Unit 6A Sigs | Baamboozle - Baamboozle | The Most Fun Classroom Games!

Describe the potential benefits and precautions for the use of CoQ10 and L-carnitine for cardiac function. (SIGS 6.3b)

CoQ10: facilitates ATP production via ETC in mitochondria; body can become dependant- do not stop abruptly; L-Carn.: "shuttle" for FA to mitochondria in L vent.

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Describe the mechanism(s) of action of diltiazem and its effect on cardiac conductivity (SIGS 6.1a)

MOA: inhibits inflow Ca2+ ions into cardiac smooth muscle (SM) during depolarization; Decr. intracellular Ca2+ --> incr. SM relaxation/vasodilation--> decr. BP

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Distinguish between cardiac conduction blocks (sinus block; bundle branch block; hemiblock) on an EKG. (SIGS 6.1b)

A: Sinus block; B: LBBB; C: RBBB; D: Hemi/fascicular (Left posterior hemiblock is associated with a frontal plane QRS axis more positive than +120°)

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Describe the role of INR monitoring in anticoagulation therapy and explain the need for bridge therapy with warfarin. (SIGS 6.1a)

monitor coagulability (maintain optimal level- not too low or too high); Bridge therapy for warfarin due to taking several days to achieve therapeutic effects

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Contrast how the distal arterioles compensate for the stenosis in their respective coronary arteries.(Sigs 6.3a)

MILD: dilation --> meet met. need; MOD: dil.--> meet met. need @ rest; exertion: max blood flow low despite dil. --> can't meet met. need;COMPLETE OCCUL: unable

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Discuss the use of ACE-inhibitors and beta-blockers to slow or reverse cardiac remodeling. (Sigs Case 6.2a)

ACE-inh.: allows heart to get more blood flow & decrease LV filing & decreases peripheral resistance; BB: decreases demand on heart and lowers BP

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What is the MOA of Colchicine and how does it relate to the management of pericarditis?(Sigs Case 6.2a)

used as a theoretical anti-inflamm. agent; inhibits IL-1 from cascading, interferes w/ NFK-B; binds to microtubular tubulin in neutrophils-> inhibits mitosis

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Explain the relationship of HCM and heart failure with preserved ejection fraction (HFpEF)(Sigs Case 6.3b)

diastolic dysfunction (early diastolic relaxation) + LV hypertrophy (concentric)- thick wall = pressure overload + less volume (EDV-ESV/EDV) = up EF

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Explain the mechanism of action of amiodarone and the rationale for its use in dysrhythmias. (SIGS 6.2b)

Class III anti-arryth; MOA: blocks VG K+ channels --> inhibit Phase 3 repol--> prolong cardiac action potential & refractoriness--> decr. SA node firing rate

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Contrast normal systolic and diastolic function in a healthy heart with the systolic and diastolic function of HCM.(Sigs Case 6.3b)

may have average systolic funct. but poor diastolic funct.; diastolic dysf. will have preserved EF; systolic dysf will have reduced EF

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