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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3736_Библиотеки_им_академика_М_И_Перельмана
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264
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C. Bennett and A. Solberg
evidence-based therapies can be initiated when
the patient is close to a euvolemic state and weaning off IV inotrope and vasopressor agents.
Afterload reduction can be transitioned to an oral
regimen based on kidney function and diagnosis.
Inotrope support may continue. Some patients
remain on long-term inotropes in the outpatient
setting as a bridge to transplant or as palliative
support for quality of life.
Clinical Pearls
• Patients with conrmed or suspected CS
should be triaged to a setting that offers PCI
capabilities and a CICU.
• Evaluation and treatment of underlying car-
diac dysfunction should continue while supporting patients in CS. ACS is the most
common etiology of CS and should be ruled
out immediately upon presentation.
• To maintain tissue perfusion, CS management
should be focused on increasing CO.Inotrope
support is the rst line for increasing stroke
volume, improving contractility, and offloading pressures working against failing
ventricles.
• Ongoing risk assessment in the setting of CS
is crucial. Risk assessment tools including the
SCAI shock stages and Killip classication
should be considered for mortality prediction.
• MCS consideration and cardiac transplant
evaluation are warranted in patients with
refractory CS.
• Early involvement of palliative care can assist
with goals of care discussions and symptom
management and can be particularly useful in
the setting of chronic end-stage heart failure.
• GDMT for the treatment for heart failure
should be considered in patients who have
recovered from CS.
References
1. O’Brien C, Beaubien-Souligny W, Amsallem M,
Denault A, Haddad F. Cardiogenic shock: reections at the crossroad between perfusion, tissue
hypoxia, and mitochondrial function. Can J Cardiol.
2020;36(2):184–96.
2. van Diepen S, Katz JN, Albert NM, Henry TD,
Jacobs AK, Kapur NK, et al. Contemporary management of cardiogenic shock: a scientic statement
from the American Heart Association. Circulation.
2017;136(16):e232–e68.
3. Brener MI, Rosenblum HR, Burkhoff
D. Pathophysiology and advanced hemodynamic
assessment of cardiogenic shock. Methodist Debakey
Cardiovasc J. 2020;16(1):7–15.
4. Vahdatpour C, Collins D, Goldberg S. Cardiogenic
shock. J Am Heart Assoc. 2019;8(8):e011991.
5. Bertini P, Guarracino F. Pathophysiology of cardiogenic shock. Curr Opin Crit Care. 2021;27(4):409–15.
6. Lim HS. Cardiogenic shock: failure of oxygen
delivery and oxygen utilization. Clin Cardiol.
2016;39(8):477–83.
7. Baran DA, Grines CL, Bailey S, Burkhoff D, Hall
SA, Henry TD, et al. SCAI clinical expert consensus statement on the classication of cardiogenic
shock: this document was endorsed by the American
College of Cardiology (ACC), the American Heart
Association (AHA), the Society of Critical Care
Medicine (SCCM), and the Society of Thoracic
Surgeons (STS) in April 2019. Catheter Cardiovasc
Interv. 2019;94(1):29–37.
8. Killip T III, Kimball JT. Treatment of myocardial infarction in a coronary care unit. A two
year experience with 250 patients. Am J Cardiol.
1967;20(4):457–64.
9. Naidu SS, Baran DA, Jentzer JC, Hollenberg SM,
van Diepen S, Basir MB, etal. SCAI SHOCK stage
classication expert consensus update: a review and
incorporation of validation studies: this statement
was endorsed by the American College of Cardiology
(ACC), American College of Emergency Physicians
(ACEP), American Heart Association (AHA),
European Society of Cardiology (ESC) Association
for Acute Cardiovascular Care (ACVC), International
Society for Heart and Lung Transplantation (ISHLT),
Society of Critical Care Medicine (SCCM), and
Society of Thoracic Surgeons (STS) in December
2021. J Am Coll Cardiol. 2022;79(9):933–46.
10. Jentzer JC, Tabi M, Burstein B. Managing the rst
120min of cardiogenic shock: from resuscitation to
diagnosis. Curr Opin Crit Care. 2021;27(4):416–25.
11. Alviar CL, Miller PE, McAreavey D, Katz JN, Lee
B, Moriyama B, et al. Positive pressure ventilation
in the cardiac intensive care unit. J Am Coll Cardiol.
2018;72(13):1532–53.
12. Argueta EE, Paniagua D.Thermodilution cardiac output: a concept over 250 years in the making. Cardiol
Rev. 2019;27(3):138–44.
13. Jentzer JC, Coons JC, Link CB, Schmidhofer
M. Pharmacotherapy update on the use of vasopressors and inotropes in the intensive care unit. J
Cardiovasc Pharmacol Ther. 2015;20(3):249–60.
Introduction toMechanical
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Support
CourtneyBennett andAmandaSolberg
25
Intro toSupport Devices
Mechanical circulatory support (MCS) devices
are designed to support patients, while they are
acutely decompensated, or to support them
through high-risk procedures to prevent decompensation. MCS devices are designed to augment
vasopressor and inotrope therapy as a way to
decrease preload, afterload, and oxygen consumption by the heart. Long-term mechanical
support devices are also available and are used as
a bridge to transplantation, bridge to decision,
destination therapy, or bridge to recovery.
There are several MCS options, each with
varying evidence supporting their use
(Table 25.1). MCS devices can be placed surgi-
cally or percutaneously. The main MCS devices
used today include intra-aortic balloon pump
(IABP), percutaneous ventricular assist device
(pVAD), extracorporeal membrane oxygenation
(ECMO), and implanted ventricular assist devices
(VAD).
Complications include death, infection, limb
ischemia, embolic events, bleeding, hemolysis,
and malposition [1]. These complications may be
worsened depending on patient comorbidities.
Careful patient selection for MCS is warranted.
Each patient should undergo a robust multidisciplinary evaluation to determine candidacy if able.
It is also recommended that prompt evaluation by
the MCS team should be made in patients with
CS to facilitate recovery [1].
C. Bennett · A. Solberg (*)
Mayo Clinic, Rochester, MN, USA
e-mail: Bennett.Courtney@mayo.edu;
Solberg.Amanda@mayo.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_25
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Table 25.1 MCS devices, their level of support, mechanism of action, and helpful information for each
Level of
support
Device Description
IABP
(temporary)
pVAD
(temporary)
V-A
ECMO
(temporary)
LVA D
(long term)
– Increase SV
– Decrease
afterload
– Perfuse
coronary
arteries
– Reduce
oxygen
consumption of
LV
– Decrease
diastolic
volume of LV
– Provides
both respiratory
and circulatory
support
– Reduce
oxygen
consumption of
LV
– Decrease
diastolic
volume of LV
(CO) Placement Mechanism of action
0.5–1L/min – Femoral access
– Sits in
descending aorta
2.5–5.5L/
min
depending
on the
device
Up to 6L/
min
Up to 8L/
min
– Femoral access
– Sits in the
ventricle, ows into
aorta
– Peripheral or
central cannulation
– Venous cannula
at the level of the
right atrium, and
arterial cannula in
the aorta or femoral
artery
– Placed via
sternotomy
– Timed balloon
ination during
diastole increases
coronary artery
perfusion, and rapid
deation during systole
reduces afterload
– An axillary ow
catheter pulls blood
from the ventricle and
pushes blood to aorta
– Blood is pumped to
an extracorporal
machine, blood is
oxygenated, and
carbon dioxide is
removed
– Blood is removed
from left ventricle and
returned to the aorta
C. Bennett and A. Solberg
Indication/
contraindication
Pros/cons
– Risk for limb and
organ ischemia,
atherosclerotic
embolization, and
hemolysis
– Monitor distal
pulses, device
placement with CXR,
CBC, and renal
function
– Used as rst-line
MCS despite mixed
evidence
– Patient is limited
to best rest with
maximum HOB
elevation to 30°
– Recent ability to
place axillary to allow
patient ambulation at
some institutions
– High risk for
hemolysis and leg
ischemia
– Monitor distal
pulses, CBC, LDH,
plasma-free
hemoglobin
– High risk for limb
ischemia with
peripheral cannulation
– The left
ventricular may
requiring venting
– Destination
therapy bridge to
decision, bridge to
transplant, or bridge
to recovery
– No pulses will be
auscultated in
continuous ow
devices
– High risk of
thrombotic events, GI
bleed, and infection
25 Introduction toMechanical Support
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Reference
1. van Diepen S, Katz JN, Albert NM, Henry TD,
Jacobs AK, Kapur NK, et al. Contemporary management of cardiogenic shock: a scientic statement
from the American Heart Association. Circulation.
2017;136(16):e232–68.
267
Part VII
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Peripheral Vascular Disease
FrankR.Arko III
Introduction
Vascular disease encompasses a wide span of disease processes involving the
arterial and venous systems. Much of the pathology in vascular surgery is
chronic in nature but each disease process can present in the acute setting and
when this occurs, we see high incidences of morbidity and mortality. In this
chapter, we will dene the common diagnoses seen in the vascular surgery
scope to include aortic dissection and aneurysms, peripheral arterial disease
(PAD), carotid artery disease, and deep vein thrombosis (DVT).
Aortic pathology can be life threatening if not appropriately managed and
regularly followed in the outpatient setting. Therefore, it is imperative that we
discuss in detail the acute management of aortic disease as well as the longterm goals of therapy for our patients. Complicated acute type B aortic dissection (TBAD) can present with life threatening end organ ischemia, aortic
rupture, spinal cord ischemia, or limb ischemia. Chronic aortic dissections
can present with aneurysmal degeneration, arterial stenosis, compressive
symptoms, and risk of aortic rupture. A mainstay of treatment in aortic disease centers around adequate blood pressure control and regular vascular surgery follow-up with imaging to survey aortic size.
PAD is a chronic process that develops over time due to atherosclerosis of
the arteries related to common risk factors including age, cholesterol, smoking history, diabetes, and hypertension. Atherosclerotic disease is important
to discuss and understand as patients present with a wide scope of symptoms
from asymptomatic, to lifestyle limiting claudication and in severe cases of
PAD, rest pain and even limb loss. PAD can affect the great vessels of the
aortic arch, the aorta, iliac arteries, arteries of the lower extremities and is
commonly seen in areas of arterial bifurcations. The mainstay of treatment is
F. R. ArkoIII
Vascular and Endovascular Surgery, Atrium Health/Sanger Heart and Vascular
Institute, Charlotte, NC, USA
e-mail: Frank.Arko@atriumhealth.org
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medical therapy and modication of risk factors and interventional therapy is
usually guided based on the patient’s quality of life with the goal of reducing
symptoms.
Initially a DVT is an acute thrombotic event that over time will develop
into chronic thrombus and scarring within the venous system. Many patients
presenting with DVT can be treated with anticoagulation alone but in the
select group of patients with proximal DVT, interventional therapy can be
recommended to reduce the long-term effects of thrombus burden. A major
goal in the treatment of DVT is to reduce post-thrombotic syndrome and
venous hypertension which can lead to chronic swelling, heaviness, leg
fatigue, hemosiderin deposition, and lastly venous ulceration.
Peripheral Vascular Disease
Carotid Artery Stenosis (CAS)
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TrentGabriel andFrankR.Arko III
26
Anatomy andPhysiology
The carotid arteries are the predominate vessels
that supply blood to the head and neck. The right
common carotid artery (RCCA) originates from
the brachiocephalic artery, whereas the left common carotid artery (LCCA) originates directly
from the aortic arch. Both CCAs bifurcate in the
neck at the level of the carotid sinus into two
branches. The external carotid arteries (ECAs) supply the neck and face with arterial blood, whereas
the internal carotid arteries (ICAs) supply the brain.
To further specify location, the carotid arteries are
located posterior to the sternoclavicular joints and
are protected as they lie within the carotid sheath,
which is a brinous connective tissue that also contains the internal jugular veins and the vagus nerve.
For most patients, the bifurcation of the CCAs into
the ECAs and ICAs occurs at the level of the upper
border of the thyroid cartilage and roughly the level
of the fourth or fth cervical vertebrae. At the bifurcation, there is the carotid body as well as the
carotid sinus. The carotid body is a chemoreceptor
that works to detect the levels of PO2, PCO2, and
pH of the blood that passes through the bifurcation
into the brain and face. This mainly works to alert
the brain of the need to increase respiratory rate.
The carotid sinus is a baroreceptor that responds to
changes in the stretch of the blood vessel and helps
to maintain blood pressure (Fig.26.1).
T. Gabriel (*)
Atrium Health/Sanger Heart and Vascular Institute,
Charlotte, NC, USA
e-mail: benjamin.gabriel@atriumhealth.org
F. R. Arko III
Vascular and Endovascular Surgery,
Atrium Health/Sanger Heart and Vascular Institute,
Charlotte, NC, USA
e-mail: Frank.Arko@atriumhealth.org
© 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_26
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T. Gabriel and F. R. Arko III
1. Brachiocephalic artery
2. Right subclavian
3. Right common carotid
artery
4. Right internal carotid
artery
5. Right external carotid
artery
6. Left common carotid
artery
7. Left internal carotid
artery
8. Left external carotid
artery
9. Left subclavian artery
Fig. 26.1 Carotid anatomy
Pathology/Pathophysiology
ofCarotid Artery Stenosis
There are several potential causes of CAS with
the most common being the development of atherosclerosis, bromuscular dysplasia, anatomical
variances, carotid artery aneurysms, Takayasu’s
arteritis, radiation therapy injuries, and carotid
body tumors.
Far and away the most common cause of CAS
is the development of atherosclerosis. One of the
prominent reasons the development of athero-
sclerosis can specically affect the CCAs is the
anatomy of the arterial bifurcation. The hemodynamics of the blood ow through this channel
with associated uctuations of shear stress can
predispose regions with lower ow velocity (i.e.,
the carotid bifurcation) to development of atherosclerotic plaques. The hemodynamics of arterial ow at the carotid bifurcation can
signicantly increase the likelihood of atherosclerotic plaque, reducing vessel lumen diameter, and increasing risk of thrombotic or embolic
event (Fig.26.2).
26 Carotid Artery Stenosis (CAS)
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273
Fig. 26.2 Turbulent
ow in CAS
development ([1],
Figure 1)
Arterial
blood vessel
↓YAP
↓TA Z
Plaques form in part due to the inammatory response (platelet deposition, smooth
muscle cell proliferation, and slow accumulation of lipoproteins) involved in the repair process. The atherosclerotic plaques form due to
several reasons, including elevated blood cholesterol, long-term damage from smoking on
the intima of the vessel wall, chronically elevated blood glucose, and genetic predisposition (Chap. 27).
Presentation ofCAS
Laminar
blood flow
Disturbed
blood flow
Endothelial
cell
↑YAP
↑TA Z
Table 26.1 Common historical features to consider with
CAS
Suggestive of symptomatic
CAS
Amaurosis fugax—loss of
vision in one eye
Difculty speaking or
understanding
Loss of strength on
contralateral side
Numbness and sensory loss
on contralateral side
Facial droop
Slurred speech
Sudden severe headache
Plaque deposit
Commonly not
associated with CAS
Dizziness/vertigo
without loss of balance
Syncope or near
syncope
Muscle tension
headache
Tinnitus
Patients with carotid artery disease can present
with or without neurological symptoms.
Symptomatology and degree of stenosis are both
considered when evaluating for surgical revascularization. Patients with symptomatic carotid
artery disease may present with a myriad of neu-
rological symptoms (Table 26.1) and may be
revascularized at a lower degree of stenosis,
whereas patients with asymptomatic carotid
artery disease may be revascularized at a higher
degree of stenosis.
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T. Gabriel and F. R. Arko III
Physical Examination
It is common to see referrals from providers for
patients that have been found to have a carotid
bruit. Bruits can be heard when there is turbulent
blood ow that must ow around an atherosclerotic plaque (stenosis) within the vessel wall.
For best clinical practice, the patient should be
evaluated with their head secure and slightly tilted
back with the chin elevated. Stand or sit next to
the patient on the right when auscultating the right
ICA and ask them to look to their left. Repeat the
same technique on the left (sit or stand to their left
and have them look right). Stethoscope should be
placed approximately 2–3cm above the clavicle,
and patient asked to briey hold their breath as
they are expiring. Reposition the stethoscope two
to three times moving caudally toward the level of
the bifurcation on both sides [2].
The presence or absence of a carotid bruit is
not diagnostic for whether the patient has signicant carotid artery stenosis. Additionally, carotid
artery bruits are most often found to be benign.
Multiple studies have shown varying degrees of
specicity and sensitivity, with a consistent trend
showing a positive bruit to be more specic than
sensitive.
Imaging/Diagnostic Testing
There are four main diagnostic tests that are
used to evaluate the degree of stenosis within
carotid arteries: cerebral angiography, carotid
duplex ultrasound (DUS), magnetic resonance
angiography, and computed tomographic angiography. Also, there are three main methods of
measuring the degree of stenosis: NASCET,
ECST, and CC.
The rst method of measuring carotid artery
stenosis, the North American Symptomatic
Carotid Endarterectomy Trial (NASCET),
measures the residual lumen diameter at the
most stenotic portion of the vessel and compares this with the lumen diameter in the normal ICA distal to the stenosis. This differs
from the European Carotid Surgery Trial
(ECST) which measures the lumen diameter at
the most stenotic portion and compares this
with the estimated probable original diameter
at the site of maximum stenosis (Fig. 26.3).
Lastly, the third most common method to measure carotid artery stenosis is the common
carotid (CC) method which measures the residual lumen diameter at the most stenotic portion
of the vessel and compares it to the lumen
diameter in the proximal CCA.
Conventional Cerebral Angiography Pros of
this diagnostic modality includes being able to
evaluate the entire carotid artery system while
also showing information about atherosclerotic
disease, plaque morphology, and collateral circulation as well. However, the downside to this
diagnostic imaging and the main reasons that it is
rarely used are that it is invasive, quite expensive,
and places patients at a slightly increased risk of
morbidity (due to CVA) and mortality.
Fig. 26.3 Assessing
carotid stenosis severity
([3], Fig4)
External
carotid
artery
B
C
Common carotid artery
NASCET ECST
A–B
A
A
Internal
carotid
artery
Estimated
position of
carotid wall
C–B
C
NASCET ECST
30
40
50
60
70
80
90
Approximate equivalent
degrees of internal carotid
artery stenosis used in
NASCET and ESCT according
to recent direct comparisons
65
70
75
80
85
91
97
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