Cardiac Muscle Action Potential

What is the approximate resting potential of a cardiac muscle cell?

Which ion plays a crucial role in creating the resting potential of a cardiac muscle cell?

In a theoretical cell with an initial equal number of positive and negative charges, what creates the charge imbalance for the resting potential?

What is the primary form of negative charge inside cardiac cells contributing to the resting potential?

Which pump is responsible for maintaining the ionic concentration gradients in cardiac muscle cells for resting potential?

What happens to the sodium gates when the membrane potential reaches between +20 and +30 mV?

During which phase of the action potential does the K+ permeability begin to increase significantly?

What role do L-type voltage gated calcium channels play in the action potential?

Why does the membrane potential not immediately fall to the equilibrium potential for potassium despite increased K+ permeability?

When does the myocyte contraction occur in relation to the action potential phases?

Which phase of the cardiac action potential is characterized by the opening of sodium gates and a hundred-fold increase in sodium permeability?

What ion has its concentration gradient reversed in the Goldman equation used to calculate the true resting potential?

During which phase of the cardiac action potential does the membrane potential depolarize to reach the threshold potential (-60 to -65mV)?

What is the primary characteristic of the plateau phase of the cardiac action potential?

Which type of muscle tissue is primarily responsible for generating the wave of excitation that triggers the opening of sodium gates in cardiac muscle membranes?

What is the main reason for the initial resting potential in the SAN being less negative compared to the rest of the heart?

What causes the pacemaker potential or 'prepotential' to drift upwards towards depolarization?

Which ion channel type is responsible for the diastolic depolarization phase in pacemaker cells?

During which phase is there an inward calcium current that accelerates depolarization towards the threshold potential?

What distinguishes the maximum depolarization level in the pacemaker cells from contractile myocardial cells?

What triggers the opening of sodium ion channel gates in cardiac muscle, leading to rapid ion permeability rise and the generation of another action potential?

Which parts of the heart exhibit automaticity, generating action potentials spontaneously?

What is the term used to describe the ability of the sinoatrial node (SAN) to have the fastest intrinsic rhythm in the human heart?

Which type of muscle cells in the heart typically do not display automaticity?

What determines the rate of contraction in cardiac muscle?

During which phase of the cardiac action potential do Na+ channels remain closed, leading to the 'absolute refractory' period of the myocytes?

What is the primary consequence of the 'absolute refractory' period in cardiac myocytes?

Where do some areas of the heart have particularly unstable 'resting potential'?

What happens to many Na+ channels during the repolarization phase of the cardiac action potential?

Why is it harder to generate a subsequent action potential during the 'relative refractory period' of the cardiac action potential?

What concept is the Nernst equation based on?

Why is the equilibrium potential for potassium in cardiac muscle cells slightly more negative than the resting membrane potential?

What is the primary ion influencing the magnitude of the resting potential in cardiac muscle cells?

Why is the membrane potential far from the Na+ equilibrium potential of +60 mV at rest?

What is responsible for maintaining the ionic concentration gradients in cardiac muscle cells?

What contributes to the resting membrane potential being slightly more negative than the potassium equilibrium potential in cardiac muscle cells?

What is the role of the Na+/K+-ATPase pump in relation to ion gradients and membrane potential?

Why is sodium far from electrochemical equilibrium at rest in cardiac muscle cells?

Why does potassium have a substantial influence on the resting membrane potential?

What determines the slightly more negative equilibrium potential for potassium in cardiac muscle cells compared to the RMP?