Intrinsic cardiac depolarization

Fig. 3.11 Intrinsic cardiac depolarization can be recorded at the pacing lead electrode and measured by the pacemaker. This signal is called an electrogram. In this example, the electrogram is measured from the ventricular lead and is caused by ventricular depolarization. The signal has an amplitude of 8mV. This signal would not be seen by the pacemaker if the sensitivity is set to 10 mV. However, by lowering the sensitivity value to 5 mV (making the pacemaker more sensitive), the intrinsic depolarization would be seen and pacemaker timing cycles would be reset when appropriate.

Stimulation or inhibition of autonomic effector cells by ACh results from interaction of ACh with muscarinic ACh receptors. In this case, the effector is coupled to the receptor by a G protein (see Chapter 1). In contrast to skeletal muscle and neurons, smooth muscle and the cardiac conduction system (sinoatrial [SA] node, atrium, atrioventricular [AV] node, and the His-Purkinje system) normally exhibit intrinsic activity, both electrical and mechanical, that is modulated but not initiated by nerve impulses. At some smooth muscle, ACh causes a decrease in the resting potential (i.e., the membrane potential becomes less negative) and an increase in the frequency of spike production, accompanied by a rise in tension. A primary action of ACh in initiating these effects through muscarinic receptors is probably partial depolarization of the cell membrane brought about by an increase in Na and, in some instances, Ca conductance activation of muscarinic receptors can also activate the G -PLC-IP pathway leading to the mobilization of stored Ccf. Hence, ACh stimulates ion fluxes across membranes and/or mobilizes intracellular Ca to cause contraction. 

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