by Mark | Sep 29, 2015 | Cardiology, Science
Constrictive Pericarditis Pathology of constriction: Thick scarred pericardium equalizes 4 chamber pressure, limits ventricular filling, reduces cardiac volume. JV pressure wave form in constriction: rapid ventricular (RV) filling causes rapid Y-descent Then, diastolic filling stops abruptly, causing a dip and plateau diastolic RV waveform Causes of constriction: Mediastinal radiation Chronic idiopathic pericarditis Cardiac surgery Tuberculous pericarditis Signs & Symptoms of Constriction: R-sided heart failure: JVD, hepatic congestion, ascites, peripheral edema Clear lungs Exercise intolerance, muscle wasting, cardiac cachexia Jugular veins with prominent X and Y descent Y descent may look like JV pulse is “falling away” from you Respiratory increase in jugular venous pressure (Kussmaul’s sign) Pericardial knock (high-pitched early diastolic sound) Imaging of Pericardial Constriction: CT with thickening +/- calcification of the pericardium CT/MRI preferred modalities to evaluate pericardial thickening Echo may show systolic discordance of LV/RV pressures, ventricular interdependence In constriction, cath of LV and RV will show discordance of LV and RV pressures Differential Diagnosis of Pericardial Constriction: Restrictive cardiomyopathy RCM and Constriction both have Kussmaul’s sign, RV cath “dip and plateau” sign in early diastole Whereas RCM has no significant respiratory mitral variation, Constriction has marked variation of mitral inflow (>25%) and hepatic flow Whereas RCM has early reduced diastolic mitral annular velocity (Ea), Constriction has normal Ea velocities Whereas RCM is associated with pulmonary congestion, Constriction usually has clear lungs Whereas RCM has a reduced mitral annular diastolic velocity < 8 cm/s, Constriction has mitral annular diastolic velocity > 8 cm/s Whereas RCM shows ventricular concordance on simultaneous LV/RV cath, Constriction has ventricular discordance on simultaneous LV/RV cath Cardiac Tamponade Constriction and Tamponade both have elevated JVP, Kussmaul’s sign, pulsus...
by Mark | Sep 29, 2015 | Cardiology, Science
Pheochromocytoma vs. Carcinoid – What’s the Difference?? Two neuroendocrine tumors affecting the cardiovascular system and often get confused are carcinoid and pheochromocytoma. I thought I would include a brief primer on the two, because both secrete some degree of catecholamines; however both are completely different in management and treatment. Carcinoid Primarily secretion of serotonin (5-HT) >> catecholamines Serotonin release: flushing, diarrhea, bronchospasm/wheezing, Carcinoid heart disease Tumors found in midgut enterochromaffin cells: small intestines, cecal, ascending colon, bronchopulmonary. Happens in 5th to 7th decade of life usually. Serotonin cycle in Carcinoid: tryptophan –(trp-OH-ase)—> 5OH-tryptophan —(AADC)–> serotonin —(MAO)–> 5-HIAA The serotonin metabolite 5-HIAA is excreted in urine and is used to diagnose Carcinoid. 24-hour urine 5-HIAA is the most important clue to Carcinoid syndrome. Carcinoid heart disease: tricuspid regurgitation with TV “frozen” midway, pulmonary stenosis > regurgitation, R>L HD, increased PFO incidence, prominent early large “v” wave in jugular veins. False-positive Ur-5-HIAA: high tryptophan diet False-negatve Ur-5-HIAA: levodopa therapy for Parkinson’s Medical therapy for Carcinoid: Octreotide (somatostatin analogue), reduces vasoactive peptide secretion. Surgical therapy for non-metastatic Carcinoid: surgical resection —————————————————————————————————————————————————- Pheochromocytoma Primarily catecholamine release >> serotonin release. Pheo catecholamines are released from the adrenal medulla (85%) or extra-adrenal chromaffin tissue (15%) Classic symptoms of Pheo: episodic hypertension, palpitations, sweating, headache, orthostatic BP, vasoconstriction, anxiety/panic. Metabolic Pheo Sequelae: hyperglycemia, lactic acidosis, weight loss Associated with genetic conditions: MEN2, VHL, NF1, and SDH B/D Remember, MEN2 = MTC, Pheo, PTH (2a) or mucosa neuroma (2b) Pheo (bio)chemical diagnosis: plasma-free metanephrines, urinary fractionated metanephrines Reason: catecholamines produced by pheo are metabolized to metanephrines, independent of quantity of pheo release Pheo imaging: CT/MRI, I123-MIBG imaging Surgical Pheo...
by Mark | Sep 23, 2015 | Cardiology
Indications for Nuclear Myocardial Perfusion Imaging (MPI): Exercise MPI: Intermediate-high risk, able to exercise, with uninterpretable ECG (class I) or interpretable ECG (class IIa) Known SIHD, able to exercise, new symptoms Contraindications to Exercise MPI: Low-risk & able to exercise –> instead do Exercise ECG Routine LV function if no new signs/symptoms No changes < 5 yr after ACB surgery or < 2 yr after PCI Essentially asymptomatic patients Pharmacological MPI: Intermediate-high risk and unable to exercise Left Bundle Branch Block (LBBB) regardless of exercise Known SIHD, unable to exercise or LBBB, new symptoms Contraindications to Pharma MPI: Low-risk & able to exercise –> instead do an Exercise ECG Intermediate-high risk, able to exercise, interpretable ECG –> instead do exercise ECG or MPI Routine LV function if no new signs/symptoms No changes < 5 yr after ACB surgery or < 2 yr after PCI Essentially asymptomatic patients Uninterpretable ECG, remember the mnemonic PELViS: P: pre-excitation (WPW) E: excess of > 1 mm ST depression L: left bundle branch block (LBBB) V: ventricular pacing i S: ST/T changes from LVH or digoxin for example Disclaimer © 2015 www.markmccauleymd.com. All rights served. ...
by Mark | Sep 8, 2015 | Cardiac Electrophysiology, Cardiology, General Public
What is atrial tachycardia? Atrial tachycardia (AT) is a disorder of fast heart rhythm that begins in the upper chambers of the heart, the left and right atria (1). AT can start from one area, or focus, in either atrium and is called focal AT. AT can also arise from multiple different areas of the atria, and is called multifocal AT. Regardless the mechanism (focal vs. multifocal), the extra early signals that start from the focus/foci spreads centrifugally out to affect the atria and ventricles, and thus speeds up heart rate. The racing heart may be felt by the patient as palpitations, dizziness, chest pain or lightheadedness, or in some people may be asymptomatic (2). Occasionally, fast AT seen in younger patients can cause them to pass out. AT has two unique characteristics that distinguish it from other similar atrial rhythm disorders: 1) they often occur in repetitive short bursts, and 2) AT episodes exhibit “warm up” and “cool down” periods where rate varies at initiation and termination of the arrhythmia (1). Although short bursts of AT are common, sustained AT is a more rare cause of sustained arrhythmias from the atria (supraventricular tachycardia, SVT). Of all episodes of SVT encountered by electrophysiologists, AT is the cause only about 5-15% of the time (2-3). The diagnosis of AT is usually straightforward and starts with a thorough medical history and physical examination. If the patient is exhibiting AT during the exam, then an electrocardiogram (ECG) may demonstrate a fast heart rhythm consistent with AT. Cardiologists would recognize AT on the ECG as 1:1 P-QRS coupling, with non-sinus P-wave morphology, and usually long R-P...
by Mark | Sep 2, 2015 | Cardiology
The Most Important Articles in Hypertension Below are what I believe to be the most important articles in hypertension in mid-2015. Each blue trial name is a link to the trial page. In many cases where the journal article is open access, the link will open the full article. Otherwise, a Pubmed or Abstract page will open. Enjoy! ALLHAT JNC7 Guidelines JNC8 Guidelines ACCOMPLISH (benazepril plus: either amlodipine or HCTZ) HYVET (indapamide diuretic) MRFIT UKPDS Compendium ABCD MDRD HOT AASK ASCOT Studies ACCORD Disclaimer © 2015 www.markmccauleymd.com. All rights served. ...
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