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
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
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 fiberoptic tests
CO= HR x SV (preload after load contractility)
Shoot CO of continuous fiber optic
Resynchronization with Biventricular Pacing
Ablation of Ventricular Fast Slow Tracks
Remodeling and RAAS
Lines the interior surface of the blood vessels,
heart and capillaries Vasoconstriction & Vasodilation to control BP Blood clotting (Thombosis and Fibrinolysis) Atherosclerosis Angiogenesis Inflammation
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
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- 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