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Collection of chest X-ray

Constrictive pericarditis Constructive pericarditis can be tricky to diagnose because its symptoms often mimic those of other conditions like restrictive cardiomyopathy or right heart failure. A multimodal approach combining clinical evaluation, imaging, and hemodynamic studies is usually needed. 1. Clinical Signs Fatigue, dyspnea, abdominal distension Peripheral edema, ascites, hepatomegaly Kussmaul’s sign (JVP rises on inspiration) Pericardial knock (early diastolic sound on auscultation) --- 2. Echocardiography Key non-invasive tool, often the first test: Septal bounce (early diastolic motion of interventricular septum) Respirophasic variation in mitral/tricuspid inflow Dilated IVC with reduced respiratory variation Normal or small ventricles, often with pericardial thickening --- 3. Cardiac CT or MRI These help confirm the diagnosis: Pericardial thickening (>4 mm) Pericardial calcification (CT) MRI may show pericardial inflammation (with gadolinium) --- 4. Cardiac Catheterization Gold standard for definitive diagnosis: Equalization of end-diastolic pressures in all chambers Square root sign (dip and plateau pattern) in ventricular pressure tracing Discordance of LV and RV pressures with respiration --- 5. Lab Tests May help rule out causes: TB, autoimmune diseases, malignancy BNP usually low or normal (vs restrictive cardiomyopathy where it's high) Pulse wave Doppler plays a crucial role in diagnosing constrictive pericarditis by identifying abnormal ventricular filling patterns, especially the exaggerated respiratory variation in inflow velocities due to the non-compliant pericardium. Here’s how pulse Doppler findings help in constrictive pericarditis: --- 1. Mitral Inflow Doppler (Apical 4-chamber view) Respiratory variation >25% in mitral E velocity: Inspiration: ↓ Mitral E velocity (↓ LV filling) Expiration: ↑ Mitral E velocity (↑ LV filling) This is due to ventricular interdependence: during inspiration, more blood goes to the RV and less to the LV (and vice versa). --- 2. Tricuspid Inflow Doppler Respiratory variation >40% in tricuspid E velocity: Inspiration: ↑ Tricuspid E velocity Expiration: ↓ Tricuspid E velocity --- 3. Hepatic Vein Flow (Subcostal view) Prominent diastolic flow reversal during expiration Indicative of elevated right atrial pressures and impaired RV compliance --- 4. Pulmonary Vein Flow Reduced or absent diastolic forward flow May show blunted or reversed diastolic flow during expiration

Oxygen Delivery System

SAVE THESE CARDS FATE stands for Focus Assessed Transthoracic Echocardiography. It is a rapid, point-of-care ultrasound protocol used primarily in critical care and emergency settings for assessing cardiac function FATE is designed to be performed by non-cardiologists, such as intensivists or emergency physicians, with basic training in ultrasound. In a nutshell OBJECTIVE ~ To provide a rapid assessment of the heart to guide immediate clinical decisions in critically ill patients. VIEWS ~ The FATE protocol entails 5 standard transthoracic echocardiography views: 1. Subcostal four-chamber view 2. Apical four-chamber view 3. Parasternal long-axis view 4. Parasternal short-axis view 5. Subcostal inferior vena cava (IVC) view Focus Areas: Evaluates: • Left and right ventricular function (e.g., systolic dysfunction, dilatation) • Pericardial effusion or tamponade • Pleural effusion • Volume status (via IVC assessment) • Gross valvular abnormalities ADVANTAGES • Quick (can be done in minutes) • Non-invasive • Portable, performed at the bedside • Guides interventions (e.g., fluid resuscitation, inotropic support) LIMITATIONS • Not a comprehensive echocardiogram • Requires basic ultrasound skills • May be limited by patient factors (e.g., obesity, poor acoustic windows)

Ebstein's Anomaly of the Tricuspid Valve

Mechanisms of Cardiovascular Benefits of Sodium Glucose Co-Transporter 2 (SGLT2) Inhibitors:

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Stable angina Vs Thick fibrous Acute coronary syndrome

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Antihyperlipidemic Drugs

However, angiotensin converting enzyme inhibitors, angiotensin II receptor blockers, angiotensin receptor-neprilysin inhibitor, and aldosterone antagonists are to be avoided, as they are contraindicated in pregnancy. HF with pulmonary congestion is treated with loop diuretics and thiazides if required; however, diuretics should be avoided in the absence of pulmonary congestion, due to the potential reduction in placental blood flow. Hydralazine and nitrates appear safe in pregnancy, although with less evidence for benefit than ACE inhibitors, and should only be used in the presence of hypertension, severe LV dysfunction, and/or evidence of congestion in decompensated HF. Beta-blockers should be initiated cautiously and gradually uptitrated to the maximum tolerated dose Additional therapeutic issues for this population may include arrhythmia management, anticoagulation therapy, mechanical support, and investigational therapies such as bromocriptine Bromocriptine The role of bromocriptine therapy in PPCM is controversial. Addition of bromocriptine to standard HF therapy may improve LV recovery and clinical outcome in women with acute severe PPCM. Bromocriptine (2.5 mg once daily) for at least 1 week may be considered in uncomplicated cases, whereas prolonged treatment (2.5 mg twice daily for 2 weeks, then 2.5 mg once daily for 6 weeks) may be considered in patients with EF <25% and/or cardiogenic shock. Bromocriptine treatment must always be accompanied by anticoagulation with heparin (LMWH or UFH), at least in prophylactic dosages Decisions regarding the timing and mode of delivery in PPCM should be made based upon combined input from cardiology, obstetrics, anesthesiology, and neonatology services. Prompt delivery is suggested in women with PPCM with advanced HF. All women with PPCM should receive counseling on the potential risk of recurrence with future pregnancies.. Peripartum cardiomyopathy(PPCM) 1-Defined as unexplained cardiomyopathy, EF less than 45% that occur in the last month of pregnancy or the first 5 months post partum 2-Pathphysiology is thought to be related to prolactin degradation product which has a myocardial toxcity which explain the benefit of anti-prolactin which is Bromocriptine Other theories include autoimmune, myocarditis, oxidative stress 3-Predictors of poor prognosis include dilated LVEDD more than 60 mm, EF less than 30% and RV involvement 4-According to the ESC guidelines for heart disease with pregnancy, Bromocriptine is a class II b indication for PPCM 5-There are two regimens I-Bromocriptine 2.5 mg once daily for 1 week II-Bromocriptine 2.5 mg twice daily for 2 weeks then 2.5 mg once daily for 6 weeks The first regimen for uncomplicated cases The second regimen is used if the patient is presenting with cardiogenic shock or EF less than 25% 6-You must give parentral anticoagulation for patients on Bromocriptine(either prophylactic or therapeutic) 7-You must continue on antifailure measures for at least 6 months after recovery of normal LV function 8-Women who did not recover LV EF Above 50% should be prohibited from further pregnancies 9-Women who have recovered normal LV function still have a higher risk than those who did not have PPCM and risk of recurrence as well 10-Levosimendan is the inotrope of the choice due to deleterious effect of beta agonist on the heart by Catecholamines release https://t.me/cardiology

Peripartum Cardiomyopathy (PPCM) PPCM is an idiopathic cardiomyopathy with the following characteristics: Development of heart failure (HF) toward the end of pregnancy or within five months following delivery. Absence of another identifiable cause for the HF. Left ventricular (LV) systolic dysfunction with LV ejection fraction (LVEF) of less than 45 percent. The LV may or may not be dilated. Etiology: The cause is uncertain, but potential aetiologies include inflammatory, angiogenic imbalance hormonal, hemodynamic, and autoimmune factors biologically active 16 kDa prolactin and other factors, such as soluble fms-like tyrosine kinase 1 (sFlt1), may initiate and drive PPCM University study reveals that one of the possible primary causes of PPCM is a functional heart cell defect. Dr. Naftali-Shani harnessed a cutting-edge genetic engineering technique, which won the Nobel Prize for medicine and physiology in 2012, to produce stem cells and beating heart cells from the skin cells of PPCM patients and healthy controls. "This is the first time that this technique was used to study the mechanism of PPCM," Dr. Naftali-Shani says. . The myocardial cells produced from the stem cells of the patients had functional defects that caused them to secrete inflammatory proteins and a protein that inhibits the formation of blood vessels in the muscle, even without stress. We hope that this discovery will pave the way for early diagnoses and new, effective prevention and treatments. Risk factors — Although the etiology of PPCM remains unclear, the following are among the factors associated with increased risk of PPCM: Age greater than 30 years. African descent Pregnancy with multiple fetuses A history of preeclampsia, eclampsia, or postpartum hypertension Maternal cocaine abuse Long-term (>4 weeks) oral tocolytic therapy with beta-adrenergic agonists such as terbutaline Although multiparity has been traditionally considered a risk factor for PPCM, studies have shown that the majority of patients who develop PPCM do so during the first or second pregnancy There are conflicting data as to whether selenium deficiency is or is not a risk factor for PPCM. Diagnosis. Careful history taking is necessary to identify and exclude other causes of HF. The LV may be non-dilated, but the EF is usually <45%. Symptoms and signs are often typical for HF with numerous phenotypes reported. Patients frequently present with acute HF, but also with ventricular arrhythmias and/or cardiac arrest. Echocardiography is the imaging modality of choice. generally reveals a global reduction in LV systolic function with LVEF nearly always <45 percent . The LV is frequently but not always dilated . Other possible echocardiographic findings include left atrial enlargement, LV or left atrial thrombus, dilated right ventricle, right ventricular hypokinesis, mitral and tricuspid regurgitation, and small pericardial effusion N.B Initial LVEF <30%, marked LV dilatation (LV end-diastolic diameter ≥6.0 cm), and RV involvement are associated with adverse outcomes Recovery of left ventricular function Partial or complete recovery of LV function is common among patients with PPCM and appears to be more frequent than with other types of dilated cardiomyopathy . Complete recovery of LV function (defined as recovery to an LVEF >50 percent) has been reported in 20 to 60 percent of patients in various series . Although nearly all recovery of LV function occurred within six months of diagnosis in some series , delayed recovery of LV function has been observed Various studies have identified the following predictors of persistent LV dysfunction at follow-up: LVEF ≤30 percent Fractional shortening less than 20 percent and an LV end-diastolic dimension ≥6 cm Black race Reduced right ventricular function MANAGEMENT Treatment of peripartum cardiomyopathy (PPCM) is largely similar to treatment for other types of heart failure (HF).