Ch21FlashCards.txt

Ischemic Heart Disease (IHD) - 35%

30%

• 1) Increasing age
• 2) Male gender
• 3) Genetic predisposition/family history

• 1) Cigarette smoking
• 2) Hypertension
• 3) Obesity
• 4) Sedentary lifestyle

• 1) Direct vascular injury
• 2) LV hypertrophy
• 3) Increased myocardial oxygen demand (MvO2)

• 1) Is it well-controlled?
• 2) Is the pt compliant with treatment?
• 3) What is the procedure?
• a. Colonoscopy vs craniotomy
• 4) What medications are being used?
• 5) What meds has the pt received before surgery?

• 1) Elevated cholesterol/triglycerides
• 2) Hyperglycemia/diabetes
• 3) Low HDL levels

• 1) Personality type
• a. Type-A are difficult to deal with
• 2) C-reactive protein: active vs bystander?
• a. Is elevated C-reactive protein causing the problem?
• b. Is the problem causing elevated C-reactive protein?

• 1) Left main coronary
• 2) Right coronary

• 1) RA
• 2) Most of the RV
• 3) LV inferior wall (varies)

70-80% of people

• 1) PDA
• 2) Posterior LV
• 3) Superior-posterior intraventricular (IV) septum
• 4) Inferior wall

10-15% of people

• 1) Circumflex artery supplies the PDA
• 2) Cx wraps around the AV groove
• a. Continues down as the PDA also supplies most of the posterior septum and inferior wall

15-20% of people

Both Cx and RCA supply PDA

• 1) LA
• 2) Most of
• a. IV septum
• i. Bundle branches here
• b. LV
• i. Septum
• ii. Anterior wall
• iii. lateral wall

• 1) LAD
• 2) Cx

• 1) Septum
• 2) Anterior wall
• What structure does the Cx supply?
• Lateral wall

• 1) RCA in 60% of people
• 2) LAD in 40% of people

• 1) RCA in 85-90% of people
• 2) Cx in 15-20% of people

• Dual blood supply
• 1) LAD
• 2) PDA

• 1) Diagonal branches of LAD
• 2) Marginal branches of Cx

PDA alone supplies these muscles

Posterior papillary muscles - singular blood supply

Anticipated papillary muscle dysfunction with vessel occlusion and subsequent MV incompetence

225-250ml/min

• The inner 0.1mm endocardial surface
• This is an insignificant amount of perfusion
• Almost no perfusion by this method during systole

Epicardial vessels - outer surface vessels

Intramuscular arteries

• A plexus of vessels located immediately beneath the endocardium
• What is unique regarding coronary blood flow during the cardiac cycle?
• Intermittent flow.
• During contraction, intramyocardial pressures in the LV approach systemic arterial pressure
• Force of LV contraction totally occludes intramyocardial part of coronary arteries
• Even during the late part of diastole, LV pressure exceeds RA pressure

During tachycardia

Diminished

ADP-LVEDP = CPP

RV has less force of contraction during systole and does not totally occlude intramyocardial vessels

5%

• 1) HR
• 2) CPP
• 3) Arterial oxygen content (CaO2)
• 4) Coronary vessel diameter

• Determines diastolic time
• Increased HR results in decrease in coronary perfusion due to disproportionate reduction in diastolic time (% of cardiac cycle)

• 1) Aortic pressure - supply side of CPP (preload)
• 2) LVEDP - resistance side of CPP (afterload)

ADP

• 1) Decreased ADP
• 2) Increased LVEDP

• 1) Arterial oxygen tension
• 2) Hgb concentration
• CaO2 = (SaO2 * Hgb * 139) + (0.0031 * PaO2)
• This formula demonstrates that oxygen saturation and hemoglobin level have a greater influence on arterial oxygen content than does partial pressure of oxygen

DO2 = CaO2 * CO

During single-lung ventilation, knowing the patient's hemoglobin level is adequate (>10) allows the patient to tolerate abnormally low PaO2 levels

• 1) Basal requirements
• 2) HR
• 3) Wall tension
• 4) Contractility

Myocardial oxygen demand

• 1) Basal requirements
• 2) Electrical activity
• 3) Volume work
• 4) Pressure work

70%

30%

• Increased coronary blood flow
• Myocardium cannot extract more oxygen from hemoglobin like other tissues

• 1) Preload (ventricular radius)
• 2) Afterload

Adenosine

• 1) Adenosine
• 2) K+ ions
• 3) H+ ions
• 4) CO2
• 5) Bradykinin
• 6) Prostaglandins
• 7) Nitric oxide

They inhibit prostaglandin synthesis and thereby decrease ability of coronary and renal artery vasodilation to a degree

• ACh released from vagus nerve stimulation
• PNS distribution is not extensive to coronary arteries, but ACh release will cause
• 1) Vasodilation
• 2) Slowed HR

• 1) Epinepherine
• 2) Norepinepherine

Extensive

• Located predominantly in epicardial vessels
• Excess stimulation can cause vasospastic myocardial ischemia and angina

• 1) Cardioacceleration (increased HR)
• 2) Positive inotropy (increased contractility)

• 1) Located mainly in
• a. Smaller intramuscular vessels
• b. Subendocardial vessels
• Vasodilator

Increased metabolic requirements caused by epi/NE offset by local blood flow regulatory mechanisms that dilate the coronary arteries.

• 1) Fat metabolism - 70%
• a. Preferential breakdown of fatty acids
• 2) Glycolysis
• a. Does not fully meet energy needs

• 1) Coronary sinus
• 2) Anterior cardiac veins
• 3) Thebsian veins

LV to RA

Anterior cardiac veins

• Account for small portion of coronary venous return
• Empty into all chambers of the heart, technically causing a right to left shunt but insignificant

• Retrograde flow through coronary veins
• Veins lack valves which allows backward flow

• 1) Atherosclerosis
• 2) Coronary thrombus
• 3) Coronary embolus
• 4) Coronary artery spasm

Because radius is raised to the 4th power in determining flow, reducing the artery's radius by 50% results in a 16-fold reduction in flow (flow becomes 1/16 of normal)

• 1) Cholesterol becomes deposited beneath endothelium of the coronary artery
• 2) Gradually these areas are invaded by fibrous tissue and frequently become calcified, becoming atherosclerotic plaques
• 3) These plaques can extend into the lumen of coronary arteries to partially or totally occlude flow

• If an atherosclerotic plaque breaks through the intima of a coronary artery and comes into contact with blood:
• 1) Platelets adhere to its unsmooth surface
• 2) Fibrin will be deposited
• 3) RBCs become entrapped
• 4) Resulting blood clot can expand to totally occlude the vessel

A thrombus breaks loose from its atherosclerotic plaque and occludes a more distal segment of a coronary artery

• Thrombus formed as the result of blood stasis from vasospasm
• Thought to be a potential source for the development of a secondary thrombus

• 1) Partial coronary obstruction
• 2) Loss of autoregulation
• 3) Angina pectoris
• a. Probably due to glycolysis and lactic acid production
• 4) Mortality
• a. Highest with left main involvement
• b. Second highest with LAD involvement

• 1) Stress EKG
• 2) Noninvasive imaging
• 3) Cardiac catheterization

• 1) Signs of ischemia and their relationship to chest pain
• 2) Appearance of a new murmur of MR
• 3) Decrease in BP during exercise

Subendocardial tissue

• Baseline voltage prior to QRS is ELEVATED
• ST-segment appears DEPRESSED relative to baseline

Full-depth tissue damage

• Baseline voltage prior to QRS is DEPRESSED
• ST-segment appears ELEVATED relative to baseline
• Q-wave seen because electricity viewed is moving in opposite direction (toward other side of heart)

• 1) Echocardiography
• 2) Nuclear stress imaging
• a. Pharmacologically induced stress (dobutamine, adenosine, dypyridamole)
• b. Imaging to assess wall motion and/or tracer uptake to assess perfusion (thallium, technetium)

Cardiac catheterization

Chest CT

• 1) Angina pectoris refractory to maximal medical therapy
• 2) Patients being considered for emergency revascularization

• 1) Behavior modifications
• 2) Medical management
• 3) Medical/surgical intervention

• 1) Stop smoking
• 2) Reform diet - lose weight
• 3) Exercise
• These 3 things alone may lower BP and improve life expectancy
• 4) Chill out

• 1) Beta blockers
• 2) Calcium-channel blockers
• 3) ACE inhibitors
• 4) Antiplatelet drugs
• 5) Nitrates

• 1) Block sympathetic beta-adrenergic receptors
• 2) Decreased sympathetic activity
• 3) Decreased HR
• 4) Decreased cardiac metabolism during stress
• 5) Decreased MvO2

• 1) Decrease HR and SVR during exercise
• 2) Dilate coronary arteries and relieve spasms
• 3) Can decrease contractility and INCREASE the rate of reinfarction

Digitalis - cardiac glycocide therapy

• 1) Low dose ASA
• 2) Plavix
• 3) Ticlid

• 1) Angioplasty
• 2) Stents
• 3) DCA
• 4) Lasers
• 5) And more

Patients with these stents require much longer antiplatelet therapy before they can safely discontinue medication prior to surgery.

• 1) Low mortality rate
• 2) High percentage of graft patency out to 10 years
• a. More with lifestyle modifications
• 3) Relieves angina in 85% of patients

• 1) Pump failure
• 2) Pulmonary edema
• 3) Ventricular fibrillation
• 4) Ventricular rupture

Systolic

Diastolic

• Ventricular stretch/cardiogenic shock, dyskinesis
• Volume of stretched bulge is immediately removed from net SV and therefore CO

Pulmonary edema

Often a delayed symptom (several days) as the result of diminished renal perfusion over days. This leads to decreased urinary excretion and subsequent increased TBV in a compromised pump.

• 1) Rapid depletion of K+ ions from ischemic musculature;
• a. increased extracellular K+ causes cardiac irritability
• 2) Injury current
• a. Ischemic muscle unable to completely repolarize membranes after each heartbeat
• 3) Increased sympathetic responses from MI cause muscle irritability
• 4) LV dilation causes increased conduction pathway and abnormal pathways

Days after an MI, dead muscle fibers begin to degenerate and the heart wall becomes stretched very thin. Dead muscle bulges outward severely with each contraction and this systolic stretch can ultimately rupture.

• 1) MONA
• 2) Thrombolytics if within window of opportunity
• 3) Anticoagulation
• 4) Beta blockers
• 5) Arrhythmia management
• 6) Rest