Class 21: Ischemic Heart Disease Flashcards
describe the filling of the heart muscle during systole & diastole
- systole = surface coronary arteries filled
- diastole = blood from surface flows deep into muscle
therefore, diastole is when heart muscle is actually nourished
when occurs if the left main coronary artery is blocked
- reminder: left main splits into circumflex & LAD
- blockage = decreased blood supply & devasting
when does the heart muscle receive blood? why?
- during diastole
- due to high pressures during systole
- also due to aortic recoil which aids perfusion into coronary arteries
what is the aortic recoil
- bulging of aorta at the end of systole
what happens to the coronary arteries when heart rate or metabolic rate increases?
- smooth muscle in arterioles supply the heart muscle (coronary arteries) relax
= vasodilation & increased blood flow
what is the local dilation of the coronary arteries caused by?
- metabolites produced by the heart muscle workload
- B-adrenergic stimulation (SNS)
- release of NO from the vascular endothelium
how does increased heart rate affect diastole
- decreases the diastolic time more than systolic
= decreased perfusion time of coronary arteries = ischemia
what are the effects of increased HR on demand, metabolic waste, and filling time? what do these cause?
- increased demands
- increased metabolic waste = vasodilation
- decreased filling time
what is the most common form of heart disease
- coronary heart disease
aka ischemic heart disease
what is the most common cause of CAD
athersclerosis
what is athersclerosis
- formation of fatty, fibrous mass (atheroma) = plaque
- within the wall of an artery
when does plaque formation usually begin
- around age 20
when does athersclerosis become symptomatic
- usually asymptomatic until vessel is 75% blocked
what happens when the vessel is 75% blocked?
= symptoms
- signs of ischemia, particularly during times of exertion when metabolic demand in higher
what is the difference between partial and full blockage of an artery
- partial = may only cause ischemia = sub lethal
- full blockage for >20 min = necrosis = lethal
what happens if we have partial blockage of the coronary arteries for a long period of time
- go from sublethal to lethal
describe the healing of necorsis tissue
how does this effect our goal?
- never heals
= want to keep necrosis as small as possible
describe the zones of injury
what is our goal of treatment?
- have lethal/necrosis surrounded by sublethal injury
- want to save area of sublethal ischemia
what is collateral circulation
- additional arterial connection that form around a blockage
what influences our ability for collaterial circulation
- genetic predisposition
2. chronic ischemia
describe collateral circulation with rapid arterial acclusion
- no time for development of collateral circulation
how do we compensate with acute ischemia
- anerobic metabolism
how might CAD manifest as.. (5)
how predictable is each?
- chronic stable angina = most predictable
- acute coronary syndrome = least predictable
- cardiac arrythmia
- HF
- sudden cardiac death
what is acute coronary syndrome divide into
- unstable angina
2. acute myocardial infarction
what are two types of MI
- stemi
2. nonstemi
what does typical myocardial O2 supply & demand look like
- normally should be able to supply as much O2 as needed
how does supply and demand change with CAD
- supply decreases due to blockage
- demand increases during activity
what are the goals of antianginal treatment
- increase supply by removing blockage or using vasodilator
- decrease demand thru rest, decreasing HR, decreasing afterload to push against
what determines myocardial O2 demand
- HR
- contractility
- afterload
- preload
describe the improtant of balance of HR
- want enough for perfusion
- but not so much you cant fill ventricles (decrease diastolic time) or feed heart
describe the importance of balance of contraction
- want enough to have a good SV
- but not so much force that workload/demand is too high (= O2 consumption)
describe the importance of balance of preload
- want enough to fill the heart
- but not so much that it is overloaded w volume = effect function
ex. think of when have too much food in mouth
describe the importance of balanced afterload
- want enough for good bp and perfusion
- but not so much its hard to push against
what does decreased contractility cause
= decreased SV = decreased CO = decreased bp = symptoms of hypotension ex. lightheaded, weak legs, pre syncope, syncope, angina
how long does it take for heart cells to stop contarcting vs die
- starts contracting within several minutes after total occlusion
- die after 20 min
cardiac ischemia may result in.. (5 things)
- diastolic dysfunction
- systolic dysfunction
- electrical dysfunction
- angina
- MI = cardiac muscle death
describe diastolic dysfunction
- ischemic muscle becomes stiff
= reduced relaxation, stretch, and filliing
= reduced preload, reduced SV, reduced CO & BP
describe systolic dysfunction
- failure of heart to properly contract
= reduced SV, CO, and BP
describe electrical disturbances in the heart due to cardiac ischemia
- conduction moves around the ischemic tissue or heart muscle is irritabloe
= ECG changes, irregular or ineffective pumping - tachy or brady can alter CO
how does tachycardia alter CO
- increased HR = decreased filling = decreased feeding = increased O2 demand = increased workload
how does bradycardia alter CO
- decreased HR = decreased CO = decreased BP
what is angina pectoris
- chest pain
what causes angina
- reversible myocardial ischemia
does angina always have symptoms?
- no, may be silent but that is unusual
how can angina be described
- pressure
- clenching
- elephant on chest
- aching
- heaviness
does angina change with position or breathing? how can we differentiate between pleuritic & muscle pain
- no it does not
- pleuritic & muscle pain changes w respiration
what symptom is associated with angina that is important to identify? how can we tell?
- may experience indigestion or burning quality
= give antacid
is ST depression common or uncommon with angina
- common
what respiratory symptom is associated with angina? why?
- SOB/dyspnea
1. compensation
2. from pulmonary edema
why might pulmonary edema occur with myocardial dysfunction
- occurs from systolic dysfunction
= failure to move blood forward = back up of fluid & pressure in lungs = pulmonary edema
describe the effects of pulmonary edema
= decreased gas exchange
= SOB and decreased O2 sats, increased RR, cough
describe the referred pain of angina
- midsternal
- down both arms
- left shoulder
- lower jaw
- neck
- intrascapular
- epigastric
describe the characteristics of stable angina
- reproducable = happens every time I ___, i get angina = can expect it everytime you do it
- intermittent = only during exertion
- caused by increased exertion
- can have it for years = chronic
how long does the feeling of angina occur during stable angina
- brief = 3-5 min
how is stable angina relieved
- rest and/or
- nitroglycerine (vasodilator)
what is the #1 way to reduce demand on the heart
- rest!
what causes stable angina
- advanced plaque that is highly fibrotic & contains little lipid
describe the pattern of angina during stable angina
- similar pattern of onset, duration, and intensity of symptoms
“my usual angina”
what is seen on ECG during stable angina
- transient ST depression
describe use of nitroglycerin
- rescue med
- can also take before the activity that causes angina
how is stable angina controlled
- usually w meds
- BUT not cured, will still be limit in activity
what is another name for stable angina
- effort or exertional angina
- can significanty reduce a persons daily functioning
what stage of atherosclerosis is present in stable angina
- fibrous plaque
what is prinzmetal’s angina
- variant angina
what causes prinzmetal’s angina? when does it occur?
- due to coronary artery spasm
- may be response to a stimulant
- occur at rest
- may occur with or without CAD
what stimulants might cause prinzmetal’s angina
- cocaine
- extreme cold
- extreme stress
is prinzmetal’s angina common? what might people have a history of?
- rare
- hx of migraine, raynaud’s syndrome
what might cause chronic stable angina to progress to acute coronary syndrome
- increased lesion size & blockage
- increased complication leison w clot
describe management of stable angina vs acute coronary sybdrom
- stable = manage at home
- acute = go to hospital or ER
what does acute coronary syndrome split intoo
- unstable angina & nonstemi MI
- stemi MI
what is the difference between unstable angina & nonstemi MI
- unstable = no necrosis
- non stemi = necrosis
describe the thickness of necrosis in stemi vs nonstemi
- nonstemi = partial thickeness = <100% blockage
- stemi = full thickness = ~100% blockage
what causes acute coronary syndrome
- develops when myocardial ischemia is prolonged & not immediately reversible
= not stable angina - typically when a coronary artery is >90% occluded
how does the size of artery impact the amount of dysfunction
- bigger with more branches = more muscle deprived = greater injury = greater dysfunction
what is the difference between MI and angina
- angina = no cardiac death = reversible
- MI = cardiac death = no reversible
what causes unstable angina?
- complicated lesion
- rapid change from stable to ustable
= rupture of plaque with coronary vasoconstriction & thrombus formation
what allows unstable angina to resolve
- followed by spontaneous thrombolysis
does unstable angina require hospitalization?
- yes requires immediate hospitalization
what are the manifestations of unstable angina
- chest pain
- dyspnea
- reduced cardiac output may occur bc of systolic dysfunction
how does systolic dysfuction cause decreased CO
- decreased contraction/stunned = decreased CO & BP
why might dyspnea occur with unstable angina
- due to myocardial dysfunction and pulmonary edema
how long does chest pain last during unstable angina? how is it relieved?
- symptoms last up to 20 min
- not relieved by nitro or rest
what happens if chest pain goes on longer than 20 min during unstable angina
= likely get necrosis = MI
what is a big difference between stable & unstable angina
- stable = relived by rest & nitro, and caused by exertion
- unstable = may occur at rest & require less exertion, not promptly relieved by nitro but once was
describe angina during unstable angina
- develops w less exertion
- can develop at rest or during sleep
- not promptly relieved by nitro but once was
- gradually worsen over days
describe the changes in biomarkers during unstable angina
- remain normal or are minimally elevated
what are cardiac biomarkers
- contents spilled by myocytes when they die
- can be measured in the blood
how can biomarkers distinguish MI vs angina
- MI = significant rise in biomarkers
- angina = no or little death = normal biomarkers
what happens if myocardial ischemia is brief during unstable angina
- ventricular dysfunction is reversible
what happens if ischemia is persistent but less than 30 min during ustable angina
- ventricle may become stunned
= mild decrease in ventricular function that can last for weeks
what happens if blood flow is not restore for 40-60 min during unstable angina
- cardiac cells begin to die = permanent myocardial dysfunction
how come during unstable angina it takes 40-60 min for cell death and not 20 min?
- if cell is completely deprived of O2 takes 20 min
- with unstable angina, usually still some blood flow = >20 min for cell death
what is myocardial infarction
- nercrotic death of cardiac muscle from prolonged ischemia (20-60 min)
is an MI irreversible?
- irreversible dysfunction = scar
what causes an MI
- plaque rupture followed by occlusive thrombus formation
NOTE: with unstable angina it is followed by spotaneous thrombolysis but not in MI
what are two kinds of MI
- non STEMI
2. STEMI
how long does it take for MI to be complete? how long until most cell death has occured?
- 12 hours to complete
- most cell death in first 6 hr
describe the progression of necrotic tissue
- begins on the endocardial (inside) and progresses to the pericardial (outside)
why does necrotic tissue first form on the inside?
- bc outer vessels travel to inner layers = furthest away from blood supply
what is a transmural infarction
- involves full thickness of ventricle
= STEMI
what is a subendocardial infarction
- only inner portion of ventricle has died
= non-STEMI
does angina or IHD always preced MI? why or why not?
- rupture-prone plaques can be less than 50% occlusive = no a history of angina does not always preced
what are manifestations of MI
- angina
- dyspnea, orthopnea
- increased JVP & leg edema (decreased CO = “back up fluid”
- syncope, presyncope (decreased CO)
- ashen, cold, clammy (with decreased bp)
- reflex tachy with decreased bp = SNS stim
- N&V (from pain)
- brady if inferior infarct = PSNS
- small temp rise from necrosis
- ECG changes
- elevated cardiac biomarkers
how might angina differ during an MI vs unstale angina
- more severe & lasts longer
- can also be silent
why might you get N&V with MI? where is this most common?
- if injury stimulated vagus nerve = triggers PSNS = lowered HR
- most common with injury to inferior aspect to heart bc its where the nerve runs
- N&V also from pain
why do we get elevated biomarkers in blood with MI
- when muscle cells die from necrosis, contents spill into the blood
what are diagnostic studies for a MI
- ECG –> see ST changes
- serum cardiac markers
- angiography
what can you see with an angiography
- direct picture of vessels
what are the 3 cardiac biomarkers
- troponin
- CK-MB
- myoglobin
what is the preferred cardiac biomarker
troponin
why is troponin the preferred biomarker
- rises fast & early = early detection
- stays elevated for long period of time = helpful if pt delays coming to hosputal
- can see elevation up to 2 days later
what is a con to the biomarker myoglobin
- not specific to heart muscle
what is a con to CK-MB
- does not go up quick = not good early indicator
why do we get a small increase in temp during a MI
- necrosis = tissue injury = inflammation = infiltration of macrophages
how come we get scar formation w MI
- cardiac cells cannot regenerate = scar tissue formation
what does the scar formation during MI cause
- cannot contract = permanent ventricular dysfunction
what does the amount of dysfunction depend on
- size of scar tissue
how does scar tissue effect conduction? how does this show during a transmural MI?
- scar tissue is not excitable = no electrical conduction
- transmural MI = permanent change in ECG = pathological Q
describe the change in Q wave seen in a transmural MI
- pathological Q –> deep.wide Q
describe SNS stimulation during & after an MI
- during: SNS stim = keep heart pumping
- after: too much SNS stim may aggrevate an injured or healing heart
describe the use of beta blockers post MI
- prevent overstimulation of heart & reduce HR/contracility
- helps the heart rest
- reduces the risk of life-threatening arrythmias
what are complications of a MI (5)
- arrythmias
- acute HF or cardiogenic shock
- pericarditis, effusion, myocardial rupture
- mural thrombosis & embolism
- valve disorders
what arrythmias may occur with MI
- atrial & ventricular rhythmns that result in tachy, brady, or AV conduction blocks
- cardiac arrest rhythmns such as VT or VF
- disrupted conduction or SNS or PSNS overstim
what do VT and VF require?
- immediate defibrillation
what is acute HF or cardiogenic shock
- stunned heart = failure to pump adequate blood
= hypotension & hypoperfusion of all organs, particularly in the brain & kidneys
what is pericarditis
- inflammation to the pericardium
what is a effusion of the heart
- exudate fills the pericardial cavity
= P on heart = tamponade
= reduced output
what is a myocardial rupture
- ventricle can perforate = blood fill the pericardial cavity
what causes mural thrombosis & embolism
- stasis of the blood in the ventricle (due to stunning) = thrombus & embolism
- the clots can be sent into cirulation = cerebral or pulmonary embolism
what causes valve disorders
- if necrosis occurs close to valve
what is a valve disorder
- damage to papillary muscle = A-V valve disorders (mitral & tricupsid)
what is sudden cardiac death
- immediate loss of CO = decreased bp = decreased perfusion = no pulse = death
how does sudden cardiac death affect the brain
= loss of cerebral blood flow
= decreased LOC
how long does it take death to occur after onset of a cardiac death
- usually within 1 hr of symptom onset
what are the highest predictors of sudden cardiac death
- vent EF <30% (so bad CO)
- vent arrhythmia post MI (catecholamines)
sudden cardiac death may the first sign of ________ in 25%
- heart disease
what are the fatal arrythmias
- acute ventricular arrhythmias
1. V tach
2. V Fib
what are other uncommon causes of sudden cardiac death
- outflow obstruction
- extreme bradycardia
what increases myocardial O2 demand?
- physical activity
- stress
- SNS input
- tachycardia
- increased afterload
- volume overload
- cardiac hypertrophy & dilation
what is cardiac hypertrophy
thickening of heart wall
what is cardiac dilation
- stretching of the heart
how does cardiac hypertrophy & dilation increase myocardial O2 demand
- cause cells to be insufficient & require O2
what decreases myocardial O2 supply
- CAD
- hypovolemia
- weakened heart muscle
- arrythmias
- cardiac injury/remodeling
- valve disease
- anemia
- resp disease
what is cardiac remodelling
- dilation or hypertrophy
how does anemia decrease O2 supply
- decreased O2 carrying capacity
how does valve disease cause decreased O2 supply
- causes leakiness
- or stenosis
how does resp disease cause decreased O2 supply
= decreased oxygenation
what are anginal managment goals
- minimize the frequenzy, duration, and intensity of anginal pain
what is the goal of anginal therapy regarding functional capacity
- improve or maintain functional capacity
what do you hope to delay or prevent with anginal therapy
- MI
- cardiac remodelling
- arrythmias
what does cardiac remodelling lead to
- HF
what is the goal of anginal therapy regarding meds
- minimize adverse effects
what are common adverse effects with anginal drugs
- bradycardia
- hypotension
- hypercalemia
(due to over effect)
what is included in non pharmacological management of angina
- diet
- lifestyle mod
- treating underlying disorder
- angioplasty
- surgery
what changes in diet can be included for management of angina
decrease intake of:
- alcohol
- cholestrol/sat fats
describe lifestyle modifications for management of angina
- exercise
- weight management
- smoking
what underlying disorders can you treat to manage angina
- DM
- HTN
- hyperlipidemia
what is angioplasty
- surgery to unblock a blood vessel
what is a surgery done for angina
CABG –> redirection of blood around a blocked artery
what does CABG stand for
- coronary artery bypass graft
why do we want to create moderate disease progression
- allow time for collateral development
what are antianginal drugs
- drugs that target cardiac vessels and worload
what is the therapeutic goal of antianginal drugs
- increase supply to ischemic heart tissue
- decrease myocardial O2 demand & workload
how can antianginal drugs increase O2 supply to ischemic tissue
- dilate coronary arteries
how can antianginal drugs decreased O2 demand & workload
- slow HR
- dilate veins in the body so the heart receievd less blood = decreased preload
- cause heart to contract w less force = reduced contractility
- dilating arterioles in the body to lower body pressue = reduced afterload
what are the antianginal drug classes
- nitrates/nitrites
- beta-blockers
- calcium channel blockers
- antilipemics
- antiplatelets, anticoagulants, thrombolytics
what are 2 types of nitrates
- nitroglycerine
- isosorbide dinitrate
what is the MOA of nitrates
- artificial NO donor
- dilate veins in the body = decreased venous return = decreased preload = decreased workload
- dilate coronary arteries = increased blood supply to myocardium
what are nitrates used for
- prevention & treatment of all types of angina
what is an important consideration w nitrates
- degrades in light = in brown bottle
how can nitroglycerine be given (routes)? why is this important?
- sl tablet
- spray
- transdermal
- iv
= no first pass effect
what is the rescue med for angina
- nitroglycerine
explain how nitroglycerine is administeres
- sit down –> to keep safe from decreased bp & decreases workload
- first dose –> wait 5 min
- if not gone then 2nd dose –> wait 5 min
- if not gone then 3rd dose
how many doses of nitro can you give in 15 min
- 3
what should you assess for an in-patient taking nitro
- angina, BP (to keep safe from falls) and HR after each dose
what should you do if the 3 rd dose of nitroglycerine does not work
= unstable angina or MI
- call ambulance
what should you for a patient in the hospital taking nitroglycerine
- return to bed or chair
- check vital signs between doses
what are side effects of nitroglycerin
- increased HR (reflex tachy)
- decreased BP –> orthostatic
- pounding headache (due to dilation of vessels in head)
- dizziness
- flushing
describe headache associated w nitroglycerin
- will go away after continued use
- due to vasodilation
does tolerance develop with nitroglycerin?
- yes if taking 24/7
how can we prevent tolerance w nitro
- nitrate holiday = nitrate free period
- remove patch nitro patch at bedtime for 8 hrs
- apply new patch in morning
describe the difference in use of patch vs spray for nitro
- patch = for maintenance
- spray = rescue
why is it important to prevent nitro tolerance
- would result in no effect of nitro spray if needed
what drug does nitro have an interaction w ? why?
- any other med w nitro in it –> viagra
- both dilate vessels = risk of dangerous drop in pressure & precipiate MI
describe the use of nitro IV
- used for urgent
- hypertensive emergencies
ex. bp control w perioperative HTN
what are 2 types of beta blockers
- metaprolol
- atenolo
what is the action of beta blockers
- decreased HR = decreased workload
- decreased contractility = decreased workload
what is the MOA of beta blockers
- selectively block beta adrenergic stimulation of the heart
what are beta blcokers used for? what are they first line for?
- decrease frequency of anginal attacks
- 1st line for chronic angina –> so if do something, HR wont automatically go up too high
- critical cardioprotective IHD med
what is one consideration for pts taking beta blocker
- bc HR is blocked from rising - must be carefulw ith exertional activity
does tolerance occur with beta blockers?
- no
what can sudden discontinuation of beta blockers cause
- may cause anginal attack
- rebound effect from HR no longer being reduced
what else do beta blockers treat
- treats HTN and angina = reduced incidence of Mi
beta blockers are _______-
cardioprotective
explain how beta blockers are also anti-arrythmic
- after an MI, high levels of catecholamine irritate the heart = imbalance in supply & demand which can lead to arrythmias
- beta blockers blcok the harmful effect of catecholamines = improve survival after MI
how do we get side effects with beta blockers
- over effect
- too big of drop in HR, BP etc.
what are the two classes of calcium channel blockers
- vascular
2. cardiac
what are cardiac CCBs known as
non-dihydropyridine
what do cardiac CCBs do
- dilate coronary arteries = increase supply
- slow conduction velocity thru the heart to reduce HR
- reduce vasospasm
- treat arrythmias thru slowing conduction
what are 2 types of cardiac CCB
- verapamil
2. diltiazem
what is the MOA of cardiac CCBs
- inhibit transport of Ca into myocardial cells = reduce conduction velocity
how can cardiac CCBs treat variant angina
- by reducing vasospasm
describe the interaction between diltiazem and digozin
- may increase digoxin levels
what are adverse effects of cardiac CCBs
- very safe
- caution with other blockers
- bradycardia
- complete heart block
what is the antidote fro complete heart block
- ca chloride IV
- competes with blocking of Ca
what are vascular CCBs
- dihydropyridine
what is the MOA of vascular CCBs
- inhibit transport of Ca in smooth muscle cells
what do vascular CCBs do
- cause peripheral arterial vasodilation = decreased afterload = decreased workload
- also helps with IHD
what are 2 types of vascular CCBs
- amlodipine
- nifedipine
what are adverse effects of vascular CCBs
- very safe
- r/t to vasodilation: headache, hypotension, dizziness, edema of ankles & feet
what is a CXR
- chest x-ray
- can also look for cardiac remodelling
= silhouette of heart
what is an ECHO
- ultrasound
- can see chambers & muscle move
- cardiac echocardiogram
- can see valves, calculate EF
what are the 2 main uses of ECGS
- arrythmias
- cardiac ischemic/damage
what is a MUGA scan
- multigated acuistion scan
- used to get EF
what is a cardiac MRI good for
- soft tissue
- no radiaition
- calculate EF
what is one important thing to look for on ECG
- St elevation or not
what is ejection fraction
“report card for heart”
what is pulmonary edema? how can we see it?
- fluid in the lung tissue
- can see on CXR
what are basic cardiac diagnostic studies
- 6 min walk test
- stress/exercise test
- angiogram
what is a PCI
- percutaneous coronary intervention
- going into an artery thru the skin & go to area of blockage in heart
- will inject dye & blow up balloon to crush plaque to the side
- may also place stent (mesh) to prevent plaque from squishing back in, or pieces from breaking off
what is revascularization? what 2 procedures are used for this?
- restoration of perfusion
1. PCI
2. CABG
what is a CABG
- coronary artery bypass graft
what does a CABG do
- open heart surgery
- use another blood vessel to divert blood flow around blockage
- may reroute a blood vessel in heart
- may harvest a vessel from leg
what is a ventricular assist device
- pump that will pump blood in heart
- often temporary
- for severe HF or heart disease, often while waiting for transplant
