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features of cardiac pain
- visceral in nature (V for Vague!!)
- hard to localize
- hard to describe
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features of pericardial pain/pericarditis
- easier to localize
- NOT made worse by palpation
- made worse by lying supine
- made better by sitting up/leaning forward
-
issue with unprovoked MFTPs
can imitate chest wall pain
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non-modifiable cardiovascular risk factors
- 1. age (men 45+, women 55+)
- 2. gender (more in men)
- 3. premature CHD
- 4. family history (male relative <55, female relative <65)
-
most people with a strong family history of heart disease also have other risk factors
true!
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normal laminar flow through a normal artery leads to:
HIGH arterial wall stress
-
Problem: decreased arterial stress
from risk factors causing endothelial activation
-
endothelial activation
increase in endothelial permeability
-
problem: sustained endothelial activation
sustained risks lead to decreased arterial stress causing the endothelium to favor vasoconstrictina nd platelet aggregation
-
most suseptible place for dysfunction???
bifurcations!
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modifiable independent risk factors for cardiovascular disease
- hypertension
- smoking/tabacco
- diabetes mellitus (#1!!)
- sedentary lifestyle
- body weight/obesity
- left ventricular hypertrophy
- cholesterol
- hypertriglyceridemia
-
significance and residual risk of: hypertension
sig: the relationship is continuous and graded. no clear cut-off. can be partially reversed.
residual: damage to the arterial endothemium. left ventrical hypertrophy.
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significance and residual risk of: tabacco smoking/environmental smoke
sig: the risk is proportional to the # of cigs smoked and how deeply they're inhaled
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significance and residual risk of: diabetes mellitus
sig: at risk even when blood glucose levels are under control
residual: increased vascular permeability
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significance and residual risk of: left ventricular hypertrophy
sig: effect of hypertension
residual: change to ventricular myocardium
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LDL risk stratification
- very high risk: prior heart attack/stroke
- low risk: 0 or 1 traditional risks
-
LDL target goals
- very high risk: target <70
- high risk: target <100
- moderate risk: target < 130
- low risk: target <160
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hypertriglyceridemia is caused by:
- poorly controlled diabetes
- obesity
- excessive alcohol consumption
-
hypertriglyceridemia can lead to:
- fatty liver disease
- pancreatitis
-
acute arterial occlusion can be caused by:
embolim or thrombi
-
embolus:
a mass traveling in the blood stream
-
embolism:
an embolus that lodges to obstruct a blood vessel
-
emboli are most often associated with??
ischemic heart disease from arterial fibrillation
-
emboli typicall lodge in?
- 50-80% in aortic bifurcation/legs
- 20% in carotid arteries
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thrombus:
a blood clot that remains attached at its origin
-
thrombi occur at:
the site of plaque
-
thrombi are precipitated by:
- inflammation of arterial wall
- chronic mechanical irritation
-
during episodes of increased oxygen demand, the myocardium:
- has a limited ability to increase oxygen extraction
- (in healthy people, the maximun is 4-6x resting flow)
-
CFR in normal arteries
-> increase in demand-> increase blood flow-> no problems
-
CFR with plaque < 50%
-> increase demand-> significant reduction in flow-> typical angina and Levines sign
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CFR with plaque >90%
-> no increase in demand-> no CFR to increase flow-> angina at rest
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most common type of angina??
typical!
-
typical angina due to?
coronary artery plaque fron decreased CFR
-
featurs of typical angina
- reproducable pattern (same level of exercise to reproduce)
- attacks start abruptly and seize the patient
- retrosternal pain (poorly localized, visceral in nature, strangling)
- attacks last 1-5 minutes
- pain relieve by rest!
-
other triggers of typical angina?
- emotion
- exposure to cold
- heavy metals
- (these triggers decrease the amount of exertion needed to cause the angina)
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is typical angina pain graded?
no, it is always the same, severity does not change
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levines sign
the patient holds a clenched fist of the sternum when describing/experiencing the discomfort.
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pattern of typical angina
- pain radiates to the left shoulder/arm (typically!)
- location can vary greatly for each individual but a persons angina is always in the same place/predictable
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when to suspect typical angina?
pain anywhere from umbilicus to eyebrows that is provoked by exercise and relieved by rest
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atypical angina due to problems with?
coronary or intramyocardial arteries (they have very low flow reserve since surrounded by heart muscle)
-
coronary artery near normal....smoking cigs:
Prinzmetal angina/coronary vasospasm-> angina at rest
-
normal intramyocardial arteries
normal coronary As--> good blood flow--> no problems
-
dysfunctinal intramyocardial arteries:
increased resistance-> less exertion needed-> angina at rest
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common symptons of atypical angina
- shortness of breathnausea
- diaphoresis (sweating)
- discomfort NOT in the chest
-
atypical angina is common among:
- older/female patients
- diabetic patients
- patients with hypertension
- patients with collagen vascular disease
-
patients with atypical angina are less likely:
to recieve rapid/aggressive treatment. once hospitalized there is no difference in mortality rates
-
prolonged myocardial ischemia= bad, bad, very bad
-
acute coronary syndrome
unstable cardiac symptoms that are happening in real time
-
end results of acute coronary syndrome:
-
signs of acute coronary syndrome
- abrupt onset
- 14% with pleuritic pain
- 33% without chest painnon-pain angina equivalents (nausea, shotrness of breath, fatigue)
- symp. activity (diaphoresis, pallor, pilomotor activity)
-
problem with a physical exam of a patient with acute coronary syndrome?
the exam might be normal!
-
at risk for acute coronary syndrome:
-
compensated congestive heart failure
C for comfortable!!
-
risks for developing compensatory CHF
- standard cardiovascular risks
- history of previous MI
- heart valve abnormalities
-
compensatory mechanism of compensated CHF:
- 1. catecholamines (symp. nervous system)
- 2. retention of Na and H2O
- 3. Cardiac remodeling
-
types of cardiac remodeling
- 1. dialated cardiomiopathy
- 2. hypertrophic cardiomiopathy
- 3. hypertrophic obstructive cardiomiopathy
-
decompensated CHF
- D for dying :(
- inadequate cardiac output even at rest!= not comfortable
-
dialated cariomiopathy
- causes reduced contractability and systolic heart failure
- most common form of heart failure
-
symptoms of systolic heart failure:
- abnormal apical impulse
- cardiac heave (from prolonged contraction)
- radiographic evidence of cariomegally
-
hypertrophic cardiomiopathy
causes muscle to be inelastic and non-compliant and diastolic heart failure
-
sympoms of diastolic heart failure
- right jugular vein distension
- radiographic evidence of pulmonary venous hypertension
-
signs of left ventricular failure:
- breathlessness
- dysphnea on exertion (may be absent in sedentary patients, not specific)
- orthopnea (early warning sign)
- paroxysmal nocturial dyspnea (patient is asleep, more specific to heart disease)
- fatigue and weakness
- nocturia
- oliguria
- cerebral symptoms
-
orthopnea
- occurs when patient is awake
- develops/resolves rapidly
- measured by the # of pillows needed to make the patient comfortable
-
paroxysmal nocturnal dyspnea
- patient is asleep
- takes hours to develop
- 30+ minutes for relief
- "cardiac asthma" from pulmonary edema
-
causes of right ventricular failure:
- left sided CHF
- Cor pulmonale (lungs)
-
symptoms of right ventricular failure
- peripheral edema
- ascites
- hepatomegaly
- anasarca
-
what to look for during a cardiac exam:
- obvious physical findings are ominous in nature
- symptomatic arrhythmias
- symptomatic cardiac murmurs
-
asculatory points
- A PET Monkey
- 1. Aortic valve: 2nd right ICS
- 2. Pulmonic valve: 2nd left ICS
- (3. Erbs point: 3rd left ICS)
- 4. Tricuspid valve: 5th left ICS
- 5. Mitral valve: 4th/5th left ICS
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