraction (Systolic dysfunction): Ischemia, myocardial fibrosis, myocarditis, ventricular aneurysm
- Characterized by low Ejection Fraction (Under 55%)

Noncompliant ventricle (Diastolic dysfunction): restricted filling due to infiltration of the muscle with amyloid, iron, or glycogen; concentric hypertrophy
- Characterized by normal to high EF (stiff ventricle) and an S4 gallop due to increase resistance to filling in late diastole

Evaluation
■ Suspect heart failure in patients with a history of dyspnea with exertion HEART FAILURE WITH
or at rest, or other symptoms of heart failure including fatigue, abdominal
distention, lower extremity swelling, orthopnea, or paroxysmal nocturnal
PULMONARY EDEMA
dyspnea. Signs may include evidence of volume overload (elevated
jugular venous pressure, peripheral edema, or rales) or diminished
perfusion (cold extremities).
■ Differential diagnosis for heart failure includes other causes of dyspnea
such as asthma, pulmonary embolism, and non-cardiogenic pulmonary
edema.
■ Consider the use of clinical prediction rules in making the diagnosis of
heart failure.
■ Obtain the following initial tests in a patient with suspected heart failure:
– 12-lead electrocardiogram (ECG)
– chest x-ray
– blood tests including complete blood count, serum chemistries,
fasting lipid profile, liver function tests, and thyroid-stimulating
hormone
– B-type natriuretic peptide (BNP) or N-terminal pro-B-type
natriuretic peptide (NT-proBNP)
– transthoracic echocardiography (TTE) to confirm diagnosis of
HFrEF and assess left ventricular ejection fraction (LVEF)
■ General physical ■ Neck
■ jugular venous distention
■ each patient encounter should include assessment
of ■ elevated jugular venous pressure (right heart failure)
– jugular venous distension approximates right atrial pressure, add 5 cm to
– volume status height above angle of Louis (that is, junction of manubrium and body of
– vital signs (pulse with manual palpation, sternum), normal is 6-8 cm H2O
blood pressure [supine and upright]) – may be present if tricuspid regurgitation present

– weight ■ hepatojugular reflux (a sign of right heart failure)

– jugular venous pressure Cardiac Palpation

■ right ventricular heave suggests right ventricular dysfunction and/or pulmonary
– presence of peripheral edema or orthopnea hypertension
■ potential indicators of heart failure with reduced ■ normal apical impulse is located in fourth or fifth intercostal space
ejection fraction (systolic dysfunction) ■ apical impulse may be palpable in < 50% of patients but palpation with patient in
– tachycardia (pulse > 90-100 beats/minute) 45 degrees left lateral decubitus position or during expiration may increase yield

– systolic blood pressure < 90 mm Hg ■ abnormal apical impulse has 31%-36% sensitivity and 89%-95% specificity for
ejection fraction < 40%, based on review of 12 studies assessing systolic
■ checking for orthostatic changes (supine and dysfunction
upright) in blood pressure and pulse may identify ■ laterally displaced or enlarged point of maximal impulse suggests ventricular
volume depletion or excessive vasodilation enlargement
Cardiac Auscultation
■ check for low perfusion at rest (cold vs. warm) with
narrow pulse pressure, cool extremities, ■ S3 - third heart sound (S3, ventricular filling gallop)
hypotension ■ occurs due to left ventricular vibration with rapid early diastolic filling (elevated
filling pressure or reduced ventricular compliance)
■ review of the role of the clinical examination in ■ sound is low-pitched, may be faint or intermittent and should be listened for with
patients with heart failure can be found in  bell of stethoscope (usually is the only mid-diastolic heart sound)
Skin ■ auscultation with patient in 45 degrees left lateral decubitus position increases
yield
■ cyanosis or pallor may be seen in severe cases ■ S3 specific but not sensitive for left ventricular dysfunction
Heart Failure
■ Four Stages of HF (ACC/AHA TREATMENT
Guidelines):
Stage A: high risk for developing HF with
no structural disorder of the heart
Stage B: structural disorder without
symptoms of HF
Stage C: past or current symptoms of HF
associated with underlying structural
heart disease
Stage D: end-stage disease who requires
specialized treatment strategies

Treat with ACEi b/c DECREASE afterload by inhibiting Angiotensin II and DECREASE preload
by inhibiting aldosterone secretion
 Stage A Stage B Stage C Stage D
At high risk, no Structural heart Structural heart Refractory HF
structural disease disease, disease with requiring
asymptomatic prior/current specialized
symptoms of HF interventions

Therapy Therapy Therapy Therapy

• Treat Hypertension • All measures • All measures • All measures
• Treat lipid under stage A under stage A under stages A,B,
disorders • ACE inhibitors in Drugs: and C

• Encourage regular appropriate • Diuretics

• Mechanical assist
exercise patients devices
• ACE inhibitors
• Beta-blockers in • Heart
• Discourage alcohol
appropriate • Beta-blockers transplantation
intake
patients • Digitalis • Continuous (not
• ACE inhibition
• Spironolactone intermittent) IV
inotropic infusions
• Dietary salt
for palliation
restriction
• Hospice care
TRAUMATIC, INFECTIOUS,
AND INFLAMMATORY
HEART CONDITIONS
Acute and subacute bacterial endocarditis
Acute pericarditis
Cardiac Tamponade
Pericardial Effusion
Acute and subacute
bacterial endocarditis

Background

■ Infective endocarditis (IE) refers to infection of the endocardial surface of

the heart, most often the heart valves, particularly prosthetic heart valves.

■ The highest incidence is reported in patients with prosthetic valves, cardiac

devices, unrepaired cyanotic heart disease, and a history of endocarditis.

■ Additional risk factors include IV drug use, prolonged bacteremia, and

certain congenital or acquired structural heart diseases.

■ Left vs. right heart involvement:

– The mitral and aortic valves are the most commonly involved in native valve
endocarditis.
– Right heart involvement, most commonly the tricuspid valve, is associated
with IV drug use or indwelling vascular catheters.

■ The great majority of cases are caused by staphylococci or streptococci.

■ Culture-negative endocarditis (CNE) refers to cases in which blood cultures

are negative due to prior antibiotic exposure or infection with fastidious
organisms and accounts for > 19% of cases.
Acute and subacute bacterial endocarditis
Signs and symptoms General physical
■ symptoms are often nonspecific and may include ■ fever, present in about 90%
– fever
HEENT
– anorexia
– malaise ■ assess for Roth spots
– weight loss – exudative, edematous lesions of retina
■ onset may be acute, subacute, or chronic – presence increases likelihood of infective endocarditis, but not diagnostic
■ patients may have protracted flu-like course ("dwindles") – reported in 2%
■ ask about recent dental procedures ( ■ conjunctival hemorrhage, present in about 5%
■ splinter hemorrhages in 8% Cardiac
■ Osler nodes (painful red lesions on hands or feet due to immune complex
deposition) in 3%
■ cardiac findings
■ Janeway lesions (painless red lesions on palms or soles indicating – new murmur, reported in 48%
microabscess formation) in 5% – worsening of preexisting murmur in about 20%
■ Roth spots in 2% ■ valves involved
■ vascular embolic event in 17% – mitral valve in about 40%
■ conjunctival hemorrhage in 5% – aortic valve in about 30%
■ splenomegaly in 11%
Abdomen
■ new heart murmur in 48%
■ assess for splenomegaly, reported in about 10%
■ worsening of preexisting murmur in 20%
■ elevated erythrocyte sedimentation rate in 61% Extremities
■ elevated C-reactive protein level in 62% ■ assess for splinter hemorrhages
■ hematuria in 26% – nonblanching, linear, reddish-brown lesions under nails
Acute and subacute bacterial endocarditis

■ Antimicrobial therapy optimal therapy based on pathogen,

antibiotic susceptibility, and absence or presence of prosthetic
materials, but typically 2-6 week IV, intramuscular, or oral
antibiotic regimen
■ Empiric antibiotic regimens vary based on valve type
– consult infectious diseases specialist prior to initiation of
antimicrobial therapy to define best empiric regimen
– for native valve endocarditis, consider vancomycin 15-20
mg/kg IV every 8-12 hours (target trough concentration of
15-20 mcg/mL) plus either ceftriaxone 2 g IV every 24
hours OR gentamicin 1 mg/kg IV or intramuscularly every
8 hours
– for prosthetic valve endocarditis, consider vancomycin 15-
20 mg/kg IV every 8-12 hours plus gentamicin 1 mg/kg IV
every 8 hours plus rifampin 300 mg orally or IV every 8
hours
 Bacterial Endocarditis Prophylaxisis
AHA/ACC Antibiotic Regimens for Dental Procedures (Given as Single Dose 30-60
Minutes before Procedure):
Situation Agent Adult Dose (30-60 Children's Dose
Minutes before (30-60 Minutes
Procedure) before Procedure)

Able to take oral • Amoxicillin • 2 g orally • 50 mg/kg orally

medications

Unable to take oral • Ampicillin • 2 g intramuscularly • 50 mg/kg

medications • Cefazolin or or IV intramuscularly or
ceftriaxone • 1 g intramuscularly IV
or IV

Able to take oral • Cephalexin* • 2 g orally • 50 mg/kg orally

medication but • Clindamycin • 600 mg orally • 20 mg/kg orally
allergic to penicillins • Azithromycin or • 500 mg orally • 15 mg/kg orally
clarithromycin

Unable to take oral • Cefazolin* or • 1 g intramuscularly • 50 mg/kg

medication and ceftriaxone* or IV intramuscularly or
allergic to penicillins • Clindamycin • 600 mg IV
intramuscularly or • 20 mg/kg
IV intramuscularly or
IV
Acute Pericarditis

Background
■ Acute pericarditis is an inflammation of the
pericardium that may occur as an isolated
condition or as a manifestation of an
underlying systemic disease.
■ Most cases of acute pericarditis are
idiopathic but other causes include
infections, metabolic disorders, myocardial
infarction, and neoplasms.
■ Acute pericarditis may be accompanied by
symptoms and laboratory evidence of
myocarditis
 Acute Pericarditis
Evaluation
■ Suspect acute pericarditis in a patient complaining of abrupt or sub-acute substernal or left-
sided chest pain that is severe, sharp, and increases with inspiration.
■ Physical exam findings may include tachycardia and pericardial friction rub.
■ Obtain the following tests to evaluate a patient with suspected acute pericarditis:
– (ECG) findings consistent with pericarditis according to stage of may include:
■ stage I (hours to several days)
– PR-segment depression, except in aVR
– PR segment elevation in lead aVR
– concave-upward ST-segment elevation with concordant (upright) T waves
– absence of reciprocal ST-segment changes
– leads aVR and V1 may have ST-segment depression
■ stage II (a few days to weeks)
– ST and PR segments return to baseline
– T waves progressively flatten and invert
■ stage III (several weeks)
– T-wave inversion persists
■ stage IV (months)
– gradual resolution of T-wave inversion
– diffuse ST-segment depression and T-wave inversion may persist up to 3 months
– echocardiography to assess for pericardial effusion and cardiac function
– blood tests for markers of inflammation and myocardial injury
■ CRP, ESR, Trop, CK-MB
– chest x-ray to evaluate cardiac silhouette and detect possible pulmonary or mediastinal
pathology
Acute Pericarditis
Pericardial Effusion
Pericardial effusion is characterized by the collection of fluid in the pericardial space.

Cardiac tamponade occurs when there is increased intrapericardial pressure due to accumulation of fluid in the pericardial space
that is often associated with impaired cardiac function, tachycardia, and hypotension.

Overview Management
■ Suspect pericardial effusion with or without tamponade in patients with ■ Admit high-risk patients (patients with fever > 38 degrees C,
diminished heart sounds, elevated jugular venous pressure, and subacute onset, large or rapidly accumulating pericardial effusion,
tachycardia. cardiac tamponade, or lack of response to aspirin or non-steroidal
anti-inflammatory drug after ≥ 1 week of therapy) to hospital
■ Use echocardiography to evaluate patients with suspected pericardial
effusion and/or cardiac tamponade. ■ Consider empirical treatment with anti-inflammatory therapy when
the underlying cause of effusion is acute pericarditis
■ Perform serial echocardiography after initial detection of pericardial
effusion to monitor the rate of accumulation of effusion and ■ Consider the temporary cessation of anticoagulants to reduce the
development of tamponade. risk of tamponade.
■ Perform a chest x-ray in all patients ■ Perform pericardiocentesis and drainage
■ In patients with pericardial effusion obtain blood tests for markers of – urgently if patient is hemodynamically compromised and/or
inflammation (such as C-reactive protein) and markers of inflammation has signs of cardiac tamponade guided by echocardiography
and myocardial injury for patients with pericarditis – if large pericardial effusion not responsive to medical therapy
■ Obtain electrocardiography (ECG) if suspicion for acute pericarditis or suspect unknown bacterial or neoplastic etiology
■ Consider pericardiotomy (open surgical drainage) - this may be
■ Additional imaging may include:
required if pericardiocentesis is not effective.
– contrast tomography (CT)/magnetic resonance imaging (MRI)
■ Consider pericardiectomy in patients with large effusion not
– cardiac catheterization
responding to repeated pericardiocentesis or intrapericardial
■ Consider performing an analysis of pericardial effusion to evaluate the therapy to promote continuous drainage.
underlying cause of effusion, particularly when infectious or neoplastic
causes are suspected.
Clinical Presentation Effusion vs Tamponade
■ Pericardial effusion - typically symptoms ■ Cardiac tamponade - typical presentation
include includes
– dyspnea during exertion, which may – hypotension
progress to orthopnea or chest pain – pulsus paradoxus
– tachypnea – increased jugular venous pressure
– additional symptoms include – quiet precordium
■ cough – additional findings may include
■ dysphagia ■ tachycardia (may be absent in
■ nausea hypothyroidism and uremia)
■ hoarseness ■ fever
■ hiccups ■ radiation of substernal pain to neck and
jaw
■ lack of appetite
■ abdominal discomfort or nausea (caused
■ weakness by local compression due to tamponade)
■ shoulder discomfort
Cardiac Tamponade
Clinical condition caused by the accumulation of blood/fluid in the pericardial space in the setting of trauma

Fluid collection causes reduced ventricular filling and cardiac output, leading to hemodynamic compromise

The rapidity of fluid collection, rather than the amount of fluid, has more of an impact on the severity of clinical
signs and symptoms

Physical
■ Examine closely the area of the “Cardiac Box”
■ Listen for breath sounds and check for chest subcutaneous crepitus,
because of likely associated hemopneumothorax
■ Evaluate for penetrating wounds and count number of entry and exit
wounds for gunshot wounds
■ Assess for concurrent injuries by performing a head-to-toe examination
of the patient, assuming time allowed based on hemodynamic stability
■ Beck’s triad (elevated jugular venous pressure, low blood pressure, and
muffled heart sounds) is a classic description of tamponade that is rarely
found in the trauma patient
■ TIP: elevated jugular venous pressure may not be present due to
hypovolemic shock
■ TIP: unexplained, persistent hypotension should heighten suspicion for
this diagnosis
Cardiac Tamponade
Diagnostic Studies Management
■ Consider obtaining a trauma panel: complete blood count ■ Swift transport to definitive care, preferably to a trauma center, is
(CBC), chemistry panel, prothrombin time/INR (PT/INR), paramount to survival for surgery or interventional radiology
type and screen, lactate, venous blood gas /arterial blood gas ■ Initial assessment: focus on the primary survey, as described in Advanced
(VBG/ABG) in the setting of cardiac injury, but will not help Trauma Life Support (ATLS), aimed at recognizing and treating immediate
in the diagnosis and initial management life threats
■ Obtain a chest x-ray – Early airway management should be considered for patients with
significant chest trauma, hypoxia, or hypotension
– May reveal an enlarged cardiac silhouette, widened
mediastinum (> 6 cm on posteroanterior [PA] or > 8 cm – Hypotension should be treated with IV crystalloid fluids and/or blood
on anteroposterior [AP] view), pneumomediastinum, or – TIP: be aware that patients with pericardial tamponade are very
associated pneumohemothoraces preload dependent and should be aggressively volume-resuscitated
before intubation, if possible
■ Obtain a cardiac view using bedside ultrasonography
Medications
– Echocardiography or Focused Assessment with
Sonography in Trauma (FAST) is a rapid, noninvasive, ■ Intravenous crystalloid fluids for findings of hypovolemia or need to
physician-performed modality allowing accurate maximize preload
diagnosis of hemopericardium – Give 1 liter boluses of isotonic fluid
– Right ventricular diastolic collapse is a sensitive finding Consultations
for cardiac tamponade
■ Trauma surgery
– If performed, entire E-FAST (Extended FAST), can
assess for concurrent intraperitoneal free fluid and ■ Cardiothoracic surgical team consultation should be considered
pneumothorax ■ Interventional Radiology/Cardiology