Cardio Flashcards
Name Pharyngeal( arches, aortic arch, pouches )?
1/2/3/4/5/6 = 5/7/9/10(s.l)/-/10(r.l) nerve= maxillary/ stapedieal(regresses)/ common carotid + prox. internal carotid/ aortic arch + subclavian/ -/ PA + DA arteries = ear/mouth/thymus + inf pth/ ultimobranchial + sup pth/-/- pouch
Diastolic heart failure change on P.V graph of LV? What initiates Sequence? HTN->LV hypertrophy->LV pressure _ + _ in SV but preserved EF ->pulmonary edema-RHF only change is elevated LV filling pressures!! to maintain normal end diastolic volume.
Diastolic heart failure change on P.V graph of LV? What initiates Sequence? HTN->LV hypertrophy->LV pressure inc + dec in SV but preserved EF ->pulmonary edema-RHFonly change is elevated LV filling pressures!! to maintain normal end diastolic volume.
Systolic HF what causes decomepensation? Chronic _overload->eccentric hypertrophy-> in volume but dec EF
Systolic HF what causes decomepensation? Chronic volume overload->eccentric hypertrophy-> in volume but dec EF
Hypertrophic/dilated heart looks like?
Hypertrophic/dilated heart looks like?
- Pulses paradoix? How calculate? Indicates what type of disease(3)?
korotkoff sounds pressure diff when put on cuff= pulses paradoxus(>10mg drop in SBP) because when inspire-> inc RV volume-> heart unable to expand well so interventricular septum bows toward LV->dec LV SV->systolic pressure dec) in disesase that constrict hearts ability to expand ( asthama, COPD because decrease space for heart to expand) !
Pulmonary edema and lung compliance? Pulmonary edema => _ surface tension( diluted surfactant) - + restrictive edema->_ lung compliance; Pulm edema presents as _ lung disease
Pulmonary edema and lung compliance? Pulmonary edema => inc surface tension( diluted surfactant) - + restrictive edema->decrease lung compliance; Pulm edema presents as restrictive lung disease
LF/RH= _/ _edema
LF/RH= pulm/ systemic edema
Antiarthymic class 1A/B/C AP looks? _. —–adenosine acts via _channels and _
Antiarthymic class 1A/B/C AP looks? like prolonged on phase 0( Na) + prolonged/ shortened/ no change on K so prolong/shorten/no change action potential form. —–adenosine acts via k channels and Ca
TTN gene for what protein in what disease? Genetics?
TTN gene for what protein in what disease? Genetics? for titin protein dorm mutation Familial dilated cardiomyopathy
Amlodipine side effect? amlodipine/amiodarone = CCB/ antiarth
Amlodipine side effect? Effects of vasodilation—Flushing, edema, dizziness; amlodipine/amiodarone = CCB/ antiarth
When deos most LV perfusion occur? So what is limiting factor( what affects it the most) for perfusion during times with hi HR( excercis)?
When deos most LV perfusion occur? So what is limiting factor( what affects it the most) for perfusion during times with hi HR( excercis); Diastole. because LV pressures inverly related perfusion. Length of diastole
PAN? Spare? PAN( segmental, transmural,( like chrons) of arteries) spares lung artereis present with GI pain, ( also cardiac & kidney & skin purpura/livedo reticularis)
PAN? Spare? PAN( segmental, transmural,( like chrons) of arteries) spares lung artereis present with GI pain, ( also cardiac & kidney & skin purpura/livedo reticularis)
neprilysin breakdown _ & _ can treat _
neprilysin breakdown ANP & BNP can treat HF
glucagon( via GS) treats _ toxicity
glucagon( via GS) treats BB toxicity
Elastin how like rubber(2)? Elastin rbber-like due to lysly _ cross-linking(after _ acts as scaffold) and many hydrophobic aa.
Elastin how like rubber(2)? Elastin rbber-like due to lysly oxidase cross-linking(after fibrilin acts as scaffold) and many hydrophobic aa.
Most people are what heart dominance? Determined by?
Most people are what heart dominance? Determined by? Right. Who supplies AV node supplied by R or left PDA form RCA or LCircumflex(from LCA) …( determines right or left dominance). SA node via RCA!
What does it mean to have decompensated HF? Decompensation occurs after what maladaptive compensations? Cause what murmur? murmur treated via?
What does it mean to have decompensated HF? Decompensation occurs after what maladaptive compensations? Cause what murmur? HF decompensation( symptomatic SOB and/or peripheral edema if L and /or RHF) -> secondary MR( diuretics and vasodilators treat this but for chorda tendinae ruptor need surgery). Chronic maladaptive compensatory mechanisms-in RAAS & sympathetic.
Nitropruside affect both a& v why?
Nitropruside affect both a& v why? Nitroglycerin, isosorbide mono/dinitrate -> NO & S-nitrosothiols via mitcho in sm so veins effects but nitropruisde metabol in bld so balanced( v & a)
What vessel has least amount of o2 in body and why?
What vessel has least amount of o2 in body and why? Heart(more than any other organ) extracts most oxygen-> coronary sinus with least O2 concentration
Class 3 vrs Class 1 antiarrythmic?
Class 3 vrs Class 1 antiarrythmic? Class 3 block K but some class 1 block K as well inaddition to Na
Atrial & ventricular action potential ions ?
Atrial & ventricular action potential ions ? for both na, Ca, K
septic shock hallmark? What must temperature be? hypovolumic shock has to do with effects of low _?
septic shock hallmark? What must temperature be? dec SVR can be either hyper or hypothermia even though septic…hypovolumic shock has to do with effects of low preload
Frank-Starling graph determined by 5 parameters looks like? How would nitroprusside look like?
Frank-Starling graph: Graph on Frank stling curve( P vrs Vol of LV) Afterload, preload, contractility, compliance SV.
hypovolumeia symptoms( _ mucous membranes, _statis _tension so _) compensatory methods include _ urine sodium & _ Bun/creatinine Difference with ATN is prerenal azotemia
hypovolumeia symptoms( dry mucous membranes, osthostatis dizz/hypotension) compensatory methods include low urine sodium & elevated Bun/creatinine