5 cardiovascular Flashcards
Arteriosclerosis definition
General term, hardening of arteries by any means including chronic disease or abnormal thickening & hardening of vessel walls
Atherosclerosis definition
Form of arteriosclerosis, specifically fibrofatty lesions in intimal lining of large and medium sized arteries
Atheroma
Thickening/hardening caused by soft intra-arterial fat and fibrin deposits
Non modifiable cardiovascular risks
Men over 45
Postmenopausal women
Family hx of CVD (death of males under 55 women under 65)
Modifiable risk factors for CAD
HTN Smoking Dyslipidemia (low HDL high LDL) Hypercholesterolemia THE BEETIES Being fat AF Inflammation
Frequency of atherosclerosis areas affected
ABD aorta and iliac Coronary arteries Thoracic aorta and lower ext Internal carotids Cerebral arteries
Order of injury
Vessel endothelial injury Migration of inflammatory cells Formation of lesions by -fatty streak -then fibrous plaque (atheroma) -lesion complications
Vessel injury
From smoking, htn, eleveated LDL, diabetes, turbulent blood, increased fibrinogen, autoimmunity
Migration of inflammatory cells
Monocytes (macrophages) adhere to damaged endothelial area and migrate between cells, then engulf LDL
Fatty streak lesion
A flat yellow discoloration created by foam cells, transformed by macrophages and filled with LDLs and cholesterol
Fibrous plaque
Lesion of advanced atherosclerosis
Consisting of lipid-laden hypertrophied smooth muscle cells surrounded by collagen, elastic fibers, and a mucoprotein matrix
Formation of scar tissue forms fibrous cap
Fibrous plaque formation part 2
Lesion is white and narrows lumen.
Core consists of debris from cell necrosis, caused by insufficient blood supply and acculmualtion of both intracellular and excracellular lipids
Fun cholesterol fact
1% decrease in serum cholesterol is associated with a 2% decrease in CHD
Methionine
With B6 and B12 produces homocysteine which inhibits the anticoagulant cascade. Abundant in animal proteins
Three types of lesions
Fatty streak
Fibrous atheromatous plaque
Complicated legion
Complicated lesions
Have thin fragile caps and possible a larger lipid core. High risk for hemorrhage and thrombosis from inflammation, injury, or turbulent blood flow
Most frequent organs effected from atherosclerosis
Heart, brain, kidneys, lower extremities, small intestine
How do atherosclerotic lesions produce their effect
Narrowing of the vessel and producing ischemia
Plaque rupture or hemorrhage causing sudden occlusion from a delicate lesion
Thrombosis and emboli
Large arteries are usually effected by atherosclerosis in what way
Thrombus formation and weakening of the vessel wall
Medium size arteries are usually effected by atherosclerosis in what way
Coronary and cerebral arteries. From ischemia and infarction due to occlusion
Cardiovascular manifestations of atherosclerosis
Stable, unstable angina MI, HF HTN Cardiac arrest aortic aneurysms
Neurological manifestations of athersclerosis
CVA, TIA, weak carotid pulses and carotid bruits
Peripheral vascular manifestations of atherosclerosis
Cyanosis Claudication Weak pulses Bruits Ulcers Limb loss
Claudication
/Cramping pain caused by too little blood flow, often set off my exercise.
Renal manifestations of atherosclerosis
Stenosis
Decreased function
HTN
Failure
Vasculitis is
Any vein/artery/capillary with inflammation. Involves endothelial cells and smooth muscle
Clinical manifestations of vasculitis
Fever, myalgia (muscle pain), arthralgia (joint pain), malaise
Causes of vasculitis
Direct tissue injury, infection agents or immune processes or secondary due to things like lupus.
Physical agents sunburn, toxins and trauma.
Physical coronary blood flow regulation
Openings for coronary arteries originate in the root of the aorta, just past the valve, and so aortic blood pressure is responsible for perfusing the coronary arteries (and the heart is responsible for creating aortic blood pressure)
The coronary arteries are perfused during diastole
Neural coronary regulation
From the ANS
Medulla Oblongata innervation at T4-T5 to influence ino, chrono and dromotropy
Metabolic effects on coronary regulation
K+. LA (?) CO2, adenosine, NO
CAD definition
Any vascular disorder that narrows or occludes CA
CAD times
Ischemia 8-10 seconds reversible
Injury 30 minutes and reversible
Infarct is greater than 30 minutes, necrosis occurs, irreversible
What effects myocardial oxygen SUPPLY
Blood flow
O2 volume within blood
RBC volume and function
Hb volume and function
Determinants of myocardial oxygen demand
Heart rate, contractility, wall tension and thickness
How does heart rate effect MVO2
Increased heart rate requires more oxygen, yet subendocardial coronary flow is reduced because of the decreased diastolic filling time
Wall tension formula
RadiusXIVP/thickness
So an increase in radius or a decrease in thickness will increase wall tension
Wall tension MVO2
Both increase preload and afterload increases MVO2
MVO2 contractility
Increased contractility increases rate of wall stress which increases MVO2
Pathology of UA/NSTEMI three phases
Development of unstable plaque that ruptures
The acute ischemic event
Long term risk of recurrent events
Inflammation ACS
Cytokines cause fibrous cap to become thinner and more vulnerable
Causes of acute ischemic event
Increased MVO2 from hypertension/tachycardia or most commonly decreased O2 supply from from platelet rich thrombi or vasospasm
Pain specific to UA (needs one of three)
Pain at rest (or minimal exertion) lasting 20 minutes
Severe and frank pain, new onset within the last month
More severe, prolonged, or frequent than previously experiences
ECG for UA NSTEMI
Normal, or depressed ST with T wave changes
Artery percentages in STEMI
30-40% RCA
40-50% LAD
15-20% LCA
Timing of damage in MI
Loss of contraction in 60 seconds
Cell structure changes in minutes
Both those reversible
Ischemic injuries cease function in minutes and necrosis occurs 20-40 minutes
Gross tissue changes aren’t apparent for hours
Ventricular remodelling
Ventricles changing shape, size, thickness comprising early wall thinning, healing, hypertrophy, dilation.
The ventricles get weak in spots, grow in others to compensate, can cause aneurysm or HF
Two groups of atherosclerotic lesions
Fixed or stable (often SA)
Unstable or vulnerable (UA, MI)
How plaque ruptures
Usually emotional or physical stress to increase sympathetic tone
Diurnal - usually most often first hour after rising (increase sympathetic tone)
Thrombosis and vessel occlusion
Plaque ruptures, exposing lipid core which provide stimulus for platelet aggregation and thrombi formation.
Smooth muscle and foam cells produce TF which starts clotting cascade
Platelets effects on ACS
Release ADP, thromboxane A2, thrombin initiates aggregation process.
Glycoprotein on platelet membrane activated
Fibrinogen binds to activated glycoprotein receptors
Poons ACS catagories
Plaque disruption and platelet aggregation in UA
Thrombus (with more fibrinogen and therefore red) in NSTEMI, STEMI
Cardiac specific biomarkers
Troponin T (Tnt) and I (Int - cardiac specific)
CK-MB (creatine kinase myoglobin)
Troponin TC and I rise 3-7 hours and can stay elevated for 7-10 days
CK-MB rises 4-8 and hit normal in 2-3 days
Myoglobin rises 1 hour and peaks at 4-8 (not cardiac specific)
ACS vs CIHD
ACS has unstable atherosclerotic plaque, which has been disrupted
CIHD has stable atheroslecrotic plaque or vasospasm
ECG changes
1mm in two contiguous leads
Q waves are 25% r wave, 0.04 long. Diminished R wave height
Which area is the first often effected and why
Subendo, least blood supply (has tips of coronary arteries)
Biomarkers specificity to cardiac
Troponin I and T are absolute
CK-MB is Highly specific but not absolute
RCA occlusion
30%, Posterior Septum involved
LCA occlusion
20%, lateral involvement
LAD occlusion
Sudden death, causes anterior infarction
STEMI layers
Transmural means all levels involved, usually from complete occlusion Partial thickenss (sub endo, non-transmural) are genereally partial occlusions
ACS presentation
Crushing, constricting
Substernal
Radiates L arm, neck, jaw
Prolonged pain not relieved by rest or nitro (need opiates)
N/V sweating SOB, syncope
Anxiety, weakness in ext, fatigue, tachy, restless, feeling of impending doom.
Pale cool moist skin
Risk factors for atypical presentations
Old beeties woman with HF
Anigina pectoris
Most common sign 70-80% have it
Pain from lactic acid or ischemic myocardium irritating the nerves
Afferent nerves enter from C3-T4
Functional changes of MI
Decrease contractility (abnormal wall motion) Altered LV compliance Decrease SV Increased LVEDP SA malfunction Dysrhythmias HF
Factors for complications in MI
Patients pre-infarct condition
Size, location, extend of necrosis
Complications from MI
Dysrhythmias (90% from MI) LV failure Lower SV (causing cardiogenic shock) Pericarditis Heart rupture
Chronic ischemic heart disease
Characterize by SA, caused by stable atherosclerotic plaque or vasospasm, causing recurrent and transient episodes of ischemia
- Stable angina
- Variant Angina
- Silent MI are all CIHD
Stable angina
From stable atherosclerotic plaque, increased MVO2 can’t be met due to narrowing of lumen/stiffening of artery wall/lack of vessel dilation.
Often a precursor to AMI
Pain differences in stable angina
Predictable causes
Relieved by rest and nitrates
Same type of pain from previous attacks
Variant angina
Prinzmetal or vasospastic. Coronary spasm from:
Endothelial damage
Hyperactive sympathetic nervous system
Defects in interaction of calcium with vascular smooth muscle
Nitric Oxide production deficits
Impaired production of prostaglanding I2 (vasoconstrictor) or thromboxane A2 (role of inflammation)
More on variant angina
Exacerbations not related to MVO2
Has nocturnal instead of diurnal relationship
Often associated with arrhythmias
Silent MI
Defined as objective evidence in absence of angina
Objective evidence includes ST segment shifts
Could be from low acuity or autonomic neuropath or increased pain thresholds
