Class 17 Flashcards
What is Coronary Artery Disease (CAD)
• Heart muscle must have adequate perfusion, via
coronary arteries, in order to contract properly. Cardiac muscle very metabolically demanding 24/7.
• When coronary artery becomes narrowed, tissue area of myocardium supplied by that artery becomes ischemic & hypotrophic; if artery becomes
blocked, myocardial infarction (heart attack) occurs.
• CAD usually caused by atherosclerosis, risk factors & clinical concerns are essentially same.
• May also be caused by vasospasm, most likely to occur in people 40-70. Condition of sensitivity of the blood vessel wall:
- Chemicals, e.g., cigarette smoke, cocaine,
amphetamines, some prescribed medications, etc.
- Cold, esp. sudden cold exposure
- Powerful emotional distress
What are Signs and Symptoms of Coronary Artery Disease (CAD)?
• CAD S/S don’t usually appear until lumen of coronary artery narrows by 75%.
• Achy chest pain and/or discomfort with exertion are most common.
• Unexplained fatigue, weakness, trouble with performing normal ADLs & trouble sleeping are S/S of CAD are sometimes missed by health care professionals.
• Can be brief episodes that never or seldom recur, or prolonged, leading to heart wall damage.
• Treated with nitroglycerine, acts quickly, possibly calcium channel blocker.
• When caused by atherosclerosis, can give rise to angina pectoris & myocardial infarction.
What is Intermittent Ischemia / Intermittent Ischemic Attack?
There are group of clinical phenomena that occur when partially occluded artery (typically from atherosclerosis) or stenotic artery (e.g., from scarred lumen or spasmy media wall) cannot deliver enough perfusion in high demand circumstances is usually fine in lower metabolic need situations.
What is Angina Pectoris?
Occurring in heart wall, producing attack of ischemic pain
What is Transient Ischemic Attack (TIA)?
Occurring in brain, producing neurological signs
What is Intermittent Claudication?
Occurring in leg muscles, causing pain & limiting
exercise tolerance (↓ walking tolerance called claudication distance)
What is Angina Pectoris?
• Episodes of perfusion insufficiency in section of heart muscle because reduced lumen space in supplying artery, d/t cause of CAD, usually atherosclerosis.
• Compromised lumen size is workable for lower demand situations, becomes insufficient when person’s heart has to work harder - e.g., sudden activity (run for bus), unusual activity (snow shoveling), onset of emotional stress, sudden shock or pain, etc.
• Some angina presentations more stable predictable & others more unstable.
• May occur from irritant-caused vasospasm, eg, lighting cigarette.
• Acute pain, pressure or discomfort in chest & heart referral pattern from imbalance between cardiac workload & available oxygen supply to working
myocardial tissue.
• May experience dyspnea (shortness of breath), nausea/indigestion feelings, belching, & anxiety/panic.
• Females have higher incidence of atypical S/S than males.
• Attack will typically subside with stopping triggering stimulus & taking nitroglycerine.
• Frequent angina attacks are concern because heart wall can become damaged.
• Atherosclerosis-caused angina pectoris is indicator of myocardial infarction (MI) risk.
What are Medications for Angina Pectoris?
• Taken at beginning of attack, typically act quickly vasodilate vessels to improve myocardial perfusion. Most common is nitroglycerin. Was initially thought that nitroglycerin selectively affects coronary arteries. Recent studies show peripheral arteries are also dilated, helping further lessen load on heart.
• Nitroglycerine, when used to rapidly relieve occasional angina symptoms, usually administered sublingually (for rapid absorption into bloodstream through mucous membranes) takes effect within 2-3 minutes. May be tablet or spray.
• More severe/unstable types of angina may involve Pt wearing nitroglycerin skin patch (provides more constant supply of meds to keep arteries dilated).
What are Massage Therapy Precautions for Angina Pectoris?
• Avoid hydrotherapy extremes & full body applications.
• Avoid significantly increasing sympathetic activation.
• Depending on how weak heart function is overall, techniques that substantially increase venous return may be enough to promote angina.
What are Clinical Issues for the RMT for Angina Pectoris?
• During intake, get clear picture of frequency & severity of attacks & person’s typical precipitators.
• Very unstable angina (erratic frequent attacks, attacks are precipitated very easily) may not be good match with massage therapy; in most cases of angina pectoris Pt can be massaged with appropriate attention to possible attack triggers.
• Medications – know in advance where medication is & prescribed dose.
- With patches – don’t physically manipulate them (can potentially increase delivery rate to Pt & can dose yourself); don’t apply temperature applications over them. Don’t wet or oil patch.
- Avoid touching patch by 10 cm/4 in all directions.
• If attack onsets during massage:
- Stop treatment
- Do what is appropriate regarding meds
- Position person in supine with trunk elevated or seated comfortably
- Monitor & maintain calm environment
• Be ready to call for medical assistance (911) if needed
Main differences Angina episode vs. heart attack?
• MI pain much more intense
• MI symptoms do not improve with rest/meds
• MI S/S do not subside
What is Myocardial Infarction (MI)?
“heart attack” layperson term. Refers to idea of heart suddenly stopping. Various reasons why this can happen: causes of acute CHF, conduction failure, ventricular dysrhythmia, etc. Most common is myocardial infarction.
MI is infarction in heart wall. 90+% occur in LV.
Other causes are possible, e.g., blood turbulence from vasospasm bringing on occluding thrombus, vast majority are atheroma + thrombosis leading to
blockage of coronary artery. Occlusive infarction means that tissue death occurs in section of heart wall supplied by that arterial vessel.
Severity of MI is determined by size & importance of coronary artery affected. If occluded vessel is small arterial branch, may be few or no clinical impacts. Central vessel occlusion can cause massive, immediately fatal situation. Most MIs fall somewhere in between. Takes about 20-40 minutes before myocardial cells sustain irreversible damage/death.
About 90% of individuals survive first MI. Surviving first year post-MI is key marker. 19% of males & 26% of females dies within year of first MI. In addition to size & location of myocardium damage & quality of medical care, other factors quitting smoking & compliance with necessary lifestyle change advice are crucial. Other survival rate factors: having pet is big one, not suffering from depression, at least one person to confide in, & social/community engagement are important & controlling blood pressure – incidence of second MI goes up significantly with BP level increases.
Fatality rate increases exponentially with each subsequent MI.
What are MI Risk Factors/Causes?
• Hypertension
• Smoking
• Excess alcohol consumption
• Obesity, sedentary lifestyle
• Other causes of atherosclerosis
• Age: risk increases in males over 45, females over 55
• Family predisposition: father or brother diagnosed with heart disease before age 55, mother or sister diagnosed before age 65
• Race predisposition: incidence is higher in black/brown & indigenous populations in Canada
• Specific health conditions, e.g., diabetes substantially increases MI risk
• Chronic high stress
• Loneliness, unhappiness, depression
Signs and Symptoms of MI (Prodromal)
Reflect early or preliminary S/S during progression of thrombosis to full occlusion. Some people have none, most have some indicators for few minutes to few days before actual MI onset.
Signs and Symptoms of MI (S/S of SNS activation)
Lists below represent S/S that can be present prodromally, what will proceed to be apparent as MI onsets.
• Cold, clammy, sweaty
• Anxiety
• Shaking
• Rapid, shallow breathing
• Pallor, cyanosis (lips, fingertips)
• Increased heart rate
• Pupil dilation
• Nausea, digestive disturbances
