BIO 426- The Heart summary notes PDF

Title BIO 426- The Heart summary notes
Author Sherika Morrison
Course Anatomy And Physiology II
Institution Borough of Manhattan Community College
Pages 6
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Summary

This document gives a brief summary of the heart and its function....


Description

BIO 426 Lecture Notes: The Heart (Chapter 19)

Introduction

The heart is located in the mediastinum of the thoracic cavity (between pleural cavities: p.708). The heart has three layers: the epicardium is a serous membrane (visceral pericardium), the myocardium is cardiac muscle tissue with intercalated discs that allow “communication” between neighboring cells, and the endocardium made of epithelium and connective tissue that lines the inside of the four chambers. The pericardium has two layers of serous membrane equivalent to the visceral and parietal pleura associated with the lungs, and the visceral and parietal peritoneum associated with the abdominopelvic organs. The visceral pericardium is the epicardium (see above). The parietal pericardium refers to the serous membrane sac (pericardial sac) that encloses the entire heart (p.692).

Path of Blood Through the Heart and Lungs LECTURE and LAB material.

The heart can be thought of as two pumps working at the same time (p.707). As the right side of the heart receives oxygen-poor blood from the body and sends it to the lungs (pulmonary circulation), the left side of the heart receives oxygen-rich blood from the lungs and sends it out to all parts of the body (systemic circulation). When oxygen binds to hemoglobin in our RBCs to form oxyhemoglobin, the blood appears bright red. After some of the oxygen is given up, the blood takes on a darker reddish-blue coloration. All arteries carry oxygen-rich blood (with one exception) away from the heart and are shown in red. All veins carry oxygen-poor blood (with one exception) towards the heart and are shown in blue. As blood is brought from the heart to all parts of the body, arteries branch into smaller arterioles and arterioles branch into microscopically small/thin vessels called capillaries. Only the capillaries are thin enough to allow exchange of materials ((oxygen, nutrients, water, electrolytes, carbon dioxide, wastes, etc.) between the blood and the cells of the body.

The capillaries then merge to form small venules and the venules merge into larger veins which return the blood to the heart. If we follow a few drops of blood on their path through the heart and lungs, the sequence of vessels, chambers and valves would be as follows (p.695 and p.697): Superior vena cava (SVC) and inferior vena cava (IVC) return oxygen-poor blood to the right atrium (from veins above the heart and below the heart, respectively). Blood in the right atrium (RA) passes through the right atrio-ventricular valve (right AV valve) called the tricuspid valve into the right ventricle (RV). The right ventricle sends blood through the pulmonary semi-lunar valve to the pulmonary arteries (PA) which carry the blood to the lungs. The pulmonary arteries (carrying oxygen-poor blood to the lungs) are the only arteries ever depicted blue! The eight underlined structures are all part of the pulmonary circulation. In the lungs, oxygen is picked up by the pulmonary capillaries and oxygen-rich blood returns to the left atrium (LA) via the pulmonary veins (PV). The pulmonary veins (carrying oxygen-rich blood from the lungs) are the only veins ever depicted red! Blood in the left atrium passes through the left atrio-ventricular valve (left AV valve) called the bicuspid/mitral valve into the left ventricle (LV). The left ventricle sends blood through the aortic semi-lunar valve to the aorta, which carries blood to all the major arteries of the body. The last six underlined structures are all part of the systemic circulation.

THE 14 STRUCTURES OF THE PULMONARY AND SYSTEMIC CIRCULATIONS SHOULD BE LEARNED IN ORDER AND RETAINED IN YOUR MEMORY BANKS FOREVER! YOU SHOULD ALSO BE ABLE TO VISUALIZE BOTH SIDES OF THE HEART FILLING AND EMPTYING AT THE SAME TIME!

The heart has its own circulatory system to ensure that every cell of the heart receives an adequate blood supply. The oxygen-rich coronary arteries branch off the aorta just above the aortic semilunar valve. They then branch into arterioles and capillaries that penetrate through all parts of the heart. The capillaries merge to form venules which combine to form the coronary veins. The oxygen-poor coronary veins empty into the coronary sinus (behind the heart) which

empties into the right atrium (similar to the SVC and IVC). This system of vessels that services the heart itself is called the coronary circulation (p.698).

Cardiac Cycle: Sequence of Contractions and Sounds

The terms systole (contraction) and diastole (relaxation) usually refer to the actions of the ventricles (even though both atria contract and relax as well). The following questions arise concerning the direction of blood flow when the ventricles undergo systole (contract): Why does blood flow from the right ventricle through the pulmonary semilunar valve into the pulmonary arteries and not back up into the right atrium? Similarly, why does blood flow from the left ventricle through the aortic semilunar valve into the aorta and not back up into the left atrium? The answer lies in the fact that on the floor of both ventricles, papillary muscles are connected to tendinous cords (chordae tendineae) which attach to their respective AV valves (p.695, 697). As the ventricles contract, blood is pushed upward, but the tendinous cords are not long enough to allow the AV valves to open back into the atria. Instead, the AV valves shut tightly so that blood can only flow through the semilunar valves. When the ventricles contract, blood flows through the open semilunar valves and the AV valves “slam shut”. The noise made by the closing of the AV valves during ventricular systole is the first sound of the cardiac cycle, the loud “LUBB”. When the ventricles relax, blood previously sent through the semilunar valves tries to “back up”, causing the semilunar valves to close upon themselves. This closing of the semilunar valves during ventricular diastole produces the second sound of the cardiac cycle, the softer “dupp”.

With respect to later discussions of blood pressure, the term systolic pressure refers to the stronger force exerted on the blood when the left ventricle contracts (systole) and sends blood into the aorta and arteries of the body. The term diastolic pressure refers to the weaker force exerted on the blood by the recoil/resistance of the arterial walls during relaxation (diastole) of the left ventricle.

Electrical Conduction System of the Heart

Cardiac muscle tissue can depolarize and repolarize on its own (autorhythmicity or automaticity). If disconnected from neural control, the heart rate would be approximately 100 beats/minute. However, the heart IS connected, and under the neural control of autonomic motor neurons (parasympathetic and sympathetic) that regulate the heart rate. The cardiac center in the medulla oblongata has two sets of neurons that regulate the heart. Parasympathetic motor neurons are in the vagus (X) nerve and release acetylcholine (Ach) onto the heart to keep it at its normal resting rate. Sympathetic motor neurons descend down the spinal cord to the thoracic level and there, cardiac accelerator nerves release norepinephrine (NE) onto the heart to adjust it to emergency or “fight-or-flight” situations. Both sets of autonomic motor neurons form neuromuscular junctions with the heart at the sinoatrial node or SA node, located where the SVC meets the right atrium. However, only one set of neurons will be functioning at a time, depending on the conditions (normal vs. emergency). When the signal arrives, the SA node depolarizes. The depolarization spreads across the atria via the intercalated discs of the cardiac muscle cells until it reaches the atrio-ventricular node or AV node, located at the base of the interatrial septum and the top of the interventricular septum. From the AV node, the depolarization spreads to the ventricles down the AV bundle or Bundle of His in the interventricular septum. Finally, the depolarization spreads from the Bundle of His throughout the ventricles via the Purkinje fibers. This sequence of depolarizations: SA node > AV node > Bundle of His > Purkinje fibers repeats itself over and over again at the rate of the existing heart rate (p.701). The fact that the depolarizations begin at the SA node is why the SA node is called the heart’s “pacemaker”. With electrodes applied to the skin, the pattern of depolarizations and repolarizations can be detected and visualized in the form of an electrocardiogram (ECG or EKG). A typical EKG is shown on p. 705: P wave: depolarization of the atria QRS wave: depolarization of the ventricles T wave: repolarization of the ventricles The reason that there is no separate peak for the repolarization of the atria is because it takes place at the same time that the ventricles are depolarizing. The QRS wave “masks” the event of

atrial repolarization. The clinical significance of the different parts of the EKG are discussed on p.705-707 (for your interest).

Cardiac Output (CMO): Amount of Blood Pumped per Minute

CMO can be measured by Heart Rate (beats/min.) x Stroke Volume (volume/beat). If the average HR = 72beats/min., and the average SV = 70mL/beat:

Average CMO = 72 beats/min. x 70 mL/beat = 5040mL/min. or approximately 5L/min.

Terminology Both atria send equal amounts of blood into both ventricles. Both ventricles send equal amounts of blood into the large arteries (PA and aorta). Emphasis is always on the left ventricle because it sends blood to the aorta and to all parts of the body. The importance of cardiac output is that it reflects the amount of blood flow to the body per minute. When the left atrium contracts (systole), blood fills the left ventricle as it relaxes (diastole). The amount of blood in the left ventricle at the end of relaxation is called End Diastolic Volume or EDV. As the left ventricle contracts, the amount of blood that leaves is called Stroke Volume or SV. The percentage or proportion of EDV that leaves the left ventricle (SV/EDV) is called the Ejection Fraction or EF. Surprisingly, an EF of 50-60% is normal. What remains in the left ventricle after it contracts (systole) is called End Systolic Volume or ESV.

Factors Affecting CMO: Anything that affects heart rate (HR) or stroke volume (SV) will affect CMO. Factors Affecting Heart Rate (HR): Acetylcholine (Ach) from the parasympathetic ns. lowers HR (to normal) and lowers CMO. Norepinephrine (NE) from the sympathetic ns. raises HR and raises CMO.

NE and epinephrine (E) from the adrenal medulla reinforce the sympathetic ns., raise HR and raise CMO. Factors Affecting Stroke Volume (SV): Preload (Frank-Starling Law/Principle): an increase in “preload” will increase SV and increase CMO. Preload refers to the amount of blood entering the right atrium from the SVC and IVC. When needed, the SVC and IVC can dilate and allow extra blood to enter the right atrium. This increase in blood entering the heart will then cause the left ventricle to stretch and fill with extra blood (increase in EDV). When the left ventricle contracts with normal strength, it will pump out extra blood (increase in SV and increase CMO). Contractility: contractility refers to the strength of contraction by the left ventricle. NE and E can cause the left ventricle to contract more strongly (increase in contractility) without an increase in EDV and, thereby, pump out more blood (increase in SV and increase CMO). NE and E cause increases In HR and SV and greatly increase CMO! Afterload: afterload refers to the resistance in the arteries that the heart must overcome to pump out normal SV. An increase in afterload (example: due to a build-up of fatty deposits in the arterial walls) will narrow the diameter of the arteries, increase the resistance and make it more difficult for the heart to pump out blood (decrease in SV and decrease in CMO). The goal is to be able to maintain adequate CMO. An individual (above example) with chronic increased afterload and reduced SV could only maintain normal CMO by increasing heart rate. However, in the long run, this can overwork the heart and cause additional problems later. In contrast, a physically fit individual with a strong heart and higher than normal SV can maintain normal CMO with a slower heart rate than a less fit individual....


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