Cardiac Diseases Flashcards
What are the 3 layers of the heart from outer to inner
epicardium
myocardium
endocardium
Where are the coronary arteries located
outside of the heart
What is the most important coronary artery
Left Coronary Artery which branches into the Left Anterior Descending - feeds most of the left ventricle (widow makers region)
Cardiac Conduction System
SA node –> AV nodie–> Bundle of His –> R and L Bundle Branches –> Purkinje fibers
SA node
pacemaker of the heart
located at top of R atrium
generate 60-100 pulses per min and is controlled by PNS and SNS
AV node
located in the lower aspect of the atrial septum - receives electrical impulses from SA node
Bundle of His
fuses with the AV node to form another pacemaker site; branches into R and L and terminates into Purkinje’s fibers
can sustain a heart rate of 40-60 beats per minute (if SA node fails)
Purkinje’s Fibers
a diffuse network of conducting strands located beneath the ventricular endocardium - they spread the wave of depolarization through the ventricles
1st heart sound
lub (S1)
AV valves close at beginning of systole d/t increased pressure in the ventricles (R - tricuspid L = Mitral)
2nd heart sound
dub (S2)
Semilunar valves shut at the end of systole due to the falling pressure in the ventricles (R = pulmonic L=aortic)
Physiologic split
Aortic vale precedes pulmonic valve closure by 0.02-0.04 seconds during expiration and 0.04-0.06 secs during inspiration
Atherosclerosis
hardening of paste
characterized by fibrofatty lesions in the intimal lining of the aorta, large and medium sized arteries, coronary arteries, and other larger vessels that supply the brain
**CORONARY ARTERIES ARE THE MOST COMMONLY EFFECTED
If atherosclerosis in veins
hard to feel pulses
If atherosclerosis in arteries
hard to feel pulses and leg pain
What is the most common cause of CAD
inflammation r/t atherosclerosis
Inflammation in Atherosclerosis
chronic inflammation condition = accumulation of fibrous plaques and lipids progressively narrows the lumen of the vessel and impedes blood flow
Progression causes vascular changes that impair diseased vessels ability to dilate (stiffens). Can result in calcification or rupture
What can trigger atherosclerotic CAD
smoking, HTN, hyperglycemia all cause release of chemicals involved in inflammatory response
What organisms have been identified to POSSIBLY contribute to atherosclerosis (they are bystanders)
Chlamydia pneumoniae
Herpes Simplex Virus
Cytomegalovirus
Is atherosclerosis problematic to the brain? Why?
yes bc its responsible for majority of cases of MI and cerebral infarction; lesions occur in the innermost layer of medium and large muscular arteries; you you have it it one part, your bound to have it in others, and since the heart pumps blood to the brain CAD can cause MI, stroke, gangrene of extremities, sudden cardiac Death
Fatty Streak Lesions
contains foam cells (macrophages filled with lipids and T cells)
migrate from smooth muscle in tunica media to tunica intema and take on the appearance of foam cells
Fibrous Plaque Lesions
connective tissue, smooth muscle cells full of lipids, macrophages, and lymphocytes; progressively thickens and may occlude the lumen
(often with necrosis and calcification)
What is Complicated Lesion?
fibrous plaque can undergo extensive degeneration and rupture. The ulcerations/cracks that occur during rupture, trigger the aggregation of platelets –> this could result in a thrombus/sudden occlusion
**takes years/decades to occur
What are some common sites of atherosclerosis
at the bifurcations
in legs (smokers and DM)
epicardial portions of coronaries
New lesions at perianastomoatic sites of CABG (bypass grafting)
Atherosclerotic Risk Factors
Men >45 Women >55 (or early menopause) Family history of CHD dyslipidemia Smoking HTN High LDL or Low HDL DM Obesity Low Birth weight in newborns
Dyslipidemia
Cholesterol >200 mg/dl and increased LDL d/t genetics, dietary, or overproduction/deficient removal
Increases risk of CAD
could also be d/t DM, renal disease, alcoholism, hypothyroidism
Smoking
accelerates atherosclerosis and 3-5X greater chance of CAD
Each year you don’t smoke you risk goes down
DM
4x greater risk for an MI
Gangrene of Lower Extremities
Women more prone than men and often goes with hyperlipidemia
Want to control Blood sure and Blood Pressure
HTN
5x great risk when 160/95 than normotensive
Tx decreases CAD, CHF or cerebrovascular disease
**MOST TREATABLE ASPECT OF ATHEROSLCEROSIS
Obesity and Inactivity
Obesisty associated with hypertryglceridemia, hypercholesterolemia, glucose intolerance, and HTN
Inactivity can lead to decreased HDLs
What are some causes of atherosclerosis
High blood serum cholesterol and triglycerides High BP Infection High blood iron levels High blood homocysteine (correlation)
Atherosclerosis raises the systolic pressure by
Decreasing arterial distensibility, and vessel lumen diameter
Coronary Artery Disease Facts
Leading cause of death and disability in US
1:3 men 1:10 women <60
Mortality/death is declining d/t CPR, HTN management, and lower cholesterol diets
Manifestations of CAD:
Sudden Cardiac Death - can occur within 1 hour and occur more frequently in AM (6am-12pm) D/T hyper coagulable state
One death every 90 seconds
Peaks btwn ages of 0-6months (SIDS) and 45-75 years
Causes of Sudden Cardiac Death
75% d/t CAD
25% d/t myocardial abnormalities (hypertrophy, valvular disease)
Narrowing of the coronary arteries >75%
Old AMI
ACUTE THROMBOSIS AT SITE OF FISSURED PLAQUE
Lethal Dysrhythmias (rhythm problem) (Ventricular fibrillation, aystole, bradycardia)
Sudden Cardiac Death Lifesaving Tx
BLS (basic life support)
ALS (advanced life support
Pacemaker
What is the primary cause of death in sudden cardiac death
lethal dysrhymias
Coronary Artery Disease
narrowing or obstruction of the coronary arteries d/t atherosclerosis which causes a decreased perfusion of myocardial tissue and myocardial O2.
Leads to HTN, angina, dysrhythmias, MI, CHF, and death
Why is occlusion of the coronary arteries in a young individual more lethal than in an older individual
The development of collateral circulation takes time; people who are older have arteries that have anastomitized which can help supply blood to occluded areas
What is the goal of tx in CAD
lather the atherosclerotic progression
CAD Manifestations: Angina
discomfort within or adjacent to the chest;
typically provoked by exertion or anxiety
Lasts for several minutes, alleviated by rest and does not result in myocardial necrosis
Potential sequelae: AMI & Death
What can decrease myocardial oxygen demand
Decreased ventricular volume
Angina
chest pain resulting from myocardial ischemia caused by inadequate myocardial blood and oxygen supply
**Imbalance btwn O2 supply and demand
Causes of Angina
obstruction of the Coronary Blood Flow d/t atherosclerosis, Coronary artery spasm, and conditions increasing myocardial oxygen consumption
Goal of Tx of Angina
provide relief of an acute attack, correct the imbalance between myocardial O2 supply and demand, and prevent the progression of the disease and further attacks to reduce the risk of MI
What is the most important concept relating to Angina
Most people have increased O2 demand and diminished O2 supply;
they hear always extracts max O2 from blood even under minimal demand; Coronary blood flow can increase up to 7x to try and meet the O2 demands. CAD prevents body from meeting it’s O2 demands
Types of Angina
Stable - person can predict that this is going to happen
Unstable - occurs at lower levels of exertion or begins to intensify at rest (can result in MI 20%)
Variant/ Prinzmetals - rest pain and V-arrhymias caused by CA spasm (no plaque; just spasms) (**could be r/t cocaine)
What are some descriptions/manifestations of Angina
Exertional chest discomfort
Lasting several minutes in duration (>20 min suspect MI)
Relieved by rest
Any area between lower jaw and epigastrium - can radiate to neck arms
“tightness” “heaviness” or “choking sensation”
Provoked by walking up hill, stairs, vigorous arm work, intercourse, following a meal etc.
Physical findings of Angina
Increased HR and BP
S4 d/t atrial contraction in a ventricle stiffened by ischemia
S3 in Left ventricular failure
Systolic mumur d/t mitral regurgitation as a result of ischemia
Diagnostic Tests for Angina
EKG during the pain
Stress Test - chest pain or changes in ECG/VS during testing may indicate ischemia
Cardiac Enzymes - normal enzymes/no random enzymes leaking = so it’s probably just angina
Cardiac Catheterization- GOLD STANDARD definitive way of looking into vessel
Cardiac Stress Test
Exercise on treadmill until ischemia EKG changes, angina, or dyspnea occur
SHOULD NOT BE PERFORMED - SIGNIFICANT AORTIC STENOSIS, UNTREATED HTN, CHF, UNSTABLE ANGINA
PERSANTINE (dypridamole thallium IV)
for pts unable to exercise this drug will dilate the coronary arteries just the like exercise does
Coronary Arteriography/Cardiac Catheterization
GOLD STANDARD - and most precise means of documenting CAD. Takes pictures of artery where the occlusion is.
Also gives measures of Left Ventricular Function
**good for people with recurrent angina or lots of angina
Management of Angina
Counseling to tell them how serious it is
Drugs can alleviate sx/ prolong survival
Modify Risk Factors - Low fat and Low cholesterol diet, stop smoking, and control BP
Search for correctable contributing factos (ex aortic stenosis, hyperthyroidism, sever anemia)
Unstable - hospitalize and catheterization
Angina Implementation
Assess Pain
AdMINISTER O2 AND 2-4 LITERS
NITROGLYCERIN -TO DILATE the coronary arteries + reduce O2 requirements (only for healthy people without/ not related to atherosclerosis)
Surgical Procedures of Angina
Percutaneous Transluminal Coronary Angioplasty (PTCA)
Laser Assisted-Angioplasty
Vascular Stent
Coronary Artery Bypass Graft (CABG)
Percutaneous Transluminal Coronary Angioplasty (PCTA)
dilate the artery/vessel with a ballon catheter to open the lumen and improved arterial blood flow
Complications of PCTA
arterial dissection/rupture
immobilization of plaque fragments
spasm
Acute MI
Contraindications to PCTA
LEFT MAIN ARTERY STENOSIS
SEVERE MULTI-VESSEL DISEASE
**if vessel completely occluded you probably can’t do this
Stent
metal cage inserted into blood vessels so it prevents the occlusion from reoccurring after the ballon is removed (maintains latency)
Laser Assisted Angioplasty
A laser probe is advanced through the artery; heat from the laser vaporizes the plaque to open the occlude artery
- *used for clients with small occlusions in (distal superficial femoral, proximal popliteal, and iliac arteries)
- If laser in wrong place it can blast the vessels
Atherectomy
USED IN THE 90s
catheter with cutting chamber that aches the plaque (packman); works best in straight lesions NOT curvy vessels
**Breaking clot is good, but the broken pieces can travel to the brain!
Coronary Artery Bypass Graft (CABG)
Attach a saphenous vein between ascending aorta and stenoic coronary artery - give the blood another way to go, except usually get occlusions there too after about a year (10%)
Coronary Revascularization has 2 forms…what are they?
CABG
PCTA
**ways of restoring blood flow to the area
Acute Myocardial Infarction Causes
**Acute MI same as MI
almost all are d/t thrombotic occlusion r/t CAD
infective endocardidtis emboli (infection of the heart muscle/valves)
atrial thrombi
vasospasm from cocaine, amphetamine use
small vessel disease in DM
trauma
Myocardial Infarction (process and tissues)
occurs when Myocardial tissue is abruptly/severely deprived of Oxygen; ischemia leads to necrosis if blood flow isn’t restored
Infarction does not occur instantly but evolves over several hours
**Obvious physical changes will not occur until 6 hours after the infarction has occurred (swollen and blue tissue)
After 48 hours the infarct turns grey with yellow streaks as neutrophils invade the tissue
8-10 days after the infarction granulation tissue forms
Over 2-3 months the necrotic area develops into a scar which permanently changes the size and shape of the left ventricle
MI Key factors
Angina (especially if pain has changed/increased when at rest)
Absence of exacerbating factors (ex anemia, htn, chf, hypothyroidism) - this could reflect changes in plaque resulting in intermittent thrombosis
Q wave infarcts = indicate the entire portion/thickness of LV is involved
Only take 20-40 minutes for muscle death to start occurring
What does the Size of the Infarct spent on
extent, severity, and duration of ischemia
amount of collateral circulation
metabolic needs of myocardium at time of the event
What does a Q wave infarct indicate?
AKA TRANSMURAL (ACROSS THE WALL) damage in the heart muscle has gone through all 3 layers of the heart muscle **damage typically begins from the inside (endocardium)
Common Locations for MI
Coronary Arteries (LAD 40-50%)
What is the result of MI on the affected portion?
decreased contractility with abnormal wall motion
altered compliance/stretch
decreased Stroke Volume –> decreased EF
Non contraction
Non Stretching
Non Filling
What does the area of infarct look like?
Central area of necrosis Surrounded by injured area Surrounded by ischemia Myocardium does NOT regenerate Replaced by scar tissue
Manifestations of MI
Onset of MI usually occurs in the early AM d/t increased platelet aggregation
Q wave infarct preceded by fatigue , chest discomfort, malaise in days preceding
May be clinically “silent” (found later on ECG)
Ex. DM damages nerves in Blood vessels, so you could not notice the symptoms
Risk Factors for MI
Athereoslcerosis CAD Elevated cholesterol levels Smoking HTN Obesity Physical Inactivity Impaired Glucose Tolerance Stress
Signs/Sx of AMI
Intense severe, crushing pain unremitting for 30-60 min
Diaphoresis
Cool, Clammy, Grey Skin
Weakness
What does impaired L ventricular filling result in
pulmonary edema/congestion (blood backs up to the lungs) = SOB, tachypnea, orthopnea and moist crackles
Will BP be increased or decreased with AMI?
BP increased initially, but with R Ventricular/L infarction may be hypotensive/drop in BP
What are some things that may happen with the heart later after an MI?
displacement of PMI
soft S1 S3 and S4
mitral regurgitation
friction rub
Diagnostic Tests for MI
Creatine Kinase
Troponin
AST (aspartate aminotransferase)
LDH (Lactic dehydrogenase)
Creatine Kinase Test
CK or CPK - enzyme found in the heart, brain, and skeletal muscles. Serum CK levels are elevated when muscle or nerve cells are injured
If you have increased muscle mass you will have more CK.
There are 3 isoenzymes
CK-MM = found in skeletal muslce
CK-MB = found in cardiac muscle
CK-BB = found in brain and lung
Elevated CK-MB can help you determine timing, quantity, and resolution of MI
Troponin T test (specific)
regulatory protein found in skeletal and cardiac muscles; specific antibody can detect cardiac troponin-T and is specific for myocardial injury
Troponin I test
GOLD STANDARD
this protein is found in cardiac muscle complex -specifically the myocardium and will return to nL sooner (8-16 hrs after onset) than Troponin T.
During an MI when do enzymes peak
fastest enzymes (Troponin-I and CK) rise within 4-6 hours after onset of MI - helps determine when person had MI
When does CK-MB peak
18 hours after onset
When does Troponin - I peak
11 hours after onset
When do CK-MB and Troponin -I return to normal?
CK-MB = 2 days Troponin-I = 4 days
Hemodynamic Monitoring
ICU related tests and catheters that can go into the heart to measure it’s pressures which can help monitor MI
On EKG what may indicated an MY
elevated ST
inverted T wave
Deep Q wave will be on there for the rest of the persons life after a MI
What is a non-Q waves infarct?
partial heart attack
Echocardiogram
ultrasound of heart - takes from 30-90 min depending on the pts condition; it evaluates:
how well the heart is moving
how well the valves are working
the size of the heart and it’s pumping chambers/ventricles
What is the most serious complication after an MI
DYSRHYTHMIAS (A-fib) d/t tissue ischemia, hypoxia, SNS and lactic acidosis
causes decreased CO and increased cardiac irritability which will further decrease myocardial perfusion
What is the most common cause of death after an MI outside of the hospital
V fib
What are other complications after an MI
CHF
Cardiogenic shock = L ventricular failure
Thromboembolism = too much bed rest - can travel to brain kidneys and spleen
Ischemic pericarditis= inflammation of the pericardium (chest hurts)
Myocardial Rupture = immediate death
Ventrical Aneurysm - thin and bulging with pressure- eventually pops and blood comes pouring out
AMI prehospital tx
ems now trained in defibrillation
AEDs are now publicly available
analgesia with morphine = venus dilation and decreased preload
aspirin therapy = anti platelet effect/reduces chances of clots
AMI hospital tx
CCUs (coronary care units) reduce mortality by 50% - Defibrillate, continuous ECG
Telemetry monitoring for arrhythmias - can go with pt and hospital can watch whats going on in the heart
Stool softeners to prevent straining
Bed rest no more than 1 day
O2 therapy to avoid hypoxemia
What do we do after an MI?
prevent recurrence with calcium channel blockers or beta blockers and aspirin
anticoagulation for 6 months
discuss risk facts
cardiac rehab - mild monitored exercise to increase tolerance
The main difference between myocardial infarction and angina is
with MI the pt is more likely to experience radiation pain to the neck and arm; with angina the pain is more localized
