ch 20 heart and neck vessels Flashcards
system consists of the heart (a muscular pump) and the blood vessels
cardiovascular (CV)
is the area on the anterior chest directly overlying the heart and great vessels
precordium
heart and great vessels are located between the lungs in the middle third of the thoracic cage
(mediastinum)
lies behind the right ventricle and forms the apex and slender area of the left border.
left ventricle
lies to the right and above the right ventricle and forms the right border
right atrium
is located posteriorly, with only a small portion, the left atrial appendage, showing anteriorly.
left atrium
blood vessels are arranged in two continuous loops, the
pulmonary circulation and the systemic circulation
“top” of the heart is the
base
bottom” is the
apex
During contraction the apex beats against the chest wall, producing an
- fifth intercostal space, 7 to 9 cm from the midsternal line.
apical impulse
lie bunched above the base of the heart.
great vessels
return unoxygenated venous blood to the right side of the heart
superior and inferior vena cava
leaves the right ventricle, bifurcates, and carries the venous blood to the lungs
pulmonary artery
return the freshly oxygenated blood to the left side of the heart
pulmonary veins
carries it out to the body
aorta
is a tough, fibrous, double-walled sac that surrounds and protects the heart
-two layers that contain a few milliliters of serous pericardial fluid. This ensures smooth, friction-free movement of the heart muscle.
pericardium (heart wall has numerous layers)
is adherent to the great vessels, esophagus, sternum, and pleurae and is anchored to the diaphragm.
pericardium
is the muscular wall of the heart; it does the pumping
myocardium
is the thin layer of endothelial tissue that lines the inner surface of the heart chambers and valves.
endocardium
two atrioventricular (AV) valves separate the
atria and the ventricles
right AV valve is the
tricuspid
left AV valve is the
bicuspid or mitral valve
are anchored by collagenous fibers (chordae tendineae) to papillary muscles embedded in the ventricle floor.
valves’ thin leaflets
open during the heart’s filling phase, or diastole, to allow the ventricles to fill with blood
AV valves
, the AV valves close to prevent regurgitation of blood back up into the atria.
-papillary muscles contract at this time so the valve leaflets meet and unite to form a perfect seal without turning themselves inside out.
pumping phase, or systole
are set between the ventricles and the arteries
-. Each valve has three cusps that look like half moons
semilunar (SL) valves
are the pulmonic valve in the right side of the heart and the aortic valve in the left side of the heart. They open during pumping (systole), when blood ejects from the heart.
SL valves
between the vena cava and the right atrium or between the pulmonary veins and the left atrium. For this reason abnormally high pressure in the left side of the heart gives a person symptoms of pulmonary congestion, and abnormally high pressure in the right side of the heart shows in the distended neck veins and abdomen.
no valves
first passive filling phase is called
early or protodiastolic filling.
active filling phase is called
presystole, or atrial systole, or sometimes the atrial kick
atrial systole occurs during
ventricular diastole
ventricular walls contract. This contraction against a closed system works to build pressure inside the ventricles to a high level
(isometric contraction)
closure of the semilunar valves causes the second heart sound
(S2) and signals the end of systole
all four valves are closed, and the ventricles relax
(called isometric or isovolumic relaxation)
pressures in the right side of the heart are much lower than those of the left side because less energy is needed to pump blood to its destination, the
pulmonary circulation
first heart sound the mitral component (M1) closes just before the tricuspid component (T1). And with(diastole) S2, aortic closure (A2) occurs slightly before pulmonic closure (P2).
Events in the Right and Left Sides. (left side close before right)
occurs with closure of the AV valves and thus signals the beginning of systole.
-mitral component of the first sound (M1) slightly precedes the tricuspid component (T1), but you usually hear these two components fused as one sound. You can hear S1 over all the precordium, but usually it is loudest at the apex.
first heart sound (S1)
occurs with closure of the semilunar valves and signals the end of systole. The aortic component of the second sound (A2) slightly precedes the pulmonic component (P2). Although it is heard over all the precordium, S2 is loudest at the base
second heart sound (S2)
That means that during inspiration, intrathoracic pressure is decreased. This pushes more blood into the vena cava, increasing venous return to the right side of the heart, which increases right ventricular stroke volume. The increased volume prolongs right ventricular systole and delays pulmonic valve closure.
Meanwhile on the left side, a greater amount of blood is sequestered in the lungs during inspiration. This momentarily decreases the amount returned to the left side of the heart, decreasing left ventricular stroke volume. The decreased volume shortens left ventricular systole and allows the aortic valve to close a bit earlier. When the aortic valve closes significantly earlier than the pulmonic valve, you can hear the two components separately
split S2.(affected by respiration)
volume of right and left ventricular systole is just about equal, but this can be affected by respiration.
MoRe to the Right heart,
Less to the Left
affected by respiration.
Normally diastole is a silent event. However, in some conditions ventricular filling creates vibrations that can be heard over the chest. These vibrations are S3. S3 occurs when the ventricles are resistant to filling during the early rapid filling phase (protodiastole)(1st part of filling). This occurs immediately after S2, when the AV valves open and atrial blood first pours into the ventricles
Third Heart Sound (S3). (extra heart sound)
S4 occurs at the end of diastole, at presystole, when the ventricle is resistant to filling. The atria contract and push blood into a noncompliant ventricle. This creates vibrations that are heard as S4. S4 occurs just before S1.
S4(extra heart sound)
turbulent blood flow and collision currents
- gentle, blowing, swooshing sound that can be heard on the chest wall
Murmurs
- Velocity of blood increases (flow murmur) (e.g., in exercise, thyrotoxicosis)
- Viscosity of blood decreases (e.g., in anemia)
- Structural defects in the valves (a stenotic or narrowed valve, an incompetent or regurgitant valve) or unusual openings occur in the chambers (dilated chamber, septal defect)
Conditions resulting Murmurs
- Frequency (pitch)—Heart sounds are described as high pitched or low pitched, although these terms are relative because all are low-frequency sounds, and you need a good stethoscope to hear them.
- Intensity (loudness)—Loud or soft
- Duration—Very short for heart sounds; silent periods are longer
- Timing—Systole or diastole
Characteristics of heart Sound
node near the superior vena cava initiate an electrical impulse. (Because the SA node has an intrinsic rhythm, it is the “pacemaker.”)
sinoatrial (SA)
across the atria to the AV node low in the atrial septum.
AV node
conduction system
bundle of His
conduction system
the right and left bundle branches, and then through the ventricles.
P wave—Depolarization of the atria
electrocardiograph (ECG)// electrical impulse stimulates the heart to do its work, which is to contract
PR interval—From the beginning of the P wave to the beginning of the QRS complex (the time necessary for atrial depolarization plus time for the impulse to travel through the AV node to the ventricles)
electrocardiograph (ECG)// electrical impulse stimulates the heart to do its work, which is to contract
QRS complex—Depolarization of the ventricles
electrocardiograph (ECG)// electrical impulse stimulates the heart to do its work, which is to contract
T wave—Repolarization of the ventricles
electrocardiograph (ECG)// electrical impulse stimulates the heart to do its work, which is to contract
is volume—it is the venous return that builds during diastole. It is the length to which the ventricular muscle is stretched at the end of diastole just before contraction
Preload
the greater the stretch, the stronger is the contraction of the heart.
Frank-Starling law
is pressure—it is the opposing pressure the ventricle must generate to open the aortic valve against the higher aortic pressure. It is the resistance against which the ventricle must pump its blood
Afterload
CV assessment
-vessels reflect the efficiency of cardiac function.
carotid artery and the jugular veins
as a pressure wave generated by each systole pumping blood into the aorta
pulse
is a central artery (i.e., it is close to the heart). Its timing closely coincides with ventricular systole.
carotid artery
is located in the groove between the trachea and the sternomastoid muscle, medial to and alongside that muscle
carotid artery
empty unoxygenated blood directly into the superior vena cava
-filling pressure and volume changes. Because volume and pressure increase when the right side of the heart fails to pump efficiently
jugular veins
larger internal jugular lies deep and medial to the sternomastoid muscle.
-not visible, although its diffuse pulsations may be seen in the sternal notch when the person is supine
internal jugular
is more superficial; it lies lateral to the sternomastoid muscle, above the clavicle.
external jugular vein
venous pulse occur because of events in the right side of the heart (no valve in superior vena cava to right aterium)
jugular pulse has 5 components
A wave reflects atrial contraction because some blood flows backward to the vena cava during right atrial contraction.
5 components of the jugular
, is backflow from the bulging upward of the tricuspid valve when it closes at the beginning of ventricular systole (not from the neighboring carotid artery pulsation)
C wave, or ventricular contraction
shows atrial relaxation when the right ventricle contracts during systole and pulls the bottom of the atria downward.
X descent
occurs with passive atrial filling because of the increasing volume in the right atria and increased pressure
V wave
reflects passive ventricular filling when the tricuspid valve opens and blood flows from the RA to the RV.
Y descent
adapts to ensure adequate blood supply to the uterus and placenta, to deliver oxygen and nutrients to the fetus, and to allow the mother to function normally during this altered state
- Blood volume increases by 30% to 50% during pregnancy, most rapid expansion occurring during the second trimester
- arterial BP decreases in pregnancy as a result of peripheral vasodilation. The BP drops to its lowest point during the second trimester and rises after that.
CV system (pregnancy)
fetal heart functions early; it begins to beat at the
end of 3 weeks’ gestation
is more horizontal in the infant than in the adult; thus the apex is higher, located at the fourth left intercostal space (Fig. 20.14). It reaches the adult position when the child reaches age 7 year
heart’s position in the chest (infant)
increase in systolic BP
-caused by thickening and stiffening of the large arteries, which in turn are caused by collagen and calcium deposits in vessel walls and loss of elastic fibers. This stiffening (arteriosclerosis) creates an increase in pulse wave velocity because the less compliant arteries cannot store the volume ejected.
isolated systolic hypertension (Aging)
left ventricular wall thickness increases.
thickens as u age
left ventricular wall thickness increases.
- creates an increased workload on the heart
- Diastolic BP may decrease after the fifth decade.1 Together with a rising systolic pressure, this increases the pulse pressure (the difference between the two).
thickens as u age
No change in resting heart rate occurs with aging.
Cardiac output at rest is not changed with aging.
NO changes occur as u age
decreased ability of the heart to augment cardiac output with exercise. This is shown by a decreased maximum heart rate with exercise and diminished sympathetic response. Noncardiac factors also cause a decrease in maximum work performance with aging: decrease in skeletal muscle performance, increase in muscle fatigue, increased sense of dyspnea. However, aerobic exercise conditioning modifies many of the aging changes in CV function.
CV alterations w/ ageing lifestyle
presence of supraventricular and ventricular dysrhythmias increases with age. Ectopic beats are common in aging people; although these are usually asymptomatic in healthy older people, they may compromise cardiac output and BP when disease is present.
Dysrhythmias.//Aging adult
may not be tolerated as well in older people
-myocardium is thicker and less compliant, and early diastolic filling is impaired at rest. Thus it may not tolerate a tachycardia as well because of shortened diastole.
Tachydysrhythmias ( shortened diastole= higher chance tachy)
- Prolonged P-R interval (first-degree AV block) and prolonged Q-T interval, but the QRS interval is unchanged.
- Left axis deviation from age-related mild LV hypertrophy and fibrosis in left bundle branch.
- Increased incidence of bundle branch block.
Age-related changes in the ECG
is the leading cause of death in those ages 65 years and older
CVD
—no current smoking, no obesity (i.e., BMI <30), physical activity at least once per week, and a healthy diet
four healthful factors (help reduce CVD )
major form of CVD (Cardiovascular disease)
coronary artery disease (CAD)
contributes to CAD because it accelerates the process of atherosclerosis;
increases the workload on the heart, and it increases the oxygen demand on the heart already compromised by atherosclerosis.
hypertension
High levels of low-density lipoprotein (LDL, or the “bad” cholesterol) add to the lipid core of plaque formation in coronary and carotid arteries
-results in MI and stroke.
Serum Cholesterol.