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Part I
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Introduction
Cardiac Anatomy, Physiology,
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andExam
RichardMusialowski andKristaAllshouse
1
Embryologic Development
The fetal heart begins as a simple tube in the third
week of gestation and develops to a four chambered beating structure by approximately week 7
to 8 [1]. Valves develop according to their location in the embryonic tube and differentiate from
the ventricle they arise within. The right ventricle
(RV) will always produce a three to four leaet
tricuspid valve (TV). The left ventricle (LV) will
always produce a two-leaet mitral valve (MV).
Septation occurs dividing both the atria and ventricles into two separate and genetically different
pairs.
Septation of the embryonic atria creates two
independent chambers with a small residual communication called the foramen ovale. Placental
blood (oxygenated) is preferentially shunted
across this structure into the left atrium, LV, and
into the fetal aorta. At delivery, the LA pressure
exceeds the RA pressure and closes this connection. Fifteen percent of the population will have a
persistent patent foramen ovale (PFO) into
adulthood.
R. Musialowski
Sanger Heart and Vascular Institute, Atrium Health,
Charlotte, NC, USA
e-mail: Richard.musialowski@atriumhealth.org
K. Allshouse (*)
Atrium Health, Levine Childrens’ Congenital Heart
Center, Charlotte, NC, USA
e-mail: Krista.allshouse@atriumhealth.org
The great vessels (aorta and pulmonary
artery) arise from the aortic arch. Through septation, the pulmonary artery and aorta divide into
two separate vessels. These tubes are in continuation with the developing and rotating ventricles.
These vessels create the semilunar valves seen in
the aortic and pulmonic positions. The coronary
arteries arise above the semilunar valves in the
developing aorta. A connection persists between
the aorta and pulmonary artery during fetal
development, called the ductus arteriosus. This
structure empties blood from the uninated fetal
lungs and pulmonary artery into the aorta in
utero. The spontaneous breathing of the infant
after birth causes a subsequent fall in the pulmonary vascular resistance (PVR) and the removal
of the placenta causes an increase in systemic
vascular resistance (SVR), resulting in abrupt
closure of the ductus, creating two separate circuits: pulmonary (unoxygenated) and systemic
(oxygenated).
Abnormalities during development can occur
at any point, resulting in a variety of congenital
cardiac defects. The advancement of surgical
techniques and medical therapies have improved
the survival of patients with congenital heart disease, and many are now living well into adulthood (see Chap. 29).
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
R. Musialowski, K. Allshouse (eds.), Cardiovascular Manual for the Advanced Practice Provider,
https://doi.org/10.1007/978-3-031-35819-7_1
3
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R. Musialowski and K. Allshouse
Excitation Contraction Coupling
(ECC)
Each cardiac cycle is a rapid process of electrical depolarization and muscle contraction with active electrical
repolarization and muscle relaxation. The timing is
well organized, and deviations of this process may
result in distinct cardiac dysfunction (Diagram 1).
ECC begins with the spontaneous phase 4
depolarization of pacemaker cells due to the
inux of sodium and calcium ions, i.e. the funny
current [2]. This is known as automaticity and
cells with this characteristic are present within
the sinoatrial node (SAN), atrial tissue, atrioventricular (AV) node, and ventricular myocytes.
The speed of spontaneous depolarization determines the heart rate, and thus the P-to-P interval.
Once the depolarization meets a threshold, phase
0 of the action potential begins (Fig. 1.1).
Propagation of the electrical impulse on the cell
membrane alters the chemical structure of trans-
membrane proteins called voltage-gated channels. These channels are ion-specic and allow
additional sodium and calcium ions into the cell,
specically at the T-tubule. The impulse then
spreads to surrounding cells via gap junctions,
microtubule structures that allow sodium and calcium ions to rapidly ow to the next cell. This ion
ow spreads rapidly throughout the whole heart
so that when one cell is depolarized, all cells
become depolarized at a speed of 0.5m/s!
At this point, the electrical excitation is completed, and repolarization begins with shifts of
other ions (mainly potassium) out of the cell.
This reset of the transmembrane potential or
refractory period is essential for the next impulse
to occur. This is seen as phase 3 on the action
potential and is associated with the QT interval
on EKG. Energy expenditure in the form of ATP
within the membrane exchange pumps is essential in this process. When the calcium enters the
cell in phase 2 of the action potential, it binds to
Diagram 1
A
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Action Potential
2
0
2+
Ca
i
4
Ca
influx
2+
Ca
ADP
+
3Na
+
2K
AT P
Fig. 1.1 Phase 4 depolarization is spontaneous due to the
funny current that determines the heart rate [2]. Phase 0
depolarization is due to rapid sodium inux that occurs
after opening of voltage-gated channels due to the funny
current depolarization. During phase 2, calcium ions
inux as well. These calcium ions are essential to cause
the muscle contraction necessary for cardiac function.
The force line is the representation of muscle contraction.
Electrical repolarization (phase 3) is occurring during
mechanical contraction. Calcium homeostasis is regulated
by the sarcoplasmic reticulum that releases and resets the
gradients for the next contraction [3]. Adapted from
Figure1Cell calcium 2020 Jan; 85:102129
Na
SR
+
Force
0.1 s
3
Ca extrusion
+
3Na
1Ca
release
Ca
Ca
uptake
+
H
Na
2+
+
the ryanodine receptors on sarcoplasmic reticulum which releases a ood of calcium throughout
the muscle cells (Diagram 1).
Cardiac muscle brils are made up of thick
myosin and thin actin laments. Intertwined
between these two structures is a protein complex called tropomyosin. This structure is composed of multiple proteins with specic
responsibilities. Troponin T is bound to the
tropomyosin, troponin C, and troponin
5
I. Troponin I can restrict the actin and myosin
interaction while in the resting state. Troponin C
binds the excitation released calcium ions causing a loosening of the troponin I/actin complex
revealing the myosin-binding sites.
In the resting state, the myosin heads have
ADP and inorganic phosphate bound to them. The
calcium-troponin directed transformation of
tropomyosin causes the presentation of the actin
binding sites. Interaction of the actin and myosin
heads releases the bound ADP and inorganic
phosphate creating cytosolic ATP. This release
causes a conformational change in the myosin
head resulting in the sliding of the actin and myosin by each other called the “power stroke” and
contraction results. Contraction is coordinated in
every cell at the same time! The reformed cytosolic ATP now binds to the contracted myosin
heads and the molecule is split back to ADP and
phosphate. This energy expenditure results in
myosin conformation changes and the brils slide
back, thus establishing the resting state. Calcium
is pumped back into the SR against a gradient by
sarcoplasmic reticulum calcium ATPase
(SERCA2A), occurring during phase 3 and repolarization of the action potential (Diagram 1).
This whole process from the initiation within
the sinus node to propagation to the AV node
takes less than 180ms, or the PR interval. This
is the moment the atria contract. This same
impulse proceeds into the ventricle in the same
ECC process with resultant QRS of 80ms and
ventricular contraction. The repolarization of
the ventricle (refractory period) takes about
300 ms and corresponds to the QT interval.
Phase 4 of the action potential is reached and
the cycle begins again.
Alterations in the SERCA2 calcium homeostasis are pathologic in HfrEF and the diastolic dysfunction of HFpEF [4]. Since diastole requires
molecular energy, disease states that reduce cellular energy (i.e., ischemia) alter calcium homeostasis and impair diastolic function (see Sect. 5).
Sympathetic nervous system innervation alters calcium ows thus increasing heart rate and contractility. Antiarrhythmic medications alter the action
potential resulting in changes in conduction, repolarization, and ekg morphology (see Chap. 7).
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R. Musialowski and K. Allshouse
Conduction System
The specialized cells of the sinoatrial node (SAN)
are located in the upper portion of the right atrium
near the entrance to the superior vena cava. The
impulse arises due to automaticity of these cells
and propagates through the atria. In the crux or
center of the heart, there is brous tissue surrounding the atrioventricular node (AVN). This brous
tissue acts as a brake to slow down and organize
the impulse. The organized impulse proceeds
through the bundle of His and continues down the
right and left bundles. The left bundle then splits
into the left anterior fascicle which is a relatively
organized structure and a diffuse left posterior fascicle. These bundles are cardiac cells that have differentiated for electrical conduction [5]. Blood
supply is important to the function of this system
and coronary ischemia can cause electrical abnormalities resulting in both tachycardia and bradycardia. Metabolic abnormalities can also alter
function of this system (see the EP Section).
Electrocardiogram (EKG or ECG)
The normal QRS complex on an EKG is seen
in Fig.1.2. This is a graphic representation of
the electrical impulse and conduction of a car-
diac cycle. The P wave originates in the SA
node and is the rst waveform of the cardiac
cycle. It is associated with atrial contraction.
The beginning of the P wave to the deection
of the QRS is called the P-R interval. This is
the time the impulse starts in the sinus node,
propagates across the atria, and is slowed down
in the AV node. This interval approximates AV
node function. Normal is less than 200 ms.
(Longer than this time suggests AV node
dysfunction.)
The QRS is the impulse proceeding through to
the right and left bundles to depolarize the ventricles, normally taking 80–100ms. Pathology of
the conduction system and ventricles causes this
interval to widen. Medication and abnormal metabolic states also affect the QRS duration.
The QT segment corresponds to phase 3 of the
action potential and is associated with repolarization of the ventricle. Atrial repolarization is hidden in the QRS complex. This interval is heart
rate dependent. It is also inuenced by many
medications, pathology, and autonomic inuences. This interval is important in the assessment and management of ventricular
arrhythmias.
The P to P and R to R intervals are used to
discuss rhythm interpretation. These intervals
link different cardiac cycles together.
Fig. 1.2 Normal EKG with intervals
Ante
e
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Cardiac Anatomy
As stated in the embryology section, two separate
circuits are created during development. The right
atrium (RA) and ventricle (RV) are separated by a
three to four leaet structure called the tricuspid
valve (TV). The RV is continuous with the pulmonary artery and its pulmonary valve. Deoxygenated
blood enters the RA and is pumped to the lungs
for oxygenation. After pulmonary capillary oxygenation, the blood collects into the left atrium
(LA) from the pulmonary veins. The left ventricle
(LV) receives the oxygen- rich blood after it
crosses a two leaet valve called the mitral valve
(MV). Ventricular systole moves blood through
the left ventricular out ow tract (LVOT) into the
aorta opening the aortic valve. Tissue perfusion
throughout the body occurs and the deoxygenated
blood returns to the RA through the superior
(SVC) or inferior vena cava (IVC) (Fig.1.4). A
detailed discussion of the important hemodynamic features is contained in Chap. 2.
The atrioventricular valves (AV) and its apparatus have specic functions necessary to generate stroke volume and thus cardiac output.
Papillary muscles are structures that are part of
the myocardial wall whose role is to contract during ventricular systole and pull the valve leaets
close to avoid regurgitation of blood backward
into the atria. The mitral valve has two muscles,
one medially and one laterally. The anterior and
posterior leaets are attached to the papillary
muscles by chordae tendineae. The leaets of the
MV are further described by their individual
cusps (Fig.1.3). Abnormalities in any part of this
apparatus will result in pathology of the valve
opening and closure. This is discussed in detail in
the Sect. 4 on structural heart disease.
The tricuspid valve is similar with papillary
muscles, chordae tendineae, and leaets. There is
a septal, anterior, and posterior leaet.
The center or crux of the heart is an important
crossroad of electrical and mechanical cardiac
function (Fig.1.4). The AVN is located within the
membranous septum. It is located near the septal
leaet of the TV and below the right and noncoronary cusps of the AV annulus. Also, the septal attachments of the MV anchor here as well. In
Fig.1.3, the approximation of the atrioventricular
and semilunar valves is seen. These valves are all
anchored in the brous crux.
This anatomy is important when infection
occurs as multiple valves may be involved,
increasing mortality. Also, aortic valve endocarditis is associated with acute conduction interruption (see Chap. 19). Intervention of the aortic
valve annulus can be complicated by disruption
of the AVN and bundle branches (see Sect. IV).
Coronary Arteries
Normal coronary artery anatomy is seen in
Fig.1.5 with three epicardial arteries. The left
main artery gives rise to the left anterior
descending (LAD) and left circumex (LCX).
rior semilunar cusp of pulmonary valve
Left semilunar cusp of pulmonary valve
Left semilunar cusp of aortic valve
Fig. 1.3 Nomenclature of the cardiac valves
Anterior cusp of mitral valve
Posterior cusp of mitral valve
AC
RC
LC
RCC
LCC
NCC
A1
P1
A2
A3
P2
P3
A
S
P
Right semilunar cusp of pulmonary valv
Right semilunar cusp of aortic valve
Posterior semilunar cusp of aortic valve
Anterior cusp of tricuspid valve
Posterior cusp of tricuspid valve
Septal cusp of tricuspid valve
8
Pulmonar
Bicuspid (Mitral)
(open)
(closed)
(closed)
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y valve
Tr icuspid valve
R. Musialowski and K. Allshouse
DIASTOLE SYSTOLE
Pulmonary valve
Bicuspid (Mitral) valve
Aortic valve
Tr icuspid valve
valve
Aortic valve
Pulmonary valve
(closed)
Left
ventricle
Bicuspid (Mitral) valve
Fig. 1.4 Work of the heart valves
Right
Left Anterior Descending
Fig. 1.5 Normal coronary anatomy
Aortic valve
(closed)
Tr icuspid valve
(open)
Left Circumflex
Right
ventricle
Pulmonary valve
(open)
Left
ventricle
Bicuspid (Mitral) valve
Aortic valve
(open)
Right
ventricle
Tr icuspid valve
The LAD branches into diagonal vessels. This
vascular distribution is the most important as it
supplies the ventricular septum, which is very
important during ventricular systole to generate
stroke volume and cardiac output. The LCX
branches into marginal vessels. This distribution
is important in blood supply to the posterior
medial papillary muscle supporting the mitral
valve. Ischemia of the RCA and LCX is associated with ischemic mitral regurgitation due to a
single blood supply from the PDA to this muscle. The right coronary artery (RCA) supplies
the SA node. The posterior descending artery
(PDA) arises from the right coronary 80% of the
time and supplies the AV node. Ischemia in the
RCA often results in bradycardia due to ischemia in these nodes.
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Physical Examination
oftheCardiovascular System:
Pearls andTechniques
The stethoscope has two options to listen to the
patient. The at surface is called the diaphragm.
It is best utilized for higher pitched sounds,
including lung and bowel sounds. The other side,
the bell, does not have a diaphragm over the contact area and is open to air. This is best utilized
for lower pitched sounds including S3 and bruits.
It is good practice to listen over an area of interest
with both the bell and the diaphragm to assess for
all frequency of sounds [7]. There are specic
locations on the chest wall to best hear specic
valves. Figures1.6 and 1.7 demonstrate the best
anatomic location and correlation with specic
valves. Every heart sound has different characteristics that need to be assessed during auscultation
(Tables 1.1 and 1.2).
The rst heart sound (S1) is at the beginning
of ventricular systole. The movement of blood
within the heart results in a closure of the mitral
and tricuspid valves. If these atrioventricular
valves are incompetent, blood ows back into the
atria and a murmur will result. The specic
pathology causing the incompetence will decide
the characteristics of the murmur. Mitral and tricuspid regurgitation are traditionally described as
holosystolic as they begin immediately after S1.
The quality is at since the pressure generated in
the ventricles is constant. Mitral valve regurgitation traditionally radiates toward the axilla from
the apex. Tricuspid regurgitation often does not
radiate but increases in intensity with inspiration.
Antegrade systolic ow across a stenotic aortic
and pulmonic valve creates a murmur that
increases in intensity as ow across the valve
increases (crescendo). As the ventricle completes
its contraction, the pressure decreases and the
intensity of the murmur decreases (decrescendo).
Radiation of the systolic murmur is essential to
determine if the pathology is atrioventricular or
semilunar valve.
Fig. 1.6 Areas of auscultation
Fig. 1.7 Heart location within thorax
Table 1.1 Murmur descriptions
Location Area Best Heard (see Fig.1.6)
Timing Systole or diastole: use radial pulse to assist
Pitch High or low
Radiation Where is it directed: neck, back, axilla,
anterior, posterior
Duration Early diastole
Holosystolic
Mid or late systolic
Intensity 1–4 for diastolic (1–3 most common)
1–6 for systolic (2–3/6 most common)
Quality Harsh, soft, blowing, crescendo,
decrescendo
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Table 1.2 Heart Sounds, Respiration, and the Cardiac
Cycle
Systolic Murmur AS, PS, MR, TR
Diastolic
murmur
Both systolic
and diastolic
Diastolic sound Softer S3 after S2, louder S4 before
Second heart
sound and
respiration
A2-P2
interaction
Pericardial
friction rub
Right-sided
murmurs PS, PI,
TR
AI, PI
AS/AI, PS/PI, patent ductus
arteriosus (PDA) “machine like”
S1
Normal splits with inspiration due to
temporary delay P2 closure
Paradoxical splits in expiration due
to LBBB and delayed A2 closure
Fixed split and independent of
respiration due to xed delay of P2
closure from pulmonary
hypertension
Rarely heard and commonly has a
systolic component sounding like
velcro™
All increase in intensity with
inspiration
After the ventricle begins to relax, it causes
negative pressure, opening the AV valves, closing
the pulmonic and aortic (semilunar) valves, and
making the second heart sound (S2). This relaxation is ventricular diastole and all sounds after
S2 are diastolic. Incompetence of the semilunar
valves will cause ow backward into the ventricles immediately following S2 causing a short
diastolic murmur. Diastolic atrioventricular murmurs are rare and out of the scope of this
discussion.
Murmurs should be described by the terms
included in Table 1.1 and should be recorded in
the medical record as such. These include timing,
pitch, radiation, location, duration, quality, and
intensity. Diastolic murmurs are graded on a
scale of 1–4 and systolic murmurs on a scale 1–6.
Grade 1 is barely audible, grade 2 is louder, grade
3 is loud but no thrill is present. Grade 4 is loud
with an associated thrill and grade 5 has a thrill
and can be heard with the stethoscope partially
off the chest. Grade 6 is the loudest, with a thrill
and heard with the stethoscope completely off the
chest.
Remember, normal inspiration causes an
increase in the venous return to the right side of
the heart. This increase in volume and ow
increases the intensity of all right-sided murmurs.
Increased venous return prolongs the right ventricular ejection time, prolonging pulmonic valve
closure (P2) and thus normally splits the second
heart sound. During exhalation, the RV ow
decreases and P2 can disappear with only A2
heard. A LBBB causes the RV to contract and
closes the PV rst. At expiration, the sounds will
be split. With inspiration, the P2 is delayed and
merges with the A2 component and thus no longer split with inspiration. This is paradoxical
splitting. If the pulmonary blood ow or pressure
is chronically elevated, the P2 component is permanently delayed, or xed, in the cardiac cycle.
This is a common nding in ASD or pulmonary
hypertension.
Since the QRS on the EKG is ventricular systole, the rst heart sound occurs shortly after the
QRS, while the diastolic second sound occurs
during ventricular repolarization and after the T
wave (see Fig.1.8).
A fourth heart sound (S4) is usually located
near the heart’s apex over the mitral area. S4 is
relatively short in duration and may occur only
intermittently. It commonly sounds like a split S1
but is located at the apex, away from the atrioventricular valves. It has a lower pitch than S1 and is
best appreciated with the bell. S4 associated with
left atrial systole and is caused by blood entering
a left ventricle already having elevated end diastolic and volume. Therefore, it is appreciated
prior to S1 and within the PR interval. It is associated with hypertensive cardiac disease and may
be intermittent depending on the afterload state
of the patient.
A sequence of S1, S2, S3 is referred to as a ventricular gallop. The S3 is heard shortly after S2 and
before the P wave which is during the rapid and
passive lling phase of the ventricles. It is softer
in intensity and can be intermittently present and
best heard with the bell. This is associated with
ventricular volume and pressure overload. A
right-sided S3 appears and varies with inspiration
due to isolated RV overload as seen in pulmonary
HTN and pulmonary embolus (PE). This is best
herd in the epigastric region (see Chap. 22). Leftsided S3 does not vary with respiration and is
associated with HFrEF (see Chap. 20).
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11
Fig. 1.8 Heart sounds in relation to EKG. Adapted from:
Jessica Shank Coviello DNP, APRN, ANP-BC, ed. 2014.
Auscultation Skills: Breath & Heart Sounds - 5th Ed.
Philadelphia, PA. Lippincott Williams & Wilkins. ISBN-
Bruit:
Blood ow within a vessel that is obstructed
creates a sound due to the higher velocity and turbulence created by the obstruction. It is like
obstructing the ow at the end of a garden hose.
The sound is higher pitched and radiated toward
the direction of ow. It is not a murmur since this
examination is occurring in the neck, legs, or
abdominal location. It is systolic in nature.
Rarely, diastolic or continuous sounds can be
heard. When listening to the neck vessels, the
bruit must be distinguished from aortic stenosis
(AS) since this murmur will often radiate to the
carotid arteries (see Chaps. 16 and 26).
Pulse Assessment
A scale from 0 to 4 is utilized. No palpable pulse
is 0/4 with normal being 4/4. Commonly, the
extremities are evaluated in assessment for
peripheral arterial disease (PAD). Signs of
10: 1–4511–8999-0, ISBN-13: 978–1–4511-8999-5.
STAT!Ref Online Electronic Medical Library. https://
online.statref.com/document/- GdzwbJZ8Qx3IotUtwjgnD
chronic arterial insufciency and specic arterial
examination are discussed in Chap. 27. The
pulses can be described as bounding in hyperdynamic states or in clinical presentation with prolonged runoff due to low afterload (see Chap.
16).
Peripheral Edema:
This is displacement of serous uids outside
the vascular space into the interstitial tissues. It is
characterized based on the severity when
depressed on a scale from 1 to 4. Commonly seen
in the legs but can progress in some disease states
like Cor pulmonale (see Chap. 22). If it is present
diffusely throughout the body of the patient, it is
called anasarca.
References
1. Sadler TW.Langman’s medical embryology. 14th ed.
Philadelphia: Wolters Kluwer; 2019.
2. DiFrancesco D.The role of the funny current in pacemaker activity. Circ Res. 2010;106:434–46.
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