Cardiovascular Physiology Electrophysiology and Muscle Contraction PDF

Week 4 & Week 5: Cardiovascular Physiology Electrophysiology and Muscle Contraction Right atrium → Right ventricle → Pulmonary arteries → Lungs → Pulmonary veins → Left atrium. Pressures in the Cardiovascular System Blood pressures are not equal throughout the cardiovascular system. If they were e...

Week 4 & Week 5: Cardiovascular Physiology Electrophysiology and Muscle Contraction Right atrium → Right ventricle → Pulmonary arteries → Lungs → Pulmonary veins → Left atrium. Pressures in the Cardiovascular System Blood pressures are not equal throughout the cardiovascular system. If they were equal, blood would not flow, since flow requires a driving force (i.e., a pressure difference). The pressure differences that exist between the heart and blood vessels are the driving force for blood flow. Table 4.1 provides a summary of pressures in the systemic circulation and pulmonary circulation. Pressure profile in the vasculature The smooth curve gives mean pressure, which is highest in the aorta and large arteries and decreases progressively as blood flows from the arteries, to the arterioles, to the capillaries, to the veins, and back to the heart. This decrease in pressure occurs as blood flows through the vasculature because energy is consumed in overcoming the frictional resistance. Cardiac electrophysiology Cardiac electrophysiology includes all of the processes involved in the electrical activation of the heart: the cardiac action potentials; the conduction of action potentials along specialized conducting tissues; excitability and the refractory periods; the modulating effects of the autonomic nervous system on heart rate, conduction velocity, and excitability; and the electrocardiogram (ECG). Ultimately, the function of the heart is to pump blood through the vasculature. To serve as a pump, the ventricles must be electrically activated and then contract. In cardiac muscle, electrical activation is the cardiac action potential, which normally originates in the sinoatrial (SA) node. The action potentials initiated in the SA node then are conducted to the entire myocardium in a specific, timed sequence. Contraction follows, also in a specific sequence. “Sequence” is especially critical because the atria must be activated and contract before the ventricles, and the ventricles must contract from apex to base for efficient ejection of blood. Week 4 & Week 5: Cardiovascular Physiology Electrophysiology and Muscle Contraction Cardiac action potentials Origin and spread of excitation within the heart The heart consists of two kinds of muscle cells: contractile cells and conducting cells. Contractile cells constitute the majority of atrial and ventricular tissues and are the working cells of the heart. Action potentials in contractile cells lead to contraction and generation of force or pressure. Conducting cells constitute the tissues of the SA node, the atrial internodal tracts, the AV node, the bundle of His, and the Purkinje system. Conducting cells are specialized muscle cells that do not contribute significantly to generation of force; instead, they function to rapidly spread action potentials over the entire myocardium. Another feature of the specialized conducting tissues is their capacity to generate action potentials spontaneously. Except for the SA node, however, this capacity normally is suppressed. Figure 4.11 is a schematic drawing showing the relationships of the SA node, atria, ventricles, and specialized conducting tissues. The action potential spreads throughout the myocardium in the following sequence: 1. SA node. Normally, the action potential of the heart is initiated in the specialized tissue of the SA node, which serves as the pacemaker. After the action potential is initiated in the SA node, there is a specific sequence and timing for the conduction of action potentials to the rest of the heart. 2. Atrial internodal tracts and atria. The action potential spreads from the SA node to the right and left atria via the atrial internodal tracts. Simultaneously, the action potential is conducted to the AV node. 3. AV node. Conduction velocity through the AV node is considerably slower than in the other cardiac tissues. Slow conduction through the AV node ensures that the ventricles have sufficient time to fill with blood before they are activated and contract. Increases in conduction velocity of the AV node can lead to decreased ventricular filling and decreased stroke volume and cardiac output. 4. Bundle of His, Purkinje system, and ventricles. From the AV node, the action potential enters the specialized conducting system of the ventricles. The action potential is first conducted to the bundle of His through the common bundle. It then invades the left and right bundle branches and then the smaller bundles of the Purkinje system. Conduction through the His-Purkinje system is extremely fast, and it rapidly distributes the action potential to the ventricles. The action potential also spreads from one ventricular muscle cell to the next, via low-resistance pathways between the cells. Rapid conduction of the action potential throughout the ventricles is essential and allows for efficient contraction and ejection of blood. The term normal sinus rhythm has a specific meaning. It means that the pattern and timing of the electrical activation of the heart are normal. To qualify as normal sinus rhythm, the following three criteria must be met: (1) The action potential must originate in the SA node. (2) The SA nodal impulses must occur regularly at a rate of 60 to 100 impulses per minute. (3) The activation of the myocardium must occur in the correct sequence and with the correct timing and delays. Week 4 & Week 5: Cardiovascular Physiology Electrophysiology and Muscle Contraction Concepts associated with cardiac action potentials The concepts applied to cardiac action potentials are the same concepts that are applied to action potentials in nerve, skeletal muscle, and smooth muscle. The following section is a summary of those principles, which are discussed in Chapter 1: 1. The membrane potential of cardiac cells is determined by the relative conductances (or permeabilities) to ions and the concentration gradients for the permeant ions. 2. If the cell membrane has a high conductance or permeability to an ion, that ion will flow down its electrochemical gradient and attempt to drive the membrane potential toward its equilibrium potential (calculated by the Nernst equation). If the cell membrane has low conductance or permeability to an ion or is impermeable to the ion, that ion will make little or no contribution to the membrane potential. 3. By convention, membrane potential is expressed in millivolts (mV), and intracellular potential is expressed relative to extracellular potential; for example, a membrane potential of −85 mV means 85 mV, cell interior negative. 4. The resting membrane potential of cardiac cells is determined primarily by potassium ions (K⁺). The conductance to K⁺ at rest is high, and the resting membrane potential is close to the K⁺ equilibrium potential. Since the conductance to sodium (Na⁺) at rest is low, Na⁺ contributes little to the resting membrane potential. 5. The role of Na⁺-K⁺ ATPase is primarily to maintain Na⁺ and K⁺ concentration gradients across the cell membrane, although it makes a small direct electrogenic contribution to the membrane potential. 6. Changes in membrane potential are caused by the flow of ions into or out of the cell. For ion flow to occur, the cell membrane must be permeable to that ion. Depolarization means the membrane potential has become less negative. Depolarization occurs when there is a net movement of positive charge into the cell, which is called an inward current. Hyperpolarization means the membrane potential has become more negative, and it occurs when there is a net movement of positive charge out of the cell, which is called an outward current. 7. Two basic mechanisms can produce a change in membrane potential: o In one mechanism, there is a change in the electrochemical gradient for a permeant ion, which changes the equilibrium potential for that ion. The permeant ion then will flow into or out of the cell in an attempt to reestablish electrochemical equilibrium, and this current flow will alter the membrane potential. § For example, consider the effect of decreasing the extracellular K⁺ concentration on the resting membrane potential of a myocardial cell. The K⁺ equilibrium potential, calculated by the Nernst equation, will become more negative. K⁺ ions will then flow out of the cell and down the now larger electrochemical gradient, driving the resting membrane potential toward the new, more negative K⁺ equilibrium potential. o In the other mechanism, there is a change in conductance to an ion. For example, the resting permeability of ventricular cells to Na⁺ is quite low, and Na⁺ contributes minimally to the resting membrane potential. However, during the upstroke of the ventricular action potential, Na⁺ conductance dramatically increases, Na⁺ flows into the cell down its electrochemical gradient, and the