Slide set 7 Flashcards
What is the levine sign
Someone gripping chest in pain
Risk factors for atheroscelrosis (8)
Smoking HTN Dyslipidemia Male Age FamHx DM Obesity
Coronary arteries represent how much of total CO
5%
When coronary artery flow decreases with exercise how stenotic is it
70% Stenotic
When coronary artery flow decreases with rest how stenotic is it
90% Stenotic
Atherosclerosis is defined as
Chronic inflammatory D/O that leads to hardening of the arteries
Ischemic heart disease defined as
Imbalance of supply and demand of blood/O2 to a portion of myocardium
Angina is defined as
chest pain induced by ischemia
Anginal equivalants
In a chest pain free pt the pt experiences SOB, Sweating, Nausea, Claudication, syncope, edema, fatigue
NL arterial wall is compsed of
I-M-A (Intima-Media-Adventitia) Endothelial cells Smooth Muscle cells Extracellular matrix
Atherosclerotic fatty streak is
Endothelial dysfunction Lipoprotein entry/modification WBC recruitment (macrophages) Foam cell formation
Plaque progression is
Fatty streak + smooth muscle recruitment and matrix metabolism
O2 content is determined by
Hgb concentraiton and sys oxygenation
Myocardial oxygenation SUPPLY relies on
Oxygen content and coronary blood flow
Coronary perfusion occurs in what phase
Diastole
Coronary blood flow relies on
Coronary perfusion pressure and coronary vascular resistance
Perfusion pressure can be approximated by
Aortic Diastolic pressure
If aortic DBP is decreased what happens to myocardial oxygenation
Myocardial oxygenation decreases due to decreased coronary artery perfuson
Coronary vascular resistance is determined by
External compression forces Intrinsic regulation
Coronary vascular resistance intrinsic regulators are due to
Local metabolites Endothelium (V-dil/V-con substances) Neural innervation
Coronary artery Vasodilators
Nitric Oxide Prostacyclin Endothelium derived polarizing factor
Coronary artery Vasoconstrictors
Endothelin 1
Coronary vasculature is innervated by
SNS with both alpha and beta2 receptors
Myocardial oxygen DEMAND is determined by
Wall stress Contractility HR
Heart wall stress is directly related to
Systolic ventricular pressure
Heart wall stress is inversely related to
Ventricular wall thickness
An increased HR does what to O2 Supply and demand
Increases O2 consumption = demand
Contractility effects supply and demand how
Increases O2 consumption = demand
What is the primary reason for ischemia when concerning vasculature
Inappropriate vasoconstriction due to metabolites and damage - not the narrowing
Lossing antithrombic properties in the blood vessels causes
A decrease in NO and Prostacyclin promoting platelt aggravation
What are the three basic consequences of Ischemic heart DZ
Myocardial injury Acute Symptoms Myocardial necrosis leading to MI
What are the 2 forms of myocardial injury
Stunned myocardium Hibernating myocardium
Acute symptoms of ischemic heart DZ include
(Un)Stable angina Variant Angina (AKA prinzmetal angina) Cardiac syndrome X
Myocardial necrosis can manifest as
Irreversible Symptomatic ischemia Silent ichemia
Variant (Prinzmetal) angina is
Coronary artery spasm occuring at rest
Cardiac syndrome X is
Classic Angina, CP, or ischemia during exercise stress test but with no occlusion or atherosclerosis
Stunned myocardium is
Short term total/near total reduction of coronary blood flow but is restablished and results in LV dysfx
Hibernating myocardium is
Basically your chronic stable angina patients. Persistantly impaired myocardial/LV function at rest but restored with improved blood flow or reducing O2 demand
What protective mechanism can you see with chronic stable angina pts
Low EF
Hibernating myocardium may require what dx test
PET or Dobutamine echo to determine perfusion ability
Stable angina is
Chronic predictable and transient during stress angina from a fixed plaque
A stable angina can be described as
Typical or Atypical
Moratility rate of stable angina is better determined by
LV fx, exercise capacity, and severity of symptoms
Classic angina is described as
Retrosternal chest pain (levine sign) Pain radiating to shoulder, arm, neck, Pt may say elephant on chest
How long is the typical classic angina
<15m
What is classic angina relieved by
Rest or nitrates
Unstable angina is essentially
A change in pattern (unpredictable) New onset Intensified S/S Prolonged episodes
Variant (Prinzmetal) Angina is
Chest pain recurrent at rest or at night and is secondary to a coronary spasm
Cardiac syndrome X is
Pt has typical S/S of angina pectoris but with no other evidence on myocardial issues
Silent ischemia is
Cardiac ischemia that occurs in the absence of discomfot or other S/S
Silent ischemia is more common with who
DM pts due to impaired pain sensations and in (elderly and women)
Three key angina questions
Is CP substernal, Retrosternal,epigastric Are S/S brought on by exercise Are S/S relieved w/in 5m of rest or NTG
Answers to key questions
3 yes = typical angina 2 yes = atypical angina <2 Yes = Non-anginal
Risk factors for CAD (5)
M >55 and F >65 Known CAD or cerebrovascular disease Pain not producible by palpitation Pain worse during exercise pt assume pain is cardiac in nature
Low risk (0-1) CAD & chest pain
Eval pt for noncardiac causes
Mod risk (2-3) CAD & chest pain
Order EKG if POS then give O2, ASA, and transport
High risk (4-5) CAD & chest pain
Order EKG and give O2, ASA, and transport
Most likely what would you find on a PE of chronic stable angina
Nothin on PE
Dx tests for high probability CAD
1st Stress imaging and if Severe or with high RFs CT angiography and revasc (PCI or CABG)
Dx tests for Intermediate probability CAD
Stress EKG or Stress imaging
Dx tests for Intermediate probability CAD
Stress EKG
Goals of chronic ischemic disease
Decrease freq Prevent acute coronary synd (AMI) Prolong Survival
Stable angina is managed by type of episode
Acute vs Chronic episode
Acute angina episode management
Rest Nitrates (SL) (1st line) Relief precipitaing/aggravating factors
Chronic angina episode management
Primary is to prevent Lifestyle mod Pharm
Pharm to prevent anginal attacks
Often used in combo (CCB, B-agonist, nitrates)
Vasculo-protective TXT regiment of pharm for stable angina
Anti-PLT Lower lipids ? Blockers ACEI (high risk pts)
What is first line therapy to reduce anginal episodes
? Blocker (goal HR is 55-60bpm)
What is the only drug to prevent re-infarct and increase survivalability
B blocker
Efx ?eta-1 have
Positive inotropic and chronotropic efx
Efx ?eta-2 have
V-dil and B-dil efx
What are the 4 types of B-Blockers
Non selective Beta1/2 (propanolol) Selective beta1 (metoprolol,atenolol) Intrinsic sympathomimetic activity Selective alpha, non selective ? block
CI to use B-Blk
Bradycardia <55HR or symptomatic PRI >0.24 or 2/3 degree heart block Decompensated HF Hx of severe asthma DM with hypoglycemia episodes
Should a BB be used for prinzmetal angina
NO
CCB are used when
Stable angina management in combo with BB or as 1st line if BB is CI
Which long acting CCB are preferred
Verapamil (Non-DHP) Diltiazem (Non-DHP) Amlodipine (DHP)
What does a non-DHP CCB do?
Decrease cardiac rate/force V-dil affect decreasing afterload
CCB are CI when
There is Bradycardia or systolic HF
What does a DHP CCB do
V-dil affect decreasing afterload 1st line for pts w/ Bradycardia or AV Blk
Nitrates are used for
Stable angina prevention and are combo w/ BB or w/ CCB
Long term use of nitrates causes
Nitrate intolerance
Ranolazine is a
Nitrate that is Na+ channel blocker and is used in combo with BB or when a BB cant be used
All pts with stable angina should counseled for
Med compliance Risk factor control Regular exercise Annual flu vaccine
Stable angina management of anti-PLT therapy consist of
ASA or Clopidogrel if there is an ASA allergy or both if there is hx of MI
Angina management w/ lipid lowering agents
All patients should be on statins >75 mod-high <75 high
Those with HTN, previous MI, or exertional angina should be on what med
BB
Will an ACEI improve an angina
NO
Who is an ACEI inhibitor good for that has an angina
HTN, DM, CKD, LVEF<40%
Coronary revascularization is pursed if
If angina S/S dont respond Rx therapy Unacceptable SEs from Rx High risk coronary disease
When is CABG more appropriate
Large amount of myocardium at risk Pts with 3 vessel disease Complexed anatomy of L-main DZ L-ventricular systolic fx
When is PCI best managed
Pts with one or two vessel disease
The COURAGE trial suggests
PCI was no better than Rx therapy at reducing mortality/events but was effective at long term symptom relief
PCI stands for
Percutaneous coronary intervention
PCI consists of
Percutaneous transluminal CA Coronary artery stents (Drug eluding)
What are the names of the drug eluding stents
Sirolemus and Paclitaxel
PCI concept is
Under fluroscopy a balloon tipped cath is manueuvered to the stenotic portion of the coronary artery and inflated
CABG concept is
Rerouting/bypassing obstructive coronary arteries via a portion of ones own saphenous vein or an internal mammary artery (better prog)
Revascularization steps
1.Pt needs coronary angiography? 2.Pt needs revascularization? 3.PCI or CABG?
In order to revascularize a pt what must be present first
Either severe or refractory angina Severe ischemia on stress testing
PCI comparison
Less invasive than CABG Shorter hospital stay/recuperation Superior to pharm in S/S relief
CABG comparison
More effective longterm than PCI/Rx Most CABG complete resvascularization Sruvival Advantage
