Module 9: Disorders of Cardiac Function Flashcards
Where is the heart located
in the left side of the mediastinum
Epicardium
covers the outer surface of the heart
has 2 layers: parietal and visceral
Myocardium
the middle layer of the heart and is the actual contracting muscle of the heart
Endocardium
is the innermost layer of the heart and lines the inner chambers and the heart valves
The epicardium is continuous with…
the pleura of the lungs
this means any leakages there can compress the heart as well
the endocardium is continuous…
with the endothelium of all vessels in the body - it ends up being a closed system to allow laminar flow
The atrioventricular valves lie between…
the atria and ventricles (the bicuspid/mitral and tricuspid valves)
The atrioventricular valves close when?
at the start of ventricular contraction (to prevent blood from flowing back into the atria from the ventricles
When do the atrioventricular valves open up?
the valves open when the ventricles relax
The bicuspid/mitral valve is located…
on the left side of the heart
The tricuspid valve is located…
on the right side of the heart
What holds leaflets of valves closed?
Papillary Muscles and Chordae Tendinea
Which AV valve has higher pressure on it?
Mitral (by a lot)
The pulmonic semilunar valve lies …
between the right ventricle and the pulmonary artery
The aortic semilunar valve lies between…
the left ventricle and aorta
When do the semilunar valves open?
they open during ventricular contraction
When do the semilunar valves closed
when the ventricles begin to relax
What is the purpose of the semilunar valves
to prevent blood from flowing back into the ventricles during relaxation
What feeds the myocardium?
NOT BLOOD IN THE VENTRICLES
it is the coronary circulation that feeds it
Where do the coronary arteries start?
they root off of the aorta
Coronary Veins
return deoxygenated blood from the heart back to the circulation so the blood can mix with systemic blood
What causes anginal pain?
In something like heart failure, the perfusion of coronary circulation is bad causing pain from tissues not being fed
Where do the vessels of coronary circulation go?
Around the heart and deep into the tissues as well
The coronary circulation has what two major branches?
Left Coronary Artery
Right Coronary Artery
What areas of the heart does the left coronary artery feed
it is the foremost facing artery due to position of the heart in the chest, so it feeds the anterior part of the septum and the anterior left ventricle
What will happen if there is a block in the left coronary artery
there will be an inability to get conduction down to the bundle of HIS
What are the parts of the Left Coronary Artery
Left Anterior Descending
Left Circumflex
what does the left anterior descending feed
the anterior septum
the anterior left ventricle
What does the left circumflex feed
the lateral wall and left ventricle
What area of the heart does the right coronary artery feed
posterior septum
posterior heart
SA and AV nodes
What can a blockage of the right coronary artery cause
it can lead to inadequate perfusion, impair the SA, AV nodes and Perkinje fibers, and stop conduction occurring in those regions
So, blockage of coronary circulation …
impacts both the myocardium tissue AND the cells responsible for electrical potential for contraction and electrical activity - a dual deficit
___ is the pacemaker of the heart
SA-Node
Where is the SA node
it starts in the right atrium
What is the pathway of heart conduction?
SA node –> left and right atria/AV Node –> bundle of HIS –> right and left bundle branches –> perkinje fibers
What happens once conduction gets to the AV node
atrial contraction
What happens once conduction gets to the perkinje fibers
ventricular contraction
What allows fast electrical conduction through the heart
intercalated discs between cardiac muscle cells
Why is it important that the signals move through the ventricles and aorta differently?
Aorta are thinner and smaller while ventricles are thicker and bigger - so signals take longer to get through them
If we did not have this then the ventricles could not contract simultaneously (since the right side of the heart is a lot thinner than the left) and we would ack ventricular contraction coordination
It also allows the SA and AV nodes to get signals at the same time and allow contractions simultaneously
P-Wave
Repolarization of the Atria in response to SA node triggering
QRS Complex
Represents Ventricular Depolarization - triggers the main pumping contractions
T Wave
represents ventricular repolarization
PR Interval
delay of the AV ode to allow filling of the ventricles
What cannot be seen in an EKG
the atrial repolarization since it is lost behind the QRS complex
If there is a malfunction of conduction from a blockage or damage to the Bundles what can occur on an EKG?
there can be a delay in getting signals to the ventricles leading to a prolonged PR interval
SA Node
pacemaker of the heart that initiates each heartbeat
Where is the SA node located
at the junction of the superior vena cava and right atrium
How fast does the SA node generate electrical impulses?
60-100 times per minute
what controls the SA node
the SNS (spinal nerve) and PNS (vagus nerve)
AV Node location
in the lower aspect of the atrial septum
AV Node
a node that gets signals from the SA node that moved through the atria in order to keep the conduction going (also sets up a slower electrical impulse if SA node is damaged)
The Bundle of HIS (AV Bundle)
Another pacemaker site from the fusion of the AV node
It branches into the right and left bundle branches which will terminate into Perkinje’s fibers
Where do the right bundle branches extend through
the right side of the interventricular septum
Where do the left bundle branches extend through
extend into the left ventricle
If the SA node and AV node fails, the bundle of HIS can initiate and sustain a heart rate of what?
40-60 BPM
What electrical impulse speed can the AV node make
50 BPM
Can the Bundle of HIS provide electrical impulses fast enough for adequate perfusion
no, 40 is rather low
What electrical impulse speed can the Perkinje Fibers make
30 BPM
The lower the control of conduction on the heart…
the lower the heart rate
Perkinje’s Fibers
a diffuse network of conducting strands located beneath the ventricular endocardium
These fibers spread the wave of depolarization throughout the ventricles
First Heart Sound
“Lub”
Made when the AV shut at the start of systole due to increased ventricular pressure
What is the actual sound of the heart coming from?
Not the valves closing but the disruption of laminar flow of blood they cause - turbulence
Second Heart Sound
Occurs when the semilunar valves shut at the end of systole from falling ventricular pressure - the pressure in the ventricles drops below that in the great vessels so these close to prevent backflow
“Dub”
Physiologic Split
The aortic valve closes slightly sooner than the pulmonic valve in order to allow the same amount of blood to go through from both areas
Atherosclerosis
Athero = Gruel/Paste ; Sclerosis = Hardening
It is the characterized by fibrofatty lesions in the intimal lining of the aorta, large and medium arteries (more than small), coronary arteries, and carotid arteries and other larger vessels that supply the brain
The most commonly affected vessel with atherosclerosis is…
the coronary arteries
The number 1 cause of death in the US is
heart disease
The third most common cause of death is
stroke
A major risk factor for atherosclerosis is…
hypercholesterolemia
The most common cause of CAD is…
inflammation r/t atherosclerosis
How does atherosclerosis cause blocks?
accumulation of fatty fibrous plaques and lipids progressively narrows the lumen of the vessel and impedes blood flow to the myocardium
Progression of atherosclerosis causes…
vascular changes that impair the diseased vessels ability to dilate
In advanced atherosclerosis what can occur?
rupture or calcification
What is another disease that is related to heart disease?
Gum disease - a portal of entry for bacteria to get through is the gums and along with non laminar flow from deposits and calcification bacteria can grow and start inflammatory processes
Atherosclerosis = ___ + ___
fat plaque build up + inflammation
Atherosclerosis was once thought of as a ___ problem, but we now know…
plumbing; now we know its inflammation thats also related
What may be high d/t the inflammation in atherosclerosis
C reactive protein levels
Evidence from research increasingly suggests that ___ is a significant part of atherosclerosis
inflammation! (with the fibrofatty plaques)
Common risk factors for the inflammation r/t to atherosclerosis?
All these release pro inflammatory cytokines
Smoking
Hypertension
Lipoproteins
Hyperglycemia
(All common heart disease risks)
What may also have a role, that we are not too sure of, in atherosclerosis?
Infection (chlamydia, herpes, CMV)
But we do not know whether they cause it or entered the disease vessel opportunistically
The majority of cases of myocardial and cerebral infarction are due to?
Atherosclerosis
The principal cause of death among men and women in the US and western Europe is
Atherosclerosis
In what layer of the blood vessels does atherosclerosis lesions tend to occur?
in the innermost layer - the intima of the medium and large muscular arteries
What are some potential sequelae of atherosclerosis?
MI (block C artery)
Stroke (block Ce Artery)
Gangrene (Block leg/arm)
Sudden Cardiac Death (instant death)
Surprisingly one of the first manifestations of atherosclerosis can be ___
death
Atherosclerosis occurs in what age groups?
ANY AGE
occurs in all ages, present at birth in some infants, and is common in young children too
As the atherosclerosis lesion develops what stages will it undergo?
Fatty streak –> fibrous plaques –> complicated lesions
Fatty Streaks
A reversible time for lesion development of atherosclerosis
It contains foam cells
During this smooth muscle from the tunica media migrate into the tunica intima and take on the appearance of foam cells
Foam Cells
macrophages filled with lipids and T cells
present in fatty streaks
Fibrous Plaques
Progressive thickening that can occlude the lumen with necrosis and calcification
it is made of connective tissue, smooth muscle cells full of lipids, macrophages, and lymphocytes
As the fibrous plaque expands, what does the artery do?
It inflames to form a fibrous cap that separates the plaque from the lumen which ends up causing decreased blood flow and increased blood pressure
Complicated Lesion
a fibrous plaque that has undergone extensive degeneration and may rupture
The softer lesions are more likely to rupture and the bleeding can cause occlusion leading to MI
How does a complicated lesion lead to occlusion for something like MI
The lesion has ulcerations, cracks from the plaque rupture serving as sites for platelet aggregation
this can allow the platelets to form a thrombus and have sudden occlusion of the vessel
___ lesions are more likely to rupture
softer
Most MI are due to what …
rupture of a vessel, bleeding, and clot formation that causes acute occlusion
Common sites for atherosclerosis vessel occlusion
Aorta
Femoral Artery
Popliteal Artery
Tibial Artery
Coronary Arteries
Carotid Arteries
Cerebral Arteries
Occlusions and Atherosclerosis most commonly occurs are ___
bifurcations (since it is more turbulent leading to debris collection or damage)
Atherosclerosis of the legs is more common in ___ and ___
smokers and DM
What is the most common region of plaque build up for the coronary arteries
the epicardial region
Can lesions occur in sites from CABG
yes. if you have bypass surgery you can get a lesion at the new stitched together vessels (perianastomotic sites)
Risk factors for Atherosclerosis
Male over 45
Women over 55 or early menopause
Family hx of premature CHD, AMI, or sudden death
Smoking
HTN (greater than 140/90)
High LDL cholesterol (greater than 160)
High triglycerides (greater than 250)
Low HDL cholesterol (lower than 35)
DM
Obesity and inactivity
Low birth weight
How does hyperlipidemia relate to atherosclerosis as a risk factor?
CAD and Chronic Hypercholesterolemia are clearly associated - with high cholesterol and LDL (and low HDL) increasing risk x5!!!
What are some causes for hypercholesterolemia?
Dietary
Genetic
Overproduction
Deficient Removal
(Familial Hypercholesterolemia gets 500-1000 mg/dL due to faulty receptors)
DM
Renal disease
alcoholism
hypothyroidism
corticosteroids
estrogens
Why do we need cholesterol?
it is an ingredient in bile and the lipoprotein bilayer of every cell
How does smoking impact heart disease and atherosclerosis?
It accelerates atherosclerosis
has a 3-5x greater risk for CAD
has a 70% death rate
(It increases BP, impacts vascular tone, decreases myocardial O2, increases LDL oxygenation, contributes to inflammation, damages the endothelial lining, etc)
Good news regarding smoking as a risk for heart disease?
Smoking cessation reduces risk to that of non smokers within 1 year (risk of heart disease; lung cancer not so much)
How is Diabetes mellitus a risk factor for atherosclerosis and CAD?
Gives a 4x greater risk of MI
Can lead to gangrene of lower extremities
Women get more prone to it than men
changes metabolism of fats leading to differing HDL and LDL issues
Often coincides with hyperlipidemia
What is the goal with DM patients
control blood sugar and blood pressure (to lower CAD risk)
Bad News about Hypertension and heart disease
risk is 5x greater when you have a BP of 160/95 than normotensive
can be idiopathic and be a silent killer
Good news regarding HTN and heart disease
treatment can decrease cardiovascular disease, CAD, and CHF significantly and there are many great treatments
The most treatable risk factor for heart issues is ___
hypertension
Reducing the risk of MI also reduces risk of ___
stroke
What is obesity associated with that contributes to heart disease risk
hypertriglyceridemia
hypercholesterolemia
glucose intolerance and DM
HTN
What is inactivity associated with that contributes to heart disease risk?
it can cause HDL levels to drop
What are some of the theories on what causes atherosclerosis to occur?
High serum cholesterol and triglycerides
High BP
Infection (and inflammation)
High Blood Iron Levels
High Blood Homocysteine Levels
(Different initiating events are involved to different degrees in different people)
What is the theory on why atherosclerosis may be higher in men than pre menopausal women?
Women lose 30 mg of iron a month and get 30 a day, so they go even but men do not leaving them potentially more predisposed to atherosclerosis if it partly from blood iron levels since it can deposit in vessels
Why is it believed high homocysteine levels contributes to atherosclerosis?
It is an AA that increases rates of heart disease and stroke and has an unclear relationship with alzheimers and osteoporosis
Also too much can irritate blood vessel linings leading to scarring, hardening, and narrowing increasing workload and coronary events and contributing to clotting
The leading cause of death and disability in the US is
CAD
(1 in 3 men, 1 in 10 women over 60; 800000 new AMIS each year, 450000 recurrences each year)
Why is the mortality rate of CAD declining some in recent years?
CPR
management of HTN
lower cholesterol diets
use of antibiotics
Risk of atherosclerosis and CAD is equal to that of men for women after…
menopause
Sometimes the first and only manifestation of CAD is
sudden cardiac death (25% of cases)
CAD r/t sudden cardiac death only takes how long to cause death?
1 hour
When is peak risk for sudden cardiac death related to CAd
between 0-6 months and 45-75 years
Why is sudden death, stroke, and MI more frequent in the morning between 6a and 12p for CAD?
that is a time of hypercoagulability and the greatest platelet aggregation can occur then
What are the major factor causes of sudden cardiac death
75% of cases are from CAD
25% are from myocardial abnormalities such as hypertrophy, dilated cardiomyopathy and valvular disease
What are some other causes of sudden cardiac death
narrowing of the coronary arteries
an old AMI
acute thrombosis at the site of fissured plaque
Sudden cardiac death can occur when ___% of the coronary artery vessel is narrowed
75%
In 90% of sudden cardiac deaht cases actual death is a result of…
LETHAL DYSRHYTHMIAS
(Ex: ventricular tachycardia, ventricular fibrillation, bradycardia, or asystole)
If Sudden Cardiac Death events are left untreated…
there is irreversible brain damage in 3-5 minutes followed by death
Possible lifesaving treatments for sudden cardiac death?
BLS (CPR)
ALS: Defibrillation, pacing for bradyarrhythmia’s, and drugs
Electrophysiologic testing to ID appropriate drug therapy
Implanted cardioverted/defibrillator
Resection of diseased myocardium
What percentage of sudden cardiac death patients are revived with defibrillation and how many discharge alive?
40-50% revive, and of those 50% leave alive
Describe CAD
a narrowing or obstruction of the coronary arteries d/t atherosclerosis, an accumulation in the arteries of fatty plaques made of lipids
This causes a decreased perfusion to the myocardium and inadequate myocardial O2 supply
What manifestations can the decreased perfusion of myocardial tissue and inadequate myocardial O2 supply lead to?
Hypertension
Angina
Dysrhythmias
MI
Congestive Heart Failure
Death
Angiogenesis
the formation of new blood vessels
especially important in coronary arteries
How does collateral circulation related back to CAD
If there is more than one artery supplying, if one is blocked then the blood can take another path
Collateral Circulation formation process
it takes time and happens when chronic ischemia occurs to meet metabolic demands
Who is more likely to die of an MI: A young person or older person
young person (does not have the collateral vessels)
When do CAD symptoms occur
when the coronary artery is occluded to the point of inadequate blood supply to the muscle, causing ischemia
When is coronary artery narrowing significant?
If the left lumen diameter is reduced 50% or any other major branch is reduced 75%
The goal of CAD treatment is to…
alter the atherosclerotic progression
The Widow Maker
This is referring to the left main artery of the coronary circulation
It feeds the anterior septum, bundle of HIS, and anterior left ventricle, and since 50% occlusion is only needed here to cause an MI, there is a much higher rate of death
Anything above ___% occlusion requires a stent
70%
Angina
discomfort within or adjacent to the chest
lasts for several minutes, is alleviated by rest, and does NOT result in myocardial necrosis
Potential Sequelae of Angina
AMI and Death
What typically provokes angina?
Exertion or Anxiety
What makes Angina different from Infarction
Angina does not cause myocardial death/necrosis (however it can turn into an MI if you keep pushing it)
What do we measure in the blood to determine if heart cells are dying?
Troponin protein levels since the cells will release that upon death
Symptoms of myocardial ischemia occur when …
O2 demand is above O2 supply
Most common causes of angina/myocardial ischemia
ASHD (Atherosclerotic Heart Disease)
Hypertrophic Cardiomyopathy
Aortic Stenosis
ASHD
Atherosclerotic Heart Disease
it is classic heart failure when the ventricular wall is thin and flabby and cannot pump well
Diastolic Heart Failure
Hypertrophic cardiomyopathy
The cells hypertrophy but on an X ray it looks like a normal heart size with a small interior left ventricle chamber
Why is hypertrophy a problem for the heart?
the cell increases in size and needs more O2, but the vessels will still be providing the same amount
Determinants of O2 demand in the heart include…
HR
Contractility
Ventricular Wall Tension (no stretch = creating greater demand)
Physiologic states that increase O2 demand
Exercise
Emotional stress
States of SNS activity
How does Anxiety decrease perfusion to the heart
it increases BP which decrease perfusion
But also SNS activity is determined by beta 1 receptors in the heart leading to a higher HR, contractility, and conduction which all contributes to decreased delivery from increased myocardial demand
Angina is chest pain resulting from…
myocardial ischemia caused by inadequate myocardial blood and O2 supply
Angina is caused by an imbalance between…
O2 demand and supply
Angina causes include…
obstruction of coronary blood flow due to atherosclerosis
Coronary artery spasm (like with drugs_
conditions increasing myocardial oxygen consumption
The goal of angina treatment is to do what?
provide relief of an acute attack
correct the imbalance between myocardial O2 supply and demand
prevent the progression of the disease and further attacks to reduce the risk of MI
4 Key concepts of Angina
- Heart always extracts near maximal O2 from blood even under minimal demand- this can only increase with more RBC
- Coronary blood flow can increase 7x as O2 demands
- In CAD, blood flow cannot get through, coronary spams occur, or plaque disruption occurs
- Most people have myocardial O2 demand AND diminished supply
Types of Angina
Stable
Unstable
Variant or Prinzmetal’s Angina
Stable Angina
Relatively constant pattern of pain with regard to severity and precipitating factors
Unstable Angina
recent onset (within the last 2 months), occurs at lower levels of exertion or at rest, has begun to intensify over time
Represents a continuum of symptoms between stable angina and MI
Also if the pattern of stable angina changes it is once again considered unstable Angina
20% of Unstable Angina progresses to…
MI within 3 months
Variant/Prinzmetal’s Angina
RESTING pain and ventricular arrhythmias caused by CA spasms
Can happen at anytime like rest, sleep, or activity
It is from coronary artery spasms
Classic angina includes..
stable and unstable angina
One drug commonly given for angina is ___
nitroglycerin
What can help control CA spasms and Prinzmetal’s Angina
Calcium Channel Blocked decreases them
The most powerful tool for diagnosing angina is…
the history and physical
When taking the H&P of a patient with potential Angina what things should be asked?
Character
location
radiation
duration
precipitating/alleviating factors
accompanying symptoms
any changes in pattern over weeks or days
Typical manifestations of Angina
exertional chest discomfort
several minutes duration
relieved by rest
in the region of the sternum (or anywhere between the lower jaw and epigastrium) - but its different in women
may radiate to neck or lower jar, arms (especially left), but not commonly in the back or epigastrium
described as a “tightness” “heaviness” or “choking sensation” rather than definite pain
Angina is provoked by…
walking uphill
stairs
vigorous arm work
intercourse
exercise in cold weather
emotions (fear, anxiety, anger)
following a meal (since more blood goes to GI tract)
Physical findings of Angina we can assess
HR and BP
S4 from atrial contraction in a ventricle stiffened by ischemia (like a baseball hitting a board than a glove_
S3 in L ventricular failure
Systolic murmur due to mitral regurgitation as a result of ischemia to the papillary muscles
The issue with Angina is many things can have similar physical findings, so what needs to be ruled out?
GERD
PUD
Cholecystitis
Asthmatic Bronchitis
PE
MI
Lab measurements for Angina
ECG (during attack)
What is seen different on an EKG during Angina
ST Segment depression or elevation
Mostly if the muscle is ischemic ST depresses, an ST elevation indicated MI
If angina occurs for more than 20 minutes…
we must suspect an impending MI or unrelated to myocardial ischemia issue and investigate
Diagnostic Studies for Angina
ECG
Stress Test
To diagnose angina, an ECG will show what during rest compared to times of activity?
Rest: ST depression or elevation and/or T wave inversion during times of pain
What will a stress test show that is indicative of angina?
Chest pain or changes in the ECG or vital signs during testing which may indicate ischemia
On an ECG if you see a tombstone shape…
that means death is imminent - very bad
Who always needs to be present for a stress test
a cardiologist in case the patient has an MI
What are the cardiac enzyme findings like in Angina
normal since none of the cells have died so no troponin has been released
What is the only way to get a definitive diagnosis of Angina by finding the cardiac enzyme levels and information about the patency of the coronary arteries?
Cardiac Catheterization
Exercise ECG AKA “Stress Test”
Exercise on a treadmill until ischemia ECG changes, angina, or dyspnea occur
May have radionuclide studies added during exercise if there’s no uptake in ischemia or prior infarctions
Persantine
an alternative to the exercise ECG stress test for patients unable to exercise
it provides dilation of the coronary arteries while lying in bed to get similar results
What are contraindications for the Stress test
significant aortic stenosis
untreated HTN
CHF
unstable Angina
The Gold standard for diagnostic testing and visualization of the heart is…
Cardiac catheterization
The most precise means to document presence of CAD is…
via a cardiac catheterization
Cardiac catheterization can give visualization of the coronary arteries and also…
measurements of left ventricular function (LVEDpressure; LVED volume; ejection fraction)
When is a cardiac catheter indicated
patients with sever angina
recurrent chest pain of uncertain etiology
survivors of cardiac arrest
If there is coronary artery stenosis of greater than 70% –> ?
there is limited flow to the myocardium and a greater risk for a coronary event
this is a significant finding
What is some general management rules for Angina
counseling and education regarding the potentially serious and unpredictable nature of the issue
drugs and other treatments to prolong survival and alleviate symptoms
hospitalization and intensive drug therapy and catheterization if angina is unstable
risk factor modification
search for correctable contributing factors
What are some risk factors for angina that can be modified?
low fat, low cholesterol diet
smoking cessation
BP control
What are some correctable contributing factors to angina
Aortic stenosis
hyperthyroidism (hyper metabolic need state)
severe anemia
tachyarrhythmias
CAD + Anemia = ??
highly lethal
Why do we need to treat tachyarrhythmias in angina patients
we should give meds to slow the heart rate and make pumping more effective since the increased heart rate will increase metabolic demand
How to implement immediate management of angina?
Assess pain
provide bed rest
administer O2 at 2-4 L nasal cannula as prescribed (this goes first!!!)
Administer nitroglycerin as prescribed
obtain a 12 lead ECG
provide cont cardiac monitoring
What does nitroglycerin do for an angina patient
dilates coronary arteries
reduces O2 requirements of myocardium
relieves chest pain
What 3 things contribute to the workload of the heart
Preload (blood volume)
the heart itself (rate and contractility)
Afterload (resistance against which it must pump)\
we wanna decrease these!!
Why is venous dilation so important for angina treatment
it will decrease preload and arterial dilation will decrease afterload and decreasing any of the 3 factors will help the heart
How do beta blockers help?
they block beta 1 receptors in the heart and cause contractility, heart rate, and conductivity to decrease
How do calcium channel blockers help?
they help prinzmetal angina in particular by stopping vasospasms
Goal of Angina pharmacologic management
restore balance between myocardial O2 demand and supply by decreased O2 demand and/or coronary blood flow
Major Drug Classifications for Angina Pharma Management
Nitrates (nitroglycerin)
Beta blockers
calcium channel blockers
How should antiplatelet therapy be done for unstable angina?
Daily aspirin to prevent new clots
hospitalization for IV heparin and aspirin if needed
Plavix if there is a stent
Invasive Angina Surgical Procedures
PTCA
Laser Angioplasty
Atherectomy
Vascular Stent
CABG
Percutaneous Transluminal Coronary Angioplasty
PTCA
One of more arteries are dilated with a balloon cath to open the lumen and improve arterial blood flow by pressing back plaque too
has a shorter hospitalization than a CABG
What can occur after a PTCA for a patient?
They can re-experience occlusion and may need the process repeated
Complications of PTCA
arterial dissection or rupture
immobilization of plaque fragments
spasm
acute MI
injury to epithelium
What is the indications for a PTCA
same as CABG with different contraindications
When is a PTCA cardiac cath contraindicated?
left main coronary artery stenosis
severe diffuse multi vessel disease
A PTCA is done via a…
cardiac catheter
PTCA can diagnose need for…
open heart surgery
Stent
something that can be placed in the Coronary artery to keep it open after PTCA
it will need to either be heparinized or take a med like Plavix to prevent clots of it
After a while the intimal layer will cover over it and the body will not longer attack it as foreign
Laser Assisted Angioplasty
a laser probe is advanced through a cannula similar to PTCA and it can vaporize the plaque rather than compress it
The heat from the laser vaporizes the plaque and opens the occluded artery
When is a Laser Assisted Angioplasty done
clients with small occlusions in the distal superficial femoral, proximal, popliteal, and common iliac arteries
Used more for small occlusions around the body
Atherectomy
removes plaque from an artery by the use of a cutting chamber on the inserted catheter or a rotating blade which pulverizes plaque
Risk of causing travelling debris though
When is Atherectomy used
to improve blood flow in those with ischemic limbs in those with Peripheral arterial disease
Intermittent Claudication
may be in those with PAD
increased O2 demand when walking leaving the legs in pain, but if the legs are in a dependent position (sitting) perfusion is aided and pain subsides
Venous Stasis
opposite to intermittent claudication
this is veins not arteries like PAD
Dependent position hurts here so the legs must be up to return blood flow to the heart
Coronary Artery Bypass Graft (CABG)
Attachment of the saphenous vein between the ascending aorta and stenotic coronary artery
coronary cath is done to detect need for this type of open heart surgery though
the blockage comes from cholesterol build up, so the surgeon makes it so the new vein goes from the aorta directly past the blocked location to provide blood
may need more than just one though, may need 2,3, 4 or more grafts
The chance of a perioperative (during surgery) AMI during CABG is
2-10%
What is common after 1 year or 6 years for CABG grafts
by one year 10% reocclude and by 6 years 2% reocclude
Angina can reoccur after CABG if…
grafts re occlude or CAD progresses
Saphenous Vein
vein taken from the leg and grafted upside down (to stop valves from blocking flow) in a CABG to provide blood flow in the heart
Mortality during a CABG is 1-3% higher when…
the patient :
has disease of left main coronary artery (LMCA)
significant left ventricular dysfunction
is over 65
Coronary Revascularization
200,000 + done a year
They are surgical methods (PTCA and CABG) to allow for reperfusion of the coronary/myocardium regions
Indications for Coronary Revascularization surgeries?
When meds have failed
If there is improved chance for survival in those with 50% stenosis of L main CA, 3 vessel disease, EF between 30-50%, and those with angina following an AMI
Basically when all else fails and you can improve survival by preserving myocardial function
Acute Myocardial Infarction
Leading cause of death in the US (30% of cardiac deaths; kills over half a million yearly and hospitalized 3/4 of a million)
many survive but often live with heart failure chronically
What is the most common cause of AMI
AMI d/t thrombotic occlusion superimposed on CAD
instability of atherosclerotic plaques with hemorrhage, fissuring, rupture – > acute thrombotic occlusion
Causes other than CAD for AMI
infective endocarditis emboli
thrombi from prosthetic valves
atrial thrombi
vasospasm from cocaine or amphetamine use
trauma
small vessel disease in DM or collagen vascular disease
anything that stops laminar flow
When does MI occur
when myocardial tissue is abruptly and severely deprived of O2
This ischemia can cause necrosis of myocardial tissue if the blood flow is not restored
How does MI progress/when does it occur?
it does not occur instantly, but rather evolves over several hours
When do obvious physical changes occur in the heart following MI?
6 HOURS LATER AFTER INFARCTION
the infarcted area appears blue and swollen at this time \
cells will release enzymes during this time that cause more damage
After 48 hours what happens to the infarct area?
the infarct turns gray with yellow streaks as neutrophils invade the itssue
8-10 Days after infarction what occurs?
granulation tissue forms (this can become necrotic)
What happens 2-3 months post infarct
necrotic area develops into a scar
the scar tissue permanently changes size and shape of the entire left ventricle causing potential bad contractions
__ is critical to a heart attack
time (the sooner you restore blood flow - like maybe in the Cath lab- the less likely morbidity is)
Manifestations of AMi
sudden death
new onset angina
unstable angina
occurrence of angina with less effort or at rest
protracted angina with pain like that of an infarct
acceleration of angina despite intense medical treatment
If the anginal pain is changed –>
pay attention and worry about an infarct
If there is an absence of anginal exacerbating factors like anemia, HTN, CHF, hypothyroidism, and obesity …
this reflects changes in plaques and resulting intermittent thrombosis that causes AMI
Transmural Infarct / Q Wave Infarct
if the clot is not broken down and thrombi persist –> ta very dangerous infarct involving the entire thickness of the left ventricle occurs
Onset of muscle death after an infarct is…
20-40 minutes (20!!!)
Size of an infarct depends on…
extent, severity, and duration of ischemic episode
amount of collateral circulation
metabolic needs of myocardium at time of event (younger die easier too; what you were doing during infarct can change impact too -shoveling v sitting)
40-50% of AMI occur…
in the LAD
this impacts the heart apex, anterior left ventricle, and interventricular septum (and papillary muscles and Bundle of HIS)
30-40Z% of AMI occur…
in the RCA
this impacts the inferior/posterior wall of the L ventricle and R ventricle (also impacts conduction like in LAD since it impacts septum and this impacts SA and AV nodes)
15-20% of AMI occur…
in the L circumflex
this impacts the lateral L ventricle
Most common MI site
LAD - the widow maker since it feeds so much
What is the result of an AMI on the affected portion
decreased contractility with abnormal wall motion
altered compliance (Stretch)
decreased stroke volume leading to decreased ejection fraction
more LVEDP
EDV
end diastolic volume
amount of blood in ventricle at end of diastole (rest period)
about 100 mL
SV
stroke volume
amount ejected from ventricles
70-75 mL normally but can be less with damage
ESV
end systolic volume
difference between EDV and SV and it is what remains in the ventricle
25-30 mL
Ejection Fraction
the % amount of ejected blood (in MI you may get a lower stroke volume causing a lower EF)
The lower the EF…
the lower the cardiac output and the lower the ability to perfuse
LVEDP
left ventricular end diastolic pressure
pressure in the ventricle at the end of diastole
the more blood left the greater the pressure
these pressures are supposed to get lower than atrial pressure when passively filling, but if the pump is affected you get higher pressures and it interferes with heart functioning
What does the area of infarct look like after an AMI?
central area of necrosis
surrounded by minimally surviving injured cell area that can come back and function if blood flow is restored
it is an area surrounded by ischemia
the myocardium will NOT regenerate and the necrosis tissues will be replaced with scar tissue
Q Wave infarcts are preceded by…
fatigue
chest discomfort
malaise in days preceding
A Q Wave infarct involves __ __ of the myocardium
full thickness (MI)
When does infarction usually occur during the day?
in the early AM since platelet aggregation and clotting is higher
What does it mean if an MI is clinically silent?
May not feel the heart attack due to impairment of the nervous system (neuropathy in DM) or having a high pain threshold (women)
However, it is usually found later on an ECG
MI that obstructs the LAD results in…
anterior or septal MI or both
MI that obstructs the circumflex artery results in ..
posterior wall MI or lateral wall MI
MI that obstructs the right coronary artery results in…
inferior wall MI
What obstruction locations impact electrical conductivity most?
LAD or RCA
Risk Factors for MI
Atherosclerosis
CAD
elevated cholesterol levels
smoking
HTN
obesity
physical inactivity
impaired glucose tolerance
glucose
many are modifiable
S/S of AMI
Pain
Diaphoresis
cool clammy gray skin
weakness
sense of impending doom
profound restlessness
confusion
fever in 24-48 hours usually above 101 r/t inflammation
respiratory issues like increased RR, cough, wheezing, frothy sputum, crackles, SOB
extremity issues like peripheral cyanosis, edema, and pallor
pre renal failure
JVD
What is the pain like in an AMI
intense, severe, crushing - like an elephant on your chest
Unremitting pain for 30-60 minutes (but only takes 20 minutes for tissue death)
retrosternal pain location
often pain radiates down the ulnar side of the arm, neck, teeth, and jaw
AMI impaired L ventricular filling —>?
pulmonary vascular congestion (pulmonary edema) –> SOB, tachypnea, orthopnea, moist crackles usually in lung bases
AMI tachycardia d/t SNS activity –> ?
dysrhythmias (EP and NEP)
BP may initially be normal in AMI, but with R ventricular or severe L infarction…
it may be hypotensive
S3 v S4 indicates
S3 is pathonomic for heart failure
S4 is more of a wall compliance issue
What sort of changes occur for the heart after an AMI
displacement of PMI
soft S1 S3 and S4
mitral regurgitation murmur
friction rub (pericardial inflammation)
dysrhythmias (PVCs and V tach)
palpitations occur
PVC - Premature Ventricular Contraction
a ventricular contraction not preceded by atrial contraction (no P wave!!)
V Tach
PVCs stack up one after another leading to ventricular tachycardia
Non Specific Diagnostic tests for AMI
CBC
ESR
Myoglobuin
CBC (AMI)
checks WBC and seeing if leukocytes are combatting infection and inflammation
ESR (AMI)
non specific measurement of infection or inflammation
rate rises with elevated levels of fibrinogen or globulins are present
RBC settle faster with inflammation
Myoglobin Test (AMI)
O2 binding protein found in striated muscle
Releases O2 at very low tensions
Any injury to skeletal muscle will cause its release into blood
non specific with limited usefulness in diagnosing AMI
Creatinine Kinase Diagnostic Test
CK or CPK - enzyme found in the heart, brain, and skeletal muscles
a non specific test for AMI
an isoenzyme with 3 types
mostly use CK-MB for MI diagnosis
What person might have higher Creatine Kinase levels
those with larger muscle masses
CK-MM
Creatine kinase in skeletal muscle
CK-MB
creatinine kinase mostly in cardiac muscle
this one is viewed for non specific MI diagnosing
CK-BB
creatine kinase in brain and lungs
What is one of the most commonly used markers for detecting MI?
Troponin
Troponin types
Troponin T
Troponin I
Troponin Test
A diagnostic test for AMI
Troponin T
a regulatory protein found in skeletal and cardiac muscle fibers
skeletal and cardiac muscle shave different forms of this protein
specific antibodies can detect cardiac troponin T and is specific for myocardial injury
Troponin I
a protein in the troponin cardiac muscle complex
specific to the myocardium
usually returns to nL sooner than troponin T
Which troponin is the gold standard
Troponin I (since T can indicate an MI from weeks ago)
AST Test
Aspartate aminotransferase
enzyme found in the heart, kidneys, brain, RBCs, liver, lungs, pancreas, & skeletal muscle
many conditions can produce elevation
not a great test for diagnosing MI but can be looked at with others
LDH test
Lactic Dehydrogenase
is present in almost all metabolizing cells, but is especially high in the heart, kidneys, brain, RBCs liver, & skeletal muscles
requires electrophoresis to separate out its 5 isoenzymes
an older and not great marker either for AMI
What replaced LDH testing
CK-MB testing
LDH is still useful, what are LHD1 and LHD2 useful for
assessing extent of myocardial damage
What is important to keep in mind about Troponin I and T rising?
They both rise at around the same time, but T lasts longer than I elevated and can indicate something old
which is more important:
CK or CK-MB?
LDH or LDH1?
CKMB
LDH1
When do the following things begin to rise, peak and return to normal: CK, CK-MB, Troponin I, Troponin T, AST, LDH, LDH 1
CK - begins rise 4-6 hours - peak 24 hour- normal 3-4 days
CK-MB- 4 hour - 18 hour peak - 2 days to normal
Troponin I - 4-6 hr - 11 hr - 4 days
Troponin T - 4-6hr - 11 hr - 10 days
AST - 8 hour - 24-48 hour - 4 days
LDH - 24 hour - 3 days - 8-9 days
LDH 1 - 24 hours - 3 days - 12 days
Hemodynamic Monitoring: CVP
central venous pressure
reflects amount of blood returning to the heart
hemodynamically monitor via a catheter in the right atrium
Hemodynamic Monitoring: CO
cardiac output
function of heart rate and stroke volume
hemodynamically monitor via a pulmonary artery catheter equipped with a special thermistor probe
Hemodynamic Monitoring: PCWP
Pulmonary capillary wedge pressure
pressure measured in the pulmonary artery; provides an indication of L ventricular function
measured via a Swan Ganz cath through the peripheral vein –> R heart –> pulmonary artery
P Wave indicates
contraction of the atrial muscles (depolarization of the atria)
QRS complex indicates
contraction of the ventricles (depolarization of the ventricles)
T Wave indicates
electrical changes during the relaxation phase of the ventricles (repolarization of ventricles)
What is lost in an ECG?
Repolarization of the atria
What EKG results may appear in damaged heart muscle
inverted T wave
Raised ST segment
Deep Q Wave
Ischemia leads to what ECG result
ST depression and T wave inversion
Infarction with death of tissue leads to what ECG result
ST elevation (tombstone) and possible T wave inversion
If you have a Q wave infarct, what happens in ECG results
whole thickness of wall is affected so the Q wave depresses - very serious
Echocardiogram
noninvasive procedure that uses sound waves
gel is applied, transducer wand moved over chest to get internal structure pic of heart
takes 30-90 minutes depending on condition and echo type
Wonderful test for how the heart works in real time - see valve opening and closing, wall movement, ventricular filling and contraction, atrial filling, can outline ventricle at end of systole and diastole and measure end diastolic volume, stroke volume, EF, and end systolic volume - can see regurgitation with leaflet movement too
Echocardiogram tests evaluate…
how well the heart is moving
how well the valves are working
the size of the heart and its pumping chambers (ventricles)
Complications d/t MI (afterward)
Dysrhythmias
CHF
Cardiogenic Shock
Thromboembolism
Ischemic pericarditis
Myocardial rupture
ventricular aneurysm
Why do dysrhythmias occur post MI
d/t tissue ischemia, hypoxia, SNS, lactic acidosis
it will cause decreased CO, cardiac irritability and further decreases in perfusion
and conduction issues from this may require a pacemaker
The most common cause of death outside of the hospital related to a complication of MI is…
ventricular fibrillation
What does CHF cause after an MI
decreased contractility and abnormal wall motions
decreased stroke volume
What does Cardiogenic shock cause after an MI
profound L ventricular failure from massive AMI (10-15 % of post MI patients with an 80% mortality rate)
What does Thromboembolism cause after an MI
may travel to the brain, kidneys, or spleen
these clots form from lack of laminar flow
bed rest and heart failure predisposes people to venous thrombus and PE (not as common with early ambulation and anticoag tho)
What does Ischemic pericarditis cause after an MI
inflammation of the pericardium
sever sudden constant pain
worse pain with inspiration
tachycardia
moderate fever
pericardial friction rub heard with every beat
Myocardial ruptures lead to…
instant death
What do ventricular aneurysms cause after an MI
late complication*
filled with clots and debris an embolus can form (like a ballooning out from the vessel)
AMI Pre Hospital Treatment
EMS personnel trained in defibrillation
AEDs
Adequate analgesia with morphine
Aspirin therapy - anti platelet effect
What is the benefit of analgesia with morphine for hospital pre treatment
it causes venous dilation dropping the preload on the heart
65% of AMI deaths are in the first hour, but 40% can be saved with ___
AED/Defibrillation
AMI Hospital Treatment
Cardiac Cath lab (CCU) to reduce mortality 50% with defib, continuous ECG, swan ganz
Diet of liquids for the first 24 hours d/t risk of aspiration with N/V and to not let blood go toward GI too much
telemetry monitoring for arrhythmias
stool softeners to prevent straining (and vagal activation)
bed rest for 1 day for uncomplicated cases
gradual monitored resumption of ambulation
oxygen therapy to avoid hypoxemia
What needs to be done in the convalescence period after an AMI?
prevent recurrence with calcium channel blockers, beta blockers, and aspirin
Anticoagulation for 6 months for high risk
Risk factor modification
Cardiac rehabilitation
Prompt detection of progression of CAD (ex: Angina)
Stenotic Valves
valves that are hard (narrowed) and calcified
Failure of the valve to OPEN completely
Regurgitant Valves
Valves that do not close like they should (leaky)
also called “Insufficiency” or “Incompetent”
Inability of valve to CLOSE completely
L Vent will have to push hard against this which can make push backward causing leaky mitral valve
Causes for Valve Disease
Myxomatous Degeneration (pathological weakening of connective tissue - mitral valve prolapse for example)
Calcific Degeneration
Congenital Defects
Ineffective Endocarditis
CAD
AMI
The pattern goes S1, ___, S2 __, S1
S1 Systole S2 Diastole S1
What are the AV valves like in Systole
closed
a problem at this time leads to mitral regurgitation
What are the SL valves like in Systole
open
a problem at this time leads to aortic stenosis
What are the AV valves like in diastole
Open
a problem at this time is mitral stenosis
What are the SL valves like in diastole
Closed
a problem at this time is aortic regurgitation
While not a definitive diagnostic, what does murmurs heard in certain areas correlate to?
All People Eat Turkey Meat
If heard on pulmonic area, its a pulmonic problem - if over tricuspid area, its a tricuspid problem
If I hear a murmur between S1 and S2 that means its a murmur in ___
systole
If I hear a murmur after S2 it is a murmur in __
diastole
If I hear a murmur when valves are closed during systole what problems could it be?
If it is the mitral or tricuspid that should be closed its a regurgitation problem
If its the pulmonic or aortic its a stenosis problem
If I hear a murmur when valves are closed during diastole what problems could it be?
If it is mitral or tricuspid its a stenosis problem
if its the pulmonic or aortic that should be closed its a regurgitation problem
What is more serious a systolic problem or diastolic problem?
Diastolic because there is less blood to inject in circulation
Systolic problems can be overcame for a time because of the strength of the ventricle forcing blood, but diastolic problems means less blood to do so with and it cannot be overcame in this case
Mitral Valve Stenosis
A diastolic murmur impeding flow from the LA –> LV
lack of passive filling is occurring
This problem occurs in diastole
Manifestations of Mitral Valve Stenosis
Atrial Fibrillation: Clotting and Embolism
Pulmonary Congestion: Orthopnea, cough, poor oxygenation
Decreased SV: Fatigue, activity intolerance, weakness
Mitral Valve Prolapse (MVP)
Mid systolic click or murmur
Blood from the atria goes into the pulmonary veins, but the chordae tendinea let go allowing blood to back up into the lungs leaving less blood flow in the left ventricle
Decreased EDV and less blood for ventricular contraction then occurs
Manifestations of MVP
palpitations
rhythm disturbances
dizziness
dyspnea
chest pain
anxiety
angina exacerbation
syncope
Why do dental procedures (or any invasive procedure) need prophylactic antibiotics?
there is a risk that organisms can get in and get to areas without laminar blood flow to grow and cause infective endocarditis
Aortic Valve Stenosis
Systolic Murmur
LV hypertrophy –> LV failure
Hard aortic valve (SL valve)
Manifestations of Aortic Valve Stenosis
angina
syncope
fatigue
hypotension
decreased peripheral pulses
Aortic Regurgitation
“Aortic Insufficiency”
Diastolic Murmur
LV hypertrophies and dilates (but valve leaflets wont close so dramatic icnrease in EDV - starlings law makes it so it can only extend and stretch so much)
(Aortic regurg on left and pulmonic regurg on right)
Manifestations of Aortic Regurgitation
Main: huge EDV
Increased SBP and decreased DBP and Widened plse pressure and bounding peripheral pulses
Ways to diagnose valvular diseases
cardiac auscultations
CXR (not super helpful with diastolic HF since you cannot see it)
echocardiography (can find SV, EDF, and EF and see valve and wall movement)
electrocardiography (check electrical activity)
coronary angiography (helpful with CAD related valve issues)
MRI (expensive)
doppler ultrasound
Medications used to reduce the workload of the heart
Digitalis
Diuretics
Anticoagulants
Beta Blockers
calcium channel blockers
Valvular Disease Surgeries
Commissurotomy
Valvuloplasty
Valve Replacement
Commissurotomy
separation of the flaps of the mitral valve to relieve mitral stenosis
Valvuloplasty
surgery performed on a heart valve
Valve Replacement
can be a donor, animal part, plastic, or metal valve put in place
What is the risk associated with replacement valves
they are foreign material so there is a risk of clots attacking it
