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USMLE Step 2 (Fach) / Cardiology (Lektion)

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• Tachycardia, stable, broad QRS, regular Likely ventricular tachycardia. Amiodarone 300 mg IV over 20-60 minutes.Followed by amiodarone 900 mg IV over 24 hours.
• Tachycardia, stable, broad QRS, irregular Seek expert help Possibilities include:- AF with bundle branch block (→ treat as for narrow complex)- Polymorphic VT (eg, torsades de pointes → give magnesium 2g over 10 min)
• Tachycardia, narrow QRS, regular Usually sinus tachycardia, AV nodal re-entry tachycardia (AVNRT), AV re-entry tachycardia (AVRT), atrial flutter with regular AV conduction. If unstable → synchronised electrical cardioversion Stable:1. Use vagal maneuvers: carotid sinus masage or Valsalva maneuver2. Adenosine 6 mg rapid IV bolus→ If unsuccessful give 12 mg
• Tachycardia, narrow QRS, irregular Probably atrial fibrillation Unstable → Synchronised electrical cardioversion Stable:- β-blocker or diltiazem- Consider digoxin or amiodarone if evidence of heart failure- Anticoagulate if duration >48 hours
• Widened QRS interval Left bundle branch block: - QRS duration >120 ms- No R wave in V1- Wide, tall R waves in I, V5, V6 Right bundle branch block:- QRS duration >120 ms- RSR' complex ("rabbit ears")- qR or R morphology with a wide R wave in V1- QRS with a wide S wave in I, V5, V6
• Axis deviations Normal (-30 – +90%):- Lead I: ↑- Lead aVF: ↑ Left axis deviation (≤-30%):- Lead I: ↑- Lead aVF: ↓ Right axis deviation (≥+90%): - Lead I: ↓- Lead aVF: ↑
• ECG - ischemia/infarction Natural progression:- Hyperacute T-waves- ST-segment changes (either depression or elevation)- Q waves > 40 msecs or more than one-third of QRS amplitude→ Q waves signify either acute or prior ischemic events and do not provide information on when an event took place- T-wave inversion Nonspecific sign: Poor R-wave progression
• ECG - Ventricular hypertrophy Left ventricular hypertrophy:- S in V1 + R in V6 or V4 is > 35 mm- Alternative criteria: The amplitude of R in aVL + S in V3 is > 28 mm in men or > 20 mm in women. Right ventricular hypertrophy:- Right axis deviation and an R wave in V1 >7 mm.
• Atrial fibrillation Risk factors:- Heart disease: Coronary artery disease, MI, hypertension, mitral valve disease, congestive heart failure- Pericarditis and pericardial trauma- Pulmonary disease, including PE and COPD- Hyperthyroidism- Systemic illness (e.g., sepsis, malignancy, DM)- Electrolyte imbalances - Excessive alcohol intake ("holiday heart syndrome")- Sick sinus syndrome- Pheochromocytoma Classification:- Stable / Instable- New-onset (< 48 h) / Paroxysmal (< 7 days) / Persistant (> 7 days) / Long-standing persistant (> 1 year) / Permanent (Untreated long-standing persistent AF)- Valvular / Non-valvular Clinical features:- Mostly asymptomatic- Symptoms of arrhythmias: Palpitations, dizziness, syncope, fatigue, and or dyspnea- Tachycardia with an irregularly irregular pulse- Complications: Acute left heart failure, thromboembolic event, ventricular tachycardia Diagnostics:- ECG (initial investigation): Irregularly irregular RR intervals, P-waves are indiscernible, tachycardia, narrow QRS complex (< 0.12 seconds)- Holter ECG monitoring may be used to detect paroxysmal AF- Echocardiography- Lab: Troponin (rule out MI), BNP (identify HF), CBC (identify anemia, infection), thyroid, electrolytes Treatment:1. Acute AFib in unstable patient: Immediate electrical cardioversion2. Acute AFib in stable patient:- Rate control with β-blockers or calcium channel blockers- Cardioversion to sinus rhythm after rate control is achieved→ If present < 48 hours → straight to cardioversion→ If present > 48 hours → 4 weeks of anticoagulation → TEE → If no thrombus, then cardiovert3. Anticoagulation- Nonvalvular: Depending on CHA2DS2-VASc score (0: Nothing, 1: choose, 2+: DOACs or warfarin)- Valvular: Warfarin 
• Stable angina pectoris Risk factors:- Diabetes mellitus – worst risk factor- Smoking- Hypertension- Hyperlipidemia- Age- Family history of premature coronary artery disease (men < 55 years, women < 65 years)- Other: Obestiy, physical inactivity, stress, excess alcohol use Clinical features:- Chest pain or retrosternal pressure→ Lasts less than 10 to 15 minutes→ Frightening chest discomfort, usually described as heaviness, pressure, squeezing, tightness; rarely sharp or stabbing pain→ Pain is often gradual in onset- Symptoms are reproducible/predictable- Complaints often subside within minutes, with rest or after administration of nitroglycerin- Common triggers: Mental or physical stress, exposure to cold Diagnostics:- ECG: normal- Stress test – useful for patients with an intermediate pretest probability of CAD based upon age, gender, and symptoms. Positive if the patient develops: ST segment depression, chest pain, hypotension, arrhythmias → catheterization.- Pharmacologic stress test – for patients who cannot exercise- Holter monitoring Treatment:- Risk factor modification: Smoking cessation, blood pressure, hyperlipidemia, DM, obesity, exercise and diet control- Aspirin or clopidogrel- β-blockers (1st line) or Ca2+-channel blockers- Nitrates - ACE inhibitors – If CHF is also present- Revascularization (PCI or CABG) – In high-risk patients
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• PCI vs. CABG Percutaneous coronary intervention (PCI):- Consists of both coronary angioplasty with a balloon and stenting.- Should be considered in patients with one-, two-, or three-vessel disease. Even with three-vessel disease, mortality and freedom from MI have been shown to be equivalent between PTCA with stenting and CABG. - Best if used for proximal lesions.- Restenosis is a significant problem (up to 40% within first 6 months). Coronary artery bypass grafting (CABG):- Main indications: → Three-vessel disease with >70% stenosis in each vessel→ Left main coronary disease with >50% stenosis→ Left ventricular dysfunction
• Unstable angina pectoris Clinical features:- Angina at rest - Symptoms are not reproducible/predictable- Usually occurs at rest or with minimal exertion and is usually not relieved by rest or nitroglycerin- Every new-onset angina- Severe, persistent, and/or worsening angina (crescendo angina)- Increasing intensity, frequency, or duration in a patient with a known stable angina Diagnostics: Same as angina- ECG – abnormalities (of the ST segment or the T wave) occur during an episode of chest pain- Stress test – if positive → catheterization- Holter monitoringThe distinction between unstable angina and NSTEMI is based entirely on cardiac enzymes. The latter has elevation of troponin or creatine kinase-MB (CK-MB). Treatment:- Hospital admission on a floor with continuous cardiac monitoring. Establish IV access and give supplemental oxygen. Provide pain control with nitrates and morphine.- Treat as in MI except for fibrinolysis.→ Aspirin + clopidogrel for 9-12 months→ β-blocker→ Low–molecular-weight heparin (LMWH) for at least 2 days – to prevent clots- Cardiac catheterization/revascularization- After acute treatment: Continue aspirin (or other antiplatelet therapy), β-blockers (atenolol or metoprolol), and nitrates
• Variant/Vasospastic/Prinzmetal angina Angina caused by transient coronary spasms (usually occurring close to areas of coronary stenosis).Episodes of angina occur at rest and are associated with ventricular dysrhythmias, some of which may be life threatening. The angina classically occurs at night. Etiology: - Cigarette smoking- Use of stimulants (e.g., cocaine, amphetamines) or sumatriptan- Alcohol, stress, hyperventilation, exposure to cold- Association with other disorders involving vasospasms (e.g., Raynaud phenomenon, migraine headaches) Diagnostics:- Ambulatory ECG: Reversible ST elevation - No troponin I or T level elevations on serial measurements- Coronary angiography: no CAD- Coronary spasms on angiography confirm the diagnosis – displays coronary vasospasm when the patient is given IV ergonovine or acetylcholine (to provoke vasoconstriction). Treatment:- Risk factor modification: Smoking cessation- Calcium channel blockers and nitrates: first-line agent for acute attacks and prophylaxis - Avoid beta-blockers!
• Myocardial infarction Clinical features:- Chest pain→ Often described as crushing and "an elephant standing on my chest"→ Radiation to neck, jaw, arms, or back, commonly to the left side- Painless infarcts or atypical presentations more likely in: postoperative patients, elderly, diabetic patients, women.- Other: Dyspnea, diaphoresis, weakness/fatigue, nausea/vomiting, sense of impending doom, syncope- Sudden cardiac death Diagnosis:- ECG→ Peaked T waves: Occur very early and may be missed→ ST segment elevation indicates transmural injury and can be diagnostic of an acute infarct→ ST segment depression: Subendocardial injury→ Q waves: Evidence for necrosis (specific)—Q waves are usually seen late; typically not seen acutely→ T-wave inversion is sensitive but not specific- Cardiac enzymes→ Troponin T/I and CK/CK-MB should me measured on admission, and again every 8 hours for 24 hours.→ Troponin T/I increases within 3 to 5 hours and returns to normal in 5 to 14 days; reaches a peak in 24 to 48 hours.→ CK/CK-MB increases within 4 to 8 hours and returns to normal in 48 to 72 hours; reaches a peak in 24 hours. Treatment:- Admit patient to a cardiac monitored floor (CCU) and establish IV access. Give supplemental oxygen and analgesics (nitrates, morphine).- Medical therapy→ Aspirin (325 mg) + ADP receptor inhibitor: Reduces mortality→ β-blocker: Reduces mortality→ ACE-inhibitor: Reduces mortality→ Statins→ Heparin- Revascularization: options include thrombolysis, PCI, or CABG- Rehabilitation
• Complications of acute myocardial infarction Early complications (within 48 h):- Arrhythmia- Acute left heart failure→ Most common cause of in-hospital mortality→ Treat with ACE inhibitor, diuretic- Cardiogenic shock Late complications:- Recurrent infarction- Rupture: (left ventricular free wall rupture → cardiac tamponade), ventricular septal rupture (→ right heart failure), papillary muscle rupture (→ mitral regurgitation)- Ventricular (pseudo-)aneurysm→ Diagnostic clue: persistent ST elevation and T-wave inversion- Acute pericarditis: within first week- Dressler syndrome: 2-10 weeks post-MI
• Congestive heart failure Etiology:- Coronary artery disease- Hypertension- Diabetes mellitus- Valvular disease- Cardiomyopathies Risk factors: Smoking, obesity, COPD, hemochromotosis, drug and alcohol abuse Stages: NYHA I-IV Diagnostic approach:1. Medical history, including pre-existing conditions and history of alcohol and recreational or prescribed drug abuse2. Initial evaluation involves laboratory tests for BNP level, ECG, and chest x-ray.3. Echocardiography is the gold standard tool for assessing cardiac morphology and function, as well as investigating the underlying cause of HF.4. Other procedures (exercise testing, angiography) may be required for further investigation.- Chest x-ray: Cardiomegaly- Echocardigram→ Systolic dysfunction = EF < 40%; Dystolic dysfunction = EF > 40% Treatment:1. Systolic dysfunction- Lifestyle modification: Sodium & fluid restriction, weight loss, smoking cessation, restrict alcohol use- All patients: ACE-i or ARB, β-blocker- Preload reduction: Diuretics, isosorbite dinitrate- Afterload reduction: Hydralazine, spironolactone (if EF < 35%)- Digitalis: Indicated for EF < 40% who continue to have symptoms despite optimal therapy. Does not improve mortality.- Hydralazine and isosorbide dinitrates: Improves mortality in African Americans- Implantable cardiac defibrillator (ICD): EF < 35% and prior MI- Cardiac transplantation: for patients with end-stage HF (NYHA class IV), ejection fraction < 20%, and no other viable treatment options2. Diastolic dysfunction: Symptomatic treatment, no medications have proven mortality benefit- β-Blockers- Diuretics- Digoxin and spironolactone should NOT be used- ACE inhibitors and ARBs – benefit is not clear
• General principals in the treatment of CHF Mild CHF (NYHA Classes I to II)- Mild restriction of sodium intake (< 4 g of sodium) and physical activitiy- Start loop diuretic if volume overload or pulmonary congestion is present- Use an ACE inhibitor as a first-line agent Mild to moderate CHF (NYHA Classes II to III)- Start a diuretic and an ACE inhibitor- Add a β-blocker is moderate disease is present and the reponse to standard treatment is suboptimal Moderate to severe CHF (NYHA Classes III to IV)- Add digoxin (to loop diuretic and ACE inhibitor)- If still symptomatic despite above, adding spironolactone can be helpful
• Atrial flutter Supraventricular tachyarrhythmia that is usually caused by a single macroreentrant rhythm within the atria. Etiology:- Heart disease: Heart failure, rheumatic heart disease, CAD- COPD- Atrial septal defect (ASD) Clinical features:- Most patients are asymptomatic- Symptoms of arrhythmias: Palpitations, dizziness, syncope, fatigue, dyspnea- Symptoms of the underlying disease (e.g., murmurs of mitral stenosis)- Tachycardia with a regular pulse Diagnostics:- ECG: Sawtooth appearance of P waves (flutter waves or F waves), at a rate of ∼ 300 bpm with a regular, narrow QRS complex appearing after every 2nd or 3rd "tooth" Treatment: similar to atrial fibrillation Complications:- Frequently degenerates into atrial fibrillation- 1:1 conduction leading to life-threatening ventricular tachycardia
• Paroxysmal supraventricular tachycardia 1. Atrioventricular nodal reentrant tachycardia (AVNRT): tachycardia caused by a dysfunctional AV node that contains two electrical pathways- Two pathways (one fast and the other slow) within the AV node, so the reentrant circuit is within the AV node 2. Atrioventricular reciprocating tachycardia (AVRT): tachycardia caused by an accessory pathway between the atria and ventricles Etiology:- Ischemic heart disease- Digoxin toxicity – paroxysmal atrial tachycardia with 2:1 block is the most common arrhythmia- AV node reentry- Atrial flutter with rapid ventricular response- AV reciprocating tachycardia (accessory pathway)- Excessive caffeine or alcohol consumption Clinical features:- Palpitations, dizziness, chest pain, dyspnea, syncopes- Urinary urgency (Irregularly activated atria contract against a closed atrioventricular valve → ↑ atrial pressures → release of atrial natriuretic peptide (ANP) → ↑ urine output through renal sodium loss) Diagnostics:- 12-lead ECG:→ Narrow QRS complexes→ AVNRT: no P waves → AVRT: Orthodromic – P wave following QRS complex. Antidromic – Delta wave. Treatment:1. Maneuvers that stimulate the vagus delay AV conduction: Valsalva maneuver, carotid sinus massage, breath holding, head immersion in cold water2. Acute treatment:- Pharmacologic therapy: IV adenosine, IV verapamil, IV esmolol3. Prevention: Verapamil or β-blockers; radiofrequency catheter ablation of either the AV node or the accessory tract if episodes are recurrent and symptomatic.
• Wolff-Parkinson-White syndrome A congenital condition characterized by intermittent tachycardias and signs of ventricular pre-excitation on ECG, which both arise from an accessory pathway known as the “bundle of Kent”. - The bundle of Kent connects the atria and ventricles, bypassing the AV node and leading to a pre-excitation of the ventricles. - Up to one-third of patients may develop paroxysmal tachycardia produced by two possible mechanisms.1. Orthodromic reciprocating tachycardia: The impulse travels through the AV node and depolarizes the ventricles. Then it travels back through the accessory pathway and redepolarizes the atria creating a reentry loop. No delta waves because conduction occurs retrograde over the accessory pathway.2. Supraventricular tachycardias (AFib or atrial flutter): Usually, AV node only allows certain impulses to get to ventricles. With an accessory pathway, all or most of the impulses may pass to the ventricles. A fast ventricular rate may occur and cause hemodynamic compromise. Diagnosis:- ECG: Narrow complex tachycardia, a short PR interval, and a delta wave Treatment:- Radiofrequency catheter ablation of one arm of the reentrant loop. - Medial options: Procainamide or quinidine.
• AV block First-degree AV block:- PR interval is prolonged (> 0.2 s)- A QRS complex follows each P wave- Benign condition that does not require treatment Second-degree AV block:1. Mobitz type I (Wenckebach)- Characterized by progressive prolongation of PR interval until a P wave fails to conduct- Site of block is usually within the AV node- Benign condition that does not require treatment2. Mobitz type II- P wave fails to conduct suddenly, without a preceding PR interval prolongation; therefore, the QRS drops suddenly- Often progresses to complete heart block- Site of block is within the His-Purkinje system- Pacemaker implantation is necesssary Third-degree (complete) AV block:- Absence of conduction of atrial impulses to ventricles; no correspondence between P waves and QRS complexes- A ventricular pacemaker maintains a ventricular rate of 25 to 40 bpm- Pacemaker implantation is necessary
• Cardioversion vs. Defibrillation Cardioversion- Delivery of a shock that is in synchrony with the QRS complex: Purpose is to terminate certain dysrhythmias such as PSVT or VT; an electric shock during T wave can cause Vfib, so the shock is timed not to hit the T wave.- Indications: AFib, atrial flutter, VT with a pulse, SVT Defibrillation- Delivery of a shock that is not in synchrony with the QRS complex: Purpose is to convert a dysrhythmia to normal sinus rhythm.- Indications: VFib, VT without a pulse Automatic implantable defibrillator- Device that is surgically placed: When it detects a lethal dysrhythmia, it delivers an electric shock to defibrillate. It delivers a set number of shocks until the dysrhythmia is terminated.- Indications: VFib and/or VT that is not controlled by medical therapy.
• Dilated cardiomyopathy Etiology:- Idiopathic (approx. 50%)- Coronary artery disease, hypertension, peripartum cardiomyopathy, valvular heart disease- Infections: Coxsackie B virus myocarditis, rheumatic heart disease, Chagas disease- Hemochromatosis- SLE- Toxins: Alcohol use, cocaine, cardiotoxic drugs (anthracyclines like doxorubicine/daunorubicine, trastuzumab) Clinical features:- Early signs: palpitations, exertional dyspnea, a feeling of pressure in the chest- Later stages: Progressive left heart failure and right heart failure, relative mitral valve regurgitation Diagnostics:- ECG: Left bundle branch block- Lab: BNP, CK-MB to rule out MI- Echocardiography: Left atrial and ventricular dilation, reduced LVEF, wall motion abnormalities- Chest x-ray: Cardiomegaly → left-sided hypertrophy with a balloon appearance, signs of heart failure decompensation: pulmonary edema Treatment:- See treatment of heart failure- Avoid cardiotoxic agents, abstain from alcohol- Anticoagulation: when atrial fibrillation and low LVEF are present- Interventional/surgical:→ If LVEF < 35%: an ICD might prevent sudden cardiac death caused by ventricular fibrillation→ Main indication for heart transplantation
• Hypertrophic cardiomyopathy Epidemiology:- Obstructive type/hypertrophic obstructive cardiomyopathy (HOCM): ∼ 70% of cases- Nonobstructive type: ∼ 30% of cases- Alongside myocarditis, hypertrophic cardiomyopathy is one of the most frequent causes of sudden cardiac death in young patients, especially young athletes. Etiology:- Primary hypertrophic cardiomyopathy (60-90% of cases)→ Mutations in genes encoding myosin heavy chain → causes disorganized myocyte architecture characterized by myofibrillar disarray and fibrosis→ Autosomal dominant inheritance with varying penetrance- Secondary hypertrophic cardiomyopathy (e.g., in Friedreich ataxia, Fabry disease, Noonan syndrome, or amyloidosis)- Pressure related hypertrophy Clinical features:- (Exertional) dyspnea- Angina pectoris- Vertigo, syncope- Cardiac arrhythmias and palpitations Diagnostics:- Auscultation findings→ Systolic ejection murmur (crescendo-decrescendo) a. Increases with valsalva maneuver and standing (decreases LV size and thus increases the outflow obstruction)b. Decreases with hand grip, squatting, or passive leg elevation (due to decreased outflow obstruction)→ S4 gallop due to thickened, non-compliant ventricle→ Possible murmur from mitral regurgitation- ECG: Signs of left ventricular hypertrophy, left bundle branch block- Echocardiogram→ Asymmetrically thickened left ventricular wall ≥ 15 mm→ Systolic anterior motion: protrusion of the anterior mitral valve cusp towards the septum→ ↑ LVOT pressure gradient via doppler echocardiography Treatment:- All patients should avoid strenuous exercise.- Asymptomatic patients usually do not require further treatment.- Symptomatic patients→ Beta blockers (1st line) or verapamil (2nd line)→ Treat possible ventricular tachycardia or atrial fibrillation→ If there is high risk of sudden cardiac death consider an implantable cardioverter defibrillator (ICD)→ Myectomy→ Transcoronary ablation of septal hypertrophy (TASH) Complications: Sudden cardiac death; heart failure; stroke
• Restrictive cardiomyopathy Etiology:- Idiopathic- Hemochromatosis- Amyloidosis- Sarcoidosis- Scleroderma- Secondary to endomyocardial fibrosis: Eosinophilic endocarditis, postradiation fibrosis, endocardial fibroelastosis Diagnostics:- Echocardiography→ Atrial enlargement and dilation→ Ventricular volume is normal or decreased, diastolic filling is reduced→ Wall-thickening is possible (symmetric)- ECG: left bundle branch block, nonspecific abnormalities, low voltage (in amyloidosis)- CXR: pleural effusions- Cardiac catheterization with pressure measurements- Possible myocardial biopsy to identify underlying cause Treatment:- Symptomatic: beta blockers, cardioselective calcium channel blockers, diuretics, ACE inhibitors- Anticoagulation and maintenance of a sinus rhythm in patients with a history of AF- Heart transplant (ultima ratio)
• Myocarditis Etiology:- Viral: Coxsackie B, parvovirus B19, human herpesvirus 6 (HHV-6), adenovirus, HCV, HIV, EBV, CMV- Bacterial: Streptococcus group A (acute rheumatic fever), Corynebacterium diphtheriae, Borrelia burgdorferi, Mycobacterium (tuberculosis)- Protozoa: Chagas disease, caused by Trypanosoma cruzi- Parasitic: Trichinella- Connective tissue diseases (e.g., SLE)- Vasculitis syndromes (e.g., Kawasaki disease)- Toxic: Radiation therapy, medication (e.g., sulfonamides), chemotherapy (eg, anthracycline), alcohol, cocaine Clinical features:- Preceding (1-2 weeks) flulike symptoms: Fever, arthralgia, myalgia, upper respiratory tract infections → indicates possible viral cause - Fatigue, weakness, dyspnea, nausea, vomiting - Cardiac arrhythmias: often sinus tachycardia, ventricular extrasystoles with palpitations or syncope, heart block with bradyarrhythmia- Chest pain: indicates pericardial involvement (perimyocarditis)- Acute decompensated congestive heart failure with dilated cardiomyopathy- Cardiogenic shock in fulminant cases Diagnostics:- ECG/24-hour Holter monitoring→ Sinus tachycardia→ Arrhythmias: atrial or ventricular ectopic beats, complex ventricular arrhythmia, atrial tachycardia→ Repolarization abnormalities: ST depression, negative T waves→ Heart block- Lab: ↑ Cardiac enzymes (CK, CK-MB, troponin T), ↑ ESR (and CRP), leukocytosis, ↑ BNP, virus serology- Chest x-ray and CT: cardiac enlargement, pulmonary congestion, pleural effusions- Echocardiography→ Ventricles: dilation, diffuse hypokinesia, reduced ejection fraction, impaired contractility, regional wall motion abnormalities → Pericardial effusion: localized or circumferential fluid surrounding the ventricles- Biopsy Treatment: Supportive
• Acute pericarditis Etiology:- Infectious: Mostly viral (e.g., coxsackie B), tuberculosis, toxoplasmosis- Post-infarction fibrinous pericarditis (1-3 days), Dressler syndrome (weeks to months)- Post-operative (post-pericardiotomy syndrome)- Collagen vascular disease: SLE, rheumatoid arthritis- Radiation- Tumors (Hodgkin lymphoma)- Renal failure: Uremia Clinical features:- Low-grade intermittent fever, tachypnea, dyspnea, nonproductive cough- Chest pain: → Often severe and pleuritic (can differentiate from pain of MI because of association with breathing).→ Often localized to the retrosternal and left precordial regions and radiates to the trapezius ridge and neck.→ Pain is positional: It is aggravated by lying supine, coughing, swallowing, and deep inspiration. Pain is relieved by sitting up and leaning forward.- Pericardial friction rub: high-pitched scratching sound best heard on auscultation over the left sternal border during expiration while the patient is sitting up and leaning forward- Pericardial effusion Diagnostics:- Blood tests: Leukocytosis, ↑ troponin I, ↑ ESR, ↑ CRP, abnormal renal parameters (BUN, creatinine, electrolytes) if caused by underlying uremia- Typical ECG changes: not present in uremic pericarditis→ Initial diffuse ST elevations, but ST depression in aVR and V1; PR segment depression- Echocardiography: often normal; possibly signs of effusion Treatment: often self-limiting and resolves within approx. 2-6 weeks.- Restricted physical activity- NSAIDs plus colchicine - Glucocorticoids if NSAIDs are ineffective
• Constrictive pericarditis Constrictive pericarditis is characterized by compromised cardiac function caused by a thickened, rigid, and fibrous pericardium secondary to acute pericarditis. Etiology:- Infectious: Viral > Bacterial - Post-infarction fibrinous pericarditis or Dressler syndrome- Postoperative (post-pericardiotomy syndrome): blunt or sharp trauma to the pericardium- Collagen vascular disease: systemic lupus erythematosus, rheumatoid arthritis- Other causes: renal failure (uremia), tumors (Hodgkin lymphoma), radiationTuberculosis is the most common cause of constrictive pericarditis in developing countries. Clinical features:- Jugular vein distention, ↑ jugular venous pressure- Kussmaul sign (the JVP increases during inspiration instead of decreasing)- Hepatic vein congestion → hepatomegaly, painful liver capsule distention, hepatojugular reflux- Peripheral edema or anasarca, ascites with abdominal discomfort- Fatigue, dyspnea on exertion- Tachycardia- Pericardial knock: sudden cessation of ventricular filling during early diastole that is heard best at the left sternal border- Pulsus paradoxus: ↓ blood pressure amplitude during deep inspiration Diagnostics:- Chest x-ray (best initial test), CT, and MRI: pericardial thickening and calcifications, normal cardiac silhouette- Echocardiography:→ ↑ Pericardial thickness→ Abnormal ventricular filling with sudden halt during early diastole→ Moderate biatrial enlargement→ Excludes right ventricular hypertrophy and cardiomyopathy- ECG shows no conclusive findings- Cardiac catheterization→ Elevated diastolic pressures in the left and right ventricles with diastolic equalization→ Square root sign (aka dip-and-plateau waveform): Sudden dip of the right and left ventricular pressure in early diastole followed by a plateau during the last stage of diastole Treatment:- Symptomatic therapy (manage fluid overload with diuretic therapy)- Pericardiectomy (complete removal of the pericardium)
• Pericardial effusion Pericardial effusion is the acute or chronic accumulation of fluid in the pericardial space (between the parietal and the visceral pericardium). Etiology: - Hemopericardium: Cardiac wall rupture, chest trauma, aortic dissection, cardiac surgery- Serous pericardial effusion: Idiopathic, acute pericarditis, malignancy, poststernotomy syndrome, uremic, autoimmune disorders Clinical features: - Shortness of breath, especially while lying down (orthopnea)- Beck's triad: Hypotension, muffled heart sounds, distended neck veins- Tachycardia, pulsus paradoxus- Retrosternal chest pain- Apical impulse difficult to locate or nonpalpable- Pallor, cold sweats Diagnostics:- Echocardiography (gold standard)→ Anechoic space between pericardium and epicardium→ Reduced ejection fraction→ Reduced wall motion- CXR: enlarged cardiac silhouette, clear lungs, in severe cases a globular "water bottle-shaped" heart contour- ECG: Low voltage; electric alternans - Pericardial fluid drainage: used to sample the effusion in cases of unclear etiology Treatment:- Hemodynamically unstable → Pericardial fluid drainage- Hemodynamically stable → Pericardial window- If the effusion is small and clinically insignificant, a repeat echocardiogram in 1 to 2 weeks is appropriate.
• Cardiac tamponade Defined as accumulation of pericardial fluid. It is the rate of fluid accumulation that is important, not the amount.- Two hundred milliliters of fluid that develops rapidly (i.e., blood secondary to trauma) can cause cardiac tamponade.- Two liters of fluid may accumulate slowly before cardiac tamponade occurs. When fluid accumulates slowly, the pericardium has the opportunity to stretch and adapt to the increased volume (ie, related to a malignancy). Etiology:- Penetrating trauma to the thorax, such as gunshot and stab wounds- Iatrogenic: Central-line placement, pacemaker insertion, pericardiocentesis- Pericarditis: Idiopathic, neoplastic, or uremic- Post-MI with free wall rupture Clinical featuers:- Beck's triad1. Hypotension2. Muffled heart sounds3. Distended neck veins- Tachycardia, pulsus paradoxus- Retrosternal chest pain- Pulsus paradoxus: Exaggerated decrease in arterial pressure during inspiration (> 10 mm Hg drop) Diagnostics:- Echocardiogram - CXR: Enlargement of cardiac silhouette when >250 mL has accumulated, clear lung fields- ECG: Electrical alternans - Cardiac catheterization: Equalization of pressures in all chambers of the heart, elevated right atrial pressure with loss of the y descent Treatment:- If stable: Hemodynamic monitoring; dialysis in renal failure; pericardial window- Not stable: Pericardiocentesis
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• Mitral stenosis Etiology- Rheumatic fever (most common)- Autoimmune diseases: systemic lupus erythematosus, rheumatoid arthritis Clinical features:- Initially asymptomatic (onset ∼ 10 years after acute rheumatic carditis) - Dyspnea (paroxysmal nocturnal dyspnea) and orthopnea, especially when supine- Hemoptysis- Atrial fibrillation, systemic thromboembolism- Voice hoarseness from recurrent laryngeal nerve compression due to left atrial enlargement (Ortner syndrome)- Later stages: signs and symptoms of right-sided heart failure Diagnostics:- Mitral facies: Pinkish-purple patches on cheecks- Auscultation→ Mid-diastolic murmur typically heard best at the apex→ Loud first heart sound (S1)→ Opening snap of the mitral valve after S2; shorter interval between opening snap and S2 indicative of more severe disease, because left atrial pressure is greater than left ventricular end diastolic pressure (LVEDP)- Chest x-ray→ Posterior-anterior image: LA enlargement with prominent left auricle (left atrial appendage) → straightening of the left cardiac border; Signs of pulmonary congestion- Lateral image: Dorsal displacement of the esophagus (visible in barium swallow test); Signs of right ventricular hypertrophy- ECG: P mitrale, atrial fibrillation, signs of right ventricular hypertrophy (Sokolow-Lyon index)- Echocardiography: Abnormal valve mobility, subvalvular thickening, leaflet thickening, calcification Treatment:- Pharmacologic:→ Diuretics: for pulmonary congestion and edema- Surgical (for severe disease)→ First-line: Percutaneous balloon commissurotomy→ Alternatives: open commissurotomy and surgical valve replacement
• Aortic stenosis Etiology:- Bicuspid aortic valve: 3:1 male predominance, predisposes the valve to dystrophic calcification, patients present with symptoms of aortic stenosis earlier than in regular aortic valve calcification- Calcific aortic stenosis- Rheumatic fever Clinical features:- Dyspnea- Angina pectoris- Dizziness and syncope- Small blood pressure amplitude, decreased pulse pressure- Delayed and weak pulse (Pulsus parvus et tardus)- Crescendo-decrescendo, late systolic ejection murmur that radiates bilaterally to the carotids→ Hand grip decreases the intensity of the murmur (increases afterload)→ Valsalva and standing from squatting decreases or does not change the intensity of the murmur (in contrast to hypertrophic cardiomyopathy) (decreases preload)- Soft S2- S4 (decreased compliance of the LV)- Early systolic ejection click (results from the abrupt stop of the valve leaflets upon opening) Diagnostics:- ECG- Chest x-ray→ Findings of left ventricular hypertrophy, and possibly left atrial enlargement as well → Narrowing of retrocardiac space (lateral view)→ Calcification of aortic valve: signs of more severe disease- Echocardiography (TTE or TEE): preferred primary test and noninvasive gold standard→ Concentric hypertrophy, narrowing of the opening of the aortic valve, and increased mean pressure gradient across the aortic valve.- Left-heart catheterization: Definitive diagnostic test Treatment:- Asymptomatic → Follow-ups- Symptomatic → Aortic valve replacement
• Aortic regurgitation Etiology:- Acute:→ Infective endocarditis→ Aortic dissection (ascending aorta)→ Chest trauma- Chronic:→ Congenital bicuspid valve: most common cause of AR in young adults and in developed countries→ Rheumatic heart disease: most common cause of AR in developing countries→ Aortic root disease: Marfan syndrome, Ehlers-Danlos syndrome, syphilitic aortitis Clinical featuers:- Dyspnea on exertion- Palpitations: worse when lying down- Angina- Orthopnea- Syncope- Symptoms of high pulse pressure (e.g., head pounding, rhythmic nodding, or bobbing of the head in synchrony with heartbeats – de Musset sign) Physical examination:- Widened pulse pressure, e.g., 150/50 mmHg- Water hammer pulse of peripheral arteries characterized by rapid upstroke and downstroke- Point of maximal impulse (PMI): displaced inferolaterally, diffuse, and hyperdynamic- S3- Diastolic decrescendo murmur→ Murmur intensity increases with sustained handgrip. Handgrip increases systemic vascular resistance (SVR), which causes an increased “backflow” through the incompetent aortic valve- Austin Flint murmur = low-pitched mid-diastolic rumble due to competing flow anterograde from the LA and retrograde from the aorta Diagnostics:- Transthoracic echocardiogram (TTE)→ Abnormal valve leaflets→ Regurgitant AR jet on Doppler→ Increased LV size and volume→ LV ejection fraction < 55%- Transesophageal echocardiogram (TEE): indicated if suboptimal or nondiagnostic TTE- Chest x-ray: Prominent aortic root/arch, enlarged cardiac silhouette Treatment:- Asymptomatic → Conservative: Salt restriction, diuretics, vasodilators, digoxin, afterload reduction (i.e., ACE inhibitors or arterial dilators), and restriction on strenuous activity- Symptomatic or significant LV dysfunction → Aortic valve replacement
• Mitral regurgitation Etiology:- Degenerative mitral valve disease: mitral valve prolapse, mitral annular calcification, ruptured chordae tendineae- Rheumatic fever- Infective endocarditis- Coronary artery disease, prior myocardial infarction causing papillary muscle involvement- Dilated cardiomyopathy  Clinical features:- Dyspnea on exertion, paroxysmal nocturnal dyspnea, orthopnea - Palpitations- Pulmonary edema Signs:- Holosystolic murmur at the apex, which radiates to the back or clavicular area→ Intensity increases with increased systemic vascular resistance (hand grip, squatting)- AFib is a common finding- Diminished S1, S3 gallop Diagnostics:- CXR: Cardiomegaly, dilated LV, pulmonary edema- Echocardiogram: MR; dilated LA and LV; decreased LV function- Coronary angiography: prior to surgical intervention Treatment:- Acute mitral regurgitation→ Hemodynamic stabilization: diuretics, nitrates, antihypertensive drugs→ Intra-aortic balloon pump if pharmacologic management is insufficient→ Urgent surgical valve repair or replacement- Chronic mitral regurgitation→ Asymptomatic → conservative→ Symptomatic → surgical valve repair or replacement
• Tricuspid regurgitation Etiology:- Secondary to RV dilation→ Left ventricular failure is the most common cause→ Right ventricular infarction→ Inferior wall MI→ Cor pulmonale, secondary to pulmonary HTN- Tricuspid endocarditis – seen in IV drug users.- Rheumatic heart disease; usually accompanied by mitral and aortic valve disease.- Epstein anomaly- Other: Carcinoid syndrome, SLE, and myxomatous valve degeneration Clinical features:- Signs and symptoms of RVF (ascites, hepatomegaly, edema, JVD)- Pulsatile liver- Prominent V waves in jugular venous pulse with rapid y descent- Blowing holosystolic murmur - AFib is usually present Diagnosis: - Echocardiogram- ECG: RV and RA enlargement
• Mitral valve prolapse Etiology:- Mostly idiopathic- Connective tissue disorders: Marfan's syndrome, osteogenesis imperfecta, Ehlers-Danlos syndrome- Myocardial infarction (Infarction of papillary muscles → rupture of chordae tendineae)- Acute rheumatic heart disease- Infective endocarditis Pathophysiology: The most common underlying pathology in the case of mitral valve prolapse is myxomatous degeneration. Clinical features:- Most patients are asymptomatic- Rarely: atypical chest pain, anxiety, palpitations- Mitral valve prolapse click: high-frequency, midsystolic click that is best heard at the mitral region- Mid-to-late systolic murmur Diagnostics:- Echocardiogram (TTE): displacement of the mitral valve during systole by more than 2 mm above the mitral valve annulus in the parasternal long-axis view Treatment:- No treatment is required in most cases.- Patients with severe mitral regurgitation: mitral valve repair or replacement
• Hypertensive crisis Hypertensive urgency: Severely increased BP (> 220 systolic and/or > 120 diastolic) Hypertensive emergency: Severely increased BP (> 220 systolic and/or > 120 diastolic) with signs of end-organ damage End-organ damage:- Cardiac presentation (chest pain, dyspnea)→ Myocardial infarction→ Congestive heart failure and dilated cardiomyopathy→ Aortic dissection- Lungs: Pulmonary edema- Neurologic presentation (headache, confusion, blurry vision)→ Hypertensive encephalopathy→ Ischemic or hemorrhagic stroke→ Retinopathy (flame hemorrhages, papilledema)- Renal presentation: azotemia and/or oliguria due to acute renal failure Treatment of hypertensive emergency- Reduce mean arterial pressure by 25% in 1 to 2 hours. The goal is not to immediately achieve normal BP, but to get the patient out of danger, then reduce BP gradually.- The most commonly used drugs to treat hypertensive emergency are IV nitroprusside, labetalol, and nicardipine.- In patients who are in less immediate danger, oral agents are appropriate. Options include captopril, clonidine, labetalol, nifedipine, and diazoxide. Treatment of hypertensive urgency- BP should be lowered within 24 hours using oral agents.
• Aortic dissection Localization:- Ascending aorta: ∼ 65% of cases- Descending aorta, distal to the left subclavian artery: 20% of cases- Aortic arch: 10% of cases- Abdominal aorta: 5% of cases Etiology:- Hypertension- Trauma- Atherosclerosis- Connective tissue disease (Marfan syndrome, Ehlers-Danlos syndrome)- Use of cocaine or amphetamines- Bicuspid aortic valve- Coarctation of the aorta Stanford Classification:- Type A (proximal): ascending aorta dissection, including retrograde extension from the descending aorta (independent of the site of origin and propagation)- Type B (distal): descending aorta dissection, originating distal to the left subclavian artery Clinical features:- Severe, tearing/ripping/stabbing pain, typically abrupt in onset, either in the anterior or back of the chest (often the interscapular region)- Diaphoresis- ↑ BP (if the patient is hypotensive, consider shock from blood loss or a cardiac tamponade)- Asymmetrical blood pressure and pulse readings between limbs- A heart murmur (an aortic regurgitation in a proximal dissection) Diagnostics:- Initial imaging: Chest x-ray: widened mediastinum (> 8 mm)- Definitive diagnostic tests (determine the type of lumen, location, and extent of the dissecting membrane)→ In stable patients → Contrast-enhanced CT angiography (gold standard) → In unstable patients, renal insufficiency, contrast allergy → Transesophageal echocardiography (TEE)→ If contrast-enhanced CT is contraindicated in stable patients → Magnetic resonance angiography (MRA)- ECG: in all patients, although normal or signs of left ventricular hypertrophy Treatment:1. Initiate medical therapy immediately- Sedation and analgesia (e.g., morphine) - Target value of the systolic blood pressure is ∼ 90-120 mm Hg- IV labetalol, esmolol, or propanolol (best initial)- ± IV sodium nitroprusside (if SBP > 120 mm Hg)- Stanford A dissections (involvement of the ascending aorta) require immediate surgery Complications due to extension:- Stroke (carotid artery)- Acute aortic regurgitation (aortic root/valve)- Horner syndrome (carotid sympathetic plexus)- Myocardial ischemia/infarction (coronary artery ostia)- Pericardial effusion/tamponade- Hemothorax (pleural cavity)- Renal injury (renal arteries)- Abdominal pain (mesenteric arteries)- Lower extremity paraplegia (spinal arteries)
• Abdominal aortic aneurysm Risk factors:- Age- Smoking (most important risk factor)- Atherosclerosis- Hypercholesterolemia and arterial hypertension- Family history- Trauma Location: Most commonly below the renal arteries Clinical features:- Pulsating mass- Back pain- Bruit on auscultation- Sense of "fullness"- Peripheral thrombosis and distal atheroembolic phenomena (e.g., blue toe syndrome and livedo reticularis)- Symptoms suggesting expansion and impending rupture include the following:→ Sudden onset of severe pain in the back or lower abdomen, radiating to the groin, buttocks, or legs→ Grey Turner sign (ecchymoses on back and flanks) and Cullen sign (ecchymoses around umbilicus)- Rupture:→ Triad of abdominal pain, hypotension, and a palpable pulsatile abdominal mass → Cardiovascular collapse→ Syncope or near-syncope, secondary to sudden hemorrhage→ Nausea and vomiting Diagnostics:- Ultrasound: best initial and confirmatory test for AAAs- CT with contrast (or MRI): only in hemodynamically stable patients; used for preoperative planning Treatment:- Conservative: Optimal blood pressure levels (< 120/80 mm Hg), cessation of smoking< 3 cm → No further follow-up3-4 cm → Ultrasound every year4-4.5 cm → Ultrasound every 6 months4.5-5.5 cm → Ultrasound every 3 months- Surgery: For symptomatic AAAs, when diameter > 5.5 cm, or if it grows > 0.5 cm/6 months- Endovascular aneurysm repair (EVAR) → Preferred over open surgery; esp. in patients with high operative risk Prevention: One-time screening in men aged 65 to 75 years with a history of smoking
• Peripheral vascular disease Risk factors: - Smoking (by far the most important risk factor)- CAD, hyperlipidemia, HTN- Diabetes Sites of occlusion/stenosis- Superficial femoral artery (in Hunter canal) is the most common site - Popliteal artery- Aortoiliac occlusive disease Fontaine Classification:I: Asymptomatic PADII: Pain on exertion- IIa: Claudication at a walking distance > 200 m - IIb: Claudication at a walking distance < 200 mIII: Pain at restIV: Necrosis/gangrene/ulcer Clinical features:- Intermittent claudication→ Femoropopiteal disease → Calf pain→ Aortoiliac disease (Leriche's sydrome) → Buttock, hip, or thigh pain→ Tibiofibular disease → Foot pain→ Worsens upon exertion, relieved by rest, reproducable- Absent or diminished arterial pulses- Trophic chainges: ↓ Hair on legs, ↓ skin temperature, ↓ perspiration, brittle nails, atrophied muscles Diagnostics:1. Ankle-brachial index (ABI) = the ratio of systolic ankle blood pressure (BP) to systolic brachial BP> 1.3 = medial sclerosis with incompressible vascular wall (generally calcified vessels)0.9-1.3 = normal value0.4-0.9 = mild to moderate PAD → claudication< 0.4 = severe PAD → resting pain, gangrene (critical limb ischemia)2. Color-coded duplex ultrasonography3. Digital subtraction angiography (DSA): gold standard Treatment:- Conservative: Smoking cessation, graduated exercise program, foot care, avoid cold temperatures- Medical: → Modify cardiovascular risks: Antiplatelets (aspirine, clopidogrel, ticagrelor), statins, antihypertensive treatment, hyperglycemia control→ PDE inhibitors: Cilostazol- Revascularization: → Percutaneous transluminal angioplasty (PTA) with or without stentingA lesion that is both in the femoral artery and < 3 cm can be stented.→ Operative vascular reconstruction (bypass surgery)→ Endarterectomy
• Acute arterial occlusion Etiology:- Heart (85%)→ Afib→ Post-MI→ Endocarditis→ Myxoma- Aneurysms- Atheromatous plaque Location of the obstruction:- Most common: femoropopliteal artery (∼ 50% of cases)- Brachial artery (∼ 20%) > Abdominal aorta (∼ 10%) > Iliac artery (∼ 10%) Clinical features (the 6 P's)- Pain - acute- Pallor- Poikilothermia (impaired ability to regulate body temperature, cold)- Paresthesias- Pulselessness- Paralysis Leriche syndrome = Occlusion at the bifurcation of the aorta usually presenting with:- Pain in both legs- Diminished inguinal or peripheral pulse- Neurological impairment- Impotence- Shock Diagnostics:- Best initial test: arterial and venous doppler- Confirmatory test: angiography (DSA is the imaging modality of choice)- Depending on the suspected etiology, other tests may be indicated (e.g., echocardiography if an arterial embolism is suspected; ECG to detect Afib, MI). Treatment:- Systemic anticoagulation with an IV heparin bolus followed by continuous infusion- Further management depends on the severity of acute limb ischemia.→ Viable, non-threatened limb: Urgent angiography and revascularization procedure within 6-24 hours→ Threatened limb: emergent revascularization procedure within 6 hoursFirst-line: catheter-directed thrombolysis and/or percutaneous mechanical thromboembolectomy (e.g., balloon catheter embolectomy)→ Non-viable limb: limb amputation
• Superficial thrombophlebitis - In upper extremities, usually occurs at the site of an IV infusion- In lower extremities, usually associated with varicose veins (in the greater saphenous system)—secondary to static blood flow in these veins Clinical features:- Pain, tenderness, induration, and erythema along the course of the vein - A tender cord may be palpated Treatment:- No anticoagulation is required – rarely causes PE. Only if thrombus extends into the deep system.- Localized thrombophlebitis – a mild analgesic (aspirin or NSAIDs) elevation, and hot compresses; continue activity.- Suppurative thrombophlebitis – septic phlebitis is usually due to infection of an IV cannula. Remove the cannula and administer systemic antibiotics.
• Deep vein thrombosis Risk factors:- History of DVT or PE (30x increased risk) - Immobilization (e.g., surgery, long-distance flights, trauma) (20x increased risk)- Age > 60 years- Malignancy- Hereditary thrombophilia (especially factor V Leiden)- Pregnancy, estrogen use (oral contraceptives)- Obesity- Smoking Clinical features:- Lower-extremity pain and swelling (worse with dependency/walking, better with elevation/rest)- Homans sign (calf pain on ankle dorsiflexion)- Palpable cord- Fever Diagnostics:- Compression ultrasonography with Doppler (test of choice)- D-dimer testing- Venography: Most accurate testInterpretation of tests:- Intermediate-to-high pretest probability of DVT→ If Doppler ultrasound is positive, begin anticoagulation→ If Doppler ultrasound is nondiagnostic, repeat ultrasound every 2 to 3 days for up to 2 weeks- Low-to-intermediate probability of DVT→ If Doppler ultrasound is negative, there is no need for anticoagulation; observation is sufficient→ Repeat ultrasound in 2 days Complications:- PE- Postthrombotic syndrome (chronic venous insufficiency)- Phlegmasia cerulea dolens (painful, blue, swollen leg) Treatment:1. Anticoagulation- Heparin bolus followed by a constant infusion titrated to maintain therapeutic aPTT- Start warfarin once the aPTT is therapeutic and continue for 3 to 6 months- Continue heparin until the INR has been therapeutic for 48 hours2. Thrombolytic therapy (streptokinase, urokinase, tissue plasminogen activator [t-PA])- Indicated mainly for patients with massive PE who are hemodynamically unstable (hypotension with SBP < 90 mm Hg), and with no contraindications3. Inferior vena cava filter placement (Greenfield filter)- Indications: If absolute contraindication to anticoagulation (bleeding) or if failure of appropriate anticoagulation
• Chronic venous insufficiency RIsk factors:- Higher age and female sex - Family history of venous disease- Ligamentous laxity- Sedentary lifestyle and prolonged standing- Obesity- Pregnancy- Smoking- Prior thrombosis (postthrombotic syndrome)- Prior extremity trauma Clinical features:- Swelling of the lower leg; worsened by heat, standing, sitting; leg elevation provides relief- Pruritus, tingling, and numbness- Yellow-brown or red-brown skin pigmentation of the medial ankle- Skin becomes thin, atrophic, shiny, and cyanotic- Lipodermosclerosis: Painful, indurated, and hardened skin; atrophie blanche- Ulcers: Ususally less painful than those associated with arteriel insufficiency; medial malleolus; recur Diagnostics: - Test of choice: duplex ultrasonography→ Presence of venous reflux confirms diagnosis of CVI (Retrograde flow lasting > 0.5 seconds.)→ Examine patency of deep vein→ Examine sufficiency of superficial and perforating veins Treatment:- Conservative: Compression stockings, elevation of legs, lymphatic drainage, avoid long periods of standing- Definite treatment: Vein ablation therapies
• tPA Contraindications Inclusion criteria:- Onset of symptoms ≤ 3 hours (therapeutic window of thrombolytic therapy)- Age ≥ 18 years Exclusion criteria- Previous intracranial hemorrhage- Head trauma or stroke (within the past 3 months)- Recent intracranial or intraspinal surgery- Arterial puncture at noncompressible site (within the past 7 days)- Intracranial neoplasm, arteriovenous malformation, or aneurysm- Intracranial bleeding- Active internal bleeding or bleeding diathesis- Hypertension > 185/110 mm Hg- Anticoagulation (prolonged PTT or INR > 1.7)- Low platelet count (< 100 000)- Hypoglycemia < 50 mg/dL or hyperglycemia > 400 mg/dL- Minor stroke or TIA
• Congenital lipid disorders Type I – Hyperchylomicronemia: Autosomal recessive condition that is not associated with an increased risk of atherosclerosis. Patients develop eruptive xanthomas, pancreatitis, and hepatosplenomegaly.- Lipoprotein lipase or apolipoprotein C-II deficiency Type IIa – Familial hypercholesterolemia: Autosomal dominant condition associated with mutations in the LDL receptor that lead to elevated LDL levels with early atherosclerotic complications (cardiovascular disease) Type III – Familial hyperlipidemia: Autosomal recessive condition associated with defective ApoE that leads to elevated LDL levels with early atherosclerotic complications (cardiovascular disease) Type IV – Familial hypertriglyceridemia: Autosomal dominant condition associated with an increased risk of acute pancreatitis- Hepatic overproduction of VLDL
• Endarterectomy Indications:- Carotid endarterectomy (CEA): treatment of choice for patients with significant (> 80%) or symptomatic carotid artery stenosis- Pulmonary endarterectomy: treatment of choice for chronic thromboembolic pulmonary hypertension- Aortoiliac endarterectomy: for aortoiliac peripheral arterial disease- Transaortic mesenteric endarterectomy: for chronic mesenteric ischemia- Femoral endarterectomy: for symptomatic lower limb claudication due to femoral artery disease that does not respond to medical management
• Guidelines for statin therapy - LDL cholesterol elevated ≥ 190 mg/dL - Clinical atherosclerotic cardiovascular disease (includes coronary heart disease, stroke, and peripheral arterial disease) - Age 40-75 with diabetes - Age 40-75 with an estimated 10-year ASCVD risk ≥ 7.5%  What statin should you give?- The goal is to be on high-intensity statin. Start a moderate-intensity and increase the dose to high-intensity.- If there’s liver disease or renal disease, start at and stay on a moderate-intensity statin.- If there are signs of statin-toxicity during treatment, stop the statin until the signs go away. Then restart the statin at a lower dose.  Evaluation:- Lipids are assessed annually- CK and LFTs are only assessed when there is evidence of disease
• Multifocal atrial tachycardia Etiology:- Exacerbation of pulmonary disease (e.g., COPD)- Electrolyte disturbance (e.g., hypokalemia)- Catecholamine surge (e.g., sepsis) Clinical features:- Typically asymptomatic- Rapid, irregular pulse- ECG: ≥ 3 P-wave forms & atrial rate > 100/min Treatment:- Correct underlying disturbance- AV nodal blockage (e.g., verapamil) if persistent
• Sternal dehiscence Relatively common complication after CABG. Soft tissue dehiscence:- Only the superficial tissues (eg, skin, muscle) separate- No signs of sternal instability or systemic illness- Treatment: Local wound care or debridement followed by primary closure Sternal dehiscence:- Separation of the edges of the approximated sternum- May occur with or without soft tissue dehiscence- Sternal instability and nonunion characterized by "clicking" or "rocking" on sternal palpation- Treatment: Surgical emergency. Requires sternal rewiring to prevent cardiac trauma. Diagnostics: Chest and sternal imaging (CT scan) Complications: Mediastinitis

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