GMS 6530 CARDIAC EXAM QUESTIONS AND ANSWERS WITH
COMPLETE SOLUTIONS GRADED A++
Sympathetic innnervation
- NE binds beta-1 receptors
- activates cAMP second-messenger system
- opens Ca2+ channels in sarcolemma
Parasympathetic innervation
- ACh binds muscarinic receptors
- opens K+ channels in nodal cells allowing outflow
- hyperpolarizes them slowing HR down
K+
- electrolyte with greatest chronotropic effect
- hyper - excess diffuses into myocytes, slowing HR & causing irregularity
- hypo - hyperpolarizes cells, causing need for incaresed stimulation
Ca2+
- hyper - increases HR & contractility
Na+
- hyper - increases HR
% of capillaries shut down at any given time
- 75%
Arteriosclerosis
,- harding of arteries with age
- decrease in elastic tissue
Atherosclerosis
- build up of lipids that form plaque
Vasomotor center of medulla
- stimulates most BV to contract with the exception of the vessels in heart
Physiologic hypertrophy
- exercise, pregnancy
- cardiomyocytes increase in length and width
- balanced enlargment of chambers
Pathologic hypertrophy
- concentric hypertrophy
- cardiomyocytes increase in width
- wall and septal thickening
- loss of chamber area
beta agaonists
- epi, isoproterenol
- dopamine
- dobutamine
dopamine
- shock
- beta 1 agonst
-increase contractility
, - increase HR
- increase renal flow
- IV only, short 1/2 life, tachycardia, tolerance, increased mortality
dobutamine
- end-stage shock
- beta 1 agonist at low dose
- alpha 1 agonist at high dose
- increase contractility
- modest decrease in afterload
- short-term cardiac support
- IV only, tolerance, pro-arrhythmic, increased mortality
Phosphodiesterase inhibitor
- PD3 inhibitors
- milrinone
Milrinone
- end-stage shock
- inhibits PDE > increases cAMP
- increase cAMP = increase in contractility & SV
- increase cAMP = decrease afterload (vasodilation)
- little/no change in HR
- hypotension, proarrhythmia, increased mortality (may be lessened with concurrent
beta blocker)
Cardiac glycosides
COMPLETE SOLUTIONS GRADED A++
Sympathetic innnervation
- NE binds beta-1 receptors
- activates cAMP second-messenger system
- opens Ca2+ channels in sarcolemma
Parasympathetic innervation
- ACh binds muscarinic receptors
- opens K+ channels in nodal cells allowing outflow
- hyperpolarizes them slowing HR down
K+
- electrolyte with greatest chronotropic effect
- hyper - excess diffuses into myocytes, slowing HR & causing irregularity
- hypo - hyperpolarizes cells, causing need for incaresed stimulation
Ca2+
- hyper - increases HR & contractility
Na+
- hyper - increases HR
% of capillaries shut down at any given time
- 75%
Arteriosclerosis
,- harding of arteries with age
- decrease in elastic tissue
Atherosclerosis
- build up of lipids that form plaque
Vasomotor center of medulla
- stimulates most BV to contract with the exception of the vessels in heart
Physiologic hypertrophy
- exercise, pregnancy
- cardiomyocytes increase in length and width
- balanced enlargment of chambers
Pathologic hypertrophy
- concentric hypertrophy
- cardiomyocytes increase in width
- wall and septal thickening
- loss of chamber area
beta agaonists
- epi, isoproterenol
- dopamine
- dobutamine
dopamine
- shock
- beta 1 agonst
-increase contractility
, - increase HR
- increase renal flow
- IV only, short 1/2 life, tachycardia, tolerance, increased mortality
dobutamine
- end-stage shock
- beta 1 agonist at low dose
- alpha 1 agonist at high dose
- increase contractility
- modest decrease in afterload
- short-term cardiac support
- IV only, tolerance, pro-arrhythmic, increased mortality
Phosphodiesterase inhibitor
- PD3 inhibitors
- milrinone
Milrinone
- end-stage shock
- inhibits PDE > increases cAMP
- increase cAMP = increase in contractility & SV
- increase cAMP = decrease afterload (vasodilation)
- little/no change in HR
- hypotension, proarrhythmia, increased mortality (may be lessened with concurrent
beta blocker)
Cardiac glycosides
