Circulation 5 Flashcards
how does depolarization travel through the heart (2)
- specialized conducting pathways
- directly between cardiomyocytes
specialized conducting pathways (3)
- modified cardiomyocytes can spread action potential rapidly throughout the myocardium
- these cells are elongated, lack contractile proteins, and are pale
- they can undergo rhythmic depolarizations
depolarization directly between cardiomyocytes (2)
- cardiomyocytes are electrically connected via gap junctions
- allows electrical signals to pass directly from cell to cell
excitation-contraction coupling
- the coupling of the action potential and the cardiomyocyte contraction
excitation-contraction coupling steps (8)
- action potential enters from adjacent cell
- voltage-gated Ca2+ channels open and Ca2+ enters the cell
- entry of Ca2+ triggers release of LOTS of Ca2+ from sarcoplasmic reticulum
- Ca2+ bind to troponin to initiate contraction
- relaxation occurs when Ca2+ unbinds from troponin
- Ca2+ is pumped back into sarcoplasmic reticulum for storage
- Ca2+ is exchanged with Na+
- Na+ gradient is maintained by Na+-K+-ATPase
conducting pathway in mammalian heart (4)
- SA node depolarizes, which spreads rapidly via the internodal pathway
- AV node delays the signals, while the depolarization spreads through atria via gap junctions and causes atria to contract
- depolarization spreads rapidly through bundles of His and Purkinje fibers
- depolarization spreads upward through ventricle, causes ventricle to contract
sequence of conduction pathway in mammalian heart (5)
- SA node
- internodal pathway
- AV node
- Bundle of His
- purkinje fibers
how do action potentials in cardiomyocytes differ from those in skeletal muscles
- cardiomyocyte APs are extended, containing a plateau phase during repolarization
what is the purpose of the plateau phase (2)
- to prevent tetanus by removing possibility for sustained contraction during rapid APs
- allow the heart to refill with blood and relax
cardiomyocyte AP plateau phase (2)
- extended repolarization that lasts as long as ventricular contraction
- caused by Ca2+ entry via L-shaped channel and temporary reduced K+ permeability
electrocardiogram (ECG/EKG) (3)
- composite recording of action potentials in cardiac muscle
- contains the P wave, QRS complex, and T wave
- used for clinical diagnosis of issues with conducting system
ECG: P wave
- atrial depolarization
ECG: QRS complex
- ventricular depolarization
ECG: T wave
- ventricular repolarization
why is the T wave positive in the ECG if it represents a repolarization event
- it is negative; ECG tracks change in membrane potential, not direction of change
heart sounds
- opening and closing of heart valves
electrical and mechanical events in cardiac cycle
- electrical events initiate contractile (mechanical) events
electrical and mechanical events in left heart cardiac cycle: P-wave (2)
- pressure is increasing in atrium and ventricle before P-wave
- P-wave initiates atrial contraction and atrial BP peaks
electrical and mechanical events in left heart cardiac cycle: QRS-complex (3)
- QRS-complex initiates ventricular contraction and ventricular BP peaks
- ventricular BP first exceeds atrial BP and then aortic diastolic BP
- atrial relaxation occurs at same time
electrical and mechanical events in left heart cardiac cycle: T-wave (2)
- T-wave initiates ventricular realization and ventricular BP falls below aortic BP, then below atrial BP
- energy stored in aorta is slowly released
end-systolic volume (ESV)
- volume after contraction
end-diastolic volume (EDV)
- volume before contraction
cardiac stroke volume (SV) (2)
SV = EDV - ESV
- volume of blood pumped with each beat
does a heartbeat fully empty the human ventricle
- no, but more can be expelled during exercise/more intense contraction
why does aortic blood pressure decrease during diastole
- falls when heart is relaxed as blood is being transported away to the extremeties
cardiac output (CO) (2)
- volume of blood pumped per unit time
- CO = HR x SV
heart rate (HR)
- rate of contraction (beats per minute)
how can cardiac output be modified (2)
- regulating heart rate
- regulating stroke volume
cardiac output modulation: heart rate (2)
- modulated by autonomic nerves and adrenal medulla
- activations of the parasympathetic (decreased HR) or the sympathetic system (increased HR)
decreased HR
- bradycardia
increased HR
- tachycardia
cardiac output modulation: stroke volume (2)
- modulated by various nervous, hormonal, and physical factors
- nervous and endocrine system an cause heart to contract more forcefully, pumping more blood each beat
control of stroke volume: pathway (8)
- binding of norepinephrine or epinephrine changes shape of beta1 adrenergic receptor, activating G protein
- G protein activates adenylate cyclase
- adenylate cyclase catalyzes ATP –> cAMP
- cAMP activates protein kinase A
- protein kinase phosphorylates L-type Ca2+, allowing Ca2+ to enter cell, stimulating contraction
- protein kinase phosphorylates Ca2+ channel on sarcoplasmic reticulum, allowing Ca2+ to move to cytoplasm, which stimulates contraction
- protein kinase phosphorylates myosin, stimulating contraction
- protein kinase phosphorylates sarcoplasmic Ca2+ ATPase speeding the removal of Ca2+ from cytoplasm during relaxation, decreasing relaxation time
how is stroke volume increased by the sympathetic nervous sytem
- more Ca2+ in cytoplasm increases contractile magnitude, promoting muscle contraction
Frank-Starling effect (2)
- increased end-diastole volume results in more forceful contraction and increased SV
- heart automatically compensates for increases in volume of blood returning to the heart (autoregulation) due to length-tension relationship for muscle
control of stroke volume: sympathetic activity levels and the Frank-Starling effect
- levels of sympathetic activity shifts positions of cardiac muscle length-tension relationship
Frank-Starling effect: increased sympathetic activity
- intensifies Frank-Starling effect, increasing the possible range of the stroke volume
Frank-Starling effect: decreased sympathetic activity
- reduces Frank-Starling effect, reducing the possible range of the stroke volume
what potentials are generated in the heart (5)
- SA node
- atrium
- AV node
- bundle of His
- ventricular cardiomyocyte
what potentials display a plateau phase in the heart (3)
- atrium
- bundle of His
- ventricular cardiomyocyte
what potentials don’t have a plateau phase in the heart (2)
- SA node
- AV node
