How does gas exchange take place

1. CARDIOVASCULAR
SYSTEM
(THE “HEART”)

2. ANATOMY of the HEART
Location
Layers of the Heart
Chambers
Valves
Coronary Vessels

3. Location…
• A hollow, cone-shaped muscular organ, about the size of
a fist.
– Size: roughly 5” (12.5 cm) long and 3 ½” (9 cm) wide
– Weight: typically 9-12 oz. (255-340 g)
• The heart is located in the chest, behind the sternum in
the mediastinal cavity (or mediastinum), between the
lungs, and in front of the spine.
• Heart lies tilted in this area like an upside-down triangle.
• The top of the heart, or its base, lies just below the
second rib; the bottom of the heart, or its apex, tilts
forward and down, toward the left side of the body, and
rests on the diaphragm.

4. Layers of the HEART
• Epicardium – outer layer w/c forms the visceral layer of the serous
percardium; squamous epithelial cells
• Myocardium – middle layer; cardiac muscles that contracts in each
heartbeat.
• Endocardium – innermost layer; endothelial tissues w/ small blood
vessels and bundles of smooth muscles.
PERICARDIUM = connective tissue layer surrounding the heart and acts
as a tough protective sac.
• Fibrous pericardium
• Serous pericardium – parietal & visceral layers
PERICARDIAL SPACE = contains 10-20 ml (or up to 30 ml) clear
pericardial fluid; lubricates the 2 surfaces and cushions the heart.

6. The Inside of the Heart…
“Chambers and Valves”

8. 4 Chambers
Right Atrium
Left Atrium
Right Ventricle
Left Ventricle
• The left ventricle is responsible for the apex beat or the point
of maximum impulse (PMI), which is normally palpable in the:
left midclavicular line of the chest wall at the 5th intercostal
space.
Serves as the pumping chambers of the
heart; thicker because they generate greater
pressures during systole.
Serves as volume reservoirs for blood being
sent into the ventricles; thin-walled because
blood returning to these chambers
generates low pressures.

10. HEART VALVES
• serve as one-way doors that keep blood flowing
through the heart in a forward direction.
• valves open and close in response to changes in
pressure within the chambers they connect.
Atrioventricular (AV) valves
= separates the atria and ventricles.
Semilunar valves
= prevents backflow of blood to the ventricles

11. When the valves close, they prevent backflow, or
regurgitation, of blood from one chamber to another.
The closing of the valves creates the heart sounds
that are heard through a stethoscope.
AV valves:
• Tricuspid – RA & RV
• Mitral – LA & LV
Semilunar valves:
• Aortic – Aorta & LV
• Pulmonary – Pulmonary trunk and RV

13. The heart has large metabolic requirements, extracting approximately 70% to
80% of the oxygen delivered (other organs consume, on average, 25%).
Coronary Arteries:
• originate from the aorta just above the aortic valve leaflets. Unlike other
arteries, the coronary arteries are perfused during diastole. An increase in
heart rate shortens diastole and can decrease myocardial perfusion.
• left and right coronary arteries and their branches supply arterial blood to the
heart.
The left coronary artery has three branches:
• Left main coronary artery – artery from the point of origin to the first major.
• Left anterior descending artery
• Circumflex artery
The right side of the heart is supplied by the right coronary artery, which
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.
BLOOD FLOW THROUGH THE HEART

15. Coronary Veins:
• Superficial to the coronary arteries are the coronary veins.
• Cardiac veins collect deoxygenated blood from the capillaries of
the myocardium. Venous blood from these veins returns to the
heart primarily through the coronary sinus, which is located
posteriorly in the right atrium.
Circulation to the heart still guaranteed…
• When two or more arteries supply the same region, they usually
connect through anastomoses (junctions that provide alternative
routes of blood flow).
• This network of smaller arteries, called collateral circulation,
provides blood to capillaries that directly feed the heart muscle.
• Collateral circulation commonly becomes so strong that even if
major coronary arteries become clogged with plaque, collateral
circulation can continue to supply blood to the heart.

16. PHYSIOLOGY OF THE
CV SYSTEM
1. Systemic vs. Pulmonary Circulation
2. Cardiac Hemodynamics
3. Control of SV and HR
4. Transmission of Electrical Impulses
5. Depolarization-repolarization Cycle
6. Conduction System of the Heart

17. Systemic vs. Pulmonary Circulation

18. Cardiac Cycle
During one heartbeat:
• ventricular diastole (relaxation)
• ventricular systole (contraction)
During diastole:
• ventricles relax,
• atria contract,
• blood is forced through the open tricuspid and mitral valves.
• aortic and pulmonic valves are closed.
During systole:
• Atria relax and fill with blood.
• Mitral and tricuspid valves are closed.
• Ventricular pressure rises, which forces open the aortic and pulmonic valves.
• Ventricles contract, and blood flows through the circulatory system.

21. Atrial kick
• The atrial contraction, or atrial kick, contributes
about 30% of the cardiac output.
• Certain arrhythmias, such as atrial fibrillation, can
cause a loss of atrial kick and a subsequent drop in
cardiac output.
• Tachycardia also affects cardiac output by shortening
diastole and allowing less time for the ventricles to
fill. Less filling time means less blood will be ejected
during ventricular systole and less will be sent
through the circulation.

22. Cardiac Output (CO)
• the amount of blood pumped by the ventricles in 1 minute.
• CO = SV x HR
• Normal cardiac output is 4 to 8 L/minute (5 L/min), depending on body size.
STROKE VOLUME (SV) = the amount of blood ejected with each ventricular
contraction
• Three factors affect stroke volume:
– preload,
– afterload, and
– myocardial contractility.
• A balance of these three factors produces optimal cardiac output.
• The average resting stroke volume is about 70 mL, and the heart rate is 60 to
80 beats per minute (bpm).
• Cardiac output can be affected by changes in either stroke volume or heart
rate.

23. Control of Stroke Volume
Preload
• stretching of muscle fibers in the ventricles and is determined by the
pressure and amount of blood remaining in the left ventricle at the
end of diastole.
Afterload
• amount of pressure the left ventricle must work against to pump
blood into the circulation. The greater this resistance, the more the
heart works to pump out blood.
Contractility
• the ability of muscle cells to contract after depolarization. This ability
depends on how much the muscle fibers are stretched at the end of
diastole. Overstretching or understretching these fibers alters
contractility and the amount of blood pumped out of the ventricles.

25. Reflex Control of Heart Rate:
• Autonomic nervous system (ANS):
– Sympathetic (adrenergic) and Parasympathetic
(cholinergic).
• SNS – heart’s accelerator
• norepinephrine and epinephrine—increase HR,
automaticity, AV conduction, and contractility.
• PNS – serves as the heart’s brakes.
• One of this system’s nerves, the vagus nerve, carries
impulses that slow HR and the conduction of impulses
through the AV node and ventricles.
• Releases the chemical acetylcholine, slowing the HR.

26. • HR is stimulated also by an increased level of circulating
catecholamines (secreted by the adrenal gland) and by excess
thyroid hormone, which produces a catecholamine-like effect.
CNS and baroreceptor activity.
• Baroreceptors are specialized nerve cells located in the aortic
arch and in both right and left internal carotid arteries (at the
point of bifurcation from the common carotid arteries).
• The baroreceptors are sensitive to changes in blood pressure
(BP).
• During elevations in BP (hypertension), these cells increase
their rate of discharge, transmitting impulses to the medulla.
• This initiates parasympathetic activity and inhibits
sympathetic response, lowering the heart rate and the BP. The
opposite is true during hypotension (low BP).

27. Transmission of Electrical Impulses
Generation and transmission of electrical impulses
depend on four characteristics of cardiac cells:
• Automaticity = refers to a cell’s ability to spontaneously
initiate an impulse. Pacemaker cells possess this ability.
• Excitability = results from ion shifts across the cell
membrane and indicates how well a cell responds to
an electrical stimulus.
• Conductivity = is the ability of a cell to transmit an
electrical impulse to another cardiac cell.
• Contractility = refers to how well the cell contracts
after receiving a stimulus.

28. Depolarization vs. Repolarization
• As impulses are transmitted, cardiac cells undergo cycles of
depolarization and repolarization.
• Cardiac cells at rest are considered polarized, meaning that no
electrical activity takes place. Cell membranes separate different
concentrations of ions, such as sodium and potassium, and create
a more negative charge inside the cell. This is called the resting
potential.
• After a stimulus occurs, ions cross the cell membrane and cause an
action potential, or cell depolarization.
• When a cell is fully depolarized, it attempts to return to its resting
state in a process called repolarization. Electrical charges in the
cell reverse and return to normal.
• A cycle of depolarization-repolarization consists of five phases—0
through 4. The action potential is represented by a curve that
shows voltage changes during the five phases.

29. • Phase 0 – the cell receives an impulse from a neighboring cell
and is depolarized.
• Phase 1 – is marked by early, rapid repolarization.
• Phase 2 – the plateau phase, is a period of slow repolarization.
• During phases 1 and 2 and at the beginning of phase 3, the
cardiac cell is said to be in its absolute refractory period.
During that period, no stimulus, no matter how strong, can
excite the cell.
• Phase 3 – the rapid repolarization phase, occurs as the cell
returns to its original state. During the last half of this phase,
when the cell is in its relative refractory period, a very strong
stimulus can depolarize it.
• Phase 4 – is the resting phase of the action potential. By the
end of phase 4, the cell is ready for another stimulus.
• All that electrical activity is represented on an
electrocardiogram (ECG). Keep in mind that the ECG represents

32. Cardiac muscle, unlike skeletal or smooth muscle, has a prolonged refractory period
during which it cannot be restimulated to contract.
Two Phases of the Refractory Period:
• absolute refractory period = is the time during which the heart cannot be
restimulated to contract regardless of the strength of the electrical stimulus. This
period corresponds with depolarization and the early part of repolarization.
• relative refractory period = During the latter part of repolarization, however, if
the electrical stimulus is stronger than normal, the myocardium can be
stimulated to contract. This short period at the end of repolarization is called the
relative refractory period.
• Refractoriness protects the heart from sustained contraction (tetany), which
would result in sudden cardiac death.
• Normal electromechanical coupling and contraction of the heart depend on the
composition of the interstitial fluid surrounding the heart muscle cells. In turn,
the composition of this fluid is influenced by the composition of the blood. A
change in serum calcium concentration may alter the contraction of the heart
muscle fibers. A change in serum potassium concentration is also important,
because potassium affects the normal electrical voltage of the cell.

33. Conducting Pathways of the Heart
• After depolarization and repolarization occur,
the resulting electrical impulse travels through
the heart along a pathway called the
conduction system.
• Impulses travel out from the SA node and
through the internodal tracts and Bachmann’s
bundle to the AV node. From there, they travel
through the bundle of His, the bundle
branches, and lastly to the Purkinje fibers.

35. Cardiac Conduction System
Sinoatrial (SA) node
• The primary pacemaker of the heart, is located at the
junction of the superior vena cava and the right atrium.
• SA node in a normal resting heart has an inherent firing
rate of 60 to 100 impulses per minute, but the rate can
change in response to the metabolic demands of the body.
• When initiated, the impulses follow a specific path through
the heart. They usually can’t flow backward because the
cells can’t respond to a stimulus immediately after
depolarization.
• Bachmann’s bundle of nerves: Impulses from the SA node
next travel through Bachmann’s bundle, tracts of tissue
extending from the SA node to the left atrium.

36. Atrioventricular (AV) node
• located in the inferior right atrium near the ostium of the coronary
sinus, is responsible for delaying the impulses that reach it.
• Although the nodal tissue itself has no pacemaker cells, the tissue
surrounding it (called junctional tissue) contains pacemaker cells that
can fire at a rate of 40 to 60 times per minute.
• The AV node’s main function is to delay impulses by 0.04 second to
keep the ventricles from contracting too quickly. This delay allows the
ventricles to complete their filling phase as the atria contract.
• It also allows the cardiac muscle to stretch to its fullest for peak cardiac
output.
Bundle of His
• a tract of tissue extending into the ventricles next to the
interventricular septum, resumes the rapid conduction of the impulse
through the ventricles.
• The bundle eventually divides into the right and left bundle branches.

37. • The right bundle branch extends down the right side of the
interventricular septum and through the right ventricle.
• The left bundle branch extends down the left side of the
interventricular septum and through the left ventricle.
• The left bundle branch then splits into two branches, or fasciculi:
the left anterior fasciculus, which extends through the anterior
portion of the left ventricle, and the left posterior fasciculus, which
runs through the lateral and posterior portions of the left ventricle.
• Impulses travel much faster down the left bundle branch (which
feeds the larger, thicker-walled left ventricle) than the right bundle
branch (which feeds the smaller, thinner- walled right ventricle).
• The difference in the conduction speed allows both ventricles to
contract simultaneously. The entire network of specialized nervous
tissue that extends through the ventricles is known as the His-
Purkinje system.

38. Purkinje fibers
• Purkinje fibers extend from the bundle branches into the
endocardium, deep into the myocardial tissue.
• These fibers conduct impulses rapidly through the
muscle to assist in its depolarization and contraction.
• Purkinje fibers can also serve as a pacemaker and are
able to discharge impulses at a rate of 20 to 40 times per
minute, some times even more slowly.
• Purkinje fibers usually aren’t activated as a pacemaker
unless conduction through the bundle of His becomes
blocked or a higher pacemaker (SA or AV node) doesn’t
generate an impulse.

40. ASSESSMENT
History
Inspection
Palpation
Auscultation

41. Subjective-Review
• Chief Complaint
• History of the present illness
• Past medical history
• Injuries/immunizations
• Medications
• Allergies
• Surgeries
• Hospitalizations
• Family history
• Social history
– Diet
– Exercise
– Smoking
– Caffeine
– Alcohol
– Nicotine
– Marrital Status
– Occupation

42. Cardiac Signs and Symptoms
Patients with cardiovascular disorders commonly have one or
more of the following signs and symptoms:
• 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 and syncope or loss of consciousness (postural
hypotension, dysrhythmias, vasovagal effect, cerebrovascular
disorders)

43. • Gordon’s 11 Functional Health Patterns:
 Health perception and management
 Nutrition and metabolism
 Elimination
 Activity and exercise
 Sleep and rest
 Cognitive and perception
 Self-perception and self-concept
 Roles and relationships
 Sexuality and reproduction
 Coping and stress tolerance
 Spiritual and Cultural beliefs

44. PHYSICAL ASSESSMENT
• In addition to observing the patient’s general appearance, a
cardiac physical examination should include an evaluation of
the following:
 • Effectiveness of the heart as a pump
 • Filling volumes and pressures
 • Cardiac output
 • Compensatory mechanisms
• Indications that the heart is not contracting sufficiently or
functioning effectively as a pump include:
– reduced pulse pressure,
– cardiac enlargement, and
– murmurs and gallop rhythms (abnormal heart sounds).

45. • The examination, which proceeds logically from
head to toe, can be performed in about 10 minutes
with practice and covers the following areas:
(1) general appearance,
(2) cognition,
(3) skin,
(4) BP,
(5) arterial pulses,
(6) jugular venous pulsations and pressures,
(7) heart,
(8) extremities,
(9) lungs, and
(10) abdomen.

46. General Appearance and Cognition
• level of distress,
• level of consciousness, and
• thought processes.
• Observe for evidence of anxiety, along with
any effects emotional factors may have on
cardiovascular status.

47. Inspection of the Skin
• Pallor—a 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, and
oral mucosa. In patients with dark skin, the nurse observes the
palms of the hands and soles of the feet.
• Peripheral cyanosis—a bluish tinge, most often of the nails and
skin of the nose, lips, earlobes, and 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 peripheral vasoconstriction associated
with a cold environment, in patients with anxiety, or in disease
states such as HF.
• Central cyanosis—a bluish tinge observed in the tongue and
buccal mucosa—denotes serious cardiac disorders (pulmonary
edema and congenital heart disease) in which venous blood
passes through the pulmonary circulation without being
oxygenated.

48. • Xanthelasma—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 (hypercholesterolemia).
• Reduced skin turgor occurs with dehydration and aging.
• Temperature and moistness are controlled by the autonomic nervous
system. 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.
• Ecchymosis (bruise)—a purplish-blue color fading to green, yellow, or brown
over time—is 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 clotting times (prothrombin or partial
thromboplastin time) caused by an anticoagulant dosage that is too high.
• Wounds, scars, and tissue surrounding implanted devices should also be
examined. Wounds are assessed for adequate healing, and any scars from
previous surgeries are noted. The skin surrounding a pacemaker or
implantable cardioverter defibrillator generator is examined for thinning,
which could indicate erosion of the device through the skin.

49. Blood Pressure
Systemic arterial BP is the pressure exerted on the walls of the arteries during
ventricular systole and diastole.
• It is affected by factors such as cardiac output, distention of the arteries, and
the volume, velocity, and viscosity of the blood.
• BP usually is expressed as the ratio of the systolic pressure over the diastolic
pressure, with normal adult values ranging from 100/60 to 140/90 mm Hg.
• average normal BP = 120/80 mm Hg
• An increase in BP above the upper normal range is called hypertension,
whereas a decrease below the lower range is called hypotension.
PULSE PRESSURE
• The difference between the systolic and the diastolic pressures.
• It is a reflection of stroke volume, ejection velocity, and systemic vascular
resistance.
• Pulse pressure, which normally is 30 to 40 mm Hg, indicates how well the
patient maintains cardiac output.

50. Arterial Pulses
• As the ventricles eject blood into he arteries, a
pressure wave is transmitted and can be felt in the
superficial arteries passing over bone. This pressure
waves is called PULSE.
• Factors to consider in assessing the pulse:
– Rate
– Rhythm
– Volume
– Character
• Common arterial pulses being examined are: radial,
brachial, carotid, femoral, popliteal, posterior tibial,
and dorsalis pedis.

51. Pulse Rhythm
• Minor variations in regularity of the pulse are normal. The pulse
rate, particularly in young people, increases during inhalation
and slows during exhalation. This is called sinus arrhythmia.
• For the initial cardiac examination, or if the pulse rhythm is
irregular, the heart rate should be counted by auscultating the
apical pulse for a full minute while simultaneously palpating the
radial pulse. Any discrepancy between contractions heard and
pulses felt is noted.
• Disturbances of rhythm (dysrhythmias) often result in a pulse
deficit, a difference between the apical rate (the heart rate
heard at the apex of the heart) and the peripheral rate.
• Pulse deficits commonly occur with atrial fibrillation, atrial
flutter, premature ventricular contractions, and varying degrees
of heart block.

52. PULSE QUALITY
• The quality, or amplitude, of the pulse can be described as absent,
diminished, normal, or bounding. It should be assessed bilaterally.
• Scales can be used to rate the strength of the pulse. The following is
an example of a 0-to-4 scale:
 0 pulse not palpable or absent
 +1 weak, thready pulse; difficult to palpate;
 obliterated with pressure
 +2 diminished pulse; cannot be obliterated
 +3 easy to palpate, full pulse; cannot be obliterated
 +4 strong, bounding pulse; may be abnormal
• The numerical classification is quite subjective; therefore, when
documenting the pulse quality, it helps to specify a scale range (eg,
“left radial +3/+4”).

53. Jugular Venous Pulsations
• An estimate of right-sided heart function can be made by observing the
pulsations of the jugular veins of the neck.
• This provides a means of estimating central venous pressure, which reflects
right atrial or right ventricular end-diastolic pressure (the pressure
immediately preceding the contraction of the right ventricle).
• Pulsations of the internal jugular veins are most commonly assessed. If they
are difficult to see, pulsations of the external jugular veins may be noted.
These veins are more superficial and are visible just above the clavicles,
adjacent to the sternocleidomastoid muscles. The external jugular veins are
frequently distended while the patient lies supine on the examining table or
bed. As the patient’s head is elevated, the distention of the veins disappears.
The veins normally are not apparent if the head of the bed or examining table
is elevated more than 30 degrees.
• Obvious distention of the veins with the patient’s head elevated 45 degrees to
90 degrees indicates an abnormal increase in the volume of the venous
system. This is associated with right-sided HF, less commonly with obstruction
of blood flow in the superior vena cava, and rarely with acute massive
pulmonary embolism.

54. Heart Inspection and Palpation
• Examination of the chest wall is performed in the following six areas:
1. Aortic area—second intercostal space to the right of the sternum. To
determine the correct intercostal space, start at the angle of Louis by
locating the bony ridge near the top of the sternum, at the junction of the
body and the manubrium. From this angle, locate the second intercostal
space by sliding one finger to the left or right of the sternum. Subsequent
intercostal spaces are located from this reference point by palpating down
the rib cage.
2. Pulmonic area—second intercostal space to the left of the sternum
3. Erb’s point—third intercostal space to the left of the sternum
4. Right ventricular or tricuspid area—fourth and fifth intercostal spaces to
the left of the sternum
5. Left ventricular or apical area—the PMI, location on the chest where
heart contractions can be palpated
6. Epigastric area—below the xiphoid process

57. Apical Pulse
(Left ventricular) Lift or Heave = broad and forceful apical impulse It is
so named because it appears to lift the hand from the chest wall
during palpation.
Left Ventricular Enlargement = apical impulse below the fifth intercostal
space or lateral to the midclavicular line; due to left ventricular
failure. Normally, the apical impulse is palpable in only one intercostal
space; palpability in two or more adjacent intercostal spaces indicates
left ventricular enlargement.
Thrill = abnormal, turbulent blood flow within the heart may be
palpated with the palm of the hand as a purring sensation; is
associated with a loud murmur.
= is always indicative of significant pathology within the heart.
= also may be palpated over vessels when blood flow is significantly
and substantially obstructed and over the carotid arteries if aortic
stenosis is present or if the aortic valve is narrowed.

58. HEART SOUNDS
Normal Heart Sounds:
S1 and S2 (Systole) = are produced primarily by the closing of the
heart valves.
S2 and S1 (Diastole)
• As the heart rate increases, diastole shortens.
• In normal physiology, the periods of systole and diastole are silent.
• Ventricular disease, however, can give rise to transient sounds in
systole and diastole that are called gallops, snaps, or clicks.
MURMURS = prolonged sounds produced when there is significant
narrowing of the valve orifices at times when they should be open,
or residual gapping of valves at times when they should be closed.

59. Heart Sounds
• S1—First Heart Sound = is produced by the closing of
the mitral and tricuspid valves and is best heard at the
apex of the heart (left ventricular or apical area).
• S2—Second Heart Sound = is produced by the closing of
the aortic and pulmonic valves and is loudest at the base
of the heart.
• The time between S1 and S2 corresponds to systole. The
time between S2 and S1 is diastole.

60. Abnormal Heart Sounds
Gallops = third heart sound (S3 or S4)
– An S3 gallop is heard immediately following the S2 and occurs when the blood filling the
ventricle is impeded during diastole, resulting in temporary vibrations. The heart sounds
come in triplets and resemble the sound of a galloping horse. Myocardial disease and heart
failure are associated with this sound.
– An S4 gallop is heard immediately preceding the S1. The S4 sound occurs during atrial
contraction and is often heard when the ventricle is enlarged or hypertrophied. Associated
conditions include coronary artery disease, hypertension, and stenosis of the aortic valve.
Snaps and Clicks:
• Opening snaps= Stenosis of the mitral valve resulting from rheumatic heart disease
gives rise to an unusual sound very early in diastole that is high-pitched and is best
heard along the left sternal border. The sound is caused by high pressure in the left
atrium with abrupt displacement of a rigid mitral valve. It occurs too long after S2 to
be mistaken for a split S2 and too early in diastole to be mistaken for a gallop. It
almost always is associated with the murmur of mitral stenosis and is specific to this
disorder.
• Ejection clicks= In a similar manner, stenosis of the aortic valve gives rise to a short,
high-pitched sound immediately after S1. This is caused by very high pressure within
the ventricle, displacing a rigid and calcified aortic valve.

62. • Murmur = created by the turbulent flow of blood. The causes
of the turbulence may be a critically narrowed valve, a
malfunctioning valve that allows regurgitant blood flow, a
congenital defect of the ventricular wall, a defect between
the aorta and the pulmonary artery, or an increased flow of
blood through a normal structure (eg, with fever, pregnancy,
hyperthyroidism).
• Friction Rub = In pericarditis, a harsh, grating sound that can
be heard in both systole and diastole is called a friction rub. It
is caused by abrasion of the pericardial surfaces during the
cardiac cycle. Because a friction rub may be confused with a
murmur, care should be taken to identify the sound and to
distinguish it from murmurs that may be heard in both
systole and diastole. A pericardial friction rub can be heard
best using the diaphragm of the stethoscope, with the
patient sitting up and leaning forward.

63. Inspection of the Extremities
The hands, arms, legs, and feet are observed for skin and vascular
changes. The most noteworthy changes include the following:
• Decreased capillary refill
• Vascular changes from decreased arterial circulation include
decrease in quality or loss of pulse, discomfort or pain,
paresthesia, numbness, decrease in temperature, pallor, and
loss of movement.
• Hematoma, or a localized collection of clotted blood in the
tissue
• Peripheral edema is fluid accumulation in dependent areas of
the body (feet and legs, sacrum in the bedridden patient).
• Clubbing of the fingers and toes
• Lower extremity ulcers

64. Other Systems
LUNGS
Findings frequently exhibited by cardiac patients include the following:
• Tachypnea: Rapid, shallow breathing may be noted in patients who have HF or
pain, and in those who are extremely anxious.
• Cheyne-Stokes respirations: Patients with severe left ventricular failure may
exhibit Cheyne-Stokes breathing, a pattern of rapid respirations alternating
with apnea. It is important to note the duration of the apnea.
• Hemoptysis: Pink, frothy sputum is indicative of acute pulmonary edema.
• Cough: A dry, hacking cough from irritation of small airways is common in
patients with pulmonary congestion from HF.
• Crackles: HF or atelectasis associated with bed rest, splinting from ischemic
pain, or the effects of pain medications and sedatives often results in the
development of crackles. Typically, crackles are first noted at the bases
(because of gravity’s effect on fluid accumulation and decreased ventilation of
basilar tissue), but they may progress to all portions of the lung fields.
• Wheezes: Compression of the small airways by interstitial pulmonary edema
may cause wheezing. Beta-adrenergic blocking agents (beta-blockers), such as
propranolol (Inderal), may precipitate airway narrowing, especially in patients
with underlying pulmonary disease.

65. ABDOMEN
For the cardiac patient, two components of the abdominal examination are
frequently performed.
• Hepatojugular reflux: Liver engorgement occurs because of decreased
venous return secondary to right ventricular failure. The liver is enlarged,
firm, nontender, and smooth. The hepatojugular reflux may be
demonstrated by pressing firmly over the right upper quadrant of the
abdomen for 30 to 60 seconds and noting a rise of 1 cm or more in jugular
venous pressure. This rise indicates an inability of the right side of the heart
to accommodate increased volume.
• Bladder distention: Urine output is an important indicator of cardiac
function, especially when urine output is reduced. This may indicate
inadequate renal perfusion or a less serious problem such as one caused by
urinary retention. When the urine output is decreased, the patient needs to
be assessed for a distended bladder or difficulty voiding. The bladder may be
assessed with an ultrasound scanner or the suprapubic area palpated for an
oval mass and percussed for dullness, indicative of a full bladder.