Coronary Artery Disease Flashcards
Cardiac output
Cardiac output = Amount of blood pumped out of the heart per minute
= HR x SV
= 3-6 L/min
Factors
- Cardiac contractility
- HR (SNS)
- Preload
- Afterload
- Blood volume
Preload
Preload/stretch - volume of blood in ventricles at end of diastole
- Left ventricular end diasoltic volume - LVED
Includes frank-sterling mechanism = recall it has limits
Increases in hypovolemia, regurgitation, HF
Afterload
Afterload/Squeeze - resistance left ventricles must overcome to eject and circulate blood
Increases in HTN, vasoconstriction
High afterload increases cardiac workload
Electrical properties
Regulate HR/rhythm
Excitability, conductivity, contractility, refractiorness
Dysrhythmias can occur if heart muscle cells die, which is life threatening
SA node is pacemaker
Coronary circualtion
1) Right coronary artery (RCA)
- Supplies RA, RV, part of LV, SA/AV/Bundle of his
- Blockage = RV failure, bradycardia
2) Left anterior descending (LAD)
- Supplies LV, heart valves
- Blockage - LV failure, dysrhythmia
3) Circumflex
- Supplies - LA, LV, SA
- Blockage - LV failure, dysrhythmia
Collateral circulation
- Arterial connections in areas o focclusion when chronic ischemia occurs
- Not enough time to create it is rapid tho
Factors = genetics, chronic ischemia
Coronary artery disease
Most common heart disease, usually due to atherosclerosis
Atherosclerosis - formation of fatty, fibrous plaque
Risk factors
- Age
- Male
- FmHx
- Elevated serum lipid
- HTN above 140/90
- Tobacco
- Sedentary
- Obesity
- DM
- Homocysteine
= Framingham risk factor can help predict risk of IM in next 10 yrs
Stages of artherosclerosis
1) Endothelium damage
- Triggered by HTN, Tobacco, hyperlipidema, diabetes, homocysteinemia, viruses/toxins
2) Fatty streaks
- LDL initiate inflammation, macrophages ingest LDL and die, becoming foam cells that create fatty streak
3) Fibrous plaque
- Platelets and LDL release growth fraction that thick arterial wall
- Collagen and elastin create cap over the fatty streak
= Harden and stiffen
4) Complicated lesions
- As fibrous cap grows, it damages artery
- Can break off and become a embolism
Clinicals manifestations of CAD
1) Stable angina pectoris
- Cardiac pain from ischemia
- Can b esilent ischemia in diabetic
- Atypical = referred such as indigestion, jaw pain, fatigue, SOB, dizzy (common in women and older adults)
- 75% occlusion, stable plaque with 3-5 minute duration
- Meds help
2) Vasospastic angina
- Aka prinzmetal/variant
- Rare from vasospasm of coronary artery
- Triggered by cocaine, eds, magnesium deficiency, allergy
Ischemia clinical manifestations
1) Angina pectoris
2) Diastolic and systolic dysfunction - SOB
3) ECG changes = ST depression
Acute coronary syndrome (ACS)
Prolonged ischemia - require immediate hospitalization
1) Unstable angina
- 90% occlusion
- Worst chest pain, unpredictable pattern for 15-20 min
- Not elevated by meds
2) Non-ST segment elevation/NSTEMI MI
- Fully occluded, with partial thickness damage
- ST depression, T inversion
3) ST segment elevation/STEMI MI
- Full thickness
- ST elevation
-> cardiac cells can tolerate 20 min of ischemia before death
Myocardial infarction - clinical manifestation
- Chest pain - usually in the morning for longer than 20 minutes, radiate to left arm etc
- Dyspnea
- Atypical = weakness, fatigue, anxious, dizzy
- Older pt - sudden delirium, atypical
- Skin - ashen, cool, diaphoretic (SNS)
- CVS - Tacky/hypertension then hypotension with loss of CO
- Resp - dyspnea, RR, crackles
- GI - N/V
- Fever up to 38 from inflammation of myocardial cell death
Serum cardiac enzymes
1) Troponin
Cardiac enzyme, most realiable as long duration
Elevated in STEMI/NSEMI but not unstable
2/3) Creatinine kinase MB and Myoglobin
Unspecific to the heart
MI Healing
Inflammation -> neutrophils/macrophages remove necrotic tissue in 2-3 days, leaving thin, unstable wall
- Collateral circulation may occur
- 2-3 mobths, scar tissue replaces and cannot contract
- Necrotic zone can be identified by EKG chanfes
= Cardiac remodelling occurs when healthy myocardium hypertrophies to compensate, which leads to heart failure
Atorvastatin (Lipitor)
HMG-CoA Reductase inhibitors
MOA - Increase LDL receptor in hepatocytes allowing for removal of LDL
Drugs that lower lipoprotein production (lower LDL, increase HDL)
AE (Well-tolerated)
- HA, rash, memory loss, GI
- Myopathy/Rhabdomyolysis
- Hepatoxicity
NC
- Significant reduction in 2 week, but goes away if drug stopped
- Evening dose
- Monitor urea/creatinine, LFT, creatinine kinase, muscle pain, GI
Colesevelam (Welchol)
Bile-acid Sequestrants
MOA - Non-absorbable resin that binds bile acid preventing reabsorption
Decrease LDL by 20% in first month
AE - Not absorbed systemically, only GI - constipation, bloating, indigestion
Can be used with statins
Metoprolol (Lopressor)
MOA - Block cardiac beta 1 adrenergic to reduce HR, force of contraction and renin
Therapeutic effect
- Slow HR - contractility
- Renin - preload
- Angiotensin 2 - Afterload
AE - bradycardia, AV heart block, HF, arrythmia from abrupt withdraw
NC
- Assess HR = DO NOT ADMINISTER IF UNDER 60 BPM
- Hold if BP under 100
- HF - edema, SOB, weight gain, crackles
-Do NOT abruptly discontinue
Precaution
- Severe allaergies
- Hypoglycemic unawareness
Verapamil (Ispoptin)
Calcium Channel Blocker
MOA - inhibit calcium influx, decreasing HR, force of contraction and vasodilate
HELPS WITH VASOGENIC ANGINA!
Therapeutic effect
- Decrease SA/AV conduction = contractility
- Vasodilates arteries = Afterload
AE - Constipation, dizziness, facial flushing (vasodilation), HA (Vasodilation), edema
NC
- Assess HR, chest pain, BP, bowels
- DO NOT give if HF or hypotension
- DO NOT give with beta blockers (heart block)
Captopril
Angiotensin Converting Enzyme Inhibitors (ACE inhibitor)
MOA - block production of angiotensin 2
Therapeutic effect
- Vasodilation from angiotensin 2 = Afterload
- Block aldosterone = preload
- Can decrease cardiac remodelling
SE
- Hyperkalemia (aldosterone)
- Hypotension
- Dry cough from bradykinin
- Renal failure, angioedema
NC
- Assess BP, hydration, blood work
- Precaution with renal function, hypovolemia
Nitroglycerin spray (Nitrate)
Antianginal
MOA - Dilate veins!!! to decrease preload and vasodilate
- ALSO USED IN VASOSPASTIC, but does NOT work on unstable
SE - HA, hypotension, tachycardia secondary to vasodilation
NC
- Patch, PO or IV, mainly sublingual spray
- VS
- Sit down, administer first dose, wait 5 min, second dose, wait 5 min and third (do not exceed 3)
- Check HR/BP before each dose as cannot administer if dropped more than 25 mmhg or less than 100 mmHg
Isosorbide dinitrate (long-acting nitrate)
Antianginal = same as nitroglycerin but in pill form for immediate or sustained release
Aspirin
Acetylsalicylic acid (Aspirin, ASA)
- Angina and MI
MOA - Suppress platelet aggregation to vasodilate and reduce risk of thrombosis
AE
- GI bleed - melena, hematemesis, low BP, pale (can use PPI)
- Abdominal pain, dyspepsia, diarrhea, rash
NC
- GI, give with food
Clopidogrel (Plavix)
P2Y12ADP Receptor antagonist
MOA - irreversible blocks receptors to prevent aggregation to prevent stenosis of stents or MI
AE
- GI bleeding, pain, dyspepsia, diarrhea, rash
NC - GI, give with food
Unfractionated Heparin (UFH)
Anticoagulant
MOA - Enhance activity of antithrombin
- Cheaper than LMWH, but more monitoring and only used in hospital
For MI, DVT, PE
AE
- Bleeding, bruises, black stool, hematuria, HA, lumbar pain
- Heparin-induced thrombosis - stop immediately
NC - Subcut/IV, only in venous clots, monito aptt and bleeding
Dalteparin (Fragmin)
Low Molecular Weight Heparin (LMWH)
- MOA - Enhance antithrombin, effective as UFH but expensive and less monitoring
Indication - Unstable angina, NSTEMI, DVT, PE (not stemi)
rest same as UFH
Alteplase (tPA)
Thrombolytic
MOA - Binds to plasminogen plasmin to digest fibrin, effective when given 4-6 hrs after onset
Indication - ONLY STEMI
AE - High risk of bleeding, esp intracranial hemorrhage
‘
NC - Bleeding, neuro check
CI - Prior intracranial hemorrhage, recent stroke in 3 months, active internal bleeding
Subjective/Objective assessment
OPQRSTUV for angina
PmHx - cariddac problems, anemia, rhaumatic heart disease,s trep infection, alcoholism, smoking, diabetes?
History of surgery?
Peripheral edema, CWSM, pale?
Juglar vein distention when pt is 45 angle? dehydration, HTN or right sided HF
Heart sounds
S3 = LV failure or mitral regurgitiaion
S4 = CAD, LV hypertrophy, aortic stenosis
= can be heard with bell only
Diagnostics for CAD blood work
Cardiac enzymes = troponin differentiated if unstable or STEMI/NSTEMI
Others include
Homocysteine - aminoacid for endothelium damage
CRP = Inflammation
Microalbuminuira
Cholesterol levels
Imaging
EKG - can be short term or telemetry
Chest xray - pulmonary edema
Cardiac MRI - contrast IV for ejection fraction
Stress test - asses cardiac ischemia, DONT USE WITH UNSTABLE ANGINA
Angiogram - catheter into artery to the heart and eject contrast then xreay
Angioplasty - insert stent
