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R. Musialowski and K. Allshouse
3. Hilgemann DW. Control of cardiac contraction by
sodium: Promises, reckonings, and new beginnings.
Cell Calcium. 2020;85:102129.
4. Chien KR, Ross J Jr, Hoshijima M.Calcium and hert
failure: the cycle game. Nat Med. 2003;9:508–9.
5. Josephson’s Clinical Cardiac Electrophysiology:
Techniques and Interpretations 6th Edition by Dr.
David Callans. Publisher, LWW.
6. Zipes DP, Libby P, Bonow RO, Mann DL, Tomaselli
GF, Braunwald E, editors. Braunwald’s heart disease:
a textbook of cardiovascular medicine, Single Volume.
11th ed. Philadelphia, PA: Elsevier; 2019.
7. Coviello JS, editor. Auscultation skills: breath & heart
sounds. 5th ed. Philadelphia, PA: Lippincott Williams
& Wilkins; 2014.
Basic Hemodynamics
CO LSVH
()
=×
S
VP
−
PV
−
EF
=×100
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CourtneyBennett andAmandaSolberg
2
Cardiac Cycle
The cardiac cycle is divided into two phases: systole and diastole (Fig. 2.1). The Wiggers diagram
demonstrates the pressure and volume changes
throughout the cardiac cycle and how these
changes correlate with the ECG and cardiac auscultation (S1-S4).
Systole occurs when the AV valves close (S1)
and the ventricles begin to contract (see Chap. 1).
During systole, ventricular pressure increases
through isovolumetric contraction and rapid ejection, and then begins to fall during isovolumetric
relaxation. The onset of systole correlates with
the R-wave on the ECG.Blood volume is ejected
through the pulmonic and aortic valves (sometimes referred to as semilunar valves) into the
systemic and pulmonary vasculature. Stroke volume (SV) is the amount of blood pumped out of
the ventricle during each systolic contraction. A
normal stroke volume is 70–80mL.The volume
of blood remaining in the ventricular chamber
after ejection is called the end systolic volume.
The cardiac output (CO) is the SV times the
heart rate (HR). CO is the volume of blood
pumped by both ventricles per unit of time. In a
normal resting heart, this would be approximately 5–6L per minute. Cardiac index (CI) is
C. Bennett · A. Solberg (*)
Mayo Clinic, Rochester, MN, USA
e-mail: Bennett.Courtney@mayo.edu;
Solberg.Amanda@mayo.edu
the cardiac output divided by body surface area
(L/min/M sq). This is a standardization tool used
especially in the management of cardiogenic
shock and transplantation.
The ejection fraction (EF) is the proportion of
end-diastolic volume that is ejected during each
systolic contraction and is commonly used as a
noninvasive assessment of stroke volume.
Afterload, or the pressure the ventricle pumps
against, can affect stroke volume. Systemic vascular resistance (SVR) impacts the left ventricle
while pulmonary vascular resistance (PVR)
impacts the right. These pressures are calculated
using the mean arterial pressure minus the CVP
or mean pulmonary artery pressure minus the
PCWP divided by the CO. These measurements
and calculations are obtained from a right heart
catheterization or pulmonary artery catheter
(Swan-Ganz) catheter placement. Normal hemodynamic values are listed in Table2.1.
VR Wood U
()
RWood U
()
()
Diastole occurs when the ventricles relax and
pressure within the ventricles decreases. The ini-
%
=
mPAP PCWP
=
SV
EDV
R/min
MAPC
CO
CO
© 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_2
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Fig. 2.1 Wiggers
diagram showing a
visual representation of
the cardiac cycle
showing heart sounds,
pressure, left ventricular
(LV) volume, and ECG
comparison during.
Permission from http://
creativecommons.org/
licenses/by/4.0/
C. Bennett and A. Solberg
Table 2.1 Normal hemodynamic values
RA pressure 0–8mmHg
PA diastolic
PA systolic
PA mean
PCWP 6–15mmHg
CO 4–7L/min
CI 2.5–3.6L/min/m
SVR 800–1200 dynes/cm
SVRI 1970–2390 dynes/cm2/m
PVR 0.5–2 Woods units (W.U.)
SvO2 65–75%
15–30mmHg
4–12mmHg
10–20mmHg
2
5
5
tial phase of diastole is passive lling of the ventricles from the atria after opening of the
atrioventricular (AV) valves due to ventricular
relaxation. In a normal heart, most ventricular
lling occurs during this passive phase of diastole. Atrial contraction occurs following passive
ventricular lling and correlates with the P-wave
on the ECG. This contributes up to 20–30% of
the end diastolic volume of the ventricles. End
diastolic volume is the amount of blood the ventricles can hold at the end of diastole as the AV
valves close (S2). The end diastolic volume of an
average adult heart is approximately 130mL of
blood.
This end-diastolic volume is also known as
preload and is dened as the degree of stretching
that occurs in the ventricles at the end of diastole.
A pulmonary capillary wedge pressure (PCWP)
obtained from a pulmonary artery catheter is
used to measure left ventricular end-diastolic
pressure as a marker of left ventricular preload.
End-diastolic volume can also be measured by
2-D echocardiogram and Doppler echocardiography can be used to estimate left ventricular lling
pressures. Central venous pressure (CVP) from a
central venous catheter or right atrial pressure
(RAP) from a pulmonary artery catheter are used
to estimate right ventricular preload in the
absence of signicant tricuspid valve pathology.
Both PCWP and RAP pressure tracings consist
of positive and negative deections (Fig. 2.2).
a
v
2 Basic Hemodynamics
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Fig. 2.2 Atrial pressure
tracing; a-, c-, and
v-waves and x- and
y-descent
Fig. 2.3 RA tracing (light blue) and PA tracing (yellow) compared to the ECG and radial arterial tracing (red)
The a-wave follows the P-wave on the ECG and
correlates with atrial contraction. At the bedside,
the a-wave of the PCWP tracing is slightly
delayed when compared to the a-wave seen on
the RA tracing. This is due to the longer uid
lled tubing used while obtaining the PCWP
tracing. Pressure falls within the atria as they
empty into the ventricles and correlates with the
x-descent. A c-wave or “bump” can sometimes
be appreciated in the right atrium as the tricuspid
valve begins to close. This nding is not seen on
a PCWP tracing because the signal is diminished
as the pressure is transmitted a further distance
within the pulmonary artery catheter. The v-wave
correlates with atrial lling during ventricular
systole. The y-descent occurs during early ventricular diastole after the AV valves open and
atrial pressure begins to decrease.
Using these measurements to evaluate patients
in real-time can be valuable in the management
of advanced heart failure and cardiogenic shock
as an adjunct to standard care. Figure2.3 shows
the pulmonary artery pressure (PAP) and RAP
with ECG and arterial line data.
The Frank-Starling Law represents the relationship between stroke volume and ventricular
end-diastolic volume. As the volume of the blood
in the ventricles increases, stroke volume
increases until the volume or myocardial stretch
exceeds the ability to contract effectively. When
cardiac dysfunction occurs, ventricular enddiastolic volume increases, and stroke volume
decreases due to decreased contractility.
Figure 2.4 shows graphically representation of
the relationship of pressure and volume during
the cardiac cycle.
c
x
y
16
140
s
Left Ventricular Pressure (mmHg)
Left Ventricular Volume (mL)
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Fig. 2.4 Pressurevolume loop of the
cardiac cycle
C. Bennett and A. Solberg
120
100
80
60
40
20
0
40 50 60 70 80
Aortic valve closes
Mitral valve opens
Aortic valve open
Stroke Volume
Mitral valve closes
90 100110 120130 140
Part II
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Coronary Artery Disease
AmyWiniger GeorgeP.Rodgers
Introduction
Atherosclerosis is the development of plaques made up of fatty and proinammatory material in and on the walls of arteries. This may affect any
arterial bed, but it is especially problematic when it affects the coronary arteries. Coronary atherosclerosis is the number one cause of death in the
USA.There are several risk factors for coronary atherosclerosis. The nonmodiable risk factors are age, male gender, and family history of premature
coronary artery disease. Premature onset is dened as the onset in a rstdegree relative male before the age of 55, or rst-degree relative female
before the age of 65.
There are, however, several modiable risk factors, which include hyperlipidemia, hypertension, diabetes mellitus, metabolic syndrome, cigarette
smoking, obesity, a sedentary lifestyle, and heavy alcohol intake. There are
many laboratory and imaging markers of coronary atherosclerosis, and these
include elevated lipoprotein (a), hyper-homocystinuria, elevated highsensitive C-reactive protein, and coronary artery calcication seen on multidetector CT.
The current paradigm of atherosclerosis is an injury/inammation paradigm. First consider the structure of the artery. The intima (tunica intima) is
one layer of endothelium over the media (tunica media). The media layer
consists of smooth muscle cells. Finally, the adventitia (tunica externa) is the
outermost layer separated from the medial layer by brous elastic lamina
(Fig.1).
A. Winiger
Atrium Health/Sanger Heart and Vascular Institute, Charlotte, NC, USA
e-mail: Amy.Winger@atriumhealth.org
G. P. Rodgers
Ascension Texas Cardiovascular, Austin, TX, USA
e-mail: grodgers@austin.utexas.edu
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Coronary Artery Disease
Fig. 1 Development of atherosclerotic plaque
Coronary Artery Disease
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The development of coronary atherosclerosis begins early in life. Fatty
streaks, which are mainly intracellular lipid accumulation, are the rst pathologic evidence of atherosclerosis. These occur within the intimal lining of the
aorta and are sometimes evident within the rst decade of life. By the third
decade of life, these intracellular lipid accumulations have developed into
small extracellular pools of lipids that are the rst evidence of atheromas.
In the fourth decade of life, these emerging atheromas may become hardened and sclerotic with brosis, thus referred to as broatheroma. These
lesions further transform through increased smooth muscle and collagen
deposition and develop into mature atherosclerotic plaque (Fig.1). Thus far,
the development of coronary atherosclerosis has been silent; the individual
has no symptoms. However, if the mature plaque becomes very large, it may
obstruct the coronary artery to a degree (>70%) so that ow to the myocardium is reduced during exercise. This would produce myocardial ischemia
and the individual may experience symptoms referred to as stable exertional
angina (Fig.2).
If an atherosclerotic plaque becomes signicantly inamed, it may exhibit
a thinning of the brous cap that covers the extracellular pool of lipids. This
is referred to as a “vulnerable plaque” because if the thinned brous cap
becomes unroofed or ruptures, it will expose the lipid pool to the circulating
blood elements. This results in immediate thrombus formation. Thrombus
begets more thrombus such that the lumen of the coronary artery at this site
may become seriously obstructed. This is the underlying pathophysiology of
acute coronary syndrome (Type I MI).
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ATHEROSCLEROSIS
NORMAL AR
DISFUNCTION
FORMATION
PLAQUE FORMATION
PLAQUE FORMATION
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Coronary Artery Disease
5.
UNSTABLE
4.
STABLE (FIBROUS)
3.
FATTY STREAK
2.
ENDOTHELIAL
TERY
1.
Fig. 2 Progression of atherosclerosis over time
Acute Coronary Syndrome (ACS)
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ST Segment Elevation Myocardial
Infarction
AmyWiniger andGeorgeP.Rodgers
3
Anatomy andPhysiology
Coronary arteries supply oxygenated blood to the
myocardium of the heart. They are located on the
outer surface of the heart (epicardial), originating
from the aorta (see Chap. 1). The left main (LM)
coronary artery originates at the left coronary
cusp and bifurcates into the left anterior descending, or LAD, and the left circumex artery
(LCX). The LAD supplies the left ventricle anterior wall, anterior portion of the intraventricular
septum and a portion of the right ventricular wall.
The diagonal branches arise from the left anterior
descending. The circumex artery supplies the
lateral and posterior regions of the left ventricle
(LV). The obtuse marginal (OM) branches arise
from the circumex artery. The right coronary
artery supplies the right ventricle and the posterior lateral branch. The right coronary artery
(RCA) also supplies the sinoatrial node (SA
node) and the atrial ventricular node (AV node)
(see Fig.3.1).
Coronary blood ow occurs during ventricular
diastole. The myocardial oxygen requirement is
inuenced by the oxygen demand of the tissues:
the faster the heart rate, the higher the oxygen
demand. In addition, an increase in left ventricular contractility and left ventricular wall stress
caused by an elevation in blood pressure increases
the myocardial demand for more oxygen. This
balance between the oxygen demand of the myocardium and the ability to supply the oxygen,
through coronary blood ow, will determine
whether the downstream myocardium becomes
under-perfused, or ischemic. Different clinical
coronary syndromes can be described based on
the condition of the coronary arteries and hemodynamic requirements.
Denition of STEMI
“in the absence of left ventricular (LV) hypertrophy or left bundle branch block (LBBB) is dened
by the European Society of Cardiology/ACC/
AHA/World Heart Federation Task Force for the
universal denition of Myocardial Infarction as
new ST elevation of the J point in at least 2 contiguous leads of >(0.2 mV in men or >1.5 mm
(0.15) mV in women in leads V2–V3, and/or of
>1mm (0.1 mV) in other contiguous chest leads,
or limb leads” [8, p. e83].
A. Winiger (*)
Atrium Health/Sanger Heart and Vascular Institute,
Charlotte, NC, USA
e-mail: Amy.Winger@atriumhealth.org
G. P. Rodgers
Ascension Texas Cardiovascular, Austin, TX, USA
e-mail: grodgers@austin.utexas.edu
© 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_3
The denition of acute coronary syndrome (ACS)
is suspicion or conrmation of acute myocardial
ischemia or infarction [1]. There are three types
of ACS: ST elevation MI (STEMI), non-ST elevation MI (NSTEMI), and unstable angina pectoris (UAP) [1]. The denition of a STEMI is
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