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Key components of the cardiovascular assessment include: • Obtaining a health history • Performing a physical assessment • Monitoring a variety of laboratory and diagnostic test results
• The heart is a hollow, muscular organ located in the center of the thorax, where it occupies the space between the lungs (mediastinum) and rests on the diaphragm
• It weighs approximately 300 g, although heart weight and size are
influenced by age, gender, body weight, extent of physical exercise and conditioning, and heart disease. The heart pumps blood to the tissues, supplying them with oxygen and other nutrients
• During systole (contraction of the muscle), the chambers of the heart become smaller as the blood is ejected
• During diastole (relaxation of the muscle), the heart chambers fill with blood in preparation for the subsequent ejection
• A normal resting adult heart beats approximately 60-80/m
• Each ventricle ejects approximately 70 mL of blood per beat • Cardiac output is approximately 5 L per minute
• The inner layer, or endocardium, consists of endothelial tissue and lines the inside of the heart and valves
• The middle layer, or myocardium, is made up of muscle fibers and is responsible for the pumping action
• The exterior layer of the heart is called the epicardium
• The heart is encased in a thin, fibrous sac called the pericardium, which is composed of two layers
• Adhering to the epicardium is the visceral pericardium
• Enveloping the visceral pericardium is the parietal pericardium, a tough fibrous tissue that attaches to the great vessels, diaphragm, sternum, and vertebral column and supports the heart in the mediastinum
• The space between these two layers (pericardial space) is filled with about 30 mL of fluid, which lubricates the surface of the heart and reduces friction during systole
• The varying thicknesses of the atrial and ventricular walls relate to:
• The atria are thin-walled because
• The ventricular walls are thicker because
• The RV has thinner walls than the left ventricle
• The LV, with walls 2.5 times more muscular than those of the RV
• RV lies anteriorly (just beneath the sternum) • LV is situated posteriorly • LV is responsible for the apex beat or the point of maximum impulse
(PMI)
Point of Maximum impulse locates Left border of the heart
Typically at or just medial to the left midclavicular line The PMI may not be readily felt in a healthy patient with a normal heart, however
• The four valves in the heart permit blood to flow in
• The valves, which are composed of thin leaflets of fibrous tissue,
open and close in response to the movement of blood and pressure changes within the chambers
• There are two types of valves:
The valves that separate the atria from the ventricles are termed • Atrioventricular valves
The tricuspid valve, so named because
It is composed of three cusps or leaflets, separates the right atrium from the right ventricle
The mitral, or bicuspid (two cusps) valve, lies between the left atrium and the left ventricle
The two semilunar valves are composed of three half moonlike leaflets The valve between the right ventricle and the pulmonary artery Called the pulmonic valve
The valve between the left ventricle and the aorta
Called the aortic valve
The left and right coronary arteries and their branches supply arterial blood to the heart
These arteries originate from the aorta just above the aortic valve leaflets.
The heart has large metabolic requirements, extracting approximately of the oxygen delivered
Diastole
Heart Rate
Left Main Coronary Artery The artery from the point of origin
to the first major branch (5)
Two bifurcations arise off the left main coronary artery
LADA: Left Anterior Descending Artery, which courses down the anterior wall of the heart (3)
CA: Circumflex Artery, which circles around to the lateral left wall of the heart (4)
The right side of the heart is supplied by the right coronary artery progresses around to the bottom or inferior wall of the heart The posterior wall of the heart receives its blood supply by an additional branch from the right coronary artery called the posterior descending artery
Superficial to the coronary arteries are the coronary veins
Venous blood from these veins returns to the heart primarily through the coronary sinus, which is located posteriorly in the right atrium
Microscopically, myocardial muscle resembles striated (skeletal) muscle, which is under conscious control Functionally, however, myocardial muscle resembles smooth muscle because its contraction is involuntary
The myocardial muscle fibers are arranged in an interconnected manner (called a syncytium) that allows for coordinated myocardial contraction and relaxation
Three physiologic characteristics of the cardiac conduction cells account for this coordination:
ability to initiate an electrical impulse
ability to respond to an electrical impulse
ability to transmit an electrical impulse from one cell to another
Referred to as the primary pacemaker of the heart, is located at the junction of the superior vena cava and the right atrium Normal resting heart has an inherent firing rate of 60 to 100 impulse/Min
The AV node coordinates the incoming electrical impulses from the atria and, after a slight delay (allowing the atria time to contract and complete ventricular filling) relays the impulse to the ventricles
Left bundle branch bifurcates into: The left anterior bundle branches
and The left posterior bundle branches
Impulses travel through the bundle branches to reach the terminal point in the conduction system, called the Purkinje fibers
This is the point at which the myocardial cells are stimulated, causing ventricular contraction
The heart rate is determined by the myocardial cells with the fastest inherent firing rate Under normal circumstances
The SA node has the highest inherent rate, the AV node has the second highest inherent rate (40 to 60 impulses per minute)
Ventricular pacemaker sites have the lowest inherent rate (30 to 40 impulses per minute) If the SA node malfunctions, the AV node generally takes over the pacemaker function of the heart at its inherently lower rate Should both the SA and the AV nodes fail in their pacemaker function, a pacemaker site in the ventricle will fire at its inherent bradycardic rate of 30 to 40 impulses per minute
1. Preload 2. Afterload 3. Contractility
Degree of stretch of the cardiac muscle fibers at the end of diastole The end of diastole is the period when
and
The volume of blood within the ventricle at the end of diastole determines preload
Preload has a direct effect on stroke volume
Return of circulating blood volume to the ventricles Controlling the loss of blood or body fluids Replacing fluids Blood transfusions Intravenous fluid administration
• volume of blood returning to the ventricles
•Preload
Diuresis Venodilating agents (eg, nitrates) Loss of blood or body fluids from excessive Diaphoresis Vomiting Diarrhea
The amount of resistance to ejection of blood from the ventricle Systemic Vascular Resistance
The resistance of the systemic BP to left ventricular ejection
Pulmonary Vascular Resistance The resistance of the pulmonary BP to right ventricular ejection
There is an inverse relationship between afterload and stroke volume Arterial vasconstriction AfterLoad Stroke Volume Arterial Vasodilation AfterLoad Stroke Volume
Afterload
Stroke Volume
The force generated by the contracting myocardium under any given condition Contractility is enhanced by
Circulating Catecholamines Sympathetic Neuronal Activity Certain Medications
Digoxin Intravenous dopamine Dobutamine
Contractility is depressed by oHypoxemia oAcidosis oCertain medications
Beta-adrenergic blocking agents such as atenolol Contractility Stroke Volume
During Exercise: Preload
(through increased venous return)
Increasing contractility (through sympathetic nervous system discharge)
Decreasing afterload (through peripheral vasodilation with decreased aortic pressure)
Changes in cardiac structure and function are clearly observable in the older heart To understand the changes specifically related to aging, it is helpful to
distinguish the normal aging process from changes related to CVD
Structural Change Functional Change History & Physical
finding
↑ Size of left atrium
Thickening of the
endocardium
↑ Atrial irritability Irregular heart rhythm
from atrial
dysrhythmias
Structural Change Functional Change History & Physical
finding
Endocardial fibrosis
Myocardial thickening
(hypertrophy)
Infiltration of fat into
myocardium
Left ventricle stiff and
less Compliant
Progressive decline in
cardiac Output
↑ Risk for ventricular
dysrhythmias
Prolonged systole
Fatigue
↓ Exercise tolerance
Signs and symptoms of
HF or ventricular
dysrhythmias
PMI palpated lateral to
the midclavicular line
↓ Intensity S1, S2; split S2
S4 may be present
Structural Change Functional Change History & Physical
finding
Thickening and rigidity
of AV Valves
Calcification of aortic
valve
Abnormal blood flow
across valves
during cardiac cycle
Murmurs may be present
Thrill may be palpated if
significant murmur is
present
Structural Change Functional Change History & Physical
finding
Connective tissue collects
in SA node, AV node,
and bundle branches
↓ Number SA node cells
↓ Number AV, bundle of
His, right and left bundle
branch cells
Slower SA node rate of
impulse discharge
Slowed conduction
across AV node and
ventricular conduction
system
Bradycardia
Heart block
ECG changes consistent
with slowed conduction
(↑ PR interval, widened
QRS complex)
Structural Change Functional Change History & Physical
finding
↓ Response to beta
adrenergic stimulation
↓ Adaptive response to
exercise: contractility and
heart rate slower to
respond to exercise
demands
Heart rate takes more
time to return to baseline
Fatigue
Diminished exercise
tolerance
↓ Ability to respond to
stress
Structural Change Functional Change History & Physical
finding
Stiffening of vasculature
↓ Elasticity and widening
of aorta
Elongation of aorta,
displacing the
brachiocephalic artery
upward
Left ventricular
hypertrophy
Progressive increase in
systolic BP;
slight ↑ in diastolic BP
Widening pulse pressure
Pulsation visible above
right clavicle
Structural Change Functional Change History & Physical
finding
↓ Sensitivity of
baroreceptors in the
carotid artery and aorta
to transient episodes of
hypertension and
hypotension
Baroreceptors unable to
regulate heart rate and
vascular tone, causing
slow response to postural
changes in body position
Postural blood pressure
changes and reports
feeling dizzy, fainting
when moving from lying
to sitting or standing
position
Woman’s heart tends to be smaller Woman’s heart has smaller coronary arteries
They occlude from atherosclerosis more easily Making procedures such as cardiac catheterization and angioplasty technically more difficult, with a higher incidence of postprocedure complications
Higher than those of a man’s: Resting rate Stroke volume Ejection fraction
The conduction time of an electrical impulse coursing from the SA node through the AV node to the Purkinje fibers is briefer
Mechanisms that protect women against the development of atherosclerosis by Estrogen Hormone: Regulation of vasomotor tone Response to vascular injury Action on the liver, which results in improved lipid pro files
Increase in coagulation proteins Fibrinolytic protein
In Acute situation you should ask few specific questions about Onset Severity of chest discomfort Associated symptoms Current medications Allergies
With stable patients, a complete health history is obtained
during the initial contact
It is helpful to have the patient’s spouse or partner available during the health history interview During the interview, the nurse conveys sensitivity to the Cultural background Religious practices of the patient
Chest pain or discomfort • Angina pectoris • MI • Valvular heart disease
Shortness of breath or dyspnea MI Left ventricular failure HF
Edema and weight gain • Right ventricular failure • HF
Palpitations • Dysrhythmias resulting from myocardial ischemia • Valvular heart disease • Ventricular aneurysm • Stress • Electrolyte imbalance
Fatigue Earliest symptom associated with several cardiovascular disorders
Dizziness Syncope Loss of consciousness Postural hypotension Dysrhythmias Vasovagal effect Cerebrovascular disorders
Not all chest discomfort is related to myocardial ischemia When a patient has chest discomfort, questions should focus on differentiating: Serious, life threatening condition such as MI from Conditions that are less serious or that would be treated differently
Women are more likely to present with atypical symptoms of MI than are men There is little correlation between the severity of the chest discomfort and the gravity of its cause
There is poor correlation between the location of chest discomfort and its source The patient may have more than one clinical condition occurring simultaneously
The chest discomfort should be assumed to be secondary to ischemia until proven otherwise in patient with positive history
Character, Location and Radiation Duration Precipitating Event Relieving Measures
Substernal or retrosternal pain
spreading across chest; may radiate
to inside of arm, neck, or jaw
5–15 min Usually related to
exertion,
emotion, eating,
cold
Rest,
nitroglycerin,
oxygen
Character, Location and Radiation Duration Precipitating Event Relieving Measures
Substernal pain or pain over
precordium; may spread widely
throughout chest. Pain In
shoulders and hands may be
present
>15 min Occurs
spontaneously
but may be
sequela to
unstable angina
Morphine sulfate,
successful
reperfusion of
blocked coronary
artery
Character, Location and Radiation Duration Precipitating Event Relieving Measures
Sharp, severe substernal pain or pain
to the left of sternum; may be felt in
epigastrium and may Be referred to
neck, arms, and back
Intermittent Sudden onset. Pain
increases with
inspiration,
swallowing,
coughing, and
rotation of trunk.
Sitting upright,
analgesia,
antiinflammatory
medications
Character, Location and Radiation Duration Precipitating Event Relieving Measures
Pain arises from inferior portion of
pleura; may be referred to costal
margins or upper abdomen
Patient may be able to localize the pain
30+ min Often occurs
spontaneously
Pain occurs or
increases with
inspiration
Rest, time.
Treatment of
underlying cause,
bronchodilators
Character, Location and Radiation Duration Precipitating Event Relieving Measures
Substernal pain; may be projected
around chest to shoulders
5–60 min Recumbency, cold
liquids, exercise.
May occur
spontaneously
Food, antacid.
Nitroglycerin
relieves spasm
Character, Location and Radiation Duration Precipitating Event Relieving Measures
Pain over chest; may be variable
Does not radiate.
Patient may complain of
numbness and tingling of hands
and mouth
2–3 min Stress, emotional
tachypnea
Removal of
stimulus,
relaxation
(1) General appearance (2) Cognition (3) Skin (4) BP (5) Arterial Pulses (6) Jugular Venous Pulsations and Pressures (7) Heart (8) Extremities (9) Lungs (10) Abdomen
• Level of distress
• Level of consciousness
• Thought processes (cerebral perfusion)
• Put the anxious patient at ease throughout the examination
Starting: Finishing: with the head and with the lower extremities
Decrease in the color of the skin is caused by lack of Oxyhemoglobin
It is a result of anemia or decreased arterial perfusion Pallor is best observed around the Fingernails Lips Oral mucosa
In patients with dark skin oPalms of the hands oSoles of the feet
Bluish tinge, most often of the Nails Skin of the nose Lips Earlobes Extremities
Suggests decreased flow rate of blood to a particular area, which allows more time for the hemoglobin molecule to become desaturated This may occur normally in
Bluish tinge observed in the tongue and buccal mucosa indicates serious cardiac disorders Pulmonary edema Congenital heart disease
Yellowish, slightly raised plaques in the skin may be observed along the nasal portion of one or both eyelids and may indicate elevated cholesterol levels
Reduced skin turgor occurs with
Normally the skin is warm and dry
Under stress, the hands may become cool and moist
In cardiogenic shock Sympathetic nervous system stimulation causes vasoconstriction, and the skin becomes cold and clammy
During an acute MI, diaphoresis is common
Purplish (blue color fading to green, yellow, or brown over time)
Associated with blood outside of the blood vessels and is usually caused by trauma
Patients who are receiving anticoagulant therapy Should be carefully observed for unexplained ecchymosis In these patients, excessive bruising indicates prolonged CT (PT & PTT) caused by an Anticoagulant dosage that is too high
Wounds are assessed for adequate healing, and any scars from previous surgeries are noted The skin surrounding a pacemaker or ICD generator is examined for thinning, Which could indicate erosion of the device through the skin
97
JVP provide the astute clinician with an important clinical index of
Jugular venous pressure (JVP) reflects right atrial pressure which in turn equals Central venous pressure (CVP)
and
Right ventricular end-diastoli c pressure
The JVP is best estimated from the right internal jugular vein, which has a more direct anatomical channel into the right atrium
Careful observation of changes in these fluctuations also yields clues about Volume status
Right and left ventricular function
Patency of the tricuspid and pulmonary valves
Pressures in the pericardium
Arrhythmias such as junctional rhythms and atrioventricular blocks
you will learn to find
highest point of oscillation in the internal jugular vein
the point above which the external jugular vein appears collapsed
The JVP is usually measured in vertical distance above the sternal angle
A hypovolemic patient may have to lie flat before you see the neck
veins
n contrast, when jugular venous pressure is increased, an elevation up
to 60° or even 90° may be required. In all these positions, the sternal
angle usually remains about 5 cm above the right atrium
Make the patient comfortable. Raise the head slightly on a pillow to relax the sternomastoid muscles
Raise the head of the bed or examining table to about 30°. Turn the patient's head slightly away from the side you are inspecting
Use tangential lighting and examine both sides of the neck. Identify the external jugular vein on each side, then find the internal jugular venous pulsations
If necessary, raise or lower the head of the bed until you can see the oscillation point or meniscus of the internal jugular venous pulsations in the lower half of the neck
Focus on the right internal jugular vein
Look for pulsations in the suprasternal notch, between the attachments of the sternomastoid muscle on the sternum and clavicle, or just posterior to the sternomastoid
Identify the highest point of pulsation in the right internal jugular vein
Extend a long rectangular object or card horizontally from this point and a centimeter ruler vertically from the sternal angle, making an exact right angle
Measure the vertical distance in centimeters above the sternal angle where the horizontal object crosses the ruler
109
Angiography/cardiac catherization determines
Coronary lesion size
Location
Evaluate (L) ventricular function
Measures heart pressures
Exercise tolerance test
Radionuclide Imaging
Myoglobin, an early marker of MI, is a heme protein with a small molecular weight
This allows it to be rapidly released from damaged myocardial tissue and accounts for its early rise, within 1 to 3 hours after the onset of an acute MI. Myoglobin peaks in 4 to 12 hours and returns to normal in 24 hours.
Myoglobin is not used alone to diagnose MI, because elevations can also occur in patients with renal or musculoskeletal disease
However, negative results are helpful in ruling out an early diagnosis of MI.
Troponin I is measured in a laboratory test that has several advantages over traditional enzyme studies
Troponin I is a contractile protein found only in cardiac muscle. After myocardial injury, elevated serum troponin I concentrations can be detected Within 3 to 4 hours; they peak in 4 to 24 hours and remain elevated for 1 to 3 weeks. These early and prolonged elevations make very early diagnosis of MI possible or allow for late diagnosis if the patient has delayed seeking treatment.