28+a+30+Fisiopatología+cardiovascular+-+Manuel+Méndez.pdf

Fisiopatología
coronaria
Manuel Méndez
Dpto. de enf. cardiovasculares
mmendezl@med.puc.cl
miércoles 16 de abril de 14

introducción

introducción
• El corazón es un órgano de alto requerimiento
energético que obtiene la energía desde la oxidación

introducción
• por tanto requiere O2

introducción
• por tanto requiere O2
• Red de irrigación autorregulada: Arterias
Coronarias

Anatomía coronaria

Anatomía coronaria
• Se originan en dos ostia desde la aorta

Anatomía coronaria
• izquierda (tci) que se divide rápidamente en
ADA Y circ.

Anatomía coronaria
ADA Y circ.
• Derecha

Anatomía coronaria
ADA Y circ.
• Derecha
• Tienen un componente epicárdico de baja
resistencia y uno intramiocardico de
resistencia variable

Anatomía

Compar'mientos-funcionales
-
Arteria epicárdica ! > 400 µm
Contribuye con < 5% de la ↓ PA
R. Miogénica, Mediada por flujo,
control neuronal y paracrino
Vasos prearteriolares
(100 - 400 µm): R.
mediada por flujo y R.
Miógeno
Arteriolas ! <30
µm: R. metabólica;
30 - 60 µm: R.
Miógena; 100 - 150
µm R. mediada por
flujo. 40 – 50% de
la resistencia al
flujo.
Capilares:
• 3500/mm2
• Endocar > Epicar.
Se afecta en HVI,
DM.
Braunwald E; Tratado de cardiología 8va ed

componentes del consumo
de O2
• FC
• Tensión de la pared
• Contractilidad
• Masa miocardica

• FC: es el mayor determinante del consumo de 02no
sólo porque aumenta los requerimientos metabólicos
si no que acorta......la diástole

Tensión de la pared
T:PxR

• Tensión de la pared
• Frecuencia cardíaca
• Contractilidad
• Capacidad de transporte O2
• Regulación intrínseca
• Metabolitos locales
• Factores endoteliales
• Control neuronal
PAo

• Normalmente el corazón extrae el 60-80% del 02
• Solo aumentando el flujo es posible aumentar la
entrega

• Normalmente el corazón extrae el 60-80% del 02
• Solo aumentando el flujo es posible aumentar la
entrega
Q:dif P/r

• El aumento de metabolitos ( ac. láctico, Co2,
ADENOSINA) induce vasodilatación mediada por
ON en su mayoría
• El aumento de flujo aumenta el Shear stress y
provoca vasodilatación

Reserva coronaria
• Diferencia entre el flujo coronario basal (en reposo)
y el flujo coronario máximo (que se logra por
vasodilatación)

Resumiendo...

Resumiendo...
• Corazón es un órgano con alto requerimiento
energético, con alta extracción de O2

Resumiendo...
• La única forma de aumentar la entrega es con mayor
flujo que se logra por vasodilatación. O reserva
coronaria

Resumiendo...
coronaria
• Esto se logra gracias a fenómenos autoregulatorios

Resumiendo...
coronaria
• Esto se logra gracias a fenómenos autoregulatorios
¿Y si agoto la reserva coronaria?

• Si se agota la reserva coronaria se produce isquemia

• Si se agota la reserva coronaria se produce isquemia
• (También se produce isquemia si aumenta la masa
muscular ( hipertrofia) ya que la densidad de
capilares no se mantiene, porque no hay transporte
de O2 etc.)

Isquemia (por falta de
reserva coronaria)
• Si se produce alguna alteración de las arterias que
comprometan el flujo, se produce isquemia si esta
alteración es lo suficiente para hacer caer la presión
de perfusión
• Recuerde que Q=dif P/resistencia

Q=dP/R

Atheromatosis

Atheromatosis
• Lesión de las arterias por “PLACAS FIBROGRASAS”

Atheromatosis
• no se conoce LA causa pero si los “factores”

Atheromatosis
• no se conoce LA causa pero si los “factores”
• Factores de riesgo cardiovascular clásicos

factores de riesgo
• edad
• sexo
• hipercolesterolemia,DM,HTA
• obesidad, tabaquismo

factores de riesgo
• edad
• sexo
• hipercolesterolemia,DM,HTA
• obesidad, tabaquismo
factores
no
clásicos:
LpA
PCR
Infecciosos etc

Lipoproteinas
s (called apoproteins). These particles,
eins, transport cholesterol and triglyc-
r energy utilization, lipid deposition,
on, and bile acid formation. There are
, classified according to their densi-
centrifugation: chylomicrons, very–
VLDL), intermediate-density lipopro-
ipoprotein (LDL), and high-density
DL carries large amounts of triglyc-
density than cholesterol. LDL is the
l, whereas HDL actually is 50% pro-
ein consists of a large molecular com-
th apoproteins.5,6 The major lipid con-
esters, triglycerides, nonesterified (or
spholipids. The insoluble cholesterol
re located in the hydrophobic core of
ecule, surrounded by the soluble phos-
olesterol, and apoproteins (Fig. 22-3).
and phospholipids provide a negative
oprotein to be soluble in plasma.
classes of apoproteins: A (i.e., apoA-
, B (i.e., apoB-48, apoB-100), C (i.e.,
C-III), and apoE.4,5 The apoproteins
and ultimate metabolic fate of the
e apoproteins activate the lipolytic
he removal of lipids from the lipo-
a reactive site that cellular receptors
he endocytosis and metabolism of the
oprotein in LDL is apoB-100, whereas
search findings suggest that genetic
may be involved in hyperlipidemia and
s.5–8
of lipoprotein synthesis: the small
e chylomicrons, which are the largest
High
density
50% protein
FIGURE 22-2 • Lipoproteins are named based on their protein
content, which is measured in density. Because fats are less dense
than proteins, as the proportion of triglycerides decreases, the den-
sity increases.
Cholesterol
esters
Apoproteins
Triglycerides Phospholipids
FIGURE 22-3 • General structure of a lipoprotein. The cholesterol
esters and triglycerides are located in the hydrophobic core of the
macromolecule, surrounded by phospholipids and apoproteins.
of the lipoprotein molecules, are synthesized in the wall of the
small intestine. They are involved in the transport of dietary
(exogenous pathway) triglycerides and cholesterol that have
been absorbed from the gastrointestinal tract. Chylomicrons
transfer their triglycerides to the cells of adipose and skeletal
muscle tissue. The remnant chylomicron particles, which con-
tain cholesterol, are then taken up by the liver and the choles-
terol used in the synthesis of VLDL or excreted in the bile.

Lipoproteinas
480 Unit VI Disorders of Cardiovascular Function
metabolism, are combinations of three fatty acids condensed
with a single glycerol molecule. Phospholipids, which contain
a phosphate group, are important structural constituents of
lipoproteins, blood clotting components, the myelin sheath,
and cell membranes. Although cholesterol is not composed of
fatty acids, its steroid nucleus is synthesized from fatty acids
and thus its chemical activity is similar to that of other lipid
substances.3
Elevated levels of blood cholesterol (hypercholesterolemia)
are implicated in the development of atherosclerosis with its
attendant risk of heart attack and stroke. This is a major public
health issue that is underscored by striking statistics released by
the American Heart Association (AHA). An estimated 37.2 mil-
lion Americans have high-risk serum cholesterol levels (240 mg/
dL or greater) that could contribute to a heart attack, stroke, or
other cardiovascular event associated with atherosclerosis.4
Lipoproteins
Because cholesterol and triglyceride are insoluble in plasma,
they are encapsulated by a stabilizing coat of water-soluble
phospholipids and proteins (called apoproteins). These particles,
which are called lipoproteins, transport cholesterol and triglyc-
eride to various tissues for energy utilization, lipid deposition,
steroid hormone production, and bile acid formation. There are
five types of lipoproteins, classified according to their densi-
ties as measured by ultracentrifugation: chylomicrons, very–
low-density lipoprotein (VLDL), intermediate-density lipopro-
tein (IDL), low-density lipoprotein (LDL), and high-density
lipoprotein (HDL). VLDL carries large amounts of triglyc-
erides that have a lower density than cholesterol. LDL is the
main carrier of cholesterol, whereas HDL actually is 50% pro-
tein (Fig. 22-2).
Each type of lipoprotein consists of a large molecular com-
plex of lipids combined with apoproteins.5,6 The major lipid con-
stituents are cholesterol esters, triglycerides, nonesterified (or
free) cholesterol, and phospholipids. The insoluble cholesterol
esters and triglycerides are located in the hydrophobic core of
the lipoprotein macromolecule, surrounded by the soluble phos-
Low
density
High
density
HDL
5% triglycerides,
20% cholesterol,
50% protein
LDL
10% triglycerides,
50% cholesterol,
25% protein
Chylomicrons
80% 90% triglycerides,
2% protein
VLDL
55% 65% triglycerides,
10% cholesterol,
5% 10% protein
sity increases.
10952-22_CH22.qxd 6/25/08 2:39 PM Page 480
s (called apoproteins). These particles,
eins, transport cholesterol and triglyc-
r energy utilization, lipid deposition,
on, and bile acid formation. There are
, classified according to their densi-
centrifugation: chylomicrons, very–
VLDL), intermediate-density lipopro-
ipoprotein (LDL), and high-density
DL carries large amounts of triglyc-
density than cholesterol. LDL is the
l, whereas HDL actually is 50% pro-
ein consists of a large molecular com-
th apoproteins.5,6 The major lipid con-
esters, triglycerides, nonesterified (or
spholipids. The insoluble cholesterol
re located in the hydrophobic core of
ecule, surrounded by the soluble phos-
olesterol, and apoproteins (Fig. 22-3).
and phospholipids provide a negative
oprotein to be soluble in plasma.
classes of apoproteins: A (i.e., apoA-
, B (i.e., apoB-48, apoB-100), C (i.e.,
C-III), and apoE.4,5 The apoproteins
and ultimate metabolic fate of the
e apoproteins activate the lipolytic
he removal of lipids from the lipo-
a reactive site that cellular receptors
he endocytosis and metabolism of the
oprotein in LDL is apoB-100, whereas
search findings suggest that genetic
may be involved in hyperlipidemia and
s.5–8
of lipoprotein synthesis: the small
e chylomicrons, which are the largest
High
density
50% protein
sity increases.
Cholesterol
esters
Apoproteins
Triglycerides Phospholipids
FIGURE 22-3 • General structure of a lipoprotein. The cholesterol
esters and triglycerides are located in the hydrophobic core of the
macromolecule, surrounded by phospholipids and apoproteins.

transport are shown in Figure 22-4.
LDL, sometimes called the bad cholesterol, is the main car-
rier of cholesterol. LDL is removed from the circulation by
either LDL receptors or by scavenger cells such as monocytes or
macrophages. Approximately 70% of LDL is removed through
the LDL receptor-dependent pathway, and the rest is removed
by the scavenger pathway.1
Although LDL receptors are widely
distributed, approximately 75% are located on hepatocytes; thus,
LDL receptors. The scavenger pathway involves ingestion by
phagocytic monocytes and macrophages. These scavenger cells
have receptors that bind LDL that has been oxidized or chem-
ically modified. The amount of LDL that is removed by the
scavenger pathway is directly related to the plasma cholesterol
level. When there is a decrease in LDL receptors or when LDL
levels exceed receptor availability, the amount of LDL that is
removed by scavenger cells is greatly increased. The uptake of
Intestine
Dietary
triglycerides
and cholesterol
Bile acid
and cholesterol
Chylomicron
Liver
Chylomicron
fragments
Blood vessels
Adipose and skeletal muscle tissue
HDL
VLDL
IDL
LDL
LDL
receptor
Cholesterol
Triglycerides
Extrahepatic
tissue
Scavenger
pathway
Exogenous pathway Endogenous pathway
Reverse cholesterol transport
Receptor-
dependent
pathway
HDL
FIGURE 22-4 • Schematic representa-
tion of the exogenous and endogenous
pathways for triglyceride and cholesterol
transport.

formación placa

Isquemia: Angina
• Recordemos:
¿velocidad?
¿presión?

Síndromes coronarios
• Se dividen clínicamente en síndromes crónicos y
agudos
• Esa división tiene un sustrato fisiopatológico: La
presencia de trombos en mayor o menor medida, es
decir si la placa es Estable
o
Inestable

Placas estables
artery stents, and determine appropriateness for coronary artery
bypass graft surgery.16
Intracoronary physiologic measurements
(Doppler ultrasonography, fractional flow reserve) can also be
obtained with new sensor guide wire technology.
Coronary Atherosclerosis and the Pathogenesis
of Coronary Artery Disease
Atherosclerosis is by far the most common cause of CAD, and
begins at a very young age in the United States and other devel-
oped countries of the world (see Chapter 22). Atherosclerosis
can affect one or all three of the major epicardial coronary arter-
ies and their branches. Clinically significant lesions may be
located anywhere in these vessels, but tend to predominate in
the first several centimeters of the left anterior descending and
left circumflex or the entire length of the right coronary artery.16
Sometimes the major secondary branches also are involved.
Coronary artery disease is commonly divided into two
types of disorders: the acute coronary syndrome and chronic
ischemic heart disease. The acute coronary syndrome (ACS)
erosclerotic lesions: the fixed or stable plaque, which obstructs
blood flow, and the unstable or vulnerable plaque, which can
rupture and cause platelet adhesion and thrombus formation.
The fixed or stable plaque is commonly implicated in stable
angina and the unstable plaque in unstable angina and myo-
cardial infarction. In most cases the myocardial ischemia under-
lying unstable angina, acute myocardial infarction, and, in
many cases, sudden cardiac death, is precipitated by abrupt
plaque changes, followed by thrombosis. The major determi-
nants of plaque vulnerability to disruption include the size of
the lipid-rich core, the stability and thickness of its fibrous cap,
the presence of inflammation, and lack of smooth muscle cells9
(Fig. 24-5). Plaques with a thin fibrous cap overlaying a large
lipid core are at high risk for rupture.
Although plaque disruption may occur spontaneously, it is
often triggered by hemodynamic factors such as blood flow
characteristics and vessel tension. For example, a sudden surge
of sympathetic activity with an increase in blood pressure, heart
rate, force of cardiac contraction, and coronary blood flow is
thought to increase the risk of plaque disruption. Indeed, many
Adventitia
Media
Intima
Lumen
Stable angina
Plaque disruption
and platelet aggregation
Unstable angina Non–ST-segment
elevation MI
ST-segment
elevation MI
Asymptomatic
atherosclerotic
plaque
Stable fixed
atherosclerotic
plaque
Unstable
plaque
Thrombus
Acute coronary syndromes
FIGURE 24-5 • Atherosclerotic plaque: stable fixed
atherosclerotic plaque in stable angina and unstable
plaque with plaque disruption and platelet aggrega-
tion in the acute coronary syndromes.

placas estables
• Angina crónica, se presentan frente aumento de los
requerimientos, ejercicio por ejemplo
• Placas con cápsula fibrosa gruesa
• Escaso “centro” necrótico
• Poco inflamadas

Agudos
• Infartos: con SDST sin SDST (al ECG)
• Angina Inestable:
• angina de reciente comienzo
• angina post infarto
• angina de pequeño esfuerzo
• (angina variante)

placas inestables
studies published by Henney et al demonstrating the presence
of stromelysin mainly in macrophages in coronary arteries.41
In the mid 1990s, Zorina Galis et al demonstrated 3 matrix
metalloproteinase (MMP) classes (interstitial collagenase,
MMP-1; gelatinases, MMP-2 and MMP-9; and stromelysin,
MMP-3) expressed primarily in the shoulder regions of
advanced plaques along with their endogenous inhibitors
(tissue inhibitors of matrix metalloproteinases [TIMPs] 1 and
2).42–44 MMP enzymatic activities were demonstrated by in
location, mean luminal narrowing was least in sections with
TCFAs (59.6%), intermediate for lesions with hemorrhage
into a plaque (68.8%) and greatest in acute plaque ruptures
(73.3%) or healed plaque ruptures (72.8%). Overall, nearly
75% of lesions showed !75% cross-sectional luminal-
narrowing or (!50% diameter stenosis), which may be a
useful indicator for the detection of vulnerable plaque.
Moreover, the location is also important, as approximately
50% of the TCFAs occur in the proximal portions of the
Figure 3. Illustration empha-
sizes the importance of colla-
gen synthesis and breakdown
in the maintenance of the
integrity of the fibrous cap.
Vascular smooth muscle cells
synthesize essential extracellu-
lar matrix proteins such as col-
lagen and elastin from amino
acids. This process may be
inhibited by interferon-! (IFN-!)
secreted by activated T cells,
thereby disrupting collagen
synthesis, which may interfere
with the maintenance and
repair of collagen framework
supporting the fibrous cap.
Importantly, the expression of
CD40 ligand on T cells may
promote tissue proteolysis
through the release and activa-
tion of matrix-degrading enzymes produced by vascular smooth muscle cells and inflammatory macrophages. Activated macrophages
within the fibrous cap can secrete tissue proteases that support the breakdown of collagen and elastin to peptides and amino acids.
The loss of structural molecules provided by the extracellular matrix can thin and weaken the fibrous cap, rendering it particularly sus-
ceptible to rupture and acute coronary syndromes. Additional factors involved in the activation of macrophages include tumor necrosis
factor-" (TNF-"), macrophage colony-stimulating factor (M-CSF), and macrophage chemoattractant protein-1 (MCP-1), among others.
Reproduced with permission from the American Heart Association (Circulation 1995;91:2844–2850), with modifications by Peter Libby.
1286 Arterioscler Thromb Vasc Biol July 2010

tasa de eventos
The new engl and jour nal of medicine
thin-cap fibroatheromas identified on radiofre-
quency intravascular ultrasonography, only 26
were sites of recurrent events at a median follow-
up of 3.4 years (estimated Kaplanñ Meier event
rate, 4.9%). Specificity was similarly limited for
a plaque burden of at least 70% (event rate, 9.6%)
and a minimal luminal area of 4.0 mm2 or less
(event rate, 5.3%). Even when all three predictive
were seen on radiofrequency intravascular ultra-
sonography. Third, the use of intravascular ul-
trasonography was associated with serious ad-
verse events in 11 patients, including 10 coronary
dissections and 1 perforation, indicating that
these procedures are not without risk. Finally, it
is unclear what therapeutic approaches might be
effective in mitigating the risk associated with
4.9
10.2
16.4
18.2
1.3 1.7 1.7 1.9
Rate
of
Major
Adverse
Cardiovascular
Events
(%)
20
10
15
5
0
TCFA (all) TCFA+MLA ≤4 mm2 TCFA+PB ≥70% TCFA+PB ≥70%+
MLA ≤4 mm2
Lesion hazard ratio (95% CI)
P value
Prevalence (%)
3.90 (2.25ñ 6.76)
<0.001
46.7
6.55 (3.43ñ 12.51)
<0.001
15.9
10.83 (5.55ñ 21.10)
<0.001
10.1
11.05 (4.39ñ 27.82)
<0.001
4.2
Present Absent
Figure 2. Event Rates for Lesions That Were and Those That Were Not Thin-Cap Fibroatheromas, at a Median
Follow-up of 3.4 Years.
Event rates associated with 595 nonculprit lesions that were characterized as thin-cap fibroatheromas (TCFA) and
2114 that were not by means of radiofrequency intravascular ultrasonographic imaging are shown according to mini-
mal luminal area (MLA) and plaque burden (PB) as detected on gray-scale intravascular ultrasonography. The inset
shows an example of a thin-cap fibroatheroma imaged by radiofrequency ultrasonography. Data on prevalence are
for one or more such lesions per patient. Lesions in patients with indeterminate events were excluded. (For addi-
tional details, see Table 6 in the Supplementary Appendix.) CI denotes confidence interval.

IAM sdst
• Oclusión de una arteria epicárdica
• Produce sdst en el ECG
• Área de compromiso dependiente de una arteria,
• Nivel de daño dependiente del tiempo

área de compromiso
dependiente de la arteria
The degree of ST-segment deviation has been shown to be an
important measure of ischemia and prognosis.
ST-Segment Elevation Myocardial Infarction
Acute ST-segment elevation myocardial infarction (STEMI),
also known as heart attack, is characterized by the ischemic
death of myocardial tissue associated with atherosclerotic dis-
ease of the coronary arteries. The area of infarction is determined
by the coronary artery that is affected and by its distribution of
blood flow (Fig. 24-7). Approximately 30% to 40% of infarcts
affect the right coronary artery, 40% to 50% affect the left ante-
rior descending artery, and the remaining 15% to 20% affect the
left circumflex artery.9
Pathologic Changes. The extent of the infarct depends on the
location and extent of occlusion, amount of heart tissue sup-
the interventricular septum.
The principal biochemical consequence of myocardial in-
farction is the conversion from aerobic to anaerobic metabolism
with inadequate production of energy to sustain normal myocar-
dial function. As a result, a striking loss of contractile function
occurs within 60 seconds of onset.9 Changes in cell structure
(i.e., glycogen depletion and mitochondrial swelling) develop
within several minutes. These early changes are reversible if
blood flow is restored. Although gross tissue changes are not
apparent for hours after onset of myocardial infarction, the
ischemic area ceases to function within a matter of minutes, and
irreversible damage to cells occurs in approximately 40 minutes.
Irreversible myocardial cell death (necrosis) occurs after 20 to
40 minutes of severe ischemia.9
Microvascular injury occurs in
approximately 1 hour and follows irreversible cell injury. If the
infarct is large enough, it depresses overall left ventricular
function and pump failure ensues.
Left circumflex artery
Right coronary artery
Right coronary artery
obstruction
Left anterior descending
artery obstruction
Left circumflex artery
obstruction
Left anterior descending
artery
A B C
LV
RV
LV
RV
LV
RV
FIGURE 24-7 • Areas of the heart
affected by occlusion of the (A) right
coronary artery, (B) left anterior de-
scending coronary artery, and (C) left
circumflex coronary artery. RV, right
ventricle; LV, left ventricle.

Manifestaciones
• muerte súbita
• dolor típico, demás de 20 min de REPOSO
• ecg típico

• La terapia es la reperfusión: restablecer el flujo
sanguíneo en el vaso ocluido, LO MÁS PRONTO
POSIBLE: Tiempo es músculo

• de manera farmacológica o trombolisis

• de manera farmacológica o trombolisis
• de manera mecánica: angioplastia primaria

Infartos s/sdst
o angina instable
NO oclusión

544 Unit VI Disorders of Cardiovascular
infarction, abnormal Q waves develop because th
larizing current conduction from the necrotic tis
Serum Biomarkers. Serum biomarkers for AC
diac-specific troponin I (TnI) and troponin T (Tn
and creatine kinase MB (CK-MB). As the m
A
A B
P
T
U
Q
S
R
ST
ST
V5
Subendocardial injury:
ST depression
Almost
4 mm
10952-24_CH24.qxd 6/25/08 2:41 PM Page 544
• La diferencia entre angina e infarto esta dado por la
capacidad de reconocer el daño provocado por
necrosis
• En otras palabras por la liberación al torrente
sanguíneo de Enzimas ( Ti, Tt, Ckmb etc.)
• Para que se produzca necrosis se requiere un tiempo
mínimo

Complicaciones

Complicaciones
• Arritmias

Complicaciones
• Arritmias
• Ruptura de pared libre

Complicaciones
• Arritmias
• ruptura de músculo papilar ( insuf. valvular aguda)

Complicaciones
• Arritmias
• CIV

Complicaciones
• Arritmias
• CIV
• Pericarditis pos AMI/ Sd. Dressler

Shock

Shock
• Definición:
• Falla circulatoria aguda que determina la
incapacidad del sistema para aportar el O2 (y
los metabolitos necesarios) lo que resulta en
hipoxia celular.

Shock
• Se puede producir por falla en cualquiera de loa
componentes del sistema:
• hipovolémico
• cardiogénico
• distributivo
• obstructivo

Shock
• Mecanismos compensatorios “standar”
• Activación del simpático (principalmente B1 y
alfa)
• vasoconstricción e inotropismo
• Activación del sistema RAA

Shock
• Hipovolémico
• por perdida importante y más o menos aguda del
volumen intravascular:
• La más clásica: hemorrágica
• Diarreas
• Grandes quemados, tercer espacio

Shock
ventions can be used successfully. 500 mL or 10% of their blood without experiencing adverse
effects. As increasing amounts of blood (10% to 25%) are
removed, the stroke volume falls but arterial pressure is main-
tained because of sympathetic-mediated increases in heart rate
and vasoconstriction. Vasoconstriction results in an increased
diastolic pressure and narrow pulse pressure. Blood pressure is
the product of cardiac output and systemic vascular resistance
Left subclavian
artery
Renal arteries
n pump. (From Hudak C. M., Gallo
rsing [6th ed.]. Philadelphia: J. B.
0 10 20 30 40 50
50
0
100
% of total blood removed
Cardiac
output
and
arterial
pressure
(%
of
normal)
Mean
arterial
pressure
Cardiac
output
FIGURE 26-10 • Effect of hemorrhage on cardiac output and arte-
rial pressure. (From Guyton A. C., Hall J. E. [2006]. Textbook of med-
ical physiology [11th ed., p. 279]. Philadelphia: Elsevier Saunders.)

Shock: mecanismos
compensatorios
anisms to maintain cardiac output and blood pressure, the loss
of vascular volume would result in a rapid progression from
the initial to the progressive and irreversible stages of shock.
The most immediate of the compensatory mechanisms are the
sympathetic-mediated responses designed to maintain cardiac
output and blood pressure (Fig. 26-11). Within seconds after
the onset of hemorrhage or the loss of blood volume, tachycar-
dia, increased cardiac contractility, vasoconstriction, and other
signs of sympathetic and adrenal medullary activity appear. The
sympathetic vasoconstrictor response also mobilizes blood that
has been stored in the venous side of the circulation as a means
of increasing venous return to the heart. There is considerable
capacity for blood storage in the large veins of the abdomen,
Extracellular fluid is distributed between the interstitial spaces
and the vascular compartment. When there is a loss of vascu-
lar volume, capillary pressures decrease and water is drawn
into the vascular compartment from the interstitial spaces. The
maintenance of vascular volume is further enhanced by renal
mechanisms that conserve fluid. A decrease in renal blood flow
and glomerular filtration rate results in activation of the renin-
angiotensin-aldosterone mechanism, which produces an increase
in sodium reabsorption by the kidneys. The decrease in blood
volume also stimulates centers in the hypothalamus that regu-
late ADH release and thirst. ADH, also known as vasopressin,
constricts the peripheral arteries and veins and greatly increases
water retention by the kidneys. Although the mechanism of
FIGURE 26-11 • Compensatory mechanisms used to maintain circulatory function and blood volume
in hypovolemic shock. ADH, antidiuretic hormone.
Acute bleeding or other conditions
leading to decrease in blood volume
Heart
Increased heart rate
and cardiac contractility
Blood vessels
Vasoconstriction
of vessels in skin
and nonvital organs
Stimulation
of thirst
Posterior
pituitary
Stimulation of
ADH release
Kidney
Sodium and water
retention
Decreased urine output
Renin-angiotensin-
aldosterone mechanism
Adrenal cortex
Release of
aldosterone
Liver
Constriction of veins and
sinusoids with mobilization
of blood stored in liver
Compensatory mechanisms
Mechanisms to
maintain cardiovascular function
Mechanisms to
maintain blood volume
Hypothalamus

Shock hipovolémico
cuadro resumen
• Resistencia vascular sistémica?
• Presión de fin de diástole ( pcp)?
• Gasto cardíaco?

Shock cardiogénico
• Caída del gasto cardiaco por caída de la función de
bomba del corazón con PFD adecuadas
• No solo al función esta comprometida, también hay
respuesta inflamatoria sistémica
• (¿con ritmo adecuado?)

Causas
• Infarto
• miocardiopatías
• patología valvular
• (arritmias)

Shock Cardiogénico:
cuadro resumen
• GC?
• PFD?
• RVS?

cuadro resumen
• GC?
• PFD?
• RVS?
¿ que pasa con la perfusión de las coronarias?

cuadro resumen
• GC?
• PFD?
• RVS?
¿ que pasa con la perfusión de las coronarias?
Recuerde que Q=dP/R

Shock distributivo

• Neurogénico: por perdida del control simpático
sobre los vasos
• Anafiláctico: reacción alérgica severa
• Séptico: infeccioso

Shock séptico
• Sapsis se refiere a una respuesta INFLAMATORIA
SISTéMICA de causa infecciosa
• Una “respuesta inflamatoria sistémica”
corresponde a la respuesta del huésped frente
a una injuria que condicione destrucción
celular.

cell function secondary to decreased numbers and/or
decreased receptor signaling, an increased proportion of
naive B cells, signaling deficits in the T-cell receptor CD3
complex, increased numbers of inhibitory receptors and
innate immune response and lymphocytes
immune response frequently become d
sepsis.
Phagocytic Cell Dysfunction
Phagocytosis consists of recognition and e
pathogen and subsequent microbe killing
chanisms such as generation of reactive oxyg
bacterial proteases and peptides, and alte
Neutrophil recruitment, phagocytosis and p
varies in particular hosts as a function of hete
way each individual responds to sepsis. Th
strated in the murine cecal ligation and p
model where mice predicted to live or die, b
IL-6 levels, demonstrated equal levels of
trophils and bacteria 6 h following CLP. Howe
mice predicted to live had significantly fewer
bacteria within the peritoneum. Meanwhile,
to die demonstrated an overwhelming infl
with an increase in cytokines, cell recruitme
load. Craciun et al11 thus concluded that th
between the two host sub-populations wa
phagocytosis and enhanced cell efficiency, w
improved survival.
Although neutrophils are necessary to co
infections, a prolonged and vigorous res
Table 1 Diagnostic criteria for sepsis
Systemic inflammatory response syndrome (two or more of the following):
Temperature 438 1C or o36 1C
Heart rate 490 beats per minute
Respiratory rate 420 breaths per minute or PaCO2 o32 mm Hg
White blood cell count 412000/cu mm or o4000/cu mm or 410%
bands
Sepsis
SIRS with an infectious source
Severe sepsis
Sepsis with associated hypoperfusion, hypotension or organ dysfunction
Septic shock
Systolic blood pressure o90 mm Hg or reduction of X40 mm Hg from
baseline despite adequate fluid resuscitation along with perfusion ab-
normalities
Abbreviation: SIRS, systemic inflammatory response syndrome.
PATHOBIOLOGY IN FOCUS Pathophysiolo

• Al “invadir” un germen un territorio estéril se
encuentra con la respuesta local de los macrófagos
residentes
• estos liberan mediadores de inflamación
• IL1b
• TNF-IL6

• Estos mediadores amplifican la respuesta local
aumentando el reclutamiento de células que
colaboran con la eliminación del agente ( ej:
formación de absceso)
• Con alguna frecuencia esta respuesta sale de control
y los macrófagos se encuentran “ hiperactivados” y
con falla en la apoptosis por lo que viven más
tiempo
• Con esto aumentan los mediadores plasmáticos

• TNF a:
• Estimula la síntesis de IL-1, IL-6, IL-8, leucotrienos, txa A2 y
prostaglandinas.
• Estimula la producción de monocitos e induce su activación
• Activa la cascada de la coagulación y sistema del complemento.
• Induce la activación del endotelio, promoviendo la aparición de
moléculas de adhesión.
• Produce alteración del tono vascular y altera su permeabilidad.
• Incrementa la producción de PMN por la médula ósea, estimula
su marginación y pasaje transendotelial y estimula su
degranulación.
• Estimula la síntesis a nivel hepático de proteínas de fase aguda.
• Estimula el catabolismo proteico y la gluconeogénesis, entre
otras.

• IL1b:Estimula la síntesis de TNFa , IL-6, IL-8, PGE2, Leucotrieno B4,
además de su propia síntesis.
• Induce la producción de GMCSF, incrementando el número de
células precursoras de la médula ósea.
• Estimula la marginación de neutrófilos activados.
• Estimula la expresión de genes para colagenasas y fosfolipasas que
participan en los mecanismos de daño celular.
• Aumenta las concentraciones plasmáticas de Factor Activador
Plaquetario (PAF), favoreciendo la actividad procoagulante
endotelial.
• Estimula la síntesis de proteínas de fase aguda.
• Estimula la liberación de hormonas hipofisiarias.
• Produce fiebre, anorexia y alteraciones hemodinámicas por
inducción de síntesis de Oxido Nítrico.

Shock distributivo: cuadro
resumen
• GC?
• PFD?
• RVS?

Shock obstructivo
• como su nombre lo indica se debe a la obstrucción
del flujo sanguíneo en los grandes vasos o corazón
• Usualmente comprometen el llenado o
vaciamiento del VD peo no son las únicas causas
• TEP, Taponamiento, Neumotórax a tensión

taponamiento

Obstructivo
• GC?
• PFD VI?
• RVP?

Complicaciones del Shock
• SDRA: edema pulmonar no cardiogénico cuya causa
exacta se desconoce.
• habría acumulación de neutrófilos en los
capilares pulmonares y aumento de la
permeabilidad de los vasos

• CID:
• Activación amplia de la cascada de coagulación
que resulta en la formación de trombina
• Se suma a lo anterior la disminución de los
sistemas de fibrinolisis
• hay fenómenos hemorrágicos y trombóticos a
nivel microvascular

• Falla Renal
• túbulos especialmente sensible a hipoxia
• NTA es la manifestación mas frecuente

Falla orgánica múltiple
• falla de dos o más sistemas lo que no permite su
funcionamiento sin apoyo (mantención de la
homeostasis)
• mortalidad muy alta

28+a+30+Fisiopatología+cardiovascular+-+Manuel+Méndez.pdf

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