Key components of the cardiovascular assessment include · Key components of the cardiovascular...

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

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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

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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.