BMS200_PATMIC_Cardio9P2_Fall2023 (2) (1).pdf

BMS 200 – Cardiology 9 Pericarditis, Myocarditis, Endocarditis Orthostatic and vasovagal syndromes Outcomes Briefly describe the pathogenesis, major clinical features, and prognosis of the following clinical classifications of pericarditis: acute pericarditis, subacute pericarditis, constricti...

BMS 200 – Cardiology 9 Pericarditis, Myocarditis, Endocarditis Orthostatic and vasovagal syndromes Outcomes Briefly describe the pathogenesis, major clinical features, and prognosis of the following clinical classifications of pericarditis: acute pericarditis, subacute pericarditis, constrictive pericarditis Briefly describe the pathogenesis, major clinical features, and prognosis of infectious and non-infectious forms of myocarditis Briefly describe the pathogenesis, major clinical features, and prognosis of acute and subacute bacterial endocarditis Describe the biology, life cycle, major virulence factors, diagnosis, and clinical manifestations of infection for the following: Borrelia burgdorferi, trypanosoma cruzi, ehrlichia chaffeensis Outcomes Briefly describe the biology, major virulence factors, diagnosis, and clinical manifestations of coxsackie virus and echovirus Briefly describe the cardiac complications of COVID19 coronavirus Briefly describe the biology, major virulence factors, diagnosis, and clinical manifestations of HACEK group of bacteria Staph epidermidis and viridans streptococci Describe the pathophysiology of postural-tachycardia syndrome (POTS) and relate it to clinical features POTS – Postural Orthostatic Tachycardia Syndrome What is it? The name describes it well – when people go from lying down to standing, they experience a > 30 beat/min increase in HR That increase in heart rate cannot be accompanied by a decrease in blood pressure… ▪ Otherwise that would be known as orthostatic hypotension ▪ It is normal for BP to drop when standing – if there is a less than 20/10 mm Hg drop, then that’s considered normal This is part of a set of syndromes known as dysautonomias ▪ Include POTS, orthostatic hypotension, vasovagal syncope as the more common syndromes POTS – key clinical features Symptomatic orthostatic intolerance without hypotension ▪ Accompanied by increase in HR > 120 beats/min or > 30 beats/min over supine HR What is meant by orthostatic intolerance? ▪ In response to standing, troublesome symptoms occur, which can include: Light-headedness, weakness, blurred vision Nausea, tremulousness (shakiness), and palpitations Although pre-syncopal symptoms are the defining feature, syncope does not tend to happen Women are affected 5X more often than men This is likely the most, or at least one of the most common, dysautonomias to cause very bothersome symptoms POTS – a tricky subject Even though it requires tilt- table testing to diagnose, there are no clear single pathophysiologic mechanisms or diagnostic criteria beyond the ones mentioned in the last slide Most experts agree that there’s “more than one POTS” ▪ There are a multitude of different causes of this syndrome and each patient has a somewhat unique variant on a number of different pathophysiologic themes ▪ So, if there’s more than one POTS, some sort of standardized recognition needs to happen before you can standardize diagnosis https://www.mayoclinic.org/tests-procedures/tilt-table- test/about/pac-20395124#dialogId36740715 The baroreceptor reflex – a review POTS – why does it happen? Let’s unpack that last slide Neuropathic causes of POTS ▪ Neuropathy where? ▪ For reasons that aren’t understood, patients with POTS have “pooling” of blood in the lower vascular beds Include the pelvic, splanchnic, and lower limb vessels ▪ Interestingly, this pooling might not be due to venous vasodilation, but instead due to inappropriate arteriolar vasodilation Studies in patients with POTS seem to indicate that less NE is released in the lower limbs in response to orthostatic or pharmacologic challenges Strangely enough, NE release was the same between controls and POTS patients in the upper extremities Other studies also find an exaggerated response to exogenously administered catecholamines… why might this be? The baroreceptor reflex – a review Still unpacking… Hypovolemic POTS ▪ It’s easy to understand why reduced blood volume leads to tachycardia – see baroreceptor reflex again ▪ Some POTS patients seem to have reduced blood volume – 13 -22% lower plasma volume than health controls Why hypovolemia? ▪ Not sure - but the following experimental findings are observed: Elevated renin compared to aldosterone (a low aldosterone:renin ratio) Elevated levels of angiotensin II… What does this evidence suggest? Hypovolemic POTS Other findings in patients with “hypovolemia-predominant” POTS ▪ Patients who are deconditioned tend to reduce their blood volume. This is seen in: Subjects exposed to microgravity for extended periods of time experienced decreased blood volume and POTS-like responses to standing Decreases in blood volume can also be seen with prolonged bed rest ▪ It is thought that deconditioning may “unmask” inadequate aldosterone secretion in those predisposed to POTS Hyper-adrenergic POTS Some POTS patients secrete much more norepinephrine than patients without the disorder ▪ Experimental data suggests that in healthy controls, there is a doubling of plasma norepinephrine concentrations on standing ▪ In patients with POTS in the same study, there can be a tripling-to-quadrupling of NE release ▪ Epinephrine concentrations seem to be similar Why is there an oversecretion of NE in some? ▪ One study suggests missense mutations in catecholamine transporters → accumulation of NE in the ECF where it is released ▪ In these patients, standing actually leads to an increase in blood pressure in some Hyper-adrenergic POTS Other theories re: hyper-adrenergic POTS ▪ Activating auto-antibodies to beta-1 and beta-2 adrenoreceptors have been detected Can you think of another disorder that involves activating antibodies? How would inappropriate activation of beta-1 receptors manifest? How about beta-2? POTS – which therapies make sense for which cause? Therapies for POTS (which model?) Midodrine – alpha-1 agonist: _________________ Avoidance of SNRIs: _________________ High sodium diet: _____________ Stockings & abdominal compression: ___________ “Drink more water”: ________________ Desmopressin (AVP agonist) ______________ Lower extremity maneuvers: _________________ Beta-blockers: ______________ Exercise: ___________________