Path physiologies of the

Cardiovascular System

Ischemia, Reperfusion Injury, ACS & Stunned Myocardium,

IABP, Fast-Slow tracts, Biphasic defibrillation &
Resynchronization Therapy,
Ablation and ,Remodeling, Sepsis, Endothelium
dysfunction, And Groinology
Ischemia, Injury, and Infarction
 ST depression or T
wave inversion
 ST elevation- the
tombstones
 Pathological Q waves
greater than 0.4 and
deeper than 2 boxes
Reperfusion Injury
 A transient decrease or interruption of blood flow; the
injury is the sum of two components - the direct injury
occurring during the ischemic interval and the indirect
or reperfusion injury which follows. When there is a
long duration of ischemia, the "direct" damage
resulting from hypoxia alone is the predominant
mechanism. For shorter duration’s of ischemia, the
indirect or reperfusion mediated damage becomes
increasingly more important.
 For example, it has been shown that the intestinal injury
induced by 3 hours of ischemia (flow reduced to 20% of
normal) and one hour of reperfusion is several times
greater than that observed after 4 hours of ischemia
alone (Parks and Granger, 1986). These results
demonstrate that the injury produced by reperfusion
can be more severe than the injury induced by ischemia
per se.
What is the clinical relevance of
reperfusion injury?

Reperfusion injury is relevant to many fields of medicine. For the
cardiologist I/R injury occurs following every successfully
balloon angioplasty or tPA induced thrombolysis. For the
transplant surgeon I/R injury is the sequela of every successful
harvest. For the plastic surgeon I/R injury threatens the integrity
of every free flap. For the orthopedist it may take the form of a
decompression fasciotomy for a severe compartment syndrome
or perhaps the reattachment of a severed extremity. Finally,
every physician who has successfully resuscitated critically ill
patients knows the frustration of a multiorgan failure syndrome
in which reperfusion injury also plays a role.
What is the mechanism for
reperfusion injury?

Several studies have demonstrated that anoxic
reperfusion of ischemic tissues results in very little
damage, and it appears that the reactions initiated at
reperfusion involve the formation of cytotoxic oxidants
derived from molecular oxygen. Because oxygen
radical scavengers afford protection in models of
reperfusion injury, a lot of attention has been given to
the oxygen racial producing enzyme xanthine
oxidase. The xanthine oxidase inhibitors allopurinol
and oxypurinol have been shown to dramatically
attenuate reperfusion injury in many different tissues.
This suggests that xanthine oxidase is an important
source of oxidants produced after reperfusion.
 Mechanisms and mediators of reperfusion injury

Verma, S. et al. Circulation 2002;105:2332-2336

Copyright ©2002 American Heart Association

Plaque Rupture
Stunning
 Partially Reversible
 May be accompanied by endothelial
dysfunction (NO) causing reduced coronary
blood flow
 Results of ischemia- reperfusion insult
 Mediated by increased intracellular Ca++
accumulation
 Recovery in hours or weeks
Hibernating & Stunned Myocardium

 Hibernating - can be defined as wall abnormalities (hypo, aki,

dyskinetic segments) present in the setting of chronic ischemia,
which are potentially reversible after revascularisation. This is
actually a proof that they were not "dead", therefore
representing viable myocardium. There is a new steady state
between MBF and function, in other words, these two
parameters are matched: MBF reduced, then function is
reduced too The clinical scenario where HM may be present is,
eg., chronic stable angina and unstable angina (possibly
because of the silent ischemia)
Hibernating & Stunned Myocardium
Stunned - Acute ischemia (eg., major coronary
occlusion) can lead to stunning (segmental
dysfunction) which is persistent for a variable period
of time, up to two weeks, even after ischemia has
been relieved. There is here a mismatched situation,
in which MBF is normal, but function is depressed. (If
ischemia lasts longer than 20 minutes,
subendocardial necrosis usually begins.) The clinical
scenario is, eg., acute myocardial infarction (AMI)
and during percutaneous transluminal coronary
angioplasty (PTCA) or cardiac surgery
EF vs. CO
 Ejection Fraction- %
 Obtained in cath lab, ECHO, and new fiber-
optic tests

 CO= HR x SV (preload after load contractility)

 Shoot CO of continuous fiber optic
IABP
Biphasic Defibrillation
Resynchronization with Biventricular
Pacing
Ablation
Ablation of Ventricular Fast Slow
Tracks
Remodeling and RAAS
Endothelium functions
 Lines the interior surface of the blood vessels,
heart and capillaries
 Vasoconstriction & Vasodilation to control BP
 Blood clotting (Thombosis and Fibrinolysis)
 Atherosclerosis
 Angiogenesis
 Inflammation
Endothelium Dysfunctions
 Vasospasm
 Re-occlusion
 Hypertension
 Reperfusion injury
 CHF
 Diabetic angiopathy
 Auto immune reaction
 PAD
 Hyperlipidemia
 Thombosis
 Atherosclerosis
Endothelial cells secrete mediators
Endothelial Functions in Inflammation
Endothelium and Blood Vessel layers
Endothelium Cells
SIRS to MOF
 Systemic Inflammatory Response Syndrome (SIRS): Patient presents with two or more
of the following criteria.
 temperature > 38°C or < 36°C
 heart rate > 90 beats/minute
 respiration > 20/min or PaCO2 < 32mm Hg
 leukocyte count > 12,000/mm3, < 4,000/mm3 or > 10% immature (band) cells
 Sepsis: SIRS plus a documented infection site (documented by positive culture for
organisms from that site). Blood cultures do NOT need to be positive. While SIRS, sepsis,
and septic shock are associated commonly with bacterial infection, bacteremia may not be
present. Bacteremia is the presence of viable bacterial within the liquid component of blood.
Bacteremia may be transient, as is seen commonly after injury to a mucosal surface,
primary (without an identifiable focus of infection), or more commonly secondary, to an
intravascular or extravascular focus of infection.
 Severe Sepsis: Sepsis associated with organ dysfunction, hypoperfusion abnormalities,
OR hypotension. Hypoperfusion abnormalities include but are not limited to: lactic
acidosis,oliguria,or an acute alteration in mental status.
 Septic Shock: Sepsis-induced hypotension despite fluid resuscitation PLUS hypoperfusion
abnormalities.
 Organ Dysfunctions associated with Severe Sepsis and Septic Shock
Groinology
 Groinology- applicable after large bore catheters
have been removed from the femoral artery
 Hematoma
 Bleeding
 Pseudoaneuryam
 Retroperitoneal bleed
 Thombosis- loss of peripheral pulse
 Manual hold femstop perclose vasoseal