✅ DDx: Chest Pain, 🛫Dyspnea, Syncope, 🔥 IE, ECG 📈 Flashcards
Differential Diagnosis of Chest Pain:
Skin: Laceration, Burns, Herpes
Subq: Cellulitis, Abscess
MSK: Chostochondritis, sprains, strains, myositis
Pleural Space: Pleurisy, Pulmonary embolism, Pulmonary Tumor, Pneumothorax, Pneumonia
Pericardium: Pericarditis
Heart: Acute Coronary Syndrome, MI, myositis
Esophagus: Esophageal rupture, GERD, Esophagitis, Boerhaves
Trachea: Tracheitis, Tracheal Tear
Aorta: Aortic dissection, Aortic stenosis
Drugs: Cocaine
Psychiatric: Panic Disorder
Classic Angina
Classic:
- Typical location (eg, 🗡substernal), quality & duration
- Provoked by exercise OR emotional stress
- Relieved by rest OR nitroglycerin
Atypical
- 2 of the 3 characteristics of classic angina
Nonanginal
- <2 of the 3 characteristics of classic angina
Atypical Angina
Pain that has the quality and characteristics of angina, OR occurs with exertion, but NOT both:
May be a sense of heaviness not consistently related to exertion or relieved by rest, or it may be pain with an atypical character (sharp or stabbing) but predictably brought on by exercise and relieved by rest.
Vasospastic angina (formerly Prinzmetal angina)
Pathogenesis
- Hyperreactivity of coronary smooth muscle.
- Caused by severe spasm of an epicardial coronary artery. The area of vasospasm is often near a nonhemodynamically significant atherosclerotic lesion.
Clinical presentation
- Young patients (age <50)
- Smoking (minimal other CAD risk factors)
- Recurrent chest discomfort
- Occurs at rest or during sleep
- Spontaneous resolution <15 minutes
Diagnosis
- Ambulatory ECG: ST elevation
- Coronary angiography: No CAD
Treatment
- 🍦Calcium channel blocker (preventive)
- Sublingual nitroglycerin (abortive)
Vascular smooth muscle hyperreactivity leads to focal or diffuse spasm of the coronary arteries, transient myocardial ischemia, and resulting angina. Patients typically have recurrent episodes of chest discomfort that occur at rest or during sleep. Cigarette smoking is a known risk factor, but patients are typically young and lack other risk factors for coronary artery disease (eg, hypertension, diabetes). As the vasospasm leads to transmural myocardial ischemia, the diagnosis is typically made by ambulatory ECG showing contiguous ST elevation during an episode of chest discomfort.
The underlying pathophysiologic mechanism of vasospastic angina is similar to that of Raynaud phenomenon, a disorder characterized by cold- or stress-induced hyperreactivity of the digital arterial smooth muscle, leading to episodic vasospasm in the fingers and toes. Accordingly, calcium channel blockers are an effective first-line pharmacologic therapy for both Raynaud phenomenon and vasospastic angina. However, despite the underlying pathophysiologic similarities, an increased prevalence of Raynaud phenomenon in patients with vasospastic angina (or vice versa) has not been clearly established.
Stress Testing🏃🏽♀️🧪 Rx: 💊
Dx:
Exercise ECG 🏃🏽♀️ testing is the standard stress test for the diagnosis of CAD in patients with normal baseline ECG findings. Stress testing is most useful in patients with an intermediate pretest probability of CAD. For patients with a low pretest probability of CAD, stress testing is not useful because an abnormal test result is likely a false-positive finding and a normal test result only confirms the low pretest probability of CAD. For patients with a high pretest probability of CAD, stress testing is not useful to diagnose CAD and empiric medical therapy should be initiated.
Cx: ❗ abnormalities that limit ST-segment analysis:(left bundle branch block, left ventricular hypertrophy, paced rhythm, Wolff-Parkinson-White pattern), imaging:
🔊echocardiography (TTE) or ☢ nuclear [Thallium, dipyridamole] stress test increases diagnostic accuracy and ability to determine the site and extent of ischemia. For women in their mid 40’s, stress ECGs are often false positive, so a stress test with imaging is most appropriate. Cx: Claudication
Pharmacologic stimulation of heart rate should be used in patients who are unable to exercise. Cx: COPD (Adenosine)
🎵 Adenosine and its synthetic analogs (eg, regadenoson, apadenoson) stimulate adenosine A2A receptors on vascular smooth muscle cells, causing coronary vasodilation and increased myocardial blood flow. There is a several-fold augmentation of blood flow in nonobstructed coronary arteries. Blood flow is increased in stenosed coronary arteries as well but to a much lesser extent. This relative blood flow difference is magnified from rest, causing a detectable reduction in radioactive isotope uptake by myocardial cells in areas supplied by a stenotic coronary artery (appears as an ischemic defect on myocardial perfusion imaging).
Coronary angiography allows direct evaluation of the coronary anatomy, with possible percutaneous coronary intervention or surgical revascularization if indicated.
Rx:
β-Blockers
Used in patients with a hx of MI and in stable heart failure. The dose should be adjusted to achieve a heart rate of 50 to 60 beats/min. [Complete β-blockade typically results in a resting pulse rate of approximately 55 to 60/min.]
🍦 Dihydropyridine calcium channel blockers (eg, amlodipine, felodipine, nifedipine)
[Second-line agents] Reduce blood pressure; do not affect heart rate and can be used with β-blockers. Avoid short-acting agents (such as nifedipine).
🍦 Nondihydropyridine calcium channel blockers (verapamil, diltiazem)
Mostly used in patients who cannot take β-blockers. Avoid in patients with heart failure; use with caution in patients taking β-blockers (bradycardia).
🃏 ACE inhibitors
Reduce blood pressure and afterload by a reduction in peripheral vascular resistance. Reduce ventricular remodeling and fibrosis after infarction. Improve long-term survival in patients with LVEF ≤40% and, possibly, in patients with high cardiovascular risk (eg, diabetes mellitus, PVD).
💣Long-acting nitrates
Can be used with β-blockers and calcium channel blockers. Tachyphylaxis occurs with continued use; requires nitrate-free period (8-12 h/d). Side effects include headache. Avoid in patients taking PDE-5 inhibitors.
💣Short-acting nitrates
Dilate coronary arteries and reduce preload. Indicated for all patients with chronic stable angina for use on an as-needed basis.
👨🏽Ranolazine
Indicated as add-on therapy for patients not responding to standard therapy; used in combination with a nitrate, β-blocker, or calcium channel blocker. Avoid using with verapamil or diltiazem (prolongs QT interval).
🧯 Aspirin
Indicated for all patients with stable angina, barring contraindications; reduces major cardiovascular events by 33%.
♨ Thienopyridine derivatives (eg, clopidogrel, ticlopidine, prasugrel)
Aspirin alternatives, but significantly more expensive. Improve outcomes in patients with recent ACS or stent placement. In patients with stable CAD, thienopyridine derivatives do not improve outcomes.
Statins
In patients with mild to moderate elevations in total and LDL cholesterol and a history of MI, statins are associated with a 24% risk reduction for fatal and nonfatal MI.
Tx: Coronary revascularization has been shown to be beneficial in patients with chronic stable angina and the following conditions: angina pectoris that is refractory to medical therapy; a large area of ischemic myocardium and high-risk criteria on stress testing; high-risk coronary anatomy, including left main coronary artery stenosis or three-vessel disease; and significant coronary artery disease with reduced left ventricular systolic function. In appropriately selected patients, revascularization, with either percutaneous coronary intervention or coronary artery bypass grafting (CABG) surgery, has been shown to reduce angina, increase longevity, and improve left ventricular performance.
Pulmonary embolism (PE)
Acute-onset dyspnea and pleuritic chest pain (exacerbated by deep breathing, coughing, sneezing, or laughing🤣) are the most common symptoms, occurring in 73% and 66% of patients, respectively.
Tachypnea (70% of cases), tachycardia (30%), and low-grade fever (15%)
Sudden-onset dyspnea, nonproductive cough, tachycardia, and mild hypoxia is highly suggestive of acute pulmonary embolism (PE).
Lower extremity deep vein thrombosis (DVT) is divided into 2 categories:
- Proximal/thigh (eg, iliac, femoral, popliteal): These are the source of >90% of acute PEs, probably due to their large caliber and proximity to the lungs.
- Distal/calf: These are less likely to embolize and more likely to spontaneously resolve .
The Wells score, has been established to help the clinician assess the likelihood of DVT.
Modified Wells score
+3 points
Clinical signs of DVT: Paralysis or recent plaster cast, recent immobilization or major surgery, tenderness along the deep veins, swelling of the entire leg, a difference in calf circumference of more than 3 cm compared with the other leg, pitting edema, and collateral superficial veins.
Alternate diagnosis less likely than PE: Clinical suspicion that an alternative diagnosis is likely is assigned -2 points.
+1.5 points
Previous PE or DVT
Heart rate >100
Recent surgery or immobilization
+1 point
Hemoptysis
Cancer
Total score for clinical probability
≤4 = PE unlikely
>4 = PE likely
Dx: A D-dimer assay is a simple, relatively noninvasive test that has been shown to have a high negative predictive value, especially if suspicion for DVT is low.
If intermediate or high probability, ventilation-perfusion scan or spiral CT is indicated.
Given clinically stablity (normotensive, mild hypoxemia) with no evidence of distress, the diagnosis of PE can be confirmed with CT angiography (CTA). If CTA confirms PE, clinical judgment can dictate whether anticoagulation is initiated or other options are pursued (eg, inferior vena cava filter placement) based on the estimated risk of bleeding from the peptic ulcer.
A ventilation-perfusion scan is the most appropriate study to confirm the suspected diagnosis of pulmonary embolism in this patient with kidney failure. Ventilation-perfusion scans detect abnormalities of blood flow in comparison to the pattern of ventilation, with areas of mismatch between perfusion and ventilation being evidence of vascular occlusion due to a pulmonary embolus.
CRX shows tachycardia (only 10% S1Q3T3)
📉 RH Cath: Low or normal pulmonary capillary wedge pressure is expected in acute pulmonary embolism due to impaired blood flow through the pulmonary circulation to the left atrium.
Tx: Early, effective anticoagulation decreases the mortality risk of acute PE and should be considered in patients without absolute contraindications (eg, hemorrhagic stroke, massive gastrointestinal bleed).
Intravenous or subcutaneous unfractionated heparin, low-molecular-weight heparin, or fondaparinux. Most patients with pulmonary embolism are treated in the hospital, although carefully selected, stable patients may be candidates for outpatient treatment. Following initial therapy, patients are usually transitioned to warfarin for long-term therapy, with factor Xa and direct thrombin inhibitors being increasingly-available options for this purpose. UFH is primarily cleared by the reticuloendothelial system rather than the kidneys (CKD patients). Fondaparinux is cleared exclusively by the kidneys. Therefore, it is contraindicated in patients with poor renal function. In addition, fondaparinux is not reversible with protamine. Consequently, potential bleeding is much more difficult to treat.
Bridge: 🖐🏽5 days of overlap with LMWH and warfarin therapy and an international normalized ratio of 2 or more for 24 hours. Randomized clinical trials show that 5 to 7 days of treatment with unfractionated heparin is as effective as 10 to 14 days of treatment when transitioning to warfarin therapy. If a patient is receiving an adequate warfarin dose, it takes at least 5 days for vitamin K-dependent factor activity levels to decrease sufficiently for therapeutic anticoagulation (INR of 2-3) to occur.
Pneumothorax
Sudden onset of pleuritic chest pain and dyspnea in a smoker or COPD patient. Other findings include sudden, sharp, nonradiating pleuritic chest pain and shortness of breath with hyperresonance, decreased breath sounds, and decreased chest wall expansion on the side of the pneumothorax in a patient with underlying lung disease.
Dx: Chest radiograph (initial test of choice) or CT scan confirms the diagnosis.
Pneumothorax occurring in patients without known lung disease or a clear precipitating cause is termed primary spontaneous pneumothorax (PSP). PSP tends to occur more often in men, smokers, and those with a family history of PSP.
Aortic Dissection
Clinical features
- History of HTN, Marfan syndrome, cocaine use, turner syndrome (bicuspid aortic valve, aortic root dilation, aortic coarctation, and hypertension), pregnancy (eg, increased blood volume).
- Severe, sharp, tearing chest or back pain
- ± >20 mm Hg variation in SBP between arms
Diagnosis
- ECG: normal or nonspecific ST- & T-wave changes
- Chest x-ray: mediastinal widening
- CT angiography or TEE for definitive diagnosis
Complications due to extension (involved structure)
- Stroke (carotid artery)
- Acute aortic regurgitation (aortic root/valve)
- Horner syndrome (carotid sympathetic plexus)
- Myocardial ischemia/infarction (coronary artery ostia)
- Pericardial effusion/tamponade (pericardium)
- Hemothorax (pleural cavity)
- Renal injury (renal arteries)
- Abdominal pain (mesenteric arteries)
- Lower extremity paraplegia (spinal arteries)
Treatment
- Pain control (eg, morphine)
- Intravenous beta blockers (eg, esmolol)
- ± Sodium nitroprusside (if SBP >120 mm Hg)
- Emergent surgical repair for ascending (type A) dissection
TAA usually results from age-related degenerative changes that lead to disruption of the aortic wall medial layer with loss of elasticity and consequent aortic dilation. The changes are likely due to a combination of enzymatic breakdown of structural proteins (eg, collagen, elastin) and physical factors such as systemic hypertension and repeated stress from the pulsating arterial wave. Underlying connective tissue disease (Marfans; cystic medial necrosis (described in patients with bicuspid aortic valves), syphilis, Ehlers-Danlos syndrome, trauma, and bacterial infections also increases the risk. Although Marfan syndrome is responsible for almost 50% of the aortic dissections seen in patients age <40, it is an uncommon cause in older patients (age >60).
❗ Type A dissection involving the ascending aorta is considered a 🔪surgical emergency, with mortality rates of 1%-2% per hour following symptom onset; rapid diagnosis and treatment are critical. Most TAAs (60%) involve the ascending aorta (between the aortic valve and the brachiocephalic artery)
Type A (ascending aorta) dissections can lead to aortic rupture into the pericardial space and hemopericardium, which can rapidly progress to cardiac tamponade and cardiogenic shock.
Type B dissections occur in the proximal descending aorta (distal to the left subclavian artery), and, if stable, may be managed medically by controlling the blood pressure and heart rate to prevent extension of the dissection.
Px: Patients often have diastolic murmurs due to aortic insufficiency from a proximal dissection into the valve. A tracheal tug is considered positive if the pulsating aorta is felt when the trachea is pulled upward, a sign that the expanding aorta is contacting the left mainstem bronchus.
Tx:
The goals of initial therapy of aortic dissection include:
Adequate pain control
Reduction of systolic blood pressure (SBP) to 100-120 mm Hg.
🎺Intravenous beta blockers (eg, labetalol, propranolol, esmolol) are preferred for initial therapy to reduce heart rate, SBP, and LV contractility. These effects lead to a decrease in the rate of rise in SBP (dP/dt) and in aortic wall stress. [Decrease in left ventricular (LV) contractility to reduce aortic wall stress.]
🧨Nitroprusside 🥈 is commonly used to titrate systolic blood pressure to less than 120. Cx: Can cause reflex sympathetic stimulation with consequent rises in heart rate, LV contractility, and aortic wall stress. Used as a second-line agent only if SBP remains above goal (ie, >120 mm Hg) despite adequate beta blockade.
Dx:
- CT angiography is the initial study of choice in hemodynamically stable patients with no evidence of renal dysfunction. It can reveal an intimal flap separating the true and false lumens in the aorta.
- MR angiography is more time consuming and requires the administration of gadolinium-containing contrast agents for contrast enhancement; it should be avoided in patients with moderate to severe kidney disease due to the risk of nephrogenic systemic fibrosis.
- Transesophageal (not transthoracic) echocardiography (TEE) has excellent sensitivity and specificity and is the preferred diagnostic study in patients with ❗ hemodynamic instability or renal insufficiency; a transthoracic echocardiogram may not visualize parts of the aorta well.
Cx: Retrograde extension of the intimal tear can involve the aortic valve and cause acute aortic regurgitation (AR). As seen in this case, affected patients can develop sudden onset of worsening chest pain, hypotension, and pulmonary edema, along with the early decrescendo diastolic murmur of AR.
Ascending aortic dissection can propagate proximally into the pericardial space and lead to hemopericardium and cardiac tamponade.
Marfan syndrome
Skeletal
- Arachnodactyly
- ↓ Upper-to-lower body segment ratio, ↑ arm-to-height ratio
- Pectus deformity, scoliosis, or kyphosis
- Joint hypermobility
Ocular
- Ectopia lentis
Cardiovascular
- Aortic dilation, regurgitation, or dissection
- Mitral valve prolapse
Pulmonary
- Spontaneous pneumothorax from apical blebs
Skin
- Recurrent or incisional hernia
- Skin striae
Marfan syndrome involves mutations that affect the extracellular matrix protein fibrillin-1 and result in disruption of connective tissue structural integrity throughout the body. The effects of the disease on the aortic root are especially prominent and account for the majority of morbidity and mortality in these patients; dissection, if it occurs, usually occurs prior to age 40.
Aneurysmal aortic root dilation is extremely common in Marfan syndrome (up to 80% of cases) and can frequently lead to chronic aortic regurgitation, identified by an early decrescendo 💎diastolic murmur best heard at the right upper sternal border. Left untreated, the aneurysmal dilation can progress to a type A aortic dissection that can extend to involve the aortic valve annulus, further impairing aortic valve closure and resulting in acute aortic regurgitation. The mortality rate for type A aortic dissection is high, and treatment requires emergent surgical repair.
AAA
The incidence of AAA is higher in men than in women and in whites versus blacks, and it increases with age.
The 5-year risk of rupture is 1% to 2% if the aneurysm is less than 5 cm, but 20% to 40% if the size is greater than 5 cm. Operative repair is typically recommended in asymptomatic individuals when the AAA diameter is greater than 5.5 cm; other indications for surgery are rapid expansion or onset of symptoms.
Hx: Typically causes few symptoms until it markedly expands or ruptures. Pain is the most common initial manifestation and can vary according to aneurysm location. Proximal aneurysms tend to present with upper abdominal, flank, or back pain, whereas distal lesions present with lower abdominal or groin pain. Clasically, substernal chest pain with radiation to the back or midscapular region; often described as “tearing” or “ripping” pain.
Locally contained AAA: Severe abdominal or back pain with syncope, followed by vague discomfort is typical for a ruptured abdominal aortic aneurysm (AAA) that has been locally contained, preventing immediate death. Contained rupture of AAA, when misdiagnosed, is most often mistaken for renal colic, acute myocardial infarction, or diverticulitis.
❗Rupture: The sentinel event of sudden, severe back pain associated with loss of consciousness. Symptoms after that time are likely caused by either local irritation and inflammation related to the rupture and hemorrhage or expansion of the aneurysm against adjacent structures. Leukocytosis and anemia are common. In the event of rupture, hemorrhage usually occurs into the retroperitoneum; because the expanding hematoma may be temporarily contained within the retroperitoneum, patients may remain hemodynamically stable and have a delayed presentation.
Pulse or blood pressure differential useful but uncommonly present.
Dx: Chest radiograph may show a widened mediastinal silhouette, pleural effusion, or both.
In symptomatic patients who are hemodynamically stable, the diagnosis should be confirmed with abdominal CT. Hemodynamically unstable patients require emergency surgical repair with confirmation obtained by rapid bedside ultrasound if necessary.
TAA (Thoracic aortic aneurysm)
Most TAAs (60%) involve the ascending aorta (between the aortic valve and the brachiocephalic artery), and a minority involve the descending aorta (distal to the left subclavian artery).
Patients with TAA are usually asymptomatic until the discovery is made incidentally on chest x-ray, CT scan, or ECG. However, some patients develop chest or abdominal discomfort as the TAA grows to compress surrounding structures. The natural history of TAA is one of slow expansion with a progressive increase in the risk of aortic dissection at larger aortic sizes. Expansion rates for TAA are generally less than those of AAA.
- Share many of the same risk factors as abdominal aortic aneurysm (AAA). Approximately 25 percent of patients with TAA will also be found to have an AAA
Esophageal rupture
Intense retrosternal pain after vomiting; often associated with ethanol use. Pneumomediastinum on CXR can be seen.
Esophagitis
Burning-type chest discomfort usually precipitated by meals and not related to exertion. It is often worse upon lying down and improved with sitting.
Musculoskeletal pain
Typically more reproducible chest pain. Includes muscle strain, costochondritis, and fracture. Should be a diagnosis of exclusion.
Cocaine
Clinical features
- Sympathetic hyperactivity - tachycardia, hypertension, dilated pupils
- Chest pain due to coronary vasoconstriction
- Psychomotor agitation, seizures
Complications
- Acute myocardial ischemia
- Aortic dissection
- Intracranial hemorrhage
Management of chest pain
- Benzodiazepines for blood pressure & anxiety
- Aspirin
- Nitroglycerin & 🍦 calcium channel blockers for pain
- Beta blockers contraindicated ❌
- Fibrinolytics not preferred due to increased risk of intracranial hemorrhage
- Immediate cardiac catheterization with reperfusion when indicated
Hx: Psychomotor agitation, dilated pupils, atrophic nasal mucosa, hypertension, and acute myocardial ischemia (chest pain, electrocardiogram changes)
Cocaine potentiates sympathomimetic actions by causing inhibition of norepinephrine reuptake into the sympathetic neuron. This causes stimulation of alpha and beta adrenergic receptors and can result in coronary vasoconstriction and increase in heart rate, systemic blood pressure, and myocardial oxygen demand. It also enhances thrombus formation by promoting platelet activation and aggregation.
It can also induce spasm of the coronary circulation even if there is no preexisting coronary artery stenosis.
Tx:
🥞 All patients with acute cocaine toxicity and myocardial ischemia should be treated initially with supplemental oxygen and intravenous benzodiazepines. By reducing sympathetic outflow, benzodiazepines reduce anxiety and agitation, improve blood pressure and heart rate, and alleviate cardiovascular symptoms.
Aspirin retards thrombus formation
Nitrates and calcium channel blockers, being vasodilators, are beneficial for the cocaine-induced coronary artery vasoconstriction.
❌ Beta blockers, including cardioselective agents (eg, metoprolol, atenolol, bisoprolol), should NOT be used in patients with cocaine-induced myocardial ischemia or infarction. Their use can cause unopposed alpha adrenergic stimulation and worsen coronary vasoconstriction
Panic Disorder
May be indistinguishable from angina. Often diagnosed after a negative evaluation for ischemic heart disease. Often associated with palpitations, sweating, and anxiety.
Sudden panic attacks with acute onset of somatic symptoms that may include chest pain, palpitations, sweating, nausea, dizziness, dyspnea, and numbness.
These symptoms usually last from 5 to 60 minutes. Approximately 50% of patients with panic disorder also have associated agoraphobia, with fears of being in crowds or in places from which escape would be difficult.
Normal cardiac and pulmonary examinations
Tx: Cognitive behavioral therapy (CBT) has been shown to be the most effective psychotherapeutic intervention in controlled trials. Selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors have been shown to be effective.
Anginal Equivalent
Occurs when a patient has no chest pain, but has other symptoms of cardiac ischemia (eg,
dyspnea) that is predictably precipitated by exertion and relieved by rest.
Non Anginal Pain
“Stabbing,” “shooting,” “knifelike,” “jabbing,” and “tingling.”.
GERD
Randomized controlled trials have shown that a therapeutic trial of twice-daily PPI treatment is effective in 50% to 60% of patients with noncardiac chest pain
Differential Diagnosis Dyspnea: Cardiovascular Causes
Aortic stenosis
Mitral stenosis
Mitral regurgitation
Chronic constrictive pericarditis
Cor Pulmonale
Hypertrophic Cardiomyopathy
Benign Murmurs
Pathologic Murmurs
Intensity or grade (<3/6), timing (early and brief systolic), lack of radiation, and absence of additional abnormal heart sounds.
❗ Diastolic and continuous murmurs are usually due to an underlying pathologic cause. Their presence should prompt further evaluation with a transthoracic echocardiogram, which can identify valvular regurgitation and evaluate for any associated structural abnormalities or hemodynamic consequences.
Benign characteristics of a murmur include its intensity or grade (<3/6), timing (early and brief systolic), lack of radiation, and absence of additional abnormal heart sounds.
A midsystolic murmur can be detected occasionally in young, asymptomatic adults. This murmur is usually benign and, in the absence of symptoms or other abnormal findings, does NOT require further evaluation.
Grading the Intensity:
1 - Murmur heard with the stethoscope, but not at first (S > murmur)
2 - Faint murmur heard with the stethoscope on the chest wall (S = murmur)
3 - Murmur heard with the stethoscope on the chest wall; louder than grade 2 but without a thrill (a vibration felt on palpation over the heart) (S
4 - Murmur associated with a (palpablre) thrill
5 - Murmur heard with just the rim of the stethoscope held against the chest
6 - Murmur heard with the stethoscope held close to but not touching the chest wall
Bell of the stethoscope detects low-frequency sounds and murmurs
Aortic stenosis
History of heart murmur, chest pain, syncope, exertional dyspnea; history of rheumatic fever; history of aortic coarctation.
Hx: The three most common causes of aortic stenosis in the general population are senile calcific aortic stenosis, bicuspid aortic valve, and rheumatic heart disease.
Px: 👧🏽Mid- to late-peaking (Crescendo-decrescendo) ejection (mid) systolic murmur at right upper sternal border cardiac base with radiation to ❗❗carotid arteries, an S4 (left atrial kick against a stiff left ventricle)[the high resistance generated by the stenosed aortic valve causes concentric hypertrophy and stiffening of the left ventricle, resulting in the S4]. a single S2 as a result of loss of the aortic closure component, and delayed timing and decreased amplitude in the carotid pulses (pulsus parvus et tardus),
🔪 Surgical aortic valve replacement (AVR) should be considered in patients with severe AS and ≥1 of the following criteria:
- Presence of symptoms attributable to AS: Patients with symptomatic, severe AS have a relatively high risk of sudden cardiac death.
- Left ventricular ejection fraction (LVEF) <50%, regardless of symptoms: A depressed LVEF is often due to excessive afterload created by the stenotic valve, and it frequently normalizes with AVR.
- Undergoing other cardiac surgery (eg, coronary artery bypass grafting): The valve can be repaired concomitantly.
The definition of severe AS encompasses many patients who are asymptomatic because it was designed to identify nearly all patients who may benefit from AVR (high sensitivity). Some of these patients are truly asymptomatic. Others lack symptoms only because of a sedentary lifestyle; when subjected to exertion (eg, stress testing) they have typical severe AS symptoms.
Coarctation of aorta usually presents with a midsystolic murmur over the left interscapular space which may become continuous if the lesion in the vessel is narrowed enough to cause high-velocity jet flow. Classic to this condition are arterial hypertension in the upper extremities and normal or low blood pressure, with diminished or delayed pulsations in the lower extremities. Chest x-ray findings such as sign of 3️⃣ due to indentation of the aorta at the site of coarctation with pre and post-stenotic dilatation and rib notching due to rib erosions by dilated collateral vessels are classic findings.
Valvuloplasty:
Bioprosthetic valves are most commonly xenografts (usually porcine); homografts from cadavers and autografts (from the pulmonary position) are less commonly implanted. Thromboembolic complications are common after implantation of a mechanical heart valve. This increased risk of thromboembolic phenomena is not seen 3 months after implantation of a bioprosthetic valve. Thus, in the absence of atrial fibrillation, long-term anticoagulation is not necessary for most patients who receive a bioprosthetic valve. For many patients this confers significant advantage, as it eliminates the risk of hemorrhagic complications related to long-term anticoagulant therapy. T he major disadvantage of bioprosthetic valves is that the rate of structural deterioration is faster and the expected valve life is shorter. Most mechanical valves have an expected life of 20 to 30 years. In contrast, one-third of patients with porcine bioprosthetic valves will require repeat valve replacement in 10 years, and half will need a new valve in 15 years.
Most experts favor a bio-prosthetic valve for women who are contemplating pregnancy. Mechanical valves require long-term anticoagulation with warfarin, which is teratogenic. Women with mechanical valves who are planning pregnancy should switch to an injectable heparin (which is inconvenient and more costly) before conception and continue this during most of pregnancy. Patients with a prosthetic heart valve are at increased risk of infective endocarditis. For prosthetic heart valve patients, prophylactic antibiotics are recommended before and after some high-risk procedures. T hough official recommendations have recently eliminated many procedures for which antibiotic prophylaxis was traditionally recommended, antibiotic prophylaxis is still recommended for patients undergoing dental procedures that manipulate gingival tissue. T his is recommended for all patients with a prosthetic heart valve irrespective of valve type or location. All patients with a prosthetic heart valve need regular follow-up. Many experts recommend yearly echocardiography beginning 5 years after valve implantation.
Cx: Prosthetic valve dysfunction (PVD), which most commonly occurs in the following forms:
- Paravalvular leak (regurgitation around the valve): more commonly occurs with mechanical (rather than bioprosthetic) valves and results from dehiscence of the valve from the aortic or mitral annulus, often due to annular degeneration or underlying infective endocarditis.
- Transvalvular regurgitation (regurgitation through the valve): more commonly affects bioprosthetic (rather than mechanical) valves and can result from cusp degeneration or occasionally valvular thrombus that impairs valve closure. Patients are often initially asymptomatic but can develop severe heart failure; those with significant regurgitation generally have a poor prognosis.
PVD can also involve valvular obstruction (stenosis), which typically results from valvular thrombus or cusp malfunction (ie, failed opening) and presents with a characteristic stenotic, rather than a regurgitant, murmur.
The best initial evaluation for PVD is echocardiography, which allows visualization of the valve and surrounding anatomy. Depending on the cause and extent of dysfunction, further studies and possible surgical intervention may be indicated.
LUSB (P)
Pulmonic stenosis
Etiology
- Congenital (usually isolated defect)
- Rarely acquired (eg, carcinoid)
Clinical presentation
- Severe: Right-sided heart failure in childhood
- Mild: Symptoms (eg, dyspnea) in early adulthood
- Crescendo-decrescendo murmur (↑ on inspiration)
- Systolic ejection click & widened split of S2
Diagnosis
- Echocardiography
Treatment
- Percutaneous balloon valvulotomy (preferred)
- Surgical repair in some cases
Commonly occurs as an isolated congenital defect and rarely occurs as an acquired defect (eg, rheumatic fever, carcinoid syndrome). Severe PS is typically diagnosed early in life due to presentation of right-sided heart failure, but patients with relatively mild PS often remain asymptomatic throughout childhood and develop symptoms (eg, dyspnea with exertion) in early adulthood. Cardiac auscultation reveals a pulmonic ejection click (high-pitch sound after S1 best heard during expiration) followed by a crescendo-decrescendo systolic murmur over the left second intercostal space. The murmur intensifies with inspiration. The stenosis also causes the pulmonic valve to close later than usual, resulting in widened splitting of the aortic and pulmonic components of S2; the splitting is further increased during inspiration.
LSB
Aortic regurgitation (AR) [Insufficency]
Common etiologies
- Congenital bicuspid aortic valve
- Postinflammatory (eg, rheumatic heart disease, endocarditis)
- Aortic root dilation (eg, Marfan syndrome, syphilis)
Pathophysiology
- Backflow from aorta into LV → ↑ LV end-diastolic volume
- LV initially compensates with eccentric hypertrophy → ↑ SV & CO
- Eventual LV dysfunction → ↓ SV & CO → heart failure
Clinical findings
- Diastolic decrescendo murmur
- Widened pulse pressure (↑SBP & ↓DBP)
- Rapid rise-rapid fall (“water-hammer”) pulsation
- Abrupt carotid distension & collapse, “pistol-shot” femoral pulses
Etiologies may include dissecting aorta, Marfan syndrome, bicuspid aortic valve, rheumatic heart disease, ankylosing spondylitis, endocarditis, and syphilis.
In young patients, Bicuspid aortic valve (BAV) can cause isolated AR due to valvular leaflet abnormalities or aortic root dilation; in older patients, it usually leads to aortic stenosis. Dilation of the aortic root or the ascending aorta can progress to aortic aneurysm and dissection, sometimes causing sudden death. Although some BAV cases develop sporadically, others have a Mendelian inheritance pattern (eg, autosomal dominant with incomplete penetrance).
Px: AR leads to an early decrescendo 💎diastolic murmur [blowing](begins immediately after A2), best heard with the diaphragm of the stethoscope along the left sternal border at the third and fourth intercostal spaces while the patient is sitting up, leaning forward, and holding a breath in full expiration. (all due to the large stroke volume with fast runoff) include a wide arterial pulse pressure and a diastolic rumble (from the aortic regurgitant flow displacing the mitral valve, often called the Austin Flint murmur), Musset sign (head bobbing with the heartbeat), water-hammer pulse or Corrigan pulse (rapidly rising and collapsing pulse), Hill sign (an increase of > 40 mm Hg in femoral artery systolic BP compared to brachial artery BP), Quincke pulse (nail-bed capillary pulsations), pistol-shot pulse (booming sound heard over the femoral arteries), and Duroziez sign (bruit auscultated over the femoral artery when compressed). Carotid arteries have a rapid, accentuated upstroke, with a rapid decline (frequently referred to as a Corrigan pulse); the point of maximal impulse is displaced (suggesting left ventricular volume overload); and the pulse pressure is widened (systolic pressure minus diastolic pressure; normal is ≤40 mm Hg).
Dx: The murmur of aortic regurgitation is a soft, blowing diastolic murmur that is often heard best at the third left or second right intercostal space. It does not radiate well and may be confined to a very limited area of the chest wall. The murmur can be heard best with the patient leaning forward in end-expiration.
The left ventricle initially adapts via the Frank-Starling mechanism, with left ventricular (LV) stretch allowing for an increase in stroke volume to help maintain cardiac output. As the volume overload becomes chronic, the left ventricle further adapts via eccentric hypertrophy, which involves the addition of myocardial fibers in series. This allows for both increased LV complianceto accommodate additional LV volume and increased LV contractility to sustain increased stroke volume and maintain cardiac output.
In the short term, eccentric hypertrophy is beneficial because it allows for an initial asymptomatic periodin the setting of severe chronic AR. However, in the long term, eccentric hypertrophy is maladaptive because it causes increased LV wall stress, which eventually leads to LV contractile dysfunction and decompensated heart failure.
[HOCM] Hypertrophic Obstructive Cardiomyopathy
HCM is an autosomal dominant genetic disorder caused by mutations in one of several sarcomere genes encoding the myocardial contractile proteins of the heart. The 2 most common mutations (responsible for about 70% of identifiable mutations) occur in the cardiac myosin binding protein C gene and the cardiac beta-myosin heavy chain gene. First-degree relatives of an affected patient with a known disease-causing mutation can be offered genetic testing to identify the risk for developing HCM.
Hypertrophic cardiomyopathy (HCM) is typically asymptomatic in childhood and adolescence.
Hx: The clinical manifestations of HCM, which depend on the extent of hypertrophy and outflow tract obstruction, include:
Exertional dyspnea, chest pain, fatigue, palpitations, presyncope, or syncope
Dx: Some patients have systolic anterior motion of the mitral valve, leading to anterior motion of mitral valve leaflets toward the interventricular septum. Contact between the mitral valve and the thickened septum during systole leads to left ventricular outflow tract obstruction (LVOT) and is responsible for the Harsh crescendo-decrescendo systolic murmur heard best at the apex and lower left sternal border. Also associated with an S4
HCM is often characterized by left ventricular hypertrophy most prominent in the basal anterior septum.
Px:
Maneuvers that decrease preload (Valsalva maneuver, standing, nitroglycerin)[reduce left ventricular end diastolic volume and increase the turbulence of blood flow exiting the ventricle during systole] 📢 enhance the murmur, and
Manuvers that 💙increase venous return (leg elevation) or squatting, hand grip [elevation of arterial pressure] 🔇 diminish the murmur.
The typical murmur of hypertrophic cardiomyopathy is a harsh systolic diamond-shaped murmur heard best at the lower sternal border and apex.
Tx: Management includes avoidance of strenuous exertion, good hydration. First-degree relatives should be screened with echocardiography. Patients with symptoms (eg, syncope, heart failure, angina) should be treated with negative inotropic agents (eg, beta blockers, verapamil, disopyramide) as the initial medical therapy.
🎺Beta blockers (eg, metoprolol, atenolol) are the most commonly used agents for initial monotherapy.
ICD implantation is effective for primary prevention of sudden cardiac death in patients with HCM.
Most low-level recreational activities, such as bowling or golf, are probably permissible. High-level recreational activities, such as basketball or bodybuilding, are not advised or are strongly discouraged. Recommendations on moderate-level recreational activities vary. Some activities, such as tennis, are deemed probably permissible, whereas others, including weightlifting, are strongly discouraged. Patients with HCM require formal counseling about acceptable levels of physical activity.
T
VSD
ASD
Tricuspid regurgitation
Tricuspid regurgitation most often is caused by left-sided heart disease that causes pulmonary hypertension, which leads to right ventricular enlargement and annular dilation.
Primary pulmonary hypertension and elevated pulmonary pressure as a result of chronic lung disease also cause tricuspid regurgitation, with the term cor pulmonale describing right-sided heart failure as a result of pulmonary hypertension in the absence of left-sided heart disease. Other causes of tricuspid regurgitation include 🔥 endocarditis, injury after pacer lead placement, carcinoid disease, mediastinal irradiation, and trauma. Carcinoid disease causes direct toxicity to the tricuspid valve, seen as leaflet thickening and retraction.
Px: Characterized by a 💨blowing (holo) systolic murmur at the lower left sternal border that may increase in intensity with inspiration. The murmur does not radiate well, although it can sometimes be heard at the upper left sternal border. A finding characteristic of right-sided murmurs is augmentation in intensity with inspiration.
May be intensified during inspiration and reduced during expiration or with the Valsalva maneuver (Carvallo’s sign). Inspiration increases right heart volume and therefore augments right-sided murmurs.
This murmur is sometimes associated with a prominent right ventricular pulsation along the left parasternal region or regurgitant waves seen in the neck veins.
In mild or moderate tricuspid regurgitation, most patients are asymptomatic.
❗Severe tricuspid regurgitation may be associated with signs of advanced right-sided heart failure, including jugular venous distention (JVD), ascites, hepatomegaly (sometimes pulsatile), and lower extremity edema. Electrocardiography may show enlargement of the right atrium or the right ventricle.
M
Mitral stenosis (MS)
History of rheumatic fever, heart murmur
Hx: In a young patient from a developing country, the clinical presentation of progressive dyspnea, nocturnal cough, and hemoptysis is highly suggestive of rheumatic MS. Long-standing MS leads to an increase in left atrial pressure, which in turn leads to elevated pulmonary pressures and pulmonary vascular congestion; these changes can cause dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and hemoptysis.
Px:💎diastolic murmur with presystolic accentuation (late diastolic accentuation) of the murmur occurs because of increased flow across the mitral valve with atrial contraction. A loud first heart sound and early diastolic opening snap may also be present.
Cx: In addition, the left atrial enlargement resulting from increased left atrial pressure predisposes to the development of atrial fibrillation, PVC’s, SVT, or atrial flutter. AF increases the risk of left atrial thrombus formation and systemic thromboembolic complications (eg, stroke).
Mitral regurgitation / MVP 🏀
History of heart murmur, mitral valve prolapse, or myocardial infarction
Holosystolic murmur at cardiac base (apex), and radiates laterally or posteriorly.
The systolic murmur of chronic MR NOT due to MVP is 📢 intensified by isometric exercise (handgrip) but is REDUCED with the Valsalva maneuver.
Pulmonary edema: As the resistance to retrograde flow across the leaky mitral valve decreases, a larger proportion of stroke volume flows into the left atrium rather than across the aortic valve.
Primarily caused by retrograde flow across the MV.
To increase antegrade flow (thereby increasing cardiac output and decreasing pulmonary vascular congestion) we should reduce the left ventricular afterload. Lower resistance to flow through the LV outflow tract will increase the proportion of stroke volume that enters systemic circulation.
Tx: Vasodilators such as 🃏 ACE inhibitors and 💦hydralazine are frequently used. ☠ Nitroprusside is another consideration.
🏀 MVP: Mitral valve prolapse occurs in approximately 2% of the general population and is the most common cause of mitral regurgitation.
“Click-murmur” complex. This complex includes a midsystolic click, believed to be caused by sudden tensing of the mitral subvalvular apparatus as the leaflets prolapse into the left atrium, followed by a late systolic murmur.
Valsalva maneuver and standing from a squatting position decrease end-diastolic volume and move the click-murmur complex closer to the S1. [Maneuvers that decrease left ventricular volume which exaggerates the propensity of mitral leaflet prolapse.]
Squatting from a standing position increases venous return (ie, preload), which in turn causes an increase in left ventricular size and volume. This leads to a delay in the valve prolapse, with a later click and shorter murmur. Isometric exercise also diminish the degree of prolapse, and the click-murmur is delayed and decreases in intensity.
Surgical indications for severe chronic mitral valve regurgitation
Primary MR
- Surgery if LVEF 30%-60% (regardless of symptoms)
- Consider surgery if successful valve repair is highly likely:
- Symptomatic & LVEF <30%
- Asymptomatic & LVEF >60%
Secondary MR
- Medical management, valve surgery rarely indicated
Primary mitral regurgitation (MR) is defined as that caused by an intrinsic defect of the mitral valve apparatus (eg, leaflets, chordae tendineae) and is differentiated from secondary MR, which results from other cardiac disease (eg, myocardial ischemia, dilated cardiomyopathy).
Chronic severe MR of primary etiology is best treated with surgical repair, and the timing of surgery should precede the development of significant left ventricular (LV) dysfunction. An important consideration is that measured LV ejection fraction (LVEF) overestimates LV function in severe MR because regurgitant flow accounts for a large amount of the stroke volume. Therefore, LVEF 30%-60% is generally an indication for surgical repair or replacement in patients with primary chronic severe MR, regardless of symptoms. Patients with LVEF <30% likely have life-limiting, permanent systolic dysfunction, and surgery should be considered only when there is a high likelihood of successful valve repair (rather than replacement). Preemptive surgery can also be considered in asymptomatic patients with LVEF >60% who are excellent candidates for successful valve repair.
Ddx Acute Dyspnea: CARDIOVASCULAR
Heart failure (acute)
Myocardial infarction
Pericardial tamponade
Congestive Heart failure (acute)
<strong>I</strong> (asymptomatic) 5%-10% Mortality
<strong>II</strong> (symptomatic; slight limitation of physical activity)[are comfortable at rest, but have fatigue, palpitations, dyspnea, or angina with ordinary activity] 15%-30% Mortality
<strong>IIIa </strong>(symptomatic; marked limitation of physical activity)[less-than-ordinary activity causes symptoms] 15%-30% Mortality
<strong>IV</strong> (inability to perform any physical activity without symptoms) [symptoms at rest and increased symptoms with even minor activity] 50%-60% Mortality
Hx: Cardiovascular risk factors, CAD, paroxysmal nocturnal dyspnea
Px:
The third heart sound (S3) is a low-frequency diastolic sound produced by the passive ventricular filling during early diastole; it is best heard over the cardiac apex in the left lateral decubitus position. An abnormal S3 (louder and higher pitch, S3 gallop) is commonly heard in patients with CHF due to left ventricular systolic dysfunction, and it correlates with elevated left atrial and/or ventricular filling pressures and serum BNP levels.
S3 gallop 0.99 (specificity), Jugular venous distention 0.92, Pulmonary crackles 0.78, Hepatojugular reflux 0.96, Ascites 0.97, Edema 0.78.
Dx: EKG, Labs, BNP, CRX
BNP is a natriuretic hormone released from ventricular myocytes in response to high ventricular filling pressures and wall stress in patients with CHF. It is derived from the cleavage of the prohormone proBNP, which produces a biologically active BNP and an inert N-terminal proBNP (NT-proBNP). Elevated levels of circulating BNP or NT-proBNP correlate with the severity of left ventricular systolic dysfunction. Conversely, normal values have a very high negative predictive value for CHF as a cause of dyspnea and should prompt a search for noncardiac causes of dyspnea.
✅ BNP >100 pg/mL is highly (90%) sensitive and 73% specific in the diagnosis of patients with heart failure in the emergency department. Patients with chronic heart failure may have BNP levels <100 pg/mL. Studies indicate that a value less than 80 pg/mL has a high (99%) negative predicative value and helps rule out CHF. Most patients with dyspnea due to CHF had plasma BNP levels >400 pg/mL whereas levels <100 pg/mL
Other conditions that raise BNP levels include acute myocardial infarction, pulmonary embolism, chronic kidney disease, older age, and female sex.
BNP is reduced by oBesity. Do not routinely measure BNP in patients with typical signs and symptoms of heart failure.
Chest radiography may be helpful in determining the cause of dyspnea. Once heart failure is diagnosed, serial chest radiographs are not sensitive to small changes in pulmonary vascular congestion and are not recommended.
Echocardiography can help identify specific causes of heart failure. Echocardiography is necessary for distinguishing systolic heart failure from heart failure with preserved systolic function.
Coronary angiography for patients with new-onset heart failure who have angina are potential candidates for revascularization and evaluation for ischemia.
Poor prognositc factors:
Hyponatremia in patients with CHF usually parallels the severity of heart failure and is an independent predictor of adverse clinical outcomes.
JVP, Mitral regurgitation, LBBB,
Tx: A 5-mg dose of oral morphine given four times daily has been shown to help relieve dyspnea in patients with end-stage heart failure.
Rx: Initial therapy:
🃏 ACE inhibitor (enalapril) [EF < 40%] “CONSENSUS TRIAL” (if ACE inhibitor is not tolerated because of cough, an ARB can be used; if ACE inhibitor is contraindicated because of hyperkalemia or renal insufficiency, combined hydralazine and isosorbide dinitrate can be used)
🎺 β-Blocker (carvedilol), ER metoprolol (succinate), and bisoprolol [EF < 40%] “MERIT HF” are approved for the treatment of heart failure. interfere with the harmful effects of sustained activation of the adrenergic nervous system (α1, β1, and β2) by competitively blocking their receptors.
❗ β-blockers should NOT be initiated when a patient is acutely decompensated (hypotensive or volume overloaded w/ pulmonary edema), as initiation of therapy is associated with a transient decline in cardiac output. β-Blockers can be initiated and tolerated once euvolemia or near-euvolemia has been established. [Patients with systolic heart failure should be treated with a β-blocker, regardless of symptom status, including heart failure that is asymptomatic or mildly symptomatic.].
Additional therapy:
🎢 Diuretic as needed to maintain euvolemia [loop diuretics (eg, furosemide, bumetanide, torsemide)] Hx: Dyspnea, orthopnea, paroxysmal nocturnal dyspnea [PND], bibasilar crackles, hypoxemia) are consistent with acute pulmonary edema. ❗ Acute Decompensated Heart Failure (ADHF): Supplemental oxygen and IV loop diuretics (eg, furosemide).
Aldosterone antagonists (spironolactone or 🍎eplerenone) [EF <30%] “RALES TRIAL” [indicated for patients with severe systolic heart failure (NYHA class III-IV symptoms), serum potassium level <5 meq/L, and creatinine level <2.5 mg/dL][should include close clinical and laboratory follow-up, with particular attention to serum potassium levels.]
💣Hydralazine and 🧨isosorbide dinitrate (for black patients) “AHEFT TRIAL”‘
Digoxin is used primarily for symptom control.
A newer-generation dihydropyridine calcium channel blocker (amlodipine) may improve control of blood pressure in a patient with resistant hypertension (blood pressure that is not at the target value with three-drug therapy with different classes of drugs, including a diuretic). Older-generation calcium channel blockers, such as diltiazem, nifedipine, and verapamil, may precipitate EXACERBATION of heart failure because of their negative inotropic effects.
Tx: Limiting dietary sodium to 2 g daily and fluid to 2 liters per day and recording daily weights results in fewer hospitalizations for patients with decompensated heart failure.
Device threapy Indications:
💫Cardiac Resynchronization Therapy: Implantable Cardioverter-Defibrillator (ICD) is an internal defibrillator that senses dangerous cardiac arrhythmias and automatically converts the rhythm to sinus rhythm by either administering a high-energy shock or delivering a short series of paced beats.
Ischemic or nonischemic cardiomyopathy with ejection fraction ≤3️⃣5️⃣% (primary prevention) “DEFINITE TRIAL”
Cardiac Resynchronization Therapy: Biventricular Pacing (pacing of both the right and left ventricles that improves pump function cause by dyssynchrony because of the conduction delay)
ALL of the following:
NYHA Class III or IV
Ejection fraction ≤35%
Ventricular dyssynchrony (QRS duration >120 msec)
Cardiac transplantation improves survival, functional status, and quality of life in patients with NYHA Class III or IV heart failure. Relative contraindications to cardiac transplantation include age >65 years, end-organ damage from diabetes or vascular disease, malignancy, previous stroke, lack of psychosocial support, or active psychiatric illness.
Fu: Monitor your weight, SOB etc.
“Best practice measure” must be seen within 7 days of discharge
Cor pulmonale
Cor pulmonale refers to impaired function of the right ventricle caused by pulmonary hypertension that occurs due to underlying diseases of the lungs (COPD, interstitial lung disease), pulmonary vasculature (idiopathic pulmonary arterial hypertension), or obstructive sleep apnea.
Diseases leading to hypoxic vasoconstriction, as in cystic fibrosis; occlusion of the pulmonary vasculature, as in pulmonary thromboembolism; other pulmonary vascular problems, such as collagen-vascular disease; parenchymal destruction as in sarcoidosis; and COPD; Chest wall disorders (eg, kyphoscoliosis). COPD is the most common cause of cor pulmonale in the United States, with nearly 25% of COPD patients developing this disorder
By convention, right ventricular dysfunction due to left heart disease or congenital heart disease is NOT considered cor pulmonale.
Physical examination may show loud P2 (pulmonic component of the 2nd heart sound), tricuspid regurgitation murmur (holosystolic at the left lower sternal border), elevated jugular venous pressure (JVP), peripheral edema, hepatomegaly due to hepatic congestion, and possible ascites. COPD patients usually have distant heart sounds due to hyperinflated lungs. End-stage cor pulmonale may present with hypotension, tachycardia, and other signs of cardiogenic shock due to decreased stroke volume.
Chest x-ray may show enlarged central pulmonary arteries and loss of retrosternal air space due to right ventricular hypertrophy.
📈 The electrocardiographic findings include tall peaked P waves in leads II, III, and aVF (indicating right atrial enlargement), tall R waves in leads V1 to V3 and a deep S wave in V6 with associated ST-T wave changes (indicating right ventricular hypertrophy) and right axis deviation. Right bundle branch block occurs in 15% of patients.
Right heart catheterization is the 🥇gold standard for diagnosis and typically shows elevated central venous pressure, right ventricular end-diastolic pressure, and mean pulmonary artery systollic pressure (>25 mm Hg at rest) without left heart disease.
Tx: Involves optimizing right ventricular dynamics (preload, afterload, and contractility) with supplemental oxygen, diuretics, treatment of underlying etiology, and intravenous inotropes for severe decompensation.
Dobutamine is an adrenergic agonist with predominant activity on beta-1 receptors and minimal activity on beta-2 and alpha-1 receptors. It is used for the management of severe heart failure associated with severe left ventricular systolic dysfunction and cardiogenic shock. Stimulation of beta-1 receptors results in increased production of cAMP in cardiac myocytes, which in turn leads to enhanced calcium-mediated binding of the actin-myosin complex to troponin C and increased myocardial contractility (positive inotropic effect). Heart rate is also increased via calcium channel activation (positive chronotropic effect). The increase in myocardial contractility allows for forward ejection of a higher volume of blood and results in a decrease in left ventricular end-systolic volume. Cardiac output is increased to perfuse organs and less blood backs up into the pulmonary circulation, resulting in improvement of symptoms.
HFpEF
(diastollic dysfunction)
Diastolic dysfunction is caused by impaired myocardial relaxation or increased LV wall stiffness (decreased compliance), leading to increased LV end-diastolic pressure (LVEDP). The increase in LVEDP is transmitted to the left atrium and pulmonary veins and capillaries, causing pulmonary congestion, dyspnea, and exercise intolerance.
Hx: Exertional dyspnea, orthopnea (choking sensation/dyspnea when lying flat), bibasilar rales, lower extremity edema,
Dx: Normal ejection fraction on echocardiography
There is NOT ❓ a large body of evidence to guide the treatment of HFPEF.
Tx: Primarily focused on managing the manifestations of heart failure (volume overload) and targeting risk factors for left ventricular hypertrophy (primarily hypertension), which is strongly associated with HFPEF.
Rx: The angiotensin receptor blocker (ARB) candesartan is an agent that has been studied in a large randomized controlled trial of HFPEF treatment and was associated with a reduction in hospitalizations. Other appropriate agents for use in HFPEF include angiotensin-converting enzyme inhibitors, nondihydropyridine calcium channel blockers (verapamil, diltiazem), and β-blockers.
Dilated Cardiomyopathy
A diagnosis of dilated cardiomyopathy requires evidence of dilatation and impaired contraction of the left ventricle or both ventricles.
Dilated cardiomyopathy has many causes, with the most common being idiopathic (50%), myocarditis (9%), ischemic (7%), peripartum (4%), and toxic (3%).
Idiopathic cardiomyopathy is diagnosed if there is no evidence of coronary artery obstruction, myocarditis, or a primary or secondary form of heart muscle disease.
🍺 Alcoholic cardiomyopathy is a diagnosis of exclusion in patients with dilated cardiomyopathy and history of alcohol abuse in whom no other potential causes of cardiomyopathy (eg, coronary artery disease, valvular heart disease) are suspected or identified. The degree of LV dysfunction in alcoholic cardiomyopathy is directly related to the daily amount and overall duration of alcohol intake. The primary therapy for such patients is complete abstinence from alcohol use; this intervention is associated with improvement or normalization of LV function over time.
Viral or idiopathic myocarditis is most commonly seen following Coxsackievirus B infection, and occurs in about 3.5 - 5% of infected patients. Other viruses commonly implicated include parvovirus B19, human herpesvirus 6, adenovirus, and enterovirus. Viral myocarditis can cause dilated cardiomyopathy via direct viral damage and as a result of humoral or cellular immune responses to persistent viral infections.
Acute myocarditis is immunologically mediated damage to the myocardium; cardiac troponin levels are typically elevated, indicating some degree of myocardial necrosis, and ventricular dysfunction may be global or regional.
Peripartum cardiomyopathy occurs during the last trimester of pregnancy or up to 6 months postpartum in the absence of an identifiable cause. Peripartum cardiomyopathy is a major cause of pregnancy-related death in North America; maternal death is related to heart failure, thromboembolic events, and arrhythmias. Left ventricular function improves within 6 months after delivery in approximately 50% of women with peripartum cardiomyopathy. Subsequent pregnancies are associated with a high risk of recurrence, however. The diagnosis of PPCM can be difficult to make in late pregnancy as many symptoms and signs (eg, dyspnea, edema) are similar to the changes seen in normal pregnancy. A transthoracic echocardiogram showing a dilated left ventricular cavity with global systolic dysfunction and ejection fraction <45% can confirm the diagnosis. Management is similar to that of other forms of heart failure.
Viral myocarditis
Etiology
- Coxsackievirus B, adenovirus
Clinical features
- Viral prodrome
- Heart failure: Respiratory distress, murmur, hepatomegaly
Diagnosis
- Chest x-ray: Cardiomegaly, pulmonary edema
- ECG: Sinus tachycardia
- Echocardiogram: Decreased ejection fraction
- Biopsy (gold standard): Inflammation, necrosis
Treatment
- Supportive (eg, diuretics, inotropes)
- Intravenous immunoglobulin
Myocarditis is a potentially lethal disorder of the myocardium and is most commonly caused, in children, by viral infection (eg, Coxsackievirus B, adenovirus). Myocyte necrosis by direct viral injury and autoimmune inflammation results in impaired systolic and diastolic function.
A viral prodrome (eg, upper respiratory infection [URI]) often precedes the illness. Patients then typically develop chest pain and respiratory distress (eg, dyspnea, tachypnea, wheezing, crackles) from acute left heart failure and pulmonary edema. Dilated cardiomyopathy with mitral regurgitation can cause an S3 gallop and holosystolic murmur. In addition, hepatomegaly is a sign of passive congestion from right heart failure.
Initial workup includes ECG, chest x-ray, and echocardiogram.
CRX typically reveals cardiomegaly (cardiothoracic ratio >50%), and echocardiogram often shows global hypokinesis with decreased ejection fraction. Although endomyocardial biopsy is the diagnostic gold standard, treatment (eg, diuretics, inotropes) is typically initiated based on clinical suspicion.
Cx: In addition, patients should be monitored in the intensive care unit due to risk of shock and fatal arrhythmias.
Pericarditis
Most cases of acute pericarditis are thought to be due to viral infection, and many viruses have been implicated (eg, adenovirus, coxsackievirus, echovirus, influenza virus, HIV).
Etiology
- Viral or idiopathic
- Autoimmune disease (eg, SLE)
- Uremia (acute or chronic renal failure)
- Postmyocardial infarction
- Early: Peri-infarction pericarditis
- Late: Dressler syndrome
Viral, idiopathic, Autoimmune disease (eg, SLE), Uremia (acute or chronic renal failure), Postmyocardial infarction, Early: Peri-infarction pericarditis, Late: Dressler syndrome.
In developing countries and endemic areas (eg, Africa, India & China), tuberculosis is a common cause of constrictive pericarditis. In the United States, the most common causes include idiopathic or viral pericarditis (>40%), radiation therapy (~30%), cardiac surgery (~10%), and connective tissue disorders.
Clinical features & diagnosis
- Pleuritic chest pain (↓ when sitting up) ± fever
- Pericardial friction rub (highly specific)
- ECG: Diffuse ST elevation & PR depression
- Echocardiogram: Pericardial effusion
Cx:
Uremia Tx: Dialysis is indicated for uremic pericarditis and typically leads to resolution of symptoms.
❗Cardiac tamponade is due to fluid accumulation in the pericardial cavity that increases the intrapericardial pressure above the diastolic ventricular pressure. This restricts venous return to the heart and lowers right and left ventricular filling. The net result is decreased preload, stroke volume, and cardiac output. Inspiration worsens this condition by lowering the intrathoracic pressure and increasing venous return to the right ventricle. Under normal conditions, the right ventricle is able to accommodate this increased venous return by expanding the right ventricular free wall. Hx: Cardiac tamponade may follow trauma or surgery and also may be a complication of malignancy (ie, lung, breast, lymphoma), chronic renal failure, or hypothyroidism. Px: The three classic features of cardiac tamponade, or the Beck triad (hypOtension, soft or absent heart sounds, and JVD) with a prominent x descent but absent y descent. Lung examination typically shows clear lungs to auscultation due to decreased ventricular filling (preload) rather than volume overload. Pulsus paradoxus, an inspiratory drop (from expiration) in systolic blood pressure of more than 10 mm Hg (normal <10 mm Hg). Pulsus paradoxus may also be seen in severe asthma and constrictive pericarditis.
Dx: ECG in tamponade may show low voltage and pulsus alternans:
1) sinus tachycardia; 2) low QRS voltages; and 3) electrical alternans
Electrical alternans in cardiac tamponade is marked by beat-to-beat alternation of the QRS complex (and other waveform components) usually with sinus tachycardia. This so-called 2:1 alternans is due to mechanical effects of the heart swinging to-and-fro in the pericardial effusion. With tamponade, the heart systematically shifts in position on a beat-to-beat basis, accounting for the alternating QRS vector and amplitude in multiple leads.
Tx: Pericardiocentesis should be performed in patients with symptoms or signs suggesting cardiac tamponade.
Chest radiograph may show enlargement of the cardiac shadow (globular-shaped).
Pericardial Effusion
Pericardial effusions are accumulations of fluid between the visceral (epicardium) and parietal pericardium.
Hx: Several factors may lead to pericardial effusions including blockage of the lymphatic or venous systems by tumors, changes in osmostic or oncotic pressures due to metabolic diseases, or increased permeability of the pericardium due to inflammation. Blood in the pericardium (hemopericardium)[trauma] may be an important clue to post operative bleeding. Effusions which do not raise the intrapericardial pressure more than 3 or 4 mmHg will not cause symptoms.
Dx: The best evidence to determine if a pericardial effusion will become hemodynamically significant is to monitor how quickly it is accumulating. Best measured with echocardiography.
CRX: Radiographically, pericardial effusions appear as changes in the size and shape of the cardiac silhouette resulting a featureless, globular or “water bottle” shape.
💀 ICU: The pericardial fluid on an ICU film is generally not distinctly visible; instead it enlarges the cardiac shadow.
Causes an enlarged heart shadow that is often globular shaped (transverse diameter is disproportionately increased). A “fat pad” sign, a soft tissue stripe wider than 2 mm between the epicardial fat and the anterior mediastinal fat can be seen anterior to the heart on a lateral view. Serial films can be helpful in the diagnosis especially if rapid changes in the size of the heart shadow are observed. Approximately 400-500 ml of fluid must be in the pericardium to lead to a detectable change in the size of the heart shadow on PA CXR. Pericardial effusion can be definitively diagnosed with either echocardiography or CT.
Cx: It can be critical to diagnose pericardial effusion because if it is acute it may lead to cardiac tamponade, and poor cardiac filling. In the postoperative patient it could be a sign of bleeding, necessitating a return to the OR.
Dx: Jugular venous distention, clear lungs, pulsus paradoxus, hypotension
History of trauma, preceding “flu” symptoms, collagen vascular disease
Tamponade
Etiology
- Aortic aneurysm or postmyocardial infarction
- Malignancy or radiation therapy
- Infection (eg, viral, tuberculosis)
- Connective tissue disease (eg, SLE)
- Cardiovascular surgery
Clinical signs
- Beck triad: Hypotension, JVD, ↓ heart sounds
- Pulsus paradoxus (SBP ↓ >10 mm Hg with inspiration)
Diagnosis
- ECG: Low-voltage QRS, electrical alternans
- Chest x-ray: Enlarged cardiac silhouette, clear lungs
- Echocardiogram: Right atrial & ventricular collapse, plethora of the IVC
Subacute tamponade typically develops from chronic processes that cause the slow accumulation of pericardial fluid (eg, malignancy, renal failure), giving the pericardium time to progressively stretch. The pericardium may accommodate 1-2 L of fluid before intrapericardial pressure rises and compromises cardiac function. This large quantity of pericardial fluid causes the classic globular cardiac silhouette on x-ray.
Acute tamponade occurs due to rapid fluid accumulation (eg, accumulation of blood due to blunt cardiac injury). Because the stiff pericardium does not have time to adapt, a small amount of pericardial fluid (eg, 100-200 mL) can dramatically increase intrapericardial pressure without causing cardiomegaly on x-ray (typically seen with >200 mL). Therefore, acute tamponade is associated with normal cardiac contours.
On physical examination, patients may have hypotension with elevated jugular venous pressure (obstructive shock due to the pericardial fluid preventing adequate cardiac contraction) as well as muffled heart sounds (Beck triad, only seen in a minority of patients).
📉 RH Cath: Characteristically, there is elevation and equalization of intracardiac diastolic pressures (right atrial, right ventricular, and pulmonary capillary wedge pressure suggestive of left atrial pressure).
Constrictive pericarditis
Constrictive pericarditis impairs ventricular filling during diastole, causing patients to experience symptoms related to decreased cardiac output (fatigue and dyspnea on exertion) and signs of venous overload (elevated JVP, ascites, and pedal edema). Substernal chest discomfort that can be sharp, dull, or pressure-like in nature, often relieved with sitting forward.
Kussmaul’s sign, defined as lack of the typical inspiratory decline in central venous pressure, and the presence of a pericardial knock (early heart sound after S2) may also be seen. Sharp x and y descents are characteristically seen on central venous tracing. Pericardial calcifications can sometimes be seen on chest x-ray and, when present, help confirm the diagnosis.
Dx:
ECG characteristically shows diffuse PR depression (due to inflammation of atrial myocardium) and diffuse ST elevation (due to inflammation of ventricular myocardium), but findings can vary. Pericardial effusion is present in >50% of cases.
Echocardiographic findings of restrictive filling and ventricular interdependence (ie, diastolic filling of one ventricular chamber that impedes that of the other, as may be manifested by a to-and-fro diastolic motion of the ventricular septum).
Treatment
- 🧯 NSAIDs & 🌿colchicine for viral or idiopathic
- Idiopathic or acute viral pericarditis: 🧯Nonsteroidal anti-inflammatory drugs (eg, aspirin, naproxen, ibuprofen, indomethacin) and/or 🌿colchicine are generally used as first-line agents for most patients.
- 🌑Oral steroids are second line
MVP
Several nonspecific symptoms (atypical chest pain, dyspnea, palpitations, dizziness, anxiety, and panic disorder) and nonspecific electrocardiographic changes have been attributed to MVP. These signs and symptoms in patients with MVP is often called MVP syndrome. However, MVP syndrome is not a validated entity, and patients should be reassured about the benign nature of the symptoms.
Px:
A short systolic murmur at the cardiac apex that disappears with squatting.
Nonejection clicks and/or mid to late systolic murmurs of mitral regurgitation (MR). Squatting from a standing position increases venous return (ie, preload), which in turn causes an increase in left ventricular size and volume. This leads to a delay in the valve prolapse, with a later click and shorter murmur. However, in patients with severe MR (from MVP or otherwise), the murmur may increase in intensity with squatting due to an increase in afterload. Echocardiogram is used to confirm the diagnosis.
High-output heart failure
A-V Fistula’s can be congenital or acquired ( and creates an abnormal connection between the arterial and venous systems that bypasses the capillary beds. Shunting of a large amount of blood through the fistula decreases systemic vascular resistance, increases cardiac preload, and increases cardiac output.
Other causes of high-output cardiac failure include thyrotoxicosis, Paget disease, anemia, and thiamine deficiency.
Dx: Doppler ultrasonography is the preferred test to diagnose an AVF in the extremity, and surgical therapy is indicated for a large AVF.
Hx: Clinical signs include widened pulse pressure, strong peripheral arterial pulsation (e.g., brisk carotid upstroke), systolic flow murmur, tachycardia, and usually flushed extremities. The left ventricle hypertrophies, and the point of maximal impulse is displaced to the left.
Dx: An ECG usually shows left ventricular hypertrophy.
In patients with AVF and significant AV shunting, there is a compensatory increase in the heart rate and stroke volume to meet the oxygen requirements of the peripheral tissues. Normal hearts are usually capable of increasing the stroke volume and cardiac output without significant problems. However, cardiac function can occasionally decompensate over a period of time and result in cardiac failure. Such patients are considered to have heart failure (despite their higher cardiac output) because the circulation is unable to meet the oxygen demand of the peripheral tissues.
VSD
Defect normally causes a loud holosystolic murmur with maximal intensity over the third or fourth left intercostal space.
The intensity of the holosystolic murmur increases with squatting.
ASD
Wide and fixed splitting of the S2. An ejection systolic murmur can be heard over the left second intercostal space due to increased blood flow across the pulmonic valve. Some patients with large ASDs and significant left-to-right shunting also have a mid-diastolic (rumbling) murmur resulting from increased flow across the tricuspid valve.
Paradoxical embolism, a venous thrombus (usually from the leg or pelvic veins) passes into the systemic circulation through an intracardiac defect, typically an atrial septal defect (ASD) or less commonly through a ventricular septal defect (VSD).
Differential Diagnosis of Syncope:
Neurocardiogenic (Vasovagal) syncope
Clinical presentation
- Inciting event (eg, stress, prolonged standing)
- Prodrome (eg, pallor, nausea, diaphoresis)
- Consciousness regained rapidly (eg, <1 minute)
Diagnosis
- Mainly clinical diagnosis
- Upright tilt table testing in uncertain cases
Treatment
- Reassurance
- Avoidance of triggers
- Counterpressure techniques for recurrent episodes
Vasovagal Neurocardiogenic syncope (the common “faint”).
Occurs due to an alteration in autonomic drive.
Most commonly, abrupt parasympathetic activation leads to a cardioinhibitory response that manifests as bradycardia with sinus arrest. Less commonly, decreased sympathetic drive leads to a vasodepressor response, resulting in peripheral vasodilation and abrupt hypotension. In both scenarios, cerebral perfusion suddenly decreases and syncope occurs. The episode resolves quickly (typically <1 minute) as cerebral perfusion is rapidly restored.
Vasovagal syncope most commonly affects young patients and is often triggered by emotional stress (eg, fear of venipuncture) or prolonged standing.
🌪🌫🌦🌤⛅Presyncopal symptoms (prodrome), such as lightheadedness, nausea, warmth, diaphoresis, or blurred vision for usually longer than 10 seconds. Common triggers include micturition, defecation, cough, fear, pain, phlebotomy, prolonged standing, postural change, hot environments, emotional distress, dehydration, and use of diuretics or vasodilators.
The specific triggers for reflex syncope cause an alteration in the autonomic response and can lead to a cardioinhibitory, vasodepressor, or mixed response:
- Increased parasympathetic stimulation can manifest as profound bradycardia, varying degrees of atrioventricular block, or asystole.
- Decreased sympathetic output can lead to vasodilation, hypotension, or syncope.
+Prodrome
“Wasovagal”
visceral organs
Syncope precipitated by pressure on the carotid sinus baroreceptors (tight collar, sudden turning of head). Carotid massage may be confirmatory (Carotid sinus hypersensitivity).
psychiatric
Px: Carotid Massage; decrease in SBP 50 pts; asystole 3 sec
Dx:
12-lead electrocardiography remains the first and most widely recommended test to perform in patients being evaluated for syncope, partly owing to its noninvasive nature, availability, and low cost.
Echocardiography is recommended in patients suspected of having structural heart disease. If an arrhythmia is suspected, documentation of the arrhythmia is indicated either by inpatient telemetry or ambulatory monitoring.
Tilt-table testing is useful in evaluating recurrent syncope in the absence of heart disease to discriminate neurocardiogenic from orthostatic syncope and to evaluate frequent syncope in patients with psychiatric disease. Tilt-table testing may also have a role in evaluating patients in whom documenting neurocardiogenic syncope is important (such as in high-risk occupational settings) and differentiating the cause of syncope from neurologic (such as seizure) or psychiatric etiologies.
Tx: The prognosis is excellent.
For patients with recurrent syncope, management consists of advising patients to avoid triggers and to assume a supine position with leg raising at the onset of symptoms. Physical counterpressure maneuvers (eg, leg crossing with tensing of muscles, handgrip and tensing of arm muscles with clenched fists) during the prodromal phase can improve venous return and cardiac output, sometimes aborting syncopal episodes. Some patients in high-risk settings associated with a potential risk of physical injury (eg, airline pilots, commercial drivers) require temporary activity restriction until these maneuvers are proven to be effective.
carotid sinus hypersensitivity
“w”asovagal
Baroreceptors of the carotid sinus are activated and pass impulses through
the glossopharyngeal nerve to the medulla.
Hx: Syncope occurs in an older patient as a result of head turning, wearing a tight shirt collar, or shaving over the neck area.
Tx: Gentle massage of one carotid sinus at a time may show a period of asystole or hypotension. This should be performed in a controlled setting with monitoring and atropine available.
Orthostatic hypotension
Elderly patients often have impaired baroreceptor sensitivity (autonomic failure), making them particularly susceptible to orthostatic hypotension and orthostatic syncope in the setting of hypovolemia.
Results from insufficient constriction of resistance and capacitance blood vessels in the lower extremities on standing, which may be due to a defect in autonomic reflexes, decreased intravascular volume, or medications. Arterial stiffness, decreased norepinephrine content of sympathetic nerve endings, and reduced sensitivity of the myocardium to sympathetic stimulation all contribute to a tendency toward orthostatic hypotension with age.
Orthostatic syncope is more common in those taking vasoactive drugs, diuretics, or alcohol; and in the setting of volume depletion or autonomic failure or disorders of the autonomic nervous system (idiopathic hypotension, Shy-Drager syndrome), or idiopathic autonomic neuropathy
May be caused by hypovolemia, drugs (α-adrenergic blockers),
Hx: Syncope occurs on assuming the upright position. Patients commonly have symptoms of dizziness, weakness, and fatigue, both before and after the event.
Orthostasis
Volume depletion: D/D/D/H (Diarrhea, dehydration, diuresis, hemorrhage)
ANS dysfunction: DM (autonomic neuropathy)/Parkinsons/Elderly (multiple system atrophy)
Abnormal drop in blood pressure with standing (>20 mm Hg systolic or 10 mm Hg diastolic)
- SBP decreases 20
- DBP decreases 10
- HR increases 10
Dx: Hypovolemia causes decreased renal perfusion, leading to activation of the renin-angiotensin-aldosterone system. Aldosterone stimulates aggressive sodium reabsorptionin the collecting tubules of the kidney in an effort to sustain blood volume. Consequently, most patients with hypovolemia (unless taking diuretics or experiencing significant renal impairment) have decreased urine sodium. The fractional excretion of sodium (ratio of renal sodium clearance to renal creatinine clearance) is typically <1%.
Obstruction to outflow
Mechanical Cardiac
🏃🏽♂️ Exertional syncope usually portends an underlying pathologic cause, including ventricular arrhythmias (due to myocardial ischemia/infarction) and outflow tract obstruction (eg, aortic stenosis [AS], hypertrophic cardiomyopathy).
The clinical presentation of progressive dyspnea on exertion, fatigue, and exertional syncope is suggestive of outflow obstruction.
Patients with fixed outflow obstruction cannot increase cardiac output in response to exercise-induced vasodilation, leading to hypotension, transient cerebral hypoperfusion, and decreased exercise tolerance, presyncope, or syncope.
Specific causes include aortic stenosis, hypertrophic cardiomyopathy, mitral stenosis, myxoma, pulmonic stenosis, massive pulmonary embolism, and pulmonary hypertension. (-) Prodrome.
Mitral Stenosis: Px: An opening snap after the S2, followed by a low-frequency decrescendo murmur (diastolic “rumble”). An accentuated P2 (evidence of elevated pulmonary artery pressure), an opening snap (a high-pitched apical sound best heard with the diaphragm), and a low-pitched, rumbling diastolic murmur best heard at the apex using the bell, with the patient in the left lateral decubitus position. Presystolic accentuation of the murmur may be present in both sinus rhythm and atrial fibrillation. As the severity of the stenosis worsens, the opening snap moves closer to S2 as a result of increased left atrial pressure, and the murmur increases in duration.A prominent a wave in the jugular pulse (decreased right ventricular compliance with pulmonary hypertension), a palpable thrill at the apex, a right ventricular heave, and signs of right-sided heart failure (eg, jugular venous distention, hepatomegaly, ascites, edema).
Aortic stenosis: Murmur is diamond-shaped, loudest at the right sternal border, and radiates to the carotid arteries. Delayed (slow-rising) and diminished (weak) carotid pulse (“pulsus parvus and tardus”). Presence of single and soft second heart sound (S2). Mid- to late-peaking systolic murmur with maximal intensity at the second right intercostal space radiating to the carotids
Aortic regurgitation: Blowing diastolic murmur that is best heard at the second right and third left interspaces (left sternal border). Additionally, the carotid arteries have a rapid, accentuated upstroke, with a rapid decline (frequently referred to as a Corrigan pulse); the point of maximal impulse is displaced (suggesting left ventricular volume overload); and the pulse pressure is widened (systolic pressure minus diastolic pressure; normal is ≤40 mm Hg). Tx: Aortic valve replacement surgery is recommended in patients with severe aortic regurgitation and cardiopulmonary symptoms. In asymptomatic patients with severe regurgitation, surgery is recommended when there are signs of adverse hemodynamic effects on the left ventricle, when there is left ventricular enlargement, or when the ejection fraction is less than 55%.
Mitral stenosis :Opening snap followed by a diastolic murmur that is accentuated with atrial contraction. S1 is usually loud; S2 may be variable in intensity. Electrocardiogram in patients with mitral stenosis typically shows features of left atrial enlargement and hypertrophy and right axis deviation.
Mitral regurgitation: Holosystolic murmur that begins shortly after S1 and ends just before S2, heard loudest at the apex, and radiating to the axilla.
Mitral valve prolapse: A “click-murmur” complex. This complex includes a midsystolic click, believed to be caused by sudden tensing of the mitral subvalvular apparatus as the leaflets prolapse into the left atrium, followed by a late systolic murmur. Performing the Valsalva maneuver and standing from a squatting position decrease end-diastolic volume and move the click-murmur complex closer to the S1.
Tricuspid regurgitation: Systolic murmur, loudest at the lower left sternal border, and becomes louder with inspiration.
Benign (innocent) flow murmur: typically midsystolic grade 1 to 2/6 murmurs associated with normal heart sounds and no other findings.
Hypertrophic cardiomyopathy is associated with a harsh crescendo-decrescendo systolic murmur that begins slightly after S1 and is heard best at the apex and lower left sternal border. Performing the Valsalva maneuver and standing from a squatting position increase the intensity of the murmur. The murmur of hypertrophic cardiomyopathy is the only murmur that increases in intensity with the Valsalva maneuver [accentuated during maneuvers that decrease preload (Valsalva maneuver) but is attenuated by increasing afterload (handgrip maneuver)]. Echocardiographic findings confirm asymmetric septal hypertrophy that is consistent with hypertrophic cardiomyopathy. The hypertrophy may be concentric (particularly if marked), but may also disproportionately involve the septal, anterior, lateral, or apical walls. Dynamic left ventricular outflow tract or midcavity obstruction is a feature of hypertrophic cardiomyopathy. Additional echocardiographic features include a small left ventricular cavity and significant left atrial enlargement. Although patients with hypertrophic cardiomyopathy may present with symptoms such as dyspnea, chest pain, or dizziness, many are asymptomatic.
Dx: Transthoracic echocardiography is recommended for diagnosis of systolic murmurs that are grade 3/6 or greater in intensity, diastolic murmurs, continuous murmurs, holosystolic murmurs, late systolic murmurs, murmurs associated with ejection clicks, or murmurs that radiate to the neck or back.
Transesophageal echocardiography may be useful in patients in whom a transthoracic study does not provide adequate diagnostic information or to evaluate the feasibility of surgical repair when surgery is planned. (or cardiac MRI or CT)
Ambulatory electrocardiography may be diagnostically useful in patients with repetitive, frequent palpitations,
TachyArrhythmia (Fatal syncope)
Cardiac diseases predominate as cause of syncope in elderly adults and include bradycardias (sinus and atrioventricular node dysfunction) as well as tachyarrhythmias (supraventricular and ventricular)..
Ventricular arrhythmias causing syncope typically occur in the setting of structural heart disease (myocardial infarction–associated ventricular tachycardia) or with a family history of sudden cardiac death (long QT syndrome, Brugada syndrome). Extended electrocardiographic recording, event monitoring, or electrophysiologic studies may be required to document arrhythmia. ❗ Sudden onset (-) NO Prodrome.
Patients with an arrhythmogenic cause of syncope usually have less than 5 seconds of warning symptoms before each episode.
Dx:
ECG = Holter - Perform in all patients with unexplained syncope. Arrhythmias, conduction defects predisposing to complete heart block, and evidence of structural heart disease may be documented. Yields a diagnosis in approximately 5% of patients in whom the initial history and physical examination are nondiagnostic.
Ambulatory (24-h) ECG monitoring correlates symptoms with an arrhythmia in only 4% of patients. Increasing the duration of monitoring (ie, to 48 or 72 h) increases the number of arrhythmias detected but not the diagnostic yield. Cardiac event monitors (patient triggered or looping) worn for longer periods of time (weeks to months) may be helpful in selected patients with infrequent episodes of suspected arrhythmogenic syncope.
Event Recorder
Implantable loop recorders (ILR) - Device that is placed subcutaneously that has a looping memory capable of storing ECG rhythm events over a period of months to years. Indicated in patients with recurrent, unexplained syncope. Long-term follow-up (median, 17 mo) led to diagnosis of the cause of syncope in 41% of patients compared with 7% of patients assigned to conventional evaluation. An ILR is placed subcutaneously under local anesthesia and has a solid-state looping memory capable of storing ECG rhythm events, with a total capacity of up to 42 minutes. Battery life is approximately 3 years.
Lytes: K+ Mg++
BradyArrhythmia
Hx: Conduction system abnormalities, including prolonged PR interval and intraventricular conduction delay (prolonged QRS-complex duration). Atrioventricular block with associated bradyarrhythmia can be quite intermittent.
May be associated with symptoms of near-syncope (transient) or signs of diminished cardiac output (persistent). Can be diagnosed by electrocardiography, extended electrocardiographic monitoring, or electrophysiologic studies. Includes both sinoatrial and atrioventricular node dysfunction, which may be drug-induced (β-blockers, calcium channel blockers, antiarrhythmic drugs). ❗ Sudden onset (-) NO Prodrome.
Neurogenic
Invariably associated with neurologic signs and symptoms. Carotid Doppler ultrasonography is not indicated because ischemia of the anterior cerebral circulation rarely causes syncope.
Neurogenic (vertebrobasilar insufficiency)
Px: FND
Dx:
U/S
CT/MRA
Psychiatric disorder (eg, anxiety, depression, conversion disorder)
A high incidence (24%–35%) of Psychiatric disorders has been reported in patients with syncope.
Px: In patients faking it, preform the Face-palm maneuver
Infective Endocarditis
Hx: Injection drug use, recent procedures associated with risk of transient bacteremia, presence of a prosthetic valve, and certain cardiac abnormalities. Rheumatic fever
Px: New cardiac murmur, new-onset heart failure, focal neurologic signs, splenomegaly, and cutaneous manifestations (eg, petechiae, splinter hemorrhages). The presence of Osler nodes (violaceous, circumscribed, painful nodules found in the pulp of the fingers and toes) or Janeway lesions (painless, erythematous, macular lesions found on the soles and palms.
Mitral valve disease, usually mitral valve prolapse with coexisting mitral 💦 regurgitation, is the most common valvular abnormality detected in patients with infective endocarditis.
About 75% of patients with IE have previously damaged heart valves, with mitral valvular disease being the most common.
Aortic root disease (AR), the characteristic early 💎 diastolic murmur is best heard along the right sternal border; in contrast, when AR is due to valvular disease, the early diastolic murmur is best heard along the left sternal border (3rd and 4th intercostal spaces); cardiac conduction abnormalities are more common with aortic valve than with TV involvement
The aortic valve is the second most common cardiac valve involved in IE, usually in patients with prior history of congenital bicuspid aortic valve with associated aortic stenosis.
Tricuspid valve (TV) is a frequent site of endocarditis among patients with 💉 intravenous drug use. TV endocarditis usually presents with a holosystolic** murmur of tricuspid regurgitation** that becomes accentuated with inspiration
Dx: Leukocytosis, normocytic normochromic anemia, electrocardiographic conduction defects (atrioventricular block from extension of infection into the conduction system), hematuria, and low serum complement levels (eg, glomerulonephritis). CRX suggesting heart failure or septic emboli from right-sided endocarditis (eg, multiple bilateral small nodules on chest radiograph) raise suspicion for infective endocarditis.
Laboratory data include an elevated erythrocyte sedimentation rate (ESR). The ECG shows evidence of first-degree AV block. An antistreptolysin O antibody is necessary to document prior streptococcal infection.
Evidence of recent streptococcal infection plus two major manifestations or one major and two minor manifestations satisfy the Jones criteria for diagnosis of acute rheumatic fever.
Major criteria include ❤ carditis, polyarthritis, s. chorea, erythema marginatum, and subcutaneous nodules.
Minor manifestations include fever, polyarthralgia (Joints) elevated erythrocyte sedimentation rate, and PR prolongation on ECG.
💙 DUKE
Definite endocarditis = 2 MAJOR criteria OR 1 major + 3 minor criteria OR 5 minor criteria
Possible endocarditis = 1 major + 1 minor criterion or 3 minor criteria
DUKE MAJOR Criteria for Dx:
- Microbiologic (Bacteremia) - any of the following:
Typical microorganisms (including Staphylococcus aureus) grown from two blood cultures
A microorganism grown from persistently positive blood cultures
Positive serologic test or single positive blood culture for Coxiella burnetii (Q fever) and for Bartonella, Legionella, Brucella, Mycoplasma, and Chlamydophila.
Additional causes of culture-negative endocarditis include a group of gram-negative pathogens constituting the HACEK group:(Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella species), nutritionally variant streptococci (eg, Abiotrophiaspecies, Trophermyma whippelii), and fungi (eg, Aspergillus species, Histoplasma capsulatum).
IE due to E corrodens is usually seen in the setting of poor dentition and/or periodontal infection, along with dental procedures that involve manipulation of the gingival or oral mucosa.
- Evidence of endocardial involvement (either of the following):
Transthoracic echocardiogram (TTE):oscillating intracardiac mass, abscess, or new partial dehiscence of a prosthetic valve(vegetation). *Transesophageal echocardiography (TEE) is the[initial test of choice]when there is a moderate or high pretest probability of endocarditis (eg, in patients with staphylococcal bacteremia or fungemia, a prosthetic heart valve, or an intracardiac device).TEEis the initial imaging test in some clinical situations, such as detection of left atrial thrombus, evaluation of prostheticmitral valve dysfunction, and evaluation of suspected aortic dissection, as well as in patients with a moderate to high pretest probability of endocarditis.
Physical examination: new valve regurgitation (change in pre-existing murmur is not sufficient). The vegetations of IE usually cause regurgitant murmurs.
DUKE MINOR Criteria:
- Predisposing heart condition (RF, IVDA, endo, prosthetics) or 💉injection drug user
- Fever: Body temperature >38.0°C (100.4°F)
- Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhage, or Janeway lesions
- Immunologic phenomena (Rheumatologic): glomerulonephritis, Osler nodes, Roth spots, positive rheumatoid factor
- Microbiologic: serologic evidence of infection or positive blood cultures not meeting the major criteria (a single blood culture for coagulase-negative staphylococci is not sufficient)
Staphylococcus aureus
- Prosthetic valves
- Intravascular catheters
- Implanted devices (eg, pacemaker/defibrillator)
- Intravenous drug users
🌴Viridans group streptococci ( Streptococcus sanguinis 💦 belongs to the viridans group of streptococci, which also includes S mitis, S oralis, S mutans, S sobrinus, and the S milleri group)
- Gingival manipulation
- Respiratory tract incision or biopsy
Staphylococcus epidermidis
- Prosthetic valves
- Intravascular catheters
- Implanted devices
Enterococci**
- Nosocomial urinary tract infections
Streptococcus gallolyticus (S bovis) or Clostridium septicum
- Colon carcinoma
- Inflammatory bowel disease
Fungi (eg, Candida species)
- Immunocompromised host
- Intravascular catheters
- Prolonged antibiotic therapy
💊 Rx: Consider antibiotic prophylaxis only in patients with: High-risk cardiac conditions include the presence of a prosthetic cardiac valve, unrepaired cyanotic congenital heart disease, congenital heart disease repair with prosthetic material or device within the last 6 months, presence of palliative shunts and conduits, cardiac valvulopathy in cardiac transplant recipients, and a history of infective endocarditis. High-risk surgical procedures include dental procedures involving manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa as well as respiratory tract procedures that involve perforation of the respiratory mucosa (tonsillectomy, adenoidectomy).
Amoxicillin and cephalosporins, such as cephalexin, are frequently prescribed. Clindamycin, azithromycin, or clarithromycin are appropriate alternatives in patients with penicillin allergy.
Tx: Empiric therapy for early prosthetic valve infective endocarditis includes vancomycin, gentamicin, and rifampin for multidrug-resistant bacteria, particularly coagulase-negative staphylococci.
The Infectious Diseases Society of America Clinical has practice guidelines that recommend intravenous vancomycin (or daptomycin) for the treatment of methicillin-resistant Staphylococcus aureus (MRSA) infective endocarditis. The recommended duration of treatment for S. aureus-associated native valve infective endocarditis is 6 weeks.
Cx: ❗
Septic pulmonary emboli occur in up to 75% of patients with tricuspid endocarditis, most commonly due to Staphylococcus aureus in IVDU with IE. Imaging may show pulmonary septic emboli as pulmonary infiltrates, abscesses, infarction, pulmonary gangrene, or cavities.
Symptoms suggesting septic emboli in patients with tricuspid valve endocarditis include shortness of breath, chest pain, and cough. Blindness, focal weakness, localized back or flank pain, hematuria, and gangrenous skin lesions may be embolic manifestations of left-sided infective endocarditis.
Splenic abscess is typically due to infective endocarditis (or seeding from another site of infection). Likely mechanisms include hematogenous seeding or septic emboli to the spleen. Common causative organisms are Staphylococcus, Streptococcus, and Salmonella. Antibiotics alone for treating splenic abscess have a high mortality (up to 50% in some studies). As a result, splenectomy is recommended for all patients. Percutaneous drainage may be an option in poor surgical candidates.\
Perivalvular abscess: Conduction abnormalities on ECG should raise suspicion extending into adjacent cardiac conduction pathways; the conduction block can potentially lead to syncope.
Leads
🔽 “Inferior” II, III, aVF 🔼 (Reciprocal = aVL)
The right coronary artery (RCA) supplies blood to the right ventricle, the SA node, the inferior portions of the left ventricle, and usually to the posterior portion of the left ventricle and the AV node. Infarctions involving the SA node may produce sinus dysrhythmias, including bradycardia and sinus arrest.
Cx: The use of verapamil or beta-blockers can further worsen the sinus node dysfunction and result in hypotension or shock.
V1-V2
Septal (R ventricle)
LAD
V3-V4
Left Anterior wall
V5-V6
Left Lateral
LCx
V4Rb
Right ventricle
Right coronary artery
aOften associated with inferior and/or lateral ST-elevation infarctions and tall R wave in V1.
bIndicates a precordial lead placed at the V4 position on the right side of the chest.
Dextrocardia in the adult is most often accompanied by situs inversus or right sided malposition of the abdominal viscera. Isolated dextrocardia without abdominal visceral malposition is uncommon in the adult.
- 1) inverted P waves in 1 and aVL;
- 2) negative QRS complex and T wave in 1;
- 3) progressively decreasing voltage across the precordium.
LBBB
Associated with absent Q waves in leads I, aVL, and V6; a large, wide, and positive R wave in leads I, aVL, and V6;
- Wide QRS a (prolongation of the QRS complex to greater than 0.12 seconds)
- RSR’ in V5 or V6
The presentation of acute coronary syndrome with new left bundle branch block should be considered equivalent to ST-elevation myocardial infarction and is an indication for acute reperfusion therapy.
Bundle branch blocks usually produce “secondary” T wave changes such that the ST-T wave vector points opposite in direction of the major vector of the QRS. These secondary ST-T changes are due to the altered sequence of ventricular activation.
ST elevations
The differential diagnosis of ST elevations not only includes 1) ischemic heart disease (MI, Prinzmetal angina, ventricular aneurysm) but also 2) pericarditis, 3) left bundle branch block (LBBB) (in V1-V3) and 4) normal (“early repolarization”) variant (J point elevation).
In myocardial infarction the ST elevations tend to be localized (inferior, anterior, posterior, lateral), often, but not always with reciprocal ST depressions.
Atrial flutter
The underlying causes of atrial flutter are similar to those for atrial fibrillation and often result from atrial dilation.
Hx: Typical causes include pulmonary embolism, septal defects, mitral or tricuspid valve disease, and chronic left ventricular failure. Atrial flutter may occur in patients without underlying heart disease, however, such as those with thyrotoxicosis or alcoholism.
Dx: Characterized by a saw-tooth pattern on electrocardiogram (lead II) that is most noticeable in the inferior leads.
The atrial rate is between 250 and 300 and is usually associated with a 2:1 or 3:1 AV block, resulting in a “ventricular rate” of approximately 100/min to 150/min.
Grouped beating (“bigeminal”) pattern represents a repetitive variable block mechanism (2:1 and 4:1 conduction).
- 2:1 Conduction: most common
- 4:1 every fourth atrial depolarization is conducted through the AV node
With atrial flutter there aren’t P waves per se but “atrial waves”. So if you talk about atrial flutter do not say “the P waves….” since once you say P wave, the informed listener will probably assume it’s not atrial fibrillation or atrial flutter
Tx: Patients with hemodynamic instability due to atrial flutter should be immediately electrically cardioverted. In others, rate control involves the use of a 🍦non-dihydropyridine calcium channel blocker or a 🎺β-blocker. Preventing stroke and cardiac embolization is identical to atrial fibrillation as mentioned previously.
Atrial 📈 Fibrillation
One of the most common cardiac arrhythmias. The typical electrocardiogram (ECG) presentation of AF includes absent P waves replaced by tiny chaotic fibrillatory waves, irregularly irregular R-R intervals, and narrow QRS complexes.
The pulmonary veins (PVs) are the most frequent location of the ectopic foci that cause AF. Cardiac tissue (myocardial sleeves) extends into the PVs and normally functions like a sphincter to reduce reflux of blood into the PVs during atrial systole. This tissue has different electrical properties than the surrounding atrial myocytes and is prone to ectopic electrical foci and/or aberrant conduction, which can initiate AF. Origination of AF in the PVs is therapeutically useful in patients who cannot achieve rate and/or rhythm control with standard medical therapy. In these patients, the myocardial tissue surrounding the PVs can be disrupted by catheter-based radiofrequency ablation, thereby electrically disconnecting the PVs from the left atrium.
Atrial fibrillation is classified as paroxysmal (lasting <7 days), persistent (lasting >7 days), or long-standing persistent (permanent) (lasting >1 year or associated with failed cardioversion).
Hx: Associated with structural heart disease, such as valvular disease (especially mitral valve disease), dilated cardiomyopathy, hypertension, and coronary artery disease. Heart failure, pulmonary hypertension, and increasing age are also strongly associated. Noncardiac causes include substance abuse (eg, alcohol, caffeine, cocaine, amphetamines), inhaled β-agonists, hypoxemia, COPD, pulmonary embolization, obstructive sleep apnea, and hyperthyroidism. Alcohol excess, sometimes called “holiday heart.” A useful mnemonic for causes of atrial fibrillation is PIRATES: P-pericarditis, pulmonary disease, pulmonary embolism; I-ischemia, infarction, infection, and inflammation; R-rheumatic heart disease; A-atrial septal defect; T-thyrotoxicosis; E-elevated blood pressure, ETOH excess and withdrawal; S-sleep apnea, surgery (cardiothoracic).
Dx: All such patients with new-onset AF should have thyroid-stimulating hormone and free T4 levels measured to screen for occult hyperthyroidism as an underlying cause.
Px: Patients with atrial fibrillation will have a “pulse deficit,” or a higher apical than peripheral pulse rate, because not all ventricular beats are conducted effectively enough to produce a peripheral pulse.
Dx: Disorganized atrial activity at a rate of 350 to 600/min, with no discernible P waves. It is characteristically associated with an irregularly irregular rhythm, and the fibrillatory waves vary in amplitude, morphologic pattern, and interval, creating a rough, irregular baseline between QRS complexes.
The CHADS2 risk score is used to predict the likelihood of stroke in patients with nonvalvular atrial fibrillation.stroke risk factors (ie, Congestive heart failure, Hypertension, A2ge >75 years, Diabetes mellitus, and prior S2troke/TIA/thromboembolism).
0 points: Low stroke risk: aspirin or no treatment is used.
1 Point: Intermediate stroke risk: either warfarin or aspirin is used, based on physician and patient preference.
2 Points or more: high risk: therapeutic anticoagulation is preferred.
CHA2DS2-VASc better recognizes the influence of gender and the presence of established Vascular disease, Age (65-74), Sex)
Tx:
The term 🤠 “lone AF” is occasionally used for patients with paroxysmal, persistent, or permanent AF with no evidence of cardiopulmonary or structural heart disease. Patients with lone AF are generally age <60 and, by definition, have a CHA2DS2-VASc score of 0. The risk of systemic embolization in such patients is extremely low, and anticoagulant therapy is not indicated.
Score of 1: Either anticoagulation or antiplatelet therapy is indicated.
Score of 2 or greater: Oral anticoagulation is recommended for prevention of stroke.
Score of 3 points (hypertension and transient ischemic attack),
Score of 4 points (age range, gender, hypertension, and transient ischemic attack).
The HAS-BLED score can be used to identify patients at high risk of bleeding. Hb decrease by 2; transfusion need. Doesn’t tell us about falls.
Rate control, restoration/maintenance of sinus rhythm, and stroke prevention w/ anticoagulation.
Approximately 50% of episodes of atrial fibrillation convert to a normal rhythm spontaneously.
Rate control approach: patients aged >65 years
🍦Intravenous non-dihydropyridine calcium channel blockers (diltiazem or verapamil)
🎺β-blockers (metoprolol or esmolol).
Warfarin (target international normalized ratio [INR] of 2.0-3.0) reduces the risk of stroke by an average of 64% in patients with nonvalvular atrial fibrillation.
Maintain the INR at 2.0 to 3.0 in patients with nonvalvular atrial fibrillation or at 2.5 to 3.5 in patients with valvular atrial fibrillation.
Rhythm control approach: The antiarrhythmic agents Amiodarone, Flecainide, ibutilide, propafenone, and sotalol are used to maintain patients in sinus rhythm following cardioversion.
If the patient is symptomatic but hemodynamically stable, the initial goal is to reduce the heart rate to 60/min to 110/min with a rate control agent.
❗RVR: Management of atrial fibrillation or atrial flutter with rapid ventricular response (RVR) is determined by the patient’s hemodynamic stability.
❗Rapid (irregular) ventricular response (RVR) AND hemodynamic compromise is treated acutely with electrical synchronized cardioversion (which delivers an electric shock timed to the R wave of QRS complex on the EKG). 120 J
“Cardioversion”: Energy delivery is synchronized to the QRS complex to minimize the likelihood of the shock occurring during repolarization, which can precipitate ventricular fibrillation.
Pulmonary vein catheter radiofrequency ablation or “maze” procedure in those treated unsuccessfully
🐺 (AVRT) Atrioventricular Reciprocating Tachycardia [Ventricular preexcitation syndrome]{WPW} w/ tachycardia
A bypass tract–mediated reentrant tachycardia in which the anterograde conduction (atrium-to-ventricle) is typically via the atrioventricular node and retrograde conduction is via the bypass tract.
[Associated with an accessory pathway between the atria and ventricle that is not contained within the AV node itself.]
[The aberrant conduction tissue bypasses the normal AV node (hence the PR interval of < 0.20 seconds); it leads the electrical impulse directly to the ventricle (bypassing the His-Purkinje
fibers and widening the QRS complex)]
Dx: Heart rate is typically between 140 and 250
Because bypass tract conduction is typically faster than conduction via the atrioventricular node, atrial activation occurs rapidly after the QRS complex, resulting in a “short R-P” tachycardia, and the P wave is usually located within the ST segment.
“short R-P” tachycardia
A 🎤short PR interval and the presence of a delta wave (a sloping upstroke initiating the QRS complex, which may be wide due to sequential rather than parallel depolarization of the ventricles). This pattern on ECG is referred to as ventricular preexcitation
➕ symptomatic tachycardia (paroxysmal tachyarrhythmias), it is called the 🐺 “Wolff-Parkinson-White syndrome”.
Prolonged QRS duration
Tx: AVNRT may be terminated by maneuvers to increase 💡vagal tone, such as Valsalva or unilateral carotid massage (after careful carotid artery auscultation for bruits).
Rx:
Intravenous 🎵 adenosine, a non-dihydropyridine calcium channel blocker, and β-blockers are often successful in terminating AVRT not responding to vagal maneuvers. Intravenous adenosine has a very rapid onset and is extremely short-acting, with a half-life of 10 seconds, making it an excellent first therapeutic choice. Cx: Adenosine is contraindicated in patients with severe bronchospastic disease.
🎺β-Blockers and 🍦non-dihydropyridine calcium channel blockers can also be used long term to prevent frequent recurrence of AVRT.
In refractory cases, catheter 🔪 radiofrequency ablation is between 95% and 99% successful in preventing AVRT recurrence.
Cx:
Atrial fibrillation (AF) occurs in 10%-30% of individuals with WPW, and is a potentially life-threatening emergency; AF in WPW can bypass the usual rate-limiting function of the AV node, leading to very rapid ventricular response rates. Persistent AF with rapid ventricular response in patients with WPW can ultimately deteriorate into ventricular fibrillation (VF).
Acute treatment of AF in patients with WPW is aimed at prompt control of ventricular response and termination of AF as follows:
Hemodynamically unstable patients require immediate electrical cardioversion
For stable patients, rhythm control with anti-arrhythmic drugs such as intravenous ibutilide or 🤴🏼 procainamide is preferred
Atrioventricular nodal reentrant tachycardia (AVNRT)
AVNRT is a common type of paroxysmal supraventricular tachycardia (PSVT)
The atria and ventricles are activated simultaneously from a reentrant circuit within the atrioventricular node.
involves a slow pathway and a fast pathway within the atrioventricular node:
The slow pathway conducts slowly but repolarizes quickly.
The fast pathway conducts quickly but repolarizes slowly.
Typical AVNRT (slow-fast) often has an R-P interval so short that the P wave is buried within the QRS complex. The QRS complex is usually narrow as long as conduction below the atrioventricular node is normal.
Accounts for approximately 60% of all SVTs that present as a regular rhythm.
Dx: P wave either is seen just after the QRS complex, which accounts for a short RP interval or is concealed within the QRS complex (no visible P wave)
Tx: Vagal maneuvers (eg, carotid sinus massage, cold-water immersion or diving reflex, Valsalva maneuver, eyeball pressure) increase parasympathetic tone in the heart and result in a temporary slowing of conduction in the AV node and an increase in the AV node refractory period, leading to termination of AVNRT.
Rx: Intravenous adenosine, a non-dihydropyridine calcium channel blocker, and β-blockers are often successful in terminating AVNRT not responding to vagal maneuvers. Intravenous adenosine has a very rapid onset and is extremely short-acting, with a half-life of 10 seconds, making it an excellent first therapeutic choice. Adenosine is contraindicated in patients with severe bronchospastic disease. β-Blockers and non-dihydropyridine calcium channel blockers can also be used long term to prevent frequent recurrence of AVNRT.
In refractory cases, catheter radiofrequency ablation is between 95% and 99% successful in preventing AVNRT recurrence.
Ventricular tachycardia (VT)
Wide-complex tachycardia (QRS duration > 0.120 sec)
Ventricular rate typically ranges from 140/min to 250/min
In a patient with wide-complex tachycardia and a history of coronary artery disease or cardiomyopathy, ventricular tachycardia is the assumed diagnosis.
- A monophasic wide R wave in V1 (or an Rsr~ or qR-type morphology)
- Very wide QRS (>140-160 ms,
- An rS or QS in V6.
Hx: VT often accompanies structural heart disease (prior MI, CAD, cardiomyopathy), most commonly ischemic heart disease, and it is associated with electrolyte disorders (eg, hypokalemia, hypomagnesemia), drug toxicity, valvular heart disease, nonischemic cardiomyopathy, and long QT syndrome.
Dx: Precordial concordance?
Monomorphic VT is usually originates in the vicinity of an underlying ventricular scar.
Nonsustained VT: has ≥ 3 beats but is <30 seconds in duration.
Hx: Usually are asymptomatic but may experience palpitations, dizziness, or syncope.
Sustained VT: Persists >3️⃣0️⃣ seconds or requires termination due to hemodynamic collapse.
Hx: Syncope or near syncope and can also present with sudden cardiac death.
Long QT syndrome is characterized by prolonged ventricular repolarization and a predisposition to the development of polymorphic VT and sudden cardiac death.
Torsades de pointes is a special subset of polymorphic VT where the ventricular rate ranges from 200/min to 300/min. Tx: Magnesium sulfate
Rx:
Sustained:
🍡👒 IV amiodarone has largely replaced other antiarrhythmic agents (sotalol) for hemodynamically stable VT in the acute setting, although lidocaine can be useful in patients with coronary ischemia.
🤴🏽Procainamide and sotalol are also acceptable
🤥Lidocaine can be used as a second-line agent.
Nonsustained: Medical therapy does not improve survival in patients with nonsustained VT, and thus pharmacologic therapy is avoided unless the patient has a history of structural heart disease or long QT syndrome or (rarely) intolerable symptoms.
🎺 β-Blockers are the mainstay of treatment for those with symptomatic nonsustained VT
🍦non-dihydropyridine calcium channel blockers may also be used in patients with structurally normal hearts.
❗Hemodynamically unstable: Epinephrine or vasopressin is recommended for hemodynamic support,
Patients in whom drug therapy for nonsustained VT fails or is not tolerated can be referred for catheter-directed radiofrequency ablation or ICD placement.
Implantable cardioverter-defibrillator (ICD) is an internal defibrillator that senses dangerous cardiac arrhythmias and automatically converts the rhythm to sinus rhythm by either administering a high-energy shock or delivering a short series of paced beats.
An ICD is also indicated in patients with sustained VT in the setting of structural heart disease or when a completely reversible risk factor cannot be identified (such as in patients with hypertrophic cardiomyopathy at increased risk for sudden cardiac death).
ICD placement is also indicated for the primary prevention of sudden cardiac death in patients with (1) NYHA Class II or III heart failure AND an ejection fraction of less than 35% or (2) a prior MI and an ejection fraction of less than 30% (after a waiting period of 40 days).
Catheter-directed radiofrequency ablation of VT is useful in patients with idiopathic VT (those without structural heart disease or another clear etiology) as well as those with frequent recurrences of VT.
Cx: VT is a potentially life-threatening arrhythmia due to rapid, depolarizing impulses originating from the His-Purkinje system, the ventricular myocardium, or both.
♨♨♨ Hypertension (primary)
Dx: Obtain the following studies in all patients: hematocrit, glucose, creatinine, electrolytes, urinalysis, fasting lipid profile, and electrocardiography. Blood or protein in the urine may indicate kidney damage or suggest secondary hypertension.
An electrocardiogram showing left ventricular hypertrophy and/or signs of previous infarction (Q waves) is evidence of cardiovascular damage. Although echocardiography is more sensitive in diagnosing ventricular hypertrophy, it is not routinely recommended in all patients with a new diagnosis of hypertension.
Tx: Weight reduction is most beneficial, and systolic blood pressure can fall from up to 20 mm Hg for each 10 lb of weight lost.
Dietary recommendations to lower BP consist of consuming a diet that emphasizes the intake of fruits, vegetables, and whole grains; includes poultry, fish, legumes, nuts, nontropical vegetable oils, and low-fat dairy products; and restricts the consumption of red meat, sweets, and sugar-sweetened beverages.
DASH (Dietary Approaches to Stop Hypertension) diet can help to achieve these goals.
Dietary sodium reduction: Sodium should be restricted to <2400 mg/day (<1500 mg/day results in greater reductions) or by at least 1000 mg/day. [can lower blood pressure between 8 and 14 mm Hg]
Three to four sessions averaging 40 minutes in duration per week of moderate to vigorous aerobic physical activity may also lower BP. [Less than 10 mmHg]
Rx: In the general adult population <60 years of age, pharmacologic treatment is recommended when the systolic BP is ≥140 mm Hg or the diastolic BP is ≥90 mm Hg. In patients ≥60 years of age, therapy is recommended if the systolic BP is ≥150 mm Hg or the diastolic BP is ≥90 mm Hg. Typically, a single agent decreases systolic BP by 12 to 15 mm Hg and diastolic BP by 8 to 10 mm Hg.
In the general non-African American population, thiazide diuretics, angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), and calcium channel blockers (CCBs) may all be considered for initial treatment of hypertension, and all reduce the complications of hypertension.
For African Americans, initial therapy should be a thiazide diuretic or CCB, including those with diabetes.
For all patients (regardless of race or the presence or absence of diabetes) >18 years of age with chronic kidney disease (including those with and those without proteinuria), initial therapy should be an ACEI or ARB because these agents are renoprotective and improve renal outcomes.
In blacks with chronic kidney disease but without proteinuria, the initial agent can be a CCB, thiazide diuretic, ACEI, or ARB. Diuretics may equalize the response of black patients to ACEIs and ARBs. Loop diuretics are preferred for patients with chronic kidney disease and a serum creatinine level >1.5 mg/dL or a glomerular filtration rate <30-50 mL/min/1.73 m2. Thiazide diuretics are much more likely than loop diuretics to cause significant hyponatremia, particularly in elderly women.
In patients with hypertension and ❤ coronary artery disease, 🎺β-blockers are the drugs of choice because they decrease cardiovascular mortality.
The presence of asthma or chronic bronchitis may limit the use of β-blockers.
#1 ACEIs are preferred for use in patients with asymptomatic ventricular dysfunction and symptomatic heart failure because they decrease cardiovascular mortality.
#2 Combination ACEIs and thiazide diuretic therapy reduces recurrent stroke rates.
#3 Compared with β-blockers, ARBs may be specifically beneficial in patients with left ventricular hypertrophy.
🃏 ACEIs and ARBs reduce albuminuria and the progression of chronic kidney disease, including 🍭diabetic nephropathy.
ACEIs produce greater reductions in cardiac morbidity and mortality compared with calcium channel blockers. An increase of up to 33% in serum creatinine is acceptable and not a reason to discontinue ACEI therapy; however, hyperkalemia may limit the use of ACEIs.
Parenteral drugs are usually not necessary in hypertensive urgency, unless symptoms or progressive end-organ damage is present. Initial treatment is with one or more rapid-onset oral anti-hypertensive drugs (such as clonidine or a short-acting ACEI such as captopril) followed by a longer-acting formulation once BP is <180/110 mm Hg. Clonidine may be given hourly until the desired BP is achieved, although care must be taken to not excessively lower the BP. BP should be rechecked within 48 hours.
❗ Avoid short-acting calcium channel blockers in patients with ischemic heart disease (such as nifedipine), because reflex adrenergic stimulation and tachycardia may lead to myocardial ischemia.
Isolated ambulatory hypertension (masked hypertension) 🎭 These patients typically have normal blood pressure readings during clinic visits but their average blood pressure throughout the day and nighttime is elevated. Because detection is difficult, patients often initially present with evidence of hypertensive end-organ damage (eg, retinal arteriovenous nicking consistent with hypertensive retinopathy, increased QRS-complex voltage consistent with left ventricular hypertrophy).
Patients with clinical signs of hypertension but normal blood pressure readings should be tested for masked hypertension with ambulatory blood pressure monitoring (ABPM). A blood pressure cuff is worn throughout a 24-hour period, and blood pressure is measured and recorded at routine intervals (eg, every 20 minutes while awake and every 60 minutes while sleeping). An average 24-hour blood pressure >135/85 mm Hg is diagnostic of hypertension
Resistant hypertension is BP that is not at target level despite maximal doses of 3️⃣ antihypertensive agents, one being a diuretic. Important causes include medication nonadherence, inadequate therapy, excessive alcohol consumption, and other drugs (eg, NSAIDs, sympathomimetic agents).
A patient with resistant hypertension and systolic heart failure should begin taking a newer-generation dihydropyridine calcium channel blocker, such as amlodipine, to improve control of blood pressure (amlodipine and felodipine to have little or no negative inotropic effect (nodal) and a neutral effect on morbidity and mortality rates). However, because they do not decrease morbidity or mortality rates, calcium channel blockers are not first-line treatment for systolic heart failure. Use of calcium channel blockers in systolic heart failure is generally reserved for treatment of conditions such as hypertension or angina that are not optimally managed with maximal doses of evidence-based medications such as ACE inhibitors and β-blockers. Many calcium channel blockers are relatively contraindicated in patients with systolic heart failure because of an associated increased risk of exacerbation of heart failure. Older-generation calcium channel blockers, such as diltiazem, nifedipine, and verapamil, may precipitate exacerbation of heart failure because of their negative inotropic effects.
Cx:
Hypertensive urgency is a severe elevation in BP without acute end-organ damage.
Malignant hypertension is usually seen in patients with long-standing and uncontrolled hypertension. It is associated with retinal hemorrhages, exudates, and/or papilledema.
❗Hypertensive emergency is defined as markedly elevated BP (≥180/120 mm Hg) combined with symptoms or signs of end-organ damage, such as encephalopathy, papilledema, retinal hemorrhages or exudates, stroke, myocardial ischemia or infarction, aortic dissection, pulmonary edema, or acute kidney injury.
Hypertensive encephalopathy is associated with cerebral edema due to breakthrough vasodilation from failure of autoregulation. Patients usually develop insidious onset of headache, nausea, and vomiting followed by non-localizing neurologic symptoms (eg, restlessness, confusion, seizures/coma if untreated). Patients also can develop subarachnoid or intracerebral hemorrhage.
Tx:
🎺Intravenous labetalol is often used in hypertensive urgencies but, as a nonselective beta-blocker, is relatively Cx: asthma
🧨Nitroprusside in the ICU setting is indicated. Cx: Renal insufficiency would be a contraindication.
Intravenous Nitroglycerin, fenoldopam, or enalapril.
Dx: Shock
Shock should be strongly considered in ill-appearing patients with vital sign abnormalities (particularly tachycardia and hypotension), altered mental status, or signs of organ hypoperfusion.
Studies should determine whether end organ damage (neurologic, cardiac, renal, GI) is present. In shock patients, the following tests should be considered:
◦ CBC and coagulation studies (to determine anemia/blood loss, infection, hypocoagulability)
◦ electrolytes
◦ BUN/creatinine and urinalysis; hepatic function panel (to assess liver and renal function)
◦ chest x-ray, EKG
◦ lactate (to gauge the degree of hypoperfusion)
◦ urine pregnancy test
◦ More invasive testing is often required: arterial blood gas for O2/pH; central venous oxygen measurement, systemic vascular resistance, and cardiac output may be measured through special central venous catheters
If a particular type of shock is suspected, further studies may be directed accordingly:
◦ infectious etiology (sepsis) – blood, sputum, urine, pelvic, or wound cultures; head CT and lumbar puncture; targeted imaging (US/CT)
◦ cardiogenic – cardiac enzymes and echocardiogram
◦ obstructive – CT or V/Q scan (PE), echo (tamponade)
