Rapid Ejection (Phase 3)

Aortic and Pulmonic Valves Open; AV Valves Remain Closed

Cardiac cycle

 

 

 

 

 

 

 

http://www.cvphysiology.com/Heart%20Disease/HD002a.htm

 

Pressure Changes

The cardiac cycle diagram shown to the right depicts changes in aortic pressure (AP), left ventricular pressure (LVP), left atrial pressure (LAP), left ventricular volume (LV Vol), and heart sounds during a single cycle of cardiac contraction and relaxation. These changes are related in time to the electrocardiogram. An online video and tutorial of the cardiac cycle from the Health Education Assets Library is available: cardiac cycle video.

Aortic pressure is measured by inserting a pressure-measuring catheter into the aorta from a peripheral artery, and the left ventricular pressure is obtained by placing a catheter inside the left ventricle and measuring changes in intraventricular pressure as the heart beats. Left atrial pressure is not usually measured directly, except in investigational procedures; however, left atrial pressure can be estimated by recording the pulmonary capillary wedge pressure. Ventricular volume changes can be assessed in real time using echocardiography or radionuclide imaging, or by using a special volume conductance catheter placed within the ventricle.

1. Pre-Load - degree of stretch of cardiac muscle (venricle) before they contract is the critical factor controlling stroke volume (Frank-Starling Law od the Heart)

2. Contractility - cardiac cell contractile force due to factors other than EDV

3. Afterload - back pressure exerted by blood in the large aerteries leaving the heart

4. Slow heartbeat and exercise increase venous return to the heart, increasing stroke volume

5. Blood loss and extremely rapid heartbeat decrease stroke volume

 

Historical Perspective

One of the most fundamental causes of variations in stroke volume was described by William Howell in 1884 and by Otto Frank in 1894 and formally stated by E. H. Starling in 1918. These investigators demonstrated that, with other factors being equal, if cardiac filling increases during diastole, the volume ejected during systole also increases. As a consequence, stroke volume increases nearly in proportion to increases in end-diastolic volume. This phenomenon is commonly referred to as Starling’s law of the heart.

Image not available.

Starling’s law of the heart.

Starling’s law is a direct consequence of the intrinsic mechanical properties of cardiac muscle cells. The primary consequence is that stroke volume (and therefore cardiac output) is strongly influenced by cardiac filling during diastole. Factors that affect cardiac filling affect the regulation of cardiac output.

 

Cardiac function is influenced by neural inputs from both the sympathetic and parasympathetic divisions of the autonomic nervous system. These inputs allowmodifification of cardiac pumping as is appropriate to meet changing homeostatic needs of the body.

All portions of the heart are richly innervated by adrenergic sympathetic fibers. When active, these sympathetic nerves release norepinephrine ( noradrenaline) on cardiac cells. Norepinephrine interacts with β1-adrenergic receptors on cardiac muscle cells to increase the heart rate, increase the action potential conduction velocity, and increase the force of contraction and rates of contraction and relaxation. Overall, sympathetic activation acts to increase cardiac pumping.

Cholinergic parasympathetic nerve fibers travel to the heart via the vagus nerve and innervate the SA node, the AV node, and the atrial muscle. When active, these parasympathetic nerves release acetylcholine on cardiac muscle cells. Acetylcholine interacts with muscarinic receptors on cardiac muscle cells to decrease the heart rate (SA node) and decrease the action potential conduction velocity (AV node). Parasympathetic nerves may also act to decrease the force of contraction of atrial (not ventricular) muscle cells. Overall, parasympathetic activation acts to decrease cardiac pumping. Usually, an increase in parasympathetic nerve activity is accompanied by a decrease in sympathetic nerve activity, and vice versa.

 

 

 

  1. The contractions of individual cardiac muscle cells must occur at regular intervals and be synchronized (not arrhythmic).

  2. The valves must open fully (not stenotic).

  3. The valves must not leak (not insufficient or regurgitant).

  4. The muscle contractions must be forceful (not failing).

  5. The ventricles must fill adequately during diastole.

 

 

 

 

Factors determining myocardial oxygen supply and demand. 

Extraction of O2 from arterial blood is maximal at rest. As demand increases (with exercise or hemodynamic stress), the oxygen supply to the myocardium must also increase. Oxygen supply is determined by the oxygen content of arterial blood and by coronary blood flow.

The oxygen content of blood is dependent on hemoglobin-bound oxygen and, to a lesser extent, dissolved oxygen. Although a high hemoglobin level gives the blood high oxygen-carrying capacity, the minimum level of hemoglobin necessary to avoid ischemia has not been well defined in clinical studies. Factors that affect this limit include the severity of coronary artery disease, the heart rate, perfusion pressure, and myocardial wall thickness and tension. Furthermore, actual delivery of oxygen to myocardial tissue is dependent on release of oxygen from hemoglobin according to the oxyhemoglobin dissociation curve. A leftward shift of this curve caused by alkalosis, hypothermia, or low levels of 2,3,-diphosphoglycerate (which may be observed after the transfusion of a large volume of stored autologous blood) will decrease the release of oxygen.

The duration of diastole is another important factor affecting oxygen supply to the myocardium because 70% to 80% of coronary arterial blood flow occurs during the diastolic phase of the cardiac cycle. During the systolic phase, cardiac contraction increases intraventricular cavitary pressure and coronary vascular resistance, thus impeding myocardial perfusion. There is a nonlinear relationship between heart rate and the duration of diastole.The total time per minute spent in diastole is a function of the heart rate. This is a major reason for the use of β-blockers as anti-ischemic agents both for long-term therapy and for preventing even small increases in heart rate during the perioperative period.

Determinants of blood flow in normal coronary arteries include the pressure differential across the coronary bed (coronary perfusion pressure) and coronary vascular resistance. The coronary perfusion pressure for the left ventricle is the aortic blood pressure during diastole minus left ventricular end-diastolic pressure (LVEDP); thus, elevations in LVEDP impede subendocardial blood flow. Because coronary stenosis causes vessels to dilate maximally distal to the stenosis, manipulation of coronary perfusion pressure becomes an important factor determining coronary blood flow (and preventing or treating myocardial ischemia). However, because the determinants of myocardial oxygen balance are complex, altering any one of them can produce multiple effects. For example, an increase in blood pressure increases coronary blood flow but also increases afterload, thereby increasing wall tension and oxygen demand.

In anesthetized patients undergoing anesthesia for coronary revascularization, vigilant monitoring for myocardial ischemia is necessary throughout the perioperative period.

Pulmonary artery (pressure and flow)

Pulmoinary vein (pressure and flow)

Coronary artery pressure and time of flow)

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Detailed Video of the Cardiac Cycle

 

The cardiac cycle is usually divided into seven phases. The first phase begins with the P wave of the electrocardiogram, which represents atrial depolarization, and is the last phase of diastole. Phases 2-4 represent systole, and phases 5-7 represent early and mid-diastole. The last phase of the cardiac cycle ends with the appearance of the next P wave, which begins a new cycle. 
Image not available.

 

Detailed descriptions of each phase can be obtained by clicking on each of the seven phases listed below.

 

 

http://www.cvphysiology.com/Heart%20Disease/HD002a.htm

 

 cardiac cycle video.

Aortic pressure is measured by inserting a pressure-measuring catheter into the aorta from a peripheral artery, and the left ventricular pressure is obtained by placing a catheter inside the left ventricle and measuring changes in intraventricular pressure as the heart beats. Left atrial pressure is not usually measured directly, except in investigational procedures; however, left atrial pressure can be estimated by recording the pulmonary capillary wedge pressure. Ventricular volume changes can be assessed in real time using echocardiography or radionuclide imaging, or by using a special volume conductance catheter placed within the ventricle.

 

Volume of blood pumped by the heart each minute; approximately 3.5–5.5 L/min (adult). CO is standardized to patient size by calculation of the cardiac index (CI): CI = CO/BSA; normal CI ≈ 2.8–3.2 L/min/m2. CI < 2.5 L/min/m2 may require pharmacologic intervention if O2 delivery is inadequate.

CO is the product of heart rate and stroke volume.

Stroke volume is a function of preload, afterload, and contractility.

1. Pre-Load -

Initial length of myocardial muscle fibers is proportional to left ventricular end-diastolic volume (LVEDV), which is governed by the volume of blood remaining in the left ventricle after systole.

As LVEDV increases, the stretch on myocardial muscle fibers increases. Furthermore (Figure, top), as LVEDV increases (ie, stretch), the energy of contraction increases proportionally until an optimal tension develops (Starling law; Figure, middle). However, when the myocardial muscle fiber is overstretched, contractile strength decreases.

Image not available.

Representation of Starling law. PAOP = pulmonary artery occlusion pressure.

 

degree of stretch of cardiac muscle (venricle) before they contract is the critical factor controlling stroke volume (Frank-Starling Law od the Heart)

2. Contractility -

Cardiac cell contractile force due to factors other than EDV; Ability of heart to alter its contractile force and velocity independent of fiber length (ie, the intrinsic strength of the individual muscle fiber cells). Contractility may be increased by stimulation of beta-receptors in the heart (see following section).

3. Afterload

Resistance to ventricular ejection; measured clinically with aortic BP and calculation of systemic vascular resistance (SVR).

 

[4. Slow heartbeat and exercise increase venous return to the heart, increasing stroke volume

5. Blood loss and extremely rapid heartbeat decrease stroke volume]

 

Sympathetic Nervous System Influence on the Cardiovascular System

CO and its determinants (preload, afterload, and contractility) are influenced by the sympathetic nervous system (SNS). The SNS releases catecholamines (predominantly epinephrine and norepinephrine), which bind to end-organ receptors and exert a physiologic response.

Adrenergic receptors are divided into two major classes: alpha (α) and beta (β). Summary End-organ function after receptor activation.

Adrenergic Receptors and Their Actions on the Cardiovascular System
Receptor Location Action
Alpha (α)1 Peripheral arterioles Vasoconstriction (increased SVR)
Beta (β)1 Myocardium Increased contractility
SA node Increased heart rate
Beta (β)2 Peripheral arterioles Vasodilatation (decreased SVR)
Bronchiolar smooth muscle Bronchodilatation

Adrenergic receptors are important because many of the cardiovascular drugs used in the ICU act through their sympathomimetic properties. Such drugs have a specific receptor affinity (ie, α versus β) and consequently differ in end-organ effects. For example, drugs that act on the α1 receptors are called vasopressors because they cause nonspecific systemic vasoconstriction. Conversely, drugs that act on β1 receptors are called inotropesbecause they increase myocardial contractility and heart rate.

Because each drug exerts receptor-specific effects, use of these agents provides differential activation of receptors and ultimately end-organ effects. Through tailoring pharmacologic support, physicians provide the necessary cardiovascular assistance to critically ill patients. Commonly used sympathomimetics and their relative receptor affinities are listed in Table 20–2. A guide to administration of these agents appears in Table 20–11.

SVR = systemic vascular resistance; SA = sinoatrial.
Relative Actions of Sympathomimetic Drugs on Adrenergic Receptors
Effect On
Drug α β1 β2 D
Phenylephrine ++++ 0 0
Norepinephrine ++++ ++ 0
Epinephrine ++++ ++++ ++
Dobutamine + ++++ ++
Isoproterenol 0 ++++ +++
Dopamine (mcg/kg/min) 10–20 5–10 1–5

Key: + = Relative effect; 0 = no clinically significant effect; D=dopaminergic receptors.