CAD and Cardiac Emergencies Flashcards
CORONARY ARTERY DISEASE (CAD)
- coronary arteries deliver 250 ml oxygenated blood to the myocardium, each minute
- this translates to about 360,000 ml / day
- the heart contracts constantly (>100,000 times / day) and hence has a constant and very
large O2 demand - the heart has very little oxygen reserve, so additional needs will require an increase in
coronary artery blood flow - the term CAD is used to describe the effects of impaired coronary artery blood flow to the
myocardium - in most cases, CAD is caused by coronary artery atherosclerotic obstruction
what is atherosclerosis?…
- atherosclerosis is the primary disease that affects coronary arteries
- it is a progressive process by which fatty substances accumulate as plaque along
the inner lining of the vessels, which then narrows the artery passages - CAD exists when atherosclerosis has reached the stage where the blood flow
through the arteries is not sufficient enough to meet the O2 demands of the
myocardium - the extent of CAD depends on the amount of arterial narrowing, and the reduction in blood
flow resulting from this narrowing
- there are 4 grades of atherosclerosis
-Grade 1 - 25% narrowing and reduction in blood flow. Severity is minimal.
- Grade 2 - 50%. Moderate
- Grade 3 - 75%. Severe
- Grade 4 - 100%. Complete blockage.
- this classification is based on the degree of obstruction
- obstruction of about 75% is needed to produce significant reduction in coronary
artery blood flow, resulting in symptoms
- obstruction can occur in any, and/or all arteries
- LAD obstruction would be the most dangerous as this vessel supplies a much
larger portion of the total myocardial mass (reviewing arteries in Lesson 1 might
be useful) - an occlusion of the LCA would be even worse, but is the least common
How CAD leads to Acute Coronary Syndromes
- a piece of plaque ruptures, traveling toward the distal portion of the artery
- during the travel, platelets begin to adhere to it, as well as fibrin and thrombin
- in other words, a blood clot forms on the plaque
- this “enlarged” plaque then partially or totally occludes the distal portion of the artery
- a rough atherosclerotic lesion irritates the arterial wall causing bleeding beneath the plaque
- the hemorrhage then dislodges the plaque, and the lesion begins its travel
- the ‘travelling’ clotted plaque obstructs a distal part of the vessel
CAD RISK FACTORS
- some are modifiable (ie: diet), while others are termed non-modifiable (ie: gender)
Heredity, Genetics
- heredity ranks very high on the list of non-modifiable risk factors
- it is becoming clear that genetic influences play an important role
- the physical structure of the coronary arteries and the rate of atherosclerosis seems to
be genetically determined
Hypertension
- high BP is associated with a 2-5 time greater incidence of CAD
- it predisposes to CAD by accelerating the rate of atherosclerosis
- cumulative arterial damage occurs with sustained hypertension
Smoking
- nicotine causes vasoconstriction, thereby reducing coronary artery blood flow
- cardiac workload increases (↑HR & BP) and can therefore produce an oxygen deficiency
- associated with ↑ CO levels in the blood, interfering with O2 supply to the myocardium
- the risk factor is markedly reduced within 2-3 years of smoking cessation
Obesity
- the mechanism is not fully understood
- it is believed that the risk of CAD is increased in the overweight populace because they
are more prone to hypertension, diabetes, elevated cholesterol levels
Gender & Age
- CAD is still a little more prevalent in men than in women
- female estrogen appears to have a protective effect, however, with women’s roles
changing, and more showing type A personalities, females are closing the gap on males - after menopause, the incidence of CAD in females equals that of the male counterpart
- in both sexes, the incidence of CAD increases with age (almost doubling every 5 years)
- men are affected by CAD as early as their mid 20s
- women in childbearing years seem almost protected from CAD, unless they have some
underlying factor (ie. diabetes, smoking, hypertension)
Diet
- fats are carried in plasma in 2 forms:
1) free fatty acids
- these are used up almost immediately for energy
2) lipoproteins
- these are mostly stored in muscle
- lipoproteins can absorb into the vessel walls, leading to atherosclerosis
- cholesterol is transported in lipoproteins. The 2 types of lipoproteins are:
1) HDL (high density lipoproteins)
- these are transported away and metabolized by the liver
- sometimes called the ‘good’ cholesterol
2) LDL (low density lipoproteins)
- these are absorbed into the vessels’ walls
- sometimes called the ‘bad’ cholesterol
- some factors affect HDLs (the ‘good’ lipoprotein):
- lower HDL levels are seen in:
- diabetics
- the overweight
- cigarette smokers
- post-menopausal women
- sedentary types, with lack of exercise
- elevated HDL levels can be seen in:
- those who exercise
- pre-menopausal women
- moderate alcohol consumers (ie.1-2 glasses red wine/day)
Diabetes Mellitus
- CAD seems to develop more frequently and at an earlier age among diabetics, particularly
those with Type 2 Diabetes - diabetics seem more prone to:
- hypertension
- obesity
- disturbances in sero-lipoproteins
- (all of which are CAD risk factors)
Sedentary Life Style
- the risk of CAD among those leading a sedentary lifestyle is almost doubled
- the mechanism is not yet fully understood, but exercise appears to decrease the risk of
CAD, regardless of the presence of other risk factors, or the patient’s age - it is believed that a sedentary lifestyle is associated with:
- low HDL levels
- higher levels of LDLs
- increased triglycerides, as fats are not burned up with activity
- hypertension
Personality Type
- the coronary prone person is often referred to as a “type A personality”
- this person is rushed, aggressive and ambitious in nature
- sometimes even impatient, easily-provoked, and over-committed
- these people have as much as twice the risk of CAD than type B personalities (those
with lower keyed, relaxed and satisfied lifestyles) - type A behaviour might increase sympathetic nervous system activity
Race
- CAD affects all races
- it is lowest among those of African and Chinese origin
- it is not understood if the differing risks result from environmental factors, or genetic factors
Stress, Anxiety
- industrialized countries reveal a higher incidence of CAD
- this is probably due to the environmental stress imposed by a fast-paced lifestyle
- while trying to cope with a rapidly changing society and culture, chronic anxiety develops
and somehow promotes atherosclerosis - anxiety is often accompanied by elevated cholesterol levels and hypertension
- studies are ongoing to better understand the CAD-stress relation
MANIFESTATIONS and CLINICAL SPECTRUM OF CAD
- CAD symptoms are caused by the lower blood supply reaching the myocardium, rather
than the state of the coronary arteries - even with grossly narrowed arteries, CAD may not produce symptoms if enough blood
is reaching the myocardium through adequate collateral circulation
STABLE ANGINA (ANGINA PECTORIS)
- this is the distinctive type of chest pain that indicates impaired circulation to the myocardium
- the heart’s oxygen demand exceeds the capacity of the coronary artery supply
STABLE ANGINA (ANGINA PECTORIS) - Pain Characteristics
- usually substernal (under the breast bone)
- pain may radiate to either arm, neck, jaw, teeth, shoulders, upper back
- sometimes, pain may be absent substernally, and only experienced at sites of radiation
- it may be described as tightness, squeezing, constriction, pressure, indigestion, burning,
heaviness - the pain is not influenced by change in position or breathing pattern
STABLE ANGINA (ANGINA PECTORIS) - Occurrence & Duration of Pain
- cardiac O2 demand is related to the amount of work the heart performs, so any condition
that increases myocardial demand for O2 can produce anginal pain - physical effort or sudden emotional stress (fear, excitement) increases the HR, the cardiac
workload and therefore the O2 requirement, leading to pain - provoking factors can include exercise, eating, emotional stress, exposure to elements
(ie. heat or cold) - when provoking factors cease (ie. activity stops), the HR drops and O2 demand decreases
- consequently, the pain subsides
- cessation of pain indicates that myocardial O2 demands have been met
- pain is usually of short duration (1-5 min), and relieved with rest
- the oxygen deficit is transient and not destructive to the myocardium
- the pain is predictable and reproducible. Patients can predetermine that certain activities
will cause chest pain - associated symptoms may include pallor, nausea, vomiting
STABLE ANGINA (ANGINA PECTORIS) - Treatment
- rest
- nitroglycerine: acts by dilating the coronary vessels thereby increasing blood flow
and oxygen supply to the myocardium - beta-blockers, Ca+ channel blockers, ASA
- often diagnosed by a positive stress test
UNSTABLE ANGINA
- this is the clinical ‘stage’ between stable angina and MI
- it is a worsening of stable angina
- chest pain develops with increasing frequency and less effort
- nitroglycerine has little or no effect
- it is difficult to rule out the possibility that a small area of the myocardium was destroyed
during the longer period of time with a lack of oxygen - so, these patients are closely observed and often admitted to hospital, until a diagnosis
of MI can be excluded - signs of ischemia are often noted on the ECG
UNSTABLE ANGINA - Pain Characteristics
- pain is described with the same terms as those experienced with stable angina
(ie. crushing, heaviness, squeezing, etc) - chest pain can persist for 10-20 minutes or longer, even after using nitroglycerine
- associated phenomena often include changes in skin color, diaphoresis, nausea, vomiting,
dyspnea, anxiety
UNSTABLE ANGINA - Treatment
- the main goal is to prevent an MI from occurring
- oxygen: increasing the oxygen supply will help supply the heart’s O2 demand
- pain control (morphine is commonly used)
- cardiac monitoring, ECGs, cardiac enzymes and proteins (troponins)
- decrease stress and activity levels
- nitrates, ASA, beta-blockers, calcium-channel blockers