Chapter 10 Cardiac Pump

Preload is the term given for the pressure in a chamber when the cardiac muscle is filled (circulation into the chamber is approaching 0) but is not yet activated. Preload is the passive tension in the chamber right before it develops active tension. Preload for cardiac muscle is analogous to stretch on skeletal muscle. The pressure of preload is related to the volume and the compliance. The compliance is at its highest when the myocardium is empty and not activated. As the chamber fills with blood, passive tension starts to develop which gradually reduces compliance while increasing the volume of blood, which when combined increases pressure. Under normal circumstances this increase in pressure (higher blood volume and lower compliance) is not great enough to fully impede circulation into the chamber. The passive tension developed during preload is subsequently utilized to assist active tension. Which develops the tension necessary to change the volume and compliance of the chamber for the purpose of increasing pressure to facilitate circulation out of the chamber. The increased pressure, alone, simply directs circulation out of the chamber from an area of high to low pressure. The direction of actual circulation through the heart is dependent on properly functioning valves that limit flow ”backwards” and allow circulation ”forwards” based on cardiac anatomy (Figure 9.1.

The preload is directly related to end-diastolic pressure (EDP), which is directly related to end-diastolic volume (assuming the compliance is normal and relatively low during diastole). The volume that results in preload is from circulation. Where the circulation is coming from for preload depends on the chamber. The right atrium preload comes from the systemic veins; right ventricle preload comes from the right atrium through the tricuspid valve; left atrium preload comes from the pulmonary veins; left ventricle preload comes from the left atrium through the mitral valve.

It is most common to discuss preload from the perspective of the left ventricle (LV). Therefore, unless otherwise noted, EDV and EDP mean LVEDV and LVEDP (respectively). EDP is related to the Frank-Starling law which states that the amount of venous return influences the performance of the left ventricle (assumes all the venous return moves through the right heart circulation (RA, RV, pulmonary arteries, pulmonary capillaries, pulmonary veins to the LA and finally the LV). The Frank-Starling mechanism is based on the relationship between EDP and total tension developed from active and passive tension.

Afterload is the term given for the pressure that a chamber must overcome to cause circulation out of the chamber. Afterload for cardiac muscle is analogous with resistance (or load) for skeletal muscle. It is the resistance that the cardiac chamber must exert its tension in order to reduce the volume of the chamber. The pressure of afterload depends on which chamber must overcome that pressure. For the RA it is the pressure exerted on the tricuspid valve by the RV; for the RV it is the pressure exerted on the pulmonic valve by the pulmonary arteries; for the LA it is the pressure exerted on the mitral valve by the LV; for the LV it is the pressure exerted on the aortic valve by the aorta (first of the systemic arteries).

It is most common to discuss afterload from the perspective of the LV. Therefore, unless otherwise noted, afterload refers to aortic pressure and is best estimated as mean arterial pressure (MAP) (See Equation 9.6). MAP is related to vascular compliance and resistance. As afterload, MAP affects aortic valve opening and is the most obvious load encountered by the ejecting ventricle.

Warning: HFpEF

Long term high blood pressure (hypertension) results in left ventricular hypertrophy (LVH) that is associated with a reduced size and reduced compliance of the LV chamber. LVH is a common cause of diastolic (preserved ejection fraction (pEF)) heart failure (HFpEF).

Cardiac muscle is self excitatory (automaticity). Self excitations are rhythmic, occurring at rest approximately every 2/3 of a second (650 ms) with very little variability when not influenced by the neuroendocine system (HR of approximately 90 bpm with low heart rate variability (HRV)). Or every 60 seconds with more variability when influenced by the neuroendocrine system at rest (HR of approximately 60 bpm with a HRV of approximately 50-100 ms when measured as a standard deviation with primarily parasympathetic influence).

In normal conditions automaticity occurs in a cluster of myocardial cells in the right atrium known as the sino atrial (SA) node (pacemaker cells). SA node cells have a higher resting permeability to $N{a}^{+}$ than axonal or skeletal muscle membranes. Based on this higher permeability to $N{a}^{+}$ these cells do not have a sustained (stable) resting membrane potential (See Figure 10.2. As soon as their membrane is repolarized it begins a slow journey back to the threshold potential due to a slow influx of $N{a}^{+}$. How long it takes to reach the threshold (pacemaker potential) determines the heart rate. Under normal conditions the SA node cells have the greatest pacemaker potential.

An excitation of the SA node results in full excitation of all the cardiac muscle cells, first in the atria and after a delay, in the ventricles. There are three features of the myocardium that lead to this pattern of conductivity.

1. 1.

   There are specialized cardiac cells that form a conduction network (See Figure 10.3. The conduction network starts with the SA node sending a wave of excitation through the atria, facilitated by intra-nodal fibers (not shown in Figure 10.3) that can rapidly carry an excitation from the SA node to the atrio-ventricular (AV) node. The excitation through the atria results in the P wave of the electrocardiograph (ECG). The excitation of the AV node and its distal conduction component, the bundle of His, is slower and delays the excitation of the ventricles (the PR interval on the ECG). Once through the AV node and bundle of His the excitation travels rapidly down the right and left bundle branches to the purkinje fibers. The branching conduction network in the ventricles is critically important to rapid and synchronous excitation of the ventricles (the QRS complex in the ECG). Atrial repolarization is a minor event and is easily lost in the waves of the QRS. Ventricular repolarization is a more substantial event because the ventricles are more substantial muscles and results first in a return to baseline (ST segment on the ECG), and then the T wave on the ECG. It should be noted in Figure 10.3 that the AV node fibers have a pacemaker potential but it is smaller than the SA node pacemaker potential. The SA node is the pacemaker under normal circumstances because it has a larger pacemaker potential and reaches the excitation threshold earlier than the AV node. However, if the SA node fails, the AV node reaches the excitation threshold and initiates ventricular excitation.

2. 2.

   There is a fibrous connective tissue boundary between the atria and the ventricles that does not transmit an excitation (does not have an excitable membrane). This helps ensure that ventricular excitation occurs only through excitation of the AV node (and no other way). The AV node ensures that the ventricular contraction occurs after a delay so that there is time for atrial contraction to push the final 20-30% of blood into the ventricles for the final stretch of the ventricles which facilitates more tension, thus more pressure for circulation. The ”atrial kick” as this is referred facilitates greater tension and thus pressure during ventricular contraction.

3. 3.

   Each excitation travels from cardiac muscle fiber to the surrounding cardiac muscle fibers due to the presence of intercalated discs that have gap junctions between cardiac muscle fibers (See Figure 10.4. The presence of these gap junctions not only allows, but greatly expedites, the excitation of one fiber to the next. This is fundamentally different from skeletal muscle where each muscle fiber is insulated from nearby muscle fibers by the endomysium. In skeletal muscle this fiber to fiber excitation would be deleterious to controlled, coordinated movement. But in cardiac muscle the fiber to fiber wave of excitation facilitates a synchronized contraction of all atrial, and then ventricular fibers. Such ”all together” contraction facilitates the change in atrial and ventricular chamber size which facilitates the change in pressure necessary for circulation.

An excitation results in full tetany of the myocardium and generates enough tension to generate enough pressure for circulation. For a single excitation to result in full contraction of the atria and then the ventricles requires enough $C{a}^{2+}$ to be released with one excitation for tetany (not just a twitch). There are two related features that allow for this to occur in cardiac muscle.

1. 1.

   The cardiac muscle excitation (action potential) is prolonged (See Figure 10.6). It is prolonged due to specialized voltage gated $C{a}^{2+}$ channels that allow an inward movement of $C{a}^{2+}$ beyond the initiation of the excitation by $N{a}^{+}$. The prolonged excitation occurs all the way down to the SR which continues to release $C{a}^{2+}$.

2. 2.

   Prolonged SR release of $C{a}^{2+}$ into the cell also contributes to the prolonged excitation of the membrane itself (a positive feedback system).

The primary take away message is that an excitation of a cardiac muscle fiber is prolonged due to inward movement of $C{a}^{2+}$ across the sarcolemma, which leads to prolonged SR release of $C{a}^{2+}$ for activation that also promotes prolonged excitation.

Warning: Cardiac $C{a}^{2+}$ Pharmacological Targets

Based on the importance of $C{a}^{2+}$ in both prolonged excitation and activation of cardiac muscle fibers it is not surprising that medications influencing $C{a}^{2+}$ make up two major classes of cardiovascular medications. $C{a}^{2+}$-channel blockers decrease the influx from the membrane (anti-arrhythmic) or the SR (anti-hypertensive); and digitalis, which increases the presence of $C{a}^{2+}$ in the cardiac muscle fiber.

Cardiac reflexes influence HR and contractility and can be divided into four general categories: baroreflex (pressure) which was discussed in Chapter 9, Bainbridge reflex (stretch), chemoreflex (chemical reflex), ergoreflex (ergoreceptors).

The major coronary arteries include the left coronary (LCA) which quickly branches into the left anterior descending (LAD) and left circumflex (LCx); and the right coronary artery RCA) (See Figure 10.7). LAD distributes the anterior wall of both ventricles (L ¿ R) including the septum. LCx the left lateral and posterior walls. LAD and LCx join for distribution in the inferior myocardium. RCA distributes to the anterolateral, lateral, posterior and inferior RV. The RCA and LCA are the first two vessels off of the aorta. Blood is pumped to these large superficial coronary arteries during ventricular systole. At this time, myocardial contraction limits the flow of blood to the myocardium; therefore myocardial tissue is perfused during diastole.