CARDIO Flashcards
Oxygen Consumption Rate
CO X (arterial O2 content − venous O2 content)
Can either be measured using a spirometer or by using an assumed value (usually 250 mL O2/min (or 3.5–4.0 mL/kg/min).
↑ Pulse Pressure
Hyperthyroidism
Aortic regurgitation
Aortic stiffening (isolated systolic hypertension in elderly)
Obstructive sleep apnea (↑ sympathetic tone)
Anemia
Exercise (transient)
↓ Pulse Pressure
Aortic stenosis
Cardiogenic shock
Cardiac tamponade
Advanced HF
Loud S1
Mitral stenosis (increased transvalvular pressure gradient)
Tachycardia (short diastole)
Hyperdynamic states (e.g., left-to-right shunts [increased transvalvular blood flow])
Short PR interval (e.g., atrioventricular reentrant tachycardia (AVRT))
S1 is generally not heard in aortic and pulmonary areas. It is considered “loud” if it is as loud as S2 in aortic and pulmonary areas.
Soft S1
Severe mitral stenosis (mitral valves are severely calcified and immobile)
Conditions that impair the transmission of heart sounds to the chest wall → COPD, pneumothorax, pericardial effusion, obesity
Left bundle branch block (LBBB) (delayed onset of systole)
Prolonged PR interval (e.g., first-degree heart blocks)
S1 is considered “soft” if S2 is louder than S1 at the mitral region.
S1 with Variable Intensity
Atrial fibrillation
AV dissociation
Auscultatory alternans → severe LV failure, large pericardial effusion
Loud A2
Arterial hypertension
Coarctation of the aorta
Loud P2
Pulmonary hypertension
Atrial septal defects
P2 is a soft sound and is usually heard only in the pulmonary area; therefore, P2 is considered “loud” when it is clearly heard in the mitral area or when it is louder than A2. A loud P2 is highly specific for pulmonary hypertension.
Signs of ↑ Jugular Venous Pressure (JVP)
Jugular venous distention
Kussmaul sign → distention of the jugular veins during inspiration due to the negative intrathoracic pressure that attempts to pull blood into the right heart, which is restricted by noncompliant pericardium or myocardium (e.g., constrictive pericarditis, restrictive cardiomyopathy, right atrial tumors, ventricular tumors, right HF, massive PE)
Hepatojugular reflux
Causes of ↑ Jugular Venous Pressure (JVP)
Right heart failure Fluid overload Tricuspid valve dysfunction Pericardial effusion Constrictive pericarditis Cardiac tamponade SVC syndrome Pulmonary hypertension
Kussmaul Sign
Distention of the jugular veins (↑ JVP) during inspiration due to the negative intrathoracic pressure that attempts to pull blood into the right heart, which is restricted by noncompliant pericardium or myocardium (e.g., constrictive pericarditis, restrictive cardiomyopathy, right atrial tumors, ventricular tumors, right HF, massive PE)
Kussmaul sign is absent during pericardial tamponade because the negative intrathoracic pressure is still able to ensure filling of the right ventricle.
JVP a wave
First peak caused by atrial contraction
Absent in atrial fibrillation
Prominent in tricuspid valve atresia
JVP c wave
Second peak caused by tricuspid valve closure, contraction of the right ventricle, and bulging of the tricuspid valve into the right atrium
cv wave (merging of the c and v waves; Lancisi sign) → severe tricuspid valve regurgitation
JVP x descent
A drop in JVP caused by atrial relaxation
Absent in:
- Tricuspid valve regurgitation
- Right heart failure
JVP v wave
The third peak caused by venous refilling of the right atrium against the closed tricuspid valve
Prominent in:
- Tricuspid valve regurgitation
- Right heart failure
JVP y descent
A drop in JVP caused by decreased right atrial pressure as blood flows into the right ventricle after opening of the tricuspid valve
The y descent is sharp and deep due to rapid filling in the first half of diastole.
Prominent in:
- Tricuspid valve regurgitation
- Constrictive pericarditis
Absent in:
- Cardiac tamponade
- Tricuspid valve stenosis
Third Heart Sound (S3)
- Early diastolic sound that is heard immediately after S2
- Ventricular gallop → S1 is followed by S2 and S3 in close succession, resembling the cadence of the word “Kentucky” (Ken-TUC-ky) on auscultation. Described as a ventricular gallop because the pattern of S1-S2-S3 on auscultation resembles the sound of a galloping horse.
- Occurrence:
1. Physiological → young individuals (< 40 years of age), athletes, or pregnant women
2. Pathological: - Chronic mitral regurgitation
- Aortic regurgitation
- Heart failure (due to dilated ventricles)
- Dilated cardiomyopathy
- Thyrotoxicosis
- L → R shunt
Fourth Heart Sound (S4)
- The fourth heart sound is often called an atrial gallop because the sound originates in the atria
- S1 rapidly follows S4, resembling the cadence of the word “Tennessee” (Ten-nes-SEE) on auscultation.
Occurrence:
- Physiological → advanced age (due to reduce ventricular compliance)
- Pathological if palpable
- Ventricular hypertrophy (e.g., hypertension, aortic stenosis, cor pulmonale)
- Ischemic cardiomyopathy
- Acute myocardial infarction
Split S1
Occurs when the closure of the tricuspid valve is delayed (e.g., due to an RBBB), resulting in the sound of tricuspid valve closure heard shortly after mitral valve closure Reversed splitting (tricuspid valve closure before mitral valve closure) is rare.
Causes:
Conduction disorders
Hemodynamic cause
S2 Physiological Split
The sound of aortic valve closure (A2) precedes the sound of pulmonary valve closure (P2) during inspiration
Inspiration → fall in intrathoracic pressure → increase in venous return to the right side of the heart → prolonged right ventricular systole → delayed closure of P2
Pooling of blood in pulmonary circulation → shortened left ventricular systole → premature A2
Especially pronounced among young individuals (chest wall excursion and, therefore, the likelihood of hearing a physiological split decreases with age)
S2 Wide Split
An exaggerated physiological split, which is more pronounced during inspiration (A2 precedes P2)
Caused by any condition that increases right ventricular afterload or decreases left ventricular preload
Increased right ventricular afterload → prolonged right ventricular systole
Decreased left ventricular preload → shortened left ventricular systole
Causes: Pulmonary hypertension Pulmonary valve stenosis RBBB Massive pulmonary embolism Severe mitral regurgitation Wolff-Parkinson-White syndrome Constrictive pericarditis
S2 Fixed Split
Does not change with respiration and tends to be wide, i.e., the split is also audible during expiration (since the right and left sides of the heart communicate, the pressure difference that normally exists during respiration evens out; therefore, the duration of the split does not change with inspiration or expiration)
Left-to-right shunt in ASD → RV volume overload → delay in the closure of the pulmonary valve
Cause:
Atrial septal defect (ASD)
Severe RV failure
S2 Paradoxical Split (Reversed Split)
Audible during expiration but not inspiration
Expiration → A2 is heard after P2 during expiration due to delayed closure of the aortic valve (split reversal)
Inspiration → the closure of the pulmonary valve is also delayed, resulting in A2 and P2 occurring simultaneously (i.e., a paradoxical decrease in the split during inspiration)
Cause: Aortic stenosis Left bundle branch block HOCM (LV outflow tract obstruction) Early excitation of the right ventricle (e.g., RV pacing, Wolff-Parkinson-White syndrome)
S2 Absent split
No splitting of S2
Cause:
- Severe aortic stenosis (geriatric) (A2 is absent due to calcification and, in severe cases, immobility of the aortic valves)
- VSD with Eisenmenger syndrome (pediatric) (VSD results in communication between the left and right ventricles. They then essentially function as a single ventricle, leading to A2 and P2 occurring simultaneously, during both inspiration and expiration (fused A2-P2)).
Lancisi sign
A physical exam finding in patients with severe tricuspid regurgitation.
The V wave merges with the C wave, forming a prominent wave on jugular venous examination that can resemble the carotid-pulse wave of aortic regurgitation.
Erb point
Location → 3rd left parasternal intercostal space
The best overview of heart sounds and murmurs can be obtained at the Erb point.
Pathology:
- Diastolic murmurs → aortic regurgitation, pulmonic regurgitation
- Systolic murmurs → HOCM
Aortic area Auscultation
Location:
2nd right parasternal intercostal space
Pathology: Aortic stenosis Aortic regurgitation Coarctation of the aorta Flow murmur (eg, physiologic murmur)
Pulmonic area Auscultation
Location:
2nd left parasternal intercostal space
Pathology: Pulmonary stenosis Pulmonary regurgitation ASD Flow murmur
Mitral area Auscultation
Location:
5th left intercostal space in the midclavicular line
Pathology:
Mitral stenosis
Mitral regurgitation
Mitral valve prolapse (MVP)
Tricuspid area Auscultation
Location:
4th left parasternal intercostal space
Pathology:
Tricuspid stenosis
Tricuspid regurgitation
Aortic Ejection Click
- Opening of a stiff aortic valve (results from the abrupt stop of the valve leaflets upon opening)
- Heard best with the diaphragm of a stethoscope at the aortic region with the patient seated and leaning forward
- Timing → early systolic sound (immediately after S1)
- Etiology → aortic stenosis
Mitral Valve Prolapse Click
- Mitral valve prolapse into the left atria during systole
- Heard best with the diaphragm of a stethoscope at the mitral region with the patient in left lateral position (MVP click is a high-frequency sound)
- Timing → midsystolic sound (often accompanied by a holosystolic, uniform murmur of mitral regurgitation.)
- Etiology → mitral valve prolapse
Mitral Valve Opening Snap
- Opening of a stiff mitral valve
- Heard best with the bell of a stethoscope at the mitral region with the patient in a left lateral position (mitral valve opening snap is a high-pitched)
- Timing → early diastolic sound (immediately after S2)
- Etiology → mitral stenosis
Mechanical Valve Clicks
- S1 and S2 sound like clicks.
- Heard best with the diaphragm of a stethoscope
- Timing → coincides with a normal S1 and S2
- Etiology → prosthetic valve
Pericardial Friction Rub
- Scratching sound due to friction between the visceral and parietal pleura (similar to the sound made when walking on snow)
- Heard best over the left sternal border during expiration with the patient sitting upright and leaning forward
- Timing → systolic or diastolic sound
- Etiology → pericarditis
Pericardial Knock
- Sudden cessation of ventricular filling against a rigid pericardial sack
- Heard best at the left sternal border
- Timing → diastolic sound
- Etiology → constrictive pericarditis
Functional Heart Murmur (Physiological or Innocent)
- An ejection murmur due to increased or turbulent blood flow across normal aortic and/or pulmonary valves, e.g., due to a hyperdynamic circulation
- Most commonly occurs in children and young adults
- Cardiac pathology must be ruled out.
- Soft (grade < 3/6 without a thrill)
- Most commonly midsystolic or continuous
- Position change → position-dependent; varies in intensity or disappears
Pathological Murmur
- Caused by structural defects (valvular disease or heart defects)
- Typically grade > 3/6
- Thrill may be present
- Systolic, diastolic, or continuous
- Position change → rarely disappears
Functional (Physiological or Innocent) Systolic Murmurs
- Children
- Pregnancy
- During states of excitement or strenuous activity
- Anemia
- Fever, sepsis
- Thyrotoxicosis
- Beriberi
- Arteriovenous fistula
- Still murmur
Pathological Systolic Murmurs
- Aortic stenosis
- Pulmonary stenosis
- Mitral regurgitation
- Tricuspid regurgitation
- VSD
- Coarctation of the aorta
- HOCM
Still Murmur
- Most common innocent murmur in children (differential diagnosis includes a VSD, which is a harsh, loud, pansystolic murmur)
- Grade 1–3 midsystolic murmur heard best at the left midsternal border or between the left lower sternal border and the apex
- Louder when the patient is supine and softer when the patient is upright
- Unknown etiology
Functional (Physiological or Innocent) Continuous Murmur
Hyperdynamic state
Cervical venous hum
Pathological Continuous Murmur
PDA
Arteriovenous fistulas
Cervical Venous Hum
- Functional (Physiological or Innocent) Continuous Murmur
- Common benign finding in children due to turbulent flow in internal jugular veins
- Heard best at the infraclavicular and supraclavicular regions (more common on the right side)
- Becomes softer or disappears with flexion of the head, compression of the jugular vein, or in the supine position
- May radiate to the 1st and 2nd ICS (could be misdiagnosed as a PDA if it is heard on the left side)
Inspiration Maneuver
Effect on cardiac parameters:
- ↑ RV preload
- ↓ LV preload
- No effect on LV afterload
Effect on murmurs:
- ↑ Intensity of murmurs arising from the right side of the heart
- ↓ Intensity of murmurs arising from the left side of the heart
Opposite effect is achieved with expiration
Expiration Maneuver
Effect on cardiac parameters:
- ↑ LV preload
- ↓ RV preload
Effect on murmurs:
- ↑ Intensity of murmurs arising from the left side of the heart
- ↓ Intensity of murmurs arising from the right side of the heart
Opposite effect is achieved with inspiration
Valsalva Maneuver
Effect on cardiac parameters:
- ↓ RV preload
- ↓ LV preload
- ↓ LV afterload
Effect on murmurs:
- ↑ Intensity of MVP (with early midsystolic click) and hypertrophic cardiomyopathy (HCM) murmurs
- ↓ Intensity of murmurs arising from the left side of the heart
Opposite effect is achieved by squatting, lying down quickly or raising the legs
Abrupt Standing Maneuver
Effect on cardiac parameters:
- ↓ RV preload
- ↓ LV preload
- ↓ LV afterload
Effect on murmurs:
- ↑ Intensity of MVP (with early midsystolic click) and hypertrophic cardiomyopathy (HCM) murmurs
- ↓ Intensity of murmurs arising from the left side of the heart
Opposite effect is achieved by squatting, lying down quickly or raising the legs
Squatting Maneuver
Effect on cardiac parameters:
- ↑ RV preload
- ↑ LV preload
- No effect on LV afterload (afterload may increase with squatting)
Effect on murmurs:
- ↑ Intensity of all murmurs
- ↓ Intensity of MVP (with late midsystolic click) and HCM murmurs
- Tetralogy of Fallot: The severity of tet spells and the associated murmurs decrease with squatting.
- MVP: click occurs later in systole
Opposite effect is achieved by standing up suddenly
Lying Down Quickly Maneuver
Effect on cardiac parameters:
- ↑ RV preload
- ↑ LV preload
- No effect on LV afterload (afterload may increase with squatting)
Effect on murmurs:
- ↑ Intensity of all murmurs
- ↓ Intensity of MVP (with late midsystolic click) and HCM murmurs
- Tetralogy of Fallot: The severity of tet spells and the associated murmurs decrease with squatting.
- MVP: click occurs later in systole
Opposite effect is achieved by standing up suddenly
Raising the Legs Maneuver
Effect on cardiac parameters:
- ↑ RV preload
- ↑ LV preload
- No effect on LV afterload (afterload may increase with squatting)
Effect on murmurs:
- ↑ Intensity of all murmurs
- ↓ Intensity of MVP (with late midsystolic click) and HCM murmurs
- Tetralogy of Fallot: The severity of tet spells and the associated murmurs decrease with squatting.
- MVP: click occurs later in systole
Opposite effect is achieved by standing up suddenly
Hand grip Maneuver
Effect on cardiac parameters:
- No effect on RV preload
- No effect on LV preload
- ↑ LV afterload
Effect on murmurs:
- ↑ Intensity of murmurs resulting from backward flow of blood in the left side of the heart (e.g., aortic regurgitation, mitral regurgitation, VSD, MVP)
- ↓ Intensity of murmurs associated with forward flow of blood in the left side of the heart (e.g., mitral stenosis, aortic stenosis, HCM)
- MVP: click occurs later in systole
Opposite effect is achieved with the use of amyl nitrite (vasodilator)
Sitting and Leaning Forward Maneuver
Effect on cardiac parameters:
- No effect
Effect on murmurs:
- ↑ Intensity of murmurs at or near the aortic valve (e.g., aortic stenosis, aortic regurgitation, coarctation of the aorta, HOCM)
Lying Down in the Left Lateral Position Maneuver
Effect on cardiac parameters:
- No effect
Effect on murmurs:
- ↑ Intensity of murmurs at or near the mitral valve (e.g., mitral stenosis, mitral regurgitation, MVP)
Acute Aortic Regurgitation Etiology
- Infective endocarditis (most common valvular cause of acute aortic regurgitation)
- Aortic dissection (ascending aorta) (most common aortic cause of acute aortic regurgitation)
- Chest trauma
- Iatrogenic complications (e.g., after percutaneous aortic balloon dilation or transcatheter aortic valve replacement (TAVR))
Chronic Aortic Regurgitation Etiology
Primary valvular defect (aortic root dilation is often secondary in primary valvular defects)
- Congenital bicuspid aortic valve → most common cause of AR in young adults in high-income countries
- Calcific aortic valve disease → most common cause of AR in older patients in high-income countries (approximately 75% of patients with aortic valve stenosis also have some degree of aortic valve regurgitation)
- Rheumatic heart disease → most common cause of AR in lower-income countries
Aortic dilatation (can be caused by any disease or defect of the ascending aorta and/or the aortic root and does not always directly involve the aortic valve)
- Connective tissue disorders (e.g., Marfan syndrome, Ehlers-Danlos syndrome)
- Chronic hypertension
- Aortitis of any etiology (e.g., tertiary syphilis)
- Thoracic aortic aneurysm
Acute Aortic Regurgitation Signs & Symptoms
- Sudden, severe dyspnea
- Rapid cardiac decompensation secondary to heart failure
- Pulmonary edema
- Symptoms related to underlying disease (e.g., fever due to endocarditis, chest pain due to aortic dissection)
- Soft S1 (due to elevated LV end-diastolic pressure leading to an early closure of the mitral valve)
- Soft and short early diastolic murmur
Findings specific to acute AR:
- Reduced cardiac output
- Elevated end-diastolic left ventricular pressure
- Early mitral valve closing (the sudden and massive volume increase in the left ventricle leads to an elevation in LV pressure, which then rapidly exceeds left atrial pressure, leading to the early closing of the mitral valve)
- Rapid equilibration of aortic and left ventricular pressure
- ECG shows possible signs of the underlying cause (e.g., signs of myocardial ischemia in aortic dissection)
- Chest x-ray shows normal heart silhouette and signs of pulmonary congestion or edema
Acute Aortic Regurgitation Findings
Auscultation
- Soft S1 (due to elevated LV end-diastolic pressure leading to an early closure of the mitral valve)
- Soft and short early diastolic murmur
Findings specific to acute AR:
- Reduced cardiac output
- Elevated end-diastolic left ventricular pressure
- Early mitral valve closing (the sudden and massive volume increase in the left ventricle leads to an elevation in LV pressure, which then rapidly exceeds left atrial pressure, leading to the early closing of the mitral valve)
- Rapid equilibration of aortic and left ventricular pressure
ECG shows possible signs of the underlying cause (e.g., signs of myocardial ischemia in aortic dissection)
Chest x-ray shows normal heart silhouette and signs of pulmonary congestion or edema
Chronic Aortic Regurgitation Sign & Symptoms
May be asymptomatic for up to decades despite progressive LV dilation
Palpitations
Symptoms of high pulse pressure
- Water hammer pulse of peripheral arteries characterized by rapid upstroke and downstroke
- Pulsing of carotid arteries with rapid upstroke and downstroke
- Quincke sign → visible capillary pulse when pressure is applied to the tip of a fingernail
- De Musset sign → rhythmic nodding or bobbing of the head in synchrony with heartbeats
Symptoms of left heart failure
- Exertional dyspnea
- Angina
- Orthopnea
- Easy fatigability
- Syncope
Point of maximal impulse (PMI) → diffuse, hyperdynamic, and displaced inferolaterally (due to eccentric hypertrophy and increased stroke volume)
Chronic Aortic Regurgitation Findings
Auscultation
- S3 (sign of volume overload)
- High-pitched, blowing, decrescendo early diastolic murmur (as a result of regurgitant, retrograde blood flow over the aortic valve)
AR due to valvular disease → heard best in the left third and fourth intercostal spaces and along the left sternal border (Erb point)
AR due to aortic root disease (e.g., aortic dissection) → heard best along the right sternal border
Worsens with squatting and handgrip (these maneuvers increase afterload)
- Austin Flint murmur
Rumbling, low-pitched, middiastolic or presystolic murmur heard best at the apex
Caused by regurgitant blood striking the anterior leaflet of the mitral valve, which leads to premature closure of the mitral leaflets
- In more severe stages, possibly a harsh, crescendo-decrescendo midsystolic murmur that resembles the ejection murmur heard in aortic stenosis (as a result of a large volume of blood ejected over the aortic valve in an anterograde direction)
- Findings specific to chronic AR → increased LV size and volume due to eccentric hypertrophy and dilation. LV function is often preserved)
ECG shows signs of LVH, ST-segment depression and T-wave inversion in I, aVL, V5, and V6
Chest x-ray shows signs of LVH and enlarged cardiac silhouette
Water Hammer Pulse
Physical exam finding in which palpation of a distal arterial pulse (such as the radial pulse) shows a rapid upstroke followed by prompt collapse of the vessel, (e.g., “bounding pulse”).
Occurs due to rapid and large stroke volume ejection into the arterial system and is most commonly associated with aortic regurgitation.
Referred to as Corrigan’s pulse in the carotid artery and water hammer pulse in the limbs.
Austin Flint Murmur
Rumbling, low-pitched, middiastolic or presystolic murmur heard best at the apex
Caused by regurgitant blood striking the anterior leaflet of the mitral valve, which leads to premature closure of the mitral leaflets
Auscultated in patients with chronic mitral regurgitation
Primary Mitral Regurgitation Etiology
Mitral regurgitation caused by direct involvement of the valve leaflets or chordae tendinae
- Degenerative mitral valve disease (mitral valve prolapse, mitral annular calcification, ruptured chordae tendinae)
- Rheumatic fever
- Infective endocarditis
- Ischemic MR (e.g., papillary muscle rupture following acute MI)
Secondary Mitral Regurgitation Etiology
Caused by changes of the left ventricle that lead to valvular incompetence
- Coronary artery disease or prior myocardial infarction causing papillary muscle involvement
- Dilated cardiomyopathy (e.g., peripartum cardiomyopathy) and left-sided heart failure
Acute Mitral Regurgitation Sign & Symptoms
- Dyspnea
- Symptoms of left-sided heart failure
- Signs and symptoms of pulmonary edema (e.g., bibasilar, fine, late inspiratory crackles)
- Cardiogenic shock → poor peripheral perfusion, tachycardia, tachypnea, and hypotension
- Palpitations (new-onset atrial fibrillation is common in patients with acute MR)
Acute Mitral Regurgitation Findings
Auscultation
- Soft, decrescendo murmur
- No murmur in severe regurgitation with LV systolic dysfunction or hypotension
- Potentially → S3 heart sound
Normal Left atrium
Normal left ventricular size
Normal LV ejection fraction
Elevated pulmonary artery pressure
Normal RV ejection fraction
Troponin elevation may indicate myocardial ischemia.
BNP typically normal because of the acute onset of symptoms
ECG findings are often nonspecific.
Chest x-ray → normal-sized cardiac silhouette
Acute Mitral Regurgitation Management
- All patients with acute primary MR should undergo urgent surgical repair or valve replacement. While awaiting surgery, any symptoms of heart failure should be managed with medical therapy (e.g., diuretics, nitrates, antihypertensive drugs).
- Surgical therapy indications
1. Acute primary MR (urgent surgery)
2. Acute secondary MR that does not adequately respond to medical therapy
Surgical procedures
- Valve repair → preferred option because of the reduced risk of mortality and complications (mitral valve replacement is associated with higher rates of short- and long-term mortality than valve repair. Additionally, most mitral valve replacements are prosthetic rather than biological, because the lifespan of biological valves is short (∼ 10 years); therefore, they risk causing thromboembolism, endocarditis, and hemorrhage as a result of lifelong anticoagulation)
- Valve replacement → may be necessary if there is severe destruction of the mitral valve
- Revascularization therapy → in ischemic MR with papillary muscle rupture
Medical therapy
- For acute primary MR, medical treatment is usually only a temporizing measure while surgery is planned. The aim is to reduce the symptoms of heart failure and improve forward flow.
- Heart failure management (may worsen hypotension; use caution in hemodynamically unstable patients)
1. Vasodilators to reduce afterload and improve cardiac output - Nitroprusside (reduces both pulmonary and systemic vascular resistance, potentially reducing the degree of MR and increasing cardiac output)
- Nitrates (e.g., nitroglycerin) (decreases pulmonary artery pressure and left ventricular preload)
2. Diuretics (e.g., furosemide) for acute pulmonary edema (reduces preload, treats acute pulmonary edema, and may increase cardiac efficiency) - Hypotension → inotropes (e.g., dobutamine )
- Atrial fibrillation → consider cardiac resynchronization therapy to improve hemodynamics.
Chronic Mitral Regurgitation Management
- Management is guided by the symptoms and extent of heart failure and the cause of MR.
- Medical therapy should be initiated in all patients to optimize cardiac function but surgery is the definitive treatment option.
Medical management
- Identify and treat any underlying cause (particularly in secondary MR).
- Heart failure management (ACE inhibitors and beta blockers are thought to favorably affect left ventricular remodeling in MR)
1. Diuretics (e.g., furosemide)
2. ACE inhibitors (e.g., lisinopril)
3. Beta blockers (e.g., metoprolol tartrate)
Surgical management and transcatheter mitral repair
- Chronic primary MR indications
- Asymptomatic patients with LV dysfunction (LVEF 30–60% or LV end-systolic diameter ≥ 40 mm)
- Symptomatic patients with LVEF 30–60 %
- Contraindications → once LVEF is < 30%, surgery is generally not recommended because of the high mortality rate and low likelihood of symptom improvement. (Ventricular remodeling in MR initially appears to be reversible if the valve is repaired; however, by the time severe changes have occurred and LVEF is< 30%, the ventricle does not remodel) - Chronic secondary MR indications
- Consider for patients with severe MR and persistent symptomatic heart failure (NYHA classes III–IV) despite optimal medical management (surgical benefit is less clear because the regurgitation is driven by changes to the ventricle, not the mitral valve, which generally remains normal)
Bundle of His
- Location → directly below the cardiac skeleton, within the membranous part of the interventricular septum
- Receives impulses from the AV node
- Splits into left and right bundle branches (Tawara branches) → the right bundle travels to the right ventricle; the left bundle splits into an anterior and a posterior branch to supply the left ventricle → terminate into terminal conducting fibers (Purkinje fibers) of the left and right ventricle
- Prevents retrograde conduction
- Filters high-frequency action potentials so that high atrial rates (e.g., in atrial fibrillation) are not conducted to the myocardium
- Frequency → ca. 30–40/min
Purkinje Fibers
- Location → terminal conducting fibers in the subendocardium
- Conduct cardiac AP faster than any other cardiac cells
- Ensure synchronized contraction of the ventricles
- Purkinje fibers have a long refractory period.
- Form functional syncytium: forward incoming stimuli very quickly via gap junctions to allow coordinated contraction
- Frequency → ca. 30–40/min
PR-Segment Depression
Atrial injury or inflammation → abnormal atrial repolarization → PR-segment depression
Etiology:
- Pericarditis (note that pericarditis is also associated with ST-segment elevation in multiple leads and can be confused with STEMI. PR-segment depression in the same leads is an indicator of pericarditis)
- Pericardial effusion
- Atrial ischemia or infarction
Pathological Q Waves
Myocardial ischemia → myocyte necrosis beneath the electrode → electrical “window” resulting from dead tissue → electrode reading of electrical activity of opposite myocardial wall → Q wave
ECG findings:
- Abnormally wide (≥ 40 ms)
- Abnormally deep (≥ 0.2 mV or > 25% of the R wave amplitude) or detectable in V1–V3
Etiology:
- Myocardial injury
- Myocardial infarction
- Cardiac infiltrative disease (e.g., sarcoidosis, amyloidosis) - Ventricular enlargement
- Hypertrophic cardiomyopathy
- Hypertensive heart disease
- Other cardiomyopathies - Altered ventricular conduction
- LBBB
- WPW - Acute pulmonary embolism
- Congenital heart disease
- Incorrect placement of the upper limb leads
Dominant R Wave
Increase in the depolarization vector toward lead V1 → tall R wave
ECG findings:
- Tall R wave in lead V1
- Normal in children and young adults
Etiology:
- RVH
- RBBB
- Posterior myocardial infarction
- HCM
- WPW
Poor R-wave Progression
Ventricular depolarization vector reduced or directed posteriorly → deviation of the depolarization vector away from electrodes → insufficient increase in the size of the R wave and deep S waves
ECG findings:
- Absence of the normal increase in the size of R waves from lead V1 to V6
- May be a normal variant
Etiology:
- Anterior wall myocardial infarction
- Right heart strain (e.g., in COPD)
- RVH
- LBBB
- LAFB
- WPW
- Incorrect electrode placement
Persistent S Wave
Ventricular depolarization vector reduced or directed posteriorly → deviation of the depolarization vector away from electrodes → insufficient increase in the size of the R wave and deep S waves
ECG findings:
1. Presence of an S wave in all precordial leads
Etiology:
- Anterior wall myocardial infarction
- Right heart strain (e.g., in COPD)
- RVH
- LBBB
- LAFB
- WPW
- Incorrect electrode placement
Bundle Branch Blocks
Bundle branch blocks → transmission of impulse via remaining functional branch or fascicle → slower ventricular depolarization → long QRS complex
Incomplete bundle branch block: QRS duration of 0.1–0.12 s
Complete bundle branch block: QRS duration ≥ 0.12 s
Left bundle branch block (LBBB)
ECG findings
- No R wave in lead V1
- Deep S waves (forming a characteristic W shape)
- Wide, notched R waves in leads I, aVL, V5, V6 (forming a characteristic M shape)
- Loss of Q waves in the lateral leads
Etiology
- Cardiac
- Coronary artery disease
- Myocardial infarction
- Hypertension
- Myocardial contusion
- Restrictive cardiomyopathy
- Dilated cardiomyopathy - Hyperkalemia
- Digoxin toxicity
- Degenerative disease of the conduction tissue
Right Bundle Branch Block (RBBB)
ECG findings
- An rsr’, rsR’, or rSR’ complex (forming a characteristic “rabbit ears” or M shape) in leads V1, V2
- Tall secondary R wave in lead V1
- Wide, slurred S wave in leads I, V5, V6
- Associated feature: ST segment depression and T-wave inversion in leads V1, V2, and sometimes V3
- Usually a normal axis
- Normal variant in ∼ 5% of individuals
Etiology
- Cardiac
- Coronary artery disease
- Myocardial infarction
- Myocardial contusion
- Mitral stenosis - Pulmonary
- Pulmonary hypertension
- Pulmonary embolism
- COPD - Congenital heart defects
- Atrial septal defect
- VSD
- Pulmonary stenosis
- Tetralogy of Fallot - Brugada syndrome (a pseudo-RBBB)
- Degenerative disease of the conduction tissue
Bifascicular Block
ECG findings
- An RBBB with either of the following:
- Left anterior fascicular block (common form) (in the absence of a concurrent RBBB, the QRS complex would be < 120 ms in addition to the criteria below)
- Left axis deviation
- qR pattern in lead aVL
- Left posterior fascicular block (rare) (in the absence of a concurrent RBBB, the QRS complex would be < 120 ms in addition to the criteria below)
- Right axis deviation
- rS pattern in leads I and aVL
- qR pattern in leads III and aVF
Etiology
- Coronary artery disease
- Valvular heart disease
- Hypertension
- Cardiomyopathies
- Chagas disease
Left Ventricular Hypertrophy (LVH)
Increased muscle mass (hypertrophy) → taller R waves (in leads V5, V6) and S waves (in leads V1, V2)
The amplitude of the QRS complex in the precordial leads is used to assess for ventricular hypertrophy.
ECG findings
- Sokolow-Lyon criteria → RV5 or RV6 + SV1 or SV2 ≥ 3.5 mV
- Left ventricular strain pattern → ST depression with T wave inversion in the left precordial leads in a resting ECG
Etiology:
- Hypertension
- Aortic stenosis
- Coarctation of the aorta
- Mitral regurgitation
- Hypertrophic cardiomyopathy
- Myocarditis
- VSD
Right Ventricular Hypertrophy (RVH)
Increased muscle mass (hypertrophy) → taller R waves (in leads V1, V2) and deeper S waves (in leads V5, V6)
Any of the following may suggest RVH:
- Right axis deviation
- Dominant R wave in lead V1 (R wave > 0.6 mV or R/S > 1)
- Deep S wave in lead V5 (> 1 mV) or V6 (> 0.3 mV)
- Sokolow-Lyon criteria → RV1 or R2 + SV5 or S6 ≥ 1.05 mV
Etiology:
- Pulmonary hypertension
- Pulmonary embolism
- COPD
- Mitral stenosis
- Congenital heart defects
ST Elevation
ECG findings (one of the following):
- ≥ 0.1 mV in limb leads
- ≥ 0.2 mV in precordial leads
Etiology:
- Normal finding → small, concave ST elevations in young, healthy adults due to early repolarization
- STEMI → significant ST elevations in ≥ 2 anatomically contiguous leads (corresponding to occlusion of a specific artery)
- LBBB
- Pericarditis → widespread ST elevations
- Pulmonary embolism
- Perimyocarditis (usually, the ST elevation follows a deepS wave)
- Brugada pattern
- Left ventricular aneurysm
J Wave
Also referred to as Osborn wave
ECG findings:
1. Positive deflection at the J point
Etiology:
- Brugada syndrome
- Idiopathic ventricular fibrillation
- Hypercalcemia
- Hypothermia
Brugada Syndrome
- Rare autosomal dominant genetic mutation that leads to abnormal cardiac conduction and sudden death
- The most common identified mutation affects cardiac voltage-gated sodium channels.
- Most common in Asian men
- Symptoms mostly manifest in adulthood.
Clinical features:
- Often an incidental finding, as most patients are asymptomatic
- Syncope
- Polymorphic ventricular tachycardia
- Ventricular fibrillation
ECG findings
- Brugada pattern: pseudo-RBBB with ST elevation in leads V1–V3
- J waves in leads V1–V3
- Rule out underlying heart disease (e.g., cardiac stress test and echocardiography).
Treatment
- Avoid certain medications (e.g., certain antiarrhythmics, psychotropics, anesthetic agents).
- Avoid excessive alcohol intake, cocaine, and large meals.
- Treat fever with antipyretics.
- Implantable cardiac defibrillator (ICD)
- Screen all first-degree relatives annually with clinical examination and ECG.
Complications
- Sudden cardiac death
- Increased risk of atrial fibrillation
T-wave Inversion
May be due to any of the following:
- Ventricular repolarization vector directed away from the electrode of the ECG lead
- Changes in myocardial cellular electrophysiology (e.g., during ischemia or infarction)
- Changes in the sequence of ventricular activation (e.g., in bundle branch blocks or cardiac hypertrophy)
ECF findings
- Amplitude ≥ -0.1 mV
- May be a normal finding in:
- Leads III, aVR, or V1 (May also be normal in lead V2 if T-wave inversion in lead V1 is also present)
- Children - New-onset T-wave inversion (i.e., not present on the patient’s previous ECGs)
Etiology:
- Coronary artery disease (myocardial ischemia)
- Bundle branch blocks
- Pulmonary embolism (pulmonary embolism is known to produce an S1Q3T3 pattern: a deep S wave in lead I, Q wave in lead III, and inverted T wave in lead III)
- Perimyocarditis (pericarditis initially causes diffuse, saddle-shaped ST elevation followed by T-wave inversion)
- Ventricular hypertrophy
- Digoxin
- Intracranial hemorrhage (asymmetric T wave inversion)
- Persistent juvenile T-wave pattern
- Wellens syndrome (symmetrical T wave inversion)
T-wave Flattening
May be due to any of the following:
- Ventricular repolarization vector directed away from the electrode of the ECG lead
- Changes in myocardial cellular electrophysiology (e.g., during ischemia or infarction)
- Changes in the sequence of ventricular activation (e.g., in bundle branch blocks or cardiac hypertrophy)
ECG findings:
- Amplitude between 0.1 mV and -0.1 mV
- T wave appears flatter than normal.
Etiology:
- Hypokalemia
- Hypoglycemia
- Myocardial ischemia
- Hypothyroidism
Peaked T Wave
May be due to any of the following:
- Ventricular repolarization vector directed away from the electrode of the ECG lead
- Changes in myocardial cellular electrophysiology (e.g., during ischemia or infarction)
- Changes in the sequence of ventricular activation (e.g., in bundle branch blocks or cardiac hypertrophy)
ECG findings:
1. Tall, narrow, symmetrically peaked
Etiology:
- Hyperkalemia
- Hypermagnesemia
- High vagal tone
Hyperacute T Wave
May be due to any of the following:
- Ventricular repolarization vector directed away from the electrode of the ECG lead
- Changes in myocardial cellular electrophysiology (e.g., during ischemia or infarction)
- Changes in the sequence of ventricular activation (e.g., in bundle branch blocks or cardiac hypertrophy)
ECG findings:
1. Broad, asymmetrically peaked
Etiology:
- Early stages of a STEMI (often precedes ST elevation and Q waves)
- Prinzmetal angina (induces ischemia and leads to hyperacute T waves as in STEMI)
Biphasic T Wave
May be due to any of the following:
- Ventricular repolarization vector directed away from the electrode of the ECG lead
- Changes in myocardial cellular electrophysiology (e.g., during ischemia or infarction)
- Changes in the sequence of ventricular activation (e.g., in bundle branch blocks or cardiac hypertrophy)
ECG findings:
- T wave consisting of an upward and downward deflection
- The initial deflection is variable and can be either up or down.
Etiology:
- Initial positive deflection
- Acute myocardial ischemia
- Wellens syndrome - Initial negative deflection: hypokalemia
Shortened QT Interval
Abnormal ventricular depolarization or repolarization (depending on the etiology) → shortened QT interval
ECG findings:
1. < 390 ms (some sources describe different cutoff values for a shortened QT interval.)
Etiology:
- Hypercalcemia
- Hyperkalemia
- Digoxin effect
- Increased sympathetic tone (e.g., hyperthyroidism, fever)
- Congenital short QT syndrome
U Wave
- Small deflection after the T wave
- Polarity is the same as the T wave
- Best seen in leads V2 to V4, but not always visible
- Normal finding in athletes
Etiology
- Exact origin is unknown
- Thought to be due to delayed repolarization of the midmyocardial cells (myocardium) and the His-Purkinje system
Causes of prominent U waves
- Hypokalemia
- Hypercalcemia
- Bradycardia
Acquired Long QT Syndrome
Drug-induced LQTS (usually substances that block potassium outflow during the rapid repolarization phase)
- Antiarrhythmics
- Class Ia (e.g., quinidine, disopyramide, procainamide)
- Class III (e.g., sotalol; uncommonly, amiodarone) - Antibiotics (e.g., macrolides, fluoroquinolones)
- Antihistamines (e.g., diphenhydramine)
- Antidepressants (most tricyclic antidepressants and tetracyclic antidepressants, some SSRIs, lithium)
- Antipsychotics (e.g., haloperidol, ziprasidone)
- Anticonvulsants (e.g., fosphenytoin, felbamate)
- Antiemetics (ondansetron)
- Antifungals (e.g., azoles)
- Antiparkinson medications
- Opioids
Electrolyte imbalances → hypokalemia, hypomagnesemia, hypocalcemia
Acute CNS insult→ ischemic stroke or intracranial hemorrhage (QT prolongation is one of the most frequent ECG abnormalities seen following ischemic stroke or intracranial hemorrhage)
Endocrine disorders → hypothyroidism
Nutritional deficiencies → severe vitamin D deficiency (uncommon) (anorexia nervosa was previously thought to be associated with acquired LQTS. However, a long-term follow-up study published by the American heart association (AHA) found no evidence to support this)
Wolff-Parkinson-White Syndrome (WPW)
- Congenital condition characterized by intermittent tachycardias and signs of ventricular preexcitation on ECG, both of which arise from an accessory pathway known as the bundle of Kent
- A congenital accessory pathway, the bundle of Kent, connects the atria and ventricles, bypassing the AV node and leading to ventricular preexcitation.
- May be associated with structural abnormalities of the heart, in particular Ebstein anomaly
- ∼ 10% of patients have multiple accessory pathways (more common with coexisting structural heart disease).
- The prevalence of WPW pattern is 0.1–0.2% in the general population and 0.55% in first-degree relatives.
- A proportion of these cases is due to familial WPW syndrome, a rare autosomal-dominant genetic disorder that causes conduction abnormalities and hypertrophic cardiomyopathy.
- ♂ > ♀
- Symptoms typically develop at 20–40 years of age.
- May be asymptomatic (WPW pattern) or associated with arrhythmias (WPW syndrome), including:
1. AVRT (most common; 80%)
2. Atrial fibrillation (15–35%; incidence increases with age)
3. Atrial flutter (5%)
4. Others (rare): MAT, FAT, ventricular fibrillation
ECG findings in WPW:
While in sinus rhythm, a preexcitation pattern may be present.
- Short PR interval (this is shortened due to the earlier activation of the ventricle through the accessory pathway)
- ECG delta wave → a slurred upstroke at the start of the QRS complex, secondary to preexcitation (this reflects partial early-onset slow ventricular depolarization through the bypass tract, which is then interrupted by the rapid depolarization of the rest of the ventricle through the His-Purkinje system. ECG delta wave is not seen in all patients)
- Widened QRS (due to the abnormal depolarization of the ventricle, which occurs slowly, myocyte to myocyte, rather than through the rapidly conducting Purkinje fibers)
Can show any of the arrhythmias associated with WPW
WPW with atrial fibrillation or flutter
- Heart rate may be very high (> 200–250/minute) because impulses from the atria are transmitted via the accessory pathway directly to the ventricles, bypassing the AV node. (The refractory period of the accessory pathway may be extremely short, allowing very rapid transmission)
- Wide QRS complexes are commonly seen because of ventricular preexcitation.
- Appearance may be very similar to that of polymorphic ventricular tachycardia
Paroxysmal Supraventricular Tachycardia (PSVT)
- Any SVT with a narrow QRS complex and an abrupt onset
- Most commonly caused by AV nodal reentry
- Commonly presents with sudden-onset palpitations, diaphoresis, lightheadedness.
- Treatment → terminate re-entry by slowing AV node conduction (eg, vagal maneuvers, IV adenosine). Electrical cardioversion if hemodynamically unstable. Definitive treatment is catheter ablation of re-entry tract.
Atrial Fibrillation Risk Factors
Cardiovascular risk factors
- Advanced age
- Hypertension
- Diabetes mellitus
- Smoking
- Obesity
- Sleep apnea
Intrinsic cardiac disorders
- Coronary artery disease
- Valvular heart disease (especially mitral valve disease) (atrial fibrillation is much more common in patients with mitral stenosis than in those with mitral regurgitation. Approximately two-thirds of patients with mitral stenosis will develop atrial fibrillation at some point)
- Congestive heart failure (CHF)
- Preexcitation tachycardia. e.g., Wolff-Parkinson-White (WPW) syndrome (atrial fibrillation occurs in approx. 20% of patients with WPW syndrome)
- Sick sinus syndrome (tachycardia-bradycardia syndrome)
- Cardiomyopathies
- Pericarditis
- Congenital channelopathies
Noncardiac disorders
- Pulmonary disease → COPD, pulmonary embolism, pneumonia
- Hyperthyroidism (increases the response of the heart to sympathetic stimulation)
- Catecholamine release and/or increased sympathetic activity
- Stress → sepsis, hypovolemia, post-surgical state (especially following cardiac surgery), hypothermia
- Pheochromocytoma
- Cocaine, amphetamines
- Electrolyte imbalances (hypomagnesemia, hypokalemia)
- Drugs → e.g., adenosine, digoxin
- Holiday heart syndrome → irregular heartbeat classically triggered by excessive alcohol consumption, but also sometimes by moderate alcohol consumption, stress, dehydration, or lack of sleep
- Chronic kidney disease (reduced renal function can lead to hypertension, LVH, and, eventually, atrial stretch and fibrosis, which are predictors of Afib. CKD can also activate the renin-angiotensin-aldosterone system, which can result in atrial remodeling and fibrosis.)
Complications of Long-Standing Atrial Fibrillation
- Acute left heart failure → pulmonary edema
- Thromboembolic events → stroke/TIA, renal infarct, splenic infarct , intestinal ischemia , acute limb ischemia
- Life-threatening ventricular tachycardia
