RESP 2210 Test #4

What is a myocardial infarction (MI)?

• occurs when blood flow to the heart is blocked

• injury to heart muscles occurs

• may lead to permanent muscle cell damage due to prolonged ischemia

What is the most common cause of MI?

CAD - plaque rupture triggers a blood clot, which will fully block artery and cause prolonged ischemia and heart muscle necrosis

What are risk factors for MI?

• pre-ecamplia during pregnancy

• highest in african americains and indigenous populations

• OSA

• diet

• exercise

• smoking

How does CAD impact the body?

• affects arteries that supply the heart wiht blood

• artery blockadge leads to - decreased O2 (angina) or no O2 (MI)

what is the etiology of CAD?

• plaque builds up in arteries - aka artherosclerosis

• builds up in artery wall, causing it to harden and narrow

• leads to restriction/blockage of blood flow to heart - muscle dies

• severe cases may lead to CAD

What are the different types of CAD?

obstructive: plaque builds up in large arteries, reducing supply of O2-rich blood to the heart - most common

non-obstructive: narrowed by plaque, disease/injury to the lining of larger arteries. impacts response to physical, chemical, or electrical signals that stimulate the heart

coronary microvascular: impacts the hearts smallest arteries, molecular changes in microvascular system, tiny blood vessels of the heart prevents normal blood flow through small arteries

What is the pathophysiology of CAD?

endothelial dysfunction

• vasoconstriction: impaired release of vasodilators in predisposed patients (ie. diabetes)

• loss of antithrombic properties, resulting in inappropriate clotting + reduced space

vessel narrowing

• due to artherosclerosis and abnormal muscle tone

• Poiseuilles Law

What is the pathophysiology of MI?

• coronary artery occlusion decreases blood flow to the heart

• heart muscle becomes starved of O2

• inadequate oxygenation for 20+min leads to irreversible necrosis of cardiac myocytes

What 3 factors determine MI severity?

• level of occlusion

• length of time of occlusion

• presence/absence of collateral circulation

What are the 2 types of MI?

STEMI: MI caused by complete or near-complete blockage of a coronary artery, visible as ST-segment elevation on ECG

NSTEMI: MI involving partial blockage with subendocardial damage, showing ST depression, T-wave changes, elevated troponin

What are the characteristics of a STEMI?

• most severe

• aka “widow-maker”

• coronary artery is completely blocked

• blood flow ceases

• ischemia extends through whole thickness of heart muscle

What are the characteristics of an NSTEMI?

• aka subendocardial or non-transmural infarction

• coronary artery is partially blocked

• blood flow decreases

• ischemia involves a small area of the heart muscle

What are common symptoms of CAD?

• no symptoms during early stages

• SOB

• rapid HR

• angina

  • heaviness/pressure

  • aching/burning

  • numbness

  • fullness

  • squeezing/chest pain

What are the characteristics of unstable angina?

• not relieved with rest

• nitroglycerin does not work

• fatigue

What are the clinical signs of MI?

• chest pain

• dizziness/nausea

• heart palpitations

• SOB

• pain in arm, neck, or jaw

• diaphoresis

• Loss of consciousness

How may an MI appear differently in women?

• fatigue

• sleep difficulties

• SOB

• indigestion

• chest discomfort

• anxiety

• breathing difficulties

• radiating pain

What would be assessed on physical exam in MI patients?

vitals

• tachycardia/arrhythmia

• BP high or low

• tachypnea

assessment

• appearance: diaphoretic, elevated JVP, cyanosis

• auscultation: wheeze

• heart sounds: soft S1, palpable S4, new mitral regurgitation murmur

What would be assessed on ECG in MI patients?

• changes to ST segment

• T wave flattening/inversion

• anterior infarction: PVCs, VT, Vfib, junctional tachy

• inferior infarction: sinus brady, AV block, sinus arrest

What would be assessed on a stress test in CAD patients?

positive result

• ischemic ECG in first 3 min

• ST depression >2mm

• Systolic BP falls significantly

• patient cannot exercise >2min due to symptoms

What would be assessed on nuclear imaging studies in CAD patients?

• radioactive material injected at peak exercise on stress test

• poor perfusion: cold spots, indicates ischemia

What is radionuclide imaging?

plots and detects passage of radioactive tracers through heart region

What is radionuclide imaging used to determine?

• severity of CAD/angina

• severity of chronic CAD

• success of CAD surgeries

• whether or not an MI has occured

What is radionuclide angiography?

technique that allows for the visualization of the chambers and major blood vessels of the heart

• inject radioactive tracer during exercise, at rest, or with stress-inducting drugs

What is an echocardiogram?

noninvasive U/S test that uses high-frequency sound waves to create live moving images of the hearts chambers, valves, and surrounding blood vessels

evaluates heart function, blood flow, muscle strength, etc

What is the difference between a TTE and a TEE?

TTE

• transthoracic

• u/s across chest surface

• screens for cardiac abnormalities

• cheaper + safer

TEE

• transesophageal

• u/s with transducer inserted in esophagus

• detects source of embolism

• higher image resolution and sensitivity

What is a coronary angiogram?

invasive procedure for patients showing evidence for severe obstruction on stress/other tests or in patients with ACS

procedure:

• narrow tube inserted into arter and threaded up through body to coronary arteries

• dye injected and X-ray records flow of dye

• maps out coronary circulation, revealing blocked areas

How is CT used on the heart?

• angiography to visualize coronary arteries

• Ca score detects calcium deposits on arterial walls

  • correlates with presence of atherosclerosis

  • does not signify artery narrowing

How can blood tests be used to determine cardaic function?

• myocardial cells produce certain proteins and enzymes associated with cell function

• when cell death occurs, cell components are released into bloodstream

• increase in serum cardiac markers:

  • troponin

  • myoglobin, creatinine kinase, creatine phosphokinase

• lipoprotein profile:

  • high fats?

How will different hemodynamics typically present in MI?

• CO: decreased, V not producing same SV due to damage

• PCWP: increased as left side of heart is not pumping as well

• BP: decreased due to reduced CO

• SVR: increased due to vasoconstriction

• SVO2: reduced due to CO, inadequate O2 delivery

• CVP: normal or elevated, depending on site of infarction

What 3 classes of medications are essential to preventing CAD?

• lipid-lowering therapy: decrease LDL cholesterol

• anti-hypertensive: lower heart workload

• anti-platelet: helps prevent blood clots

What LDL drugs may be used to help prevent CAD?

• statins: reduce cholesterol

• fibrates: lower cholesterol and triglyceride

• ezetimibe: lowers cholesterol in statin intolerance

• icotinic acid: reduces cholesterol

What anti-hypertensive drugs may be used to help prevent CAD?

• beta-blockers: decrease HR, increase filling time, and decrease contractility

• ACE inhibitors: in CAD patients post MI, diabetics, LV dysfunction, or hypertension

• Angiotension Receptor blockers: inhibit angotension II receptors, decrease vasoconstriction

• Ca channel blockersL coronary vasodilation, reduce o2 demand, relieve angina symptoms

• nitrates: relax vascular smooth muscle, cause venodilation and reduce preload

What anti-platelet drugs may be used to help prevent CAD?

• aspirin

• clopidogrel

What is the difference in presentation/diagnosis of CAD versus MI?

CAD

• chronic, gradual onset

• best determined via stress test and angiopathy

• symptoms: stable angina, dyspnea

• treatment focuses on modifying risk factors

MI

• acute, sudden onset

• best determined via troponin levels, ECG, or echo

• symptoms: severe chest pain, diaphoresis, nausea

• treatment focus on reperfusion

What medications may be used to treat an acute MI?

• morphine

• O2

• aspirin

• nitroglycerin

• Beta blockers

• thrombolysis

• coronary angioplasty

What are the 3 main surgical intervetntions in acute MI?

• percutaneous coronary intervention or coronary angioplasty

• coronary artery bypass grafting

• cardiac rehabilitation

What is a coronary angioplasty and how is it used to treat acute MI?

• catheter used to place a stent to open blood vessels in the heart that have narrowed from plaque buildup

• using fluroscopy, catheter is threaded through the blood vessels into the heart where artery in narrowed

• balloon tip compresses plaque and expands the stent

What is a coronary artery bypass grafting and how is it used to treat acute MI?

• improved blood flow to the heart

• healthy artery/vein from the body is grafted to blocked coronary artery

• new vessel bypassess blocked portion

• creates a new path for O2 rich blood to flow to heart muscle

What is a transmyocardial laser revascularization and how is it used to treat acute MI?

• laser ablation to create transmural channels in ischemic myocardium to restore myocardial perfusion

• indicationns: surgical refractory angina

What is cardiac rehabilitation?

• medically supervised secondary prevention program for patients with established cardiovascular disease

• goal is to help patients with CAD to recover more quickly post-cardiac event and reduce risk of future cardiac illness

• shown to:

  • reduce risk of sudden cardiac death or re-infarction

  • control cardiac symptoms

  • stabalize/reverse atherosclerotic process

  • improve psychosocial status

What is the prognosis of CAD/MIs?

dependent on heart function, number of affected vessels, and lifestyle

one impacted vessel with good LV function: >90% 5y survival

one affected vessel with severe LV dysfunction: <5y survival rate

What is the difference in inital therapy in CAD versus acute MI?

CAD

• lifestyle changes

• antianginal meds

MI

• MONA

• morphine

• oxygen

• nitrates

• aspirin

What is the difference in medication in CAD versus acute MI?

CAD

• statins

• ACEI

• antiplatelets

• beta blockers

MI

• antiplatelet therapy

• statins

• beta blockers

• ACEI

What is the difference in revascularization techniques in CAD versus acute MI?

CAD

• PCI/stenting for symptoms if meds inadequate

• CABG if multivessel/severe

MI

• emergent PCI (<90min door-to-balloon time)

• thrombolysis if unavailable

What is the leading cause of morbidity and mortality in canda?

CHF

What are the characteristics of Class I CHF?

• no limitation of physical activity

• no undue fatigure

• normal heart beat

• no dyspnea

What are the characteristics of Class II CHF?

• slight limitation of physical activity

• comfortable at rest

• ordinary activity = fatigue, dyspnea, palpitations

What are the characteristics of Class III CHF?

• marked limitation of physical activity

• comfortable at rest

• easily fatigued, dyspneic

• palpitations

What are the characteristics of Class IV CHF?

• all physical activity comes with discumfort

• fatigue, palpitations, and dyspnea at rest

What is cardiac output?

the volume of blood pumped out by the ventricles in one minute

What is stroke volume?

vol of blood pumped in ventricle in one contraction

What is ejection fraction?

% of total blood volume expelled by ventricles each contraction

normal 50-70%, <40& in HF

What is the difference between reduced ejection fraction and preserved ejection fraction in left heart failure?

HFrEF

• “systolic” heart failure

• EF <40% with clinical signs of HF

• reduced contractility OR increased afterload

HFpEF

• “diastolic” heart failure

• impaired ventricular relaxation OR impaired ventricular filling

What are the two mechanisms of HFrEF?

increased afterload

• HTN

• LV hypertrophy

• increased O2 demand by LV

• increased muscle compressing coronary arteries

impaired ventricular contractility

• myocardium infarction

• myocardial ischemia

• dilated cardiomyopathy

What are the two main causes of HFpEF?

impaired ventricular filling

• mitral stenosis

• pericardial constriction

impaired ventricular relaxation

• Ca concentration fails to decrease, prolonging contraction + impairing active cardiac relaxation

• ventricular passive diastolic stiffness

  • amplified by fibrosis of ventricle

What are common causes of HFrEF?

• MI

• CAD

• HTN

• cardiomyopathy

• valvular heart disease

What are common causes of HFpEF?

• HTN

• A fib

• diabetes

• obesity

• kidney disease

What is the pathophysiology of CHF?

Initial event injury

• damage to the heart due to MI, vol overload, toxins, etc

Reduced CO

• reduced SV

• results in adrenergic activation - baroreceptors detects reduced SV and activates sympathetic nervous system

Compensation mechanisms

• SNS activation

• RAAS activation

• Angiotensin II

• Aldosterone

• Vasopressin release

Remodeling

• chronic stress triggers dilation or hypertrophy ventricular changes

  • myocyte hypertrophy

  • apoptosis

  • fibrosis

• worsens wall stress per Laplace’s law, further impairing ejection fraction

Heart damage

• neurohormonal/cytokine activation promotes:

  • myocyte loss

  • fibrosis

  • arrhythmias

  • ischemia

• manifests as severe edema and end-stage organ damage

What is the pathophysiology of the compensation mechanisms in CHF?

SNS activation

• triggered by decrease in BP

• tachycardia

• increased SVR

• increased contractility

RAAS activation

• triggered by decreased renal perfusion

• renin-angiotensin I - angiotensin II- aldosterone

Angiotensin II

• potent vasoconstriction - increased SVR

• stimulates sympathetic activity

Aldosterone

• sodium/water retention - hypertension

• results in increased preload and afterload

ADH (vasopressin) release

• triggered by low effective circulating volyne

• leads to water retention and vasoconstriction

What are common symptoms of CHF?

• dyspnea on extertion/at rest

• fatigue

• orthopnea

• paroxysmal nocturnal dyspnea

• cheyne stokes

• edema

• decreased urine output

• chest pain

What are common clinical signs of CHF?

• pulmonary crackles, wheeze

• tachypnea

• hypoxia, cyanosis

• tachycardia

• JVD

• decreased cap refill

• S3 gallop

What may be identified on physical exam in patients with CHF?

• dyspnea

• JVD

• tachycardia

• weak pulse

• edema

• murmurs

What may be identified on CXR in patients with CHF?

• cardiomegaly

• increased interstitial markings

• pleural effusion

What may be identified on echo in patients with CHF?

• ejection fraction

• systolic/diastolic function

• valve visualization

What may be identified on ECG in patients with CHF?

• LV hypertrophy

• a fib

• ventricular dyssynchrony

• wide QRS
  sinus tachycardia

What are common pulmonary complications of CHF?

• dyspnea

• decreased LV

• decreased Cs

• increased WOB

• decreased Dlco

How does left heart failure impact hemodynamics?

• PCWP increased due to pulmonary vein congestion

• increased SVR - compensation for BP

• CO decreased due to impaired LV contractility

• low mixed venous saturation due to low CO

What is the Framington Criteria?

set of guidelines to diagnose heart failure + assess cardiovascular risk

What pharmacological treatments may be used for CHF?

• anti-HTN (ACEI, B-blockers)

• diuretics - manage fluid

• cardiotonic glycoside - improved contractility

• vasodilators

What non-pharmacological treatments may be used for CHF?

• cardiac resynchronization therapy (pacemaker)

• LVAD - implant support main pumping chamber in LV

• heart transplant

• NIV

What are possible causes of Cor Pulmonale?

• LV failure (due to pressure and volume overload)

• pneumonia

• PE

• ARDS

• MV

• Pulm HTN

• sepsis

• diseases causing impaired filling (pericarditis, cardiac tamponade, hypovolemia)

What is the pathophysiology of cor pulmonale?

• similar to LV failure

• due to weakening of the ventricle or increased afterload that puts strain on the heart

• Frank-starling mechanism employed when compensating for the increased stretch

• eventually, RV begins to dilate from stretch

What are common signs and symptoms of cor pulmonale?

• dyspnea

• chest discomfort

• palpitations

• hepatomegaly

• ascites

• paradoxical pulse

How can cor pulmonale be managed?

• treat the cause

• diuresis/RRT for vol overload

• vasopressors

• inotropes, pulm vasodilators

• ECMA

• heart/lung transplant

How are hemodynamics impacted in cor pulmonale?

• elevated CVP due to increased RA pressure and systemic venous congestion

• elevated PAP if primary cause is increased PVR

• normal-low PCWP

• decreased CO due to inability to pump effectively

• increased SVR to compensate for CO

• decreased mixed venous O2 saturation due to reduced CO

What are the characteristics of cardiomyopathies?

• diseases of the myocardium w/ associated structural + functional abnormalities

• as cardiomyopathy worsens, heart becomes weaker resulting in:

  • decreased ability to pump blood through body

  • reduced ability to maintain normal electrical rhythm

What are the 4 types of cardiomyopathies?

• dilated

• hypertrophic

• restrictive

• arrhythmogenic RV

What is a dilated cardiomyopathy (DCM)?

one or more heart chambers become enlarged = myocardium stretches and becomes thin

leads to impairment in contractility = systolic failure

50% mortality in 5y

What is the etiology of DCM?

• ischemia - CAD, MI, HTN

• genetic abnormalities

• neuromuscular/neurologic, connective tissue, metabolic disorders

• pregnancy complications

• infection

What is the pathophysiology of DCM?

• ventricular enlargement

• leads to mitral and tricuspid insufficiency

• compensation: increased HR, peripheral resistance

• leads eventually to heart failure

What is the clinical presentation of DCM?

• chest pain

• S3 heart sound

• LV dysfunction

  • dyspnea on exertion

  • fatigue

  • high LV diastolic pressure

  • low CO

• RV dysfunction

  • peripheral edema

  • atrial arrhythmia

How can DCM be diagnosed?

• pt hx/physical exam

• echo: dilated hypokinetic cardiac chambers

• CXR: cardiomegaly, pulmonary edema

• serology: elevated troponin, myocardial injury, elevated BNP

How can DCM be managed?

• address underlying cause

• meds: beta blockers, digoxin, diuretics, prophylactic anticoagulation

• surgery

  • implanted cardioverter-defib (ICD): controls arrhythmia

  • cardiac resychronization therapy (CRT): patients with wide QRS and low EF

  • LV assist device (LVAD): mechanical pump preserved contracile function

  • heart transplant: last resport

What is hypertrophic cardiomyopathy (HCM)?

abnormally thick myocardium leads to impingement of chamber space, reducing filling capacity = diastolic failure

pts typically have normal life expectancy with no significant complications with appropriate treatment

What is the etiology of HCM?

• genetics: most common, autosomal dominant

• HTN

• diabetes

• thyroid disease

What is the pathophysiology of HCM?

wall thickens near interventricular septal wall

contributing factors:

1. dynamic LV outflow tract obstruction - due to thickness and damage to mitral valve

2. mitral regurgitation - due to obstruction

3. diastolic dysfunction- due to LV fibrosis and stiffness

4. myocardial ischemia - impaired coronary artery perfusion

5. autonomic dysfunction - abnormal BP response leads to inappropriate LV receptor firing

What is the clinical presentation of HCM?

• SOB

• dizziness/syncope

• palpitations

• S3/S4 sounds

How can HCM be diagnosed?

• hx + physical exam

• echo: increased septum to ventricular wall ratio

• stress test: obstructive blood flow at rest

• biopsy

• CXR and ECG will be normal

How may HCM be treated?

meds

• beta blockers

• antiarrhythmics

• diuretics

• anticoagulants

• mavacamten - blocks interaction b/w myosin and actin in cardiac muscle cells, exerting neg inotropic effect and reliewing obstruction

non-surgical

• alcohol septal ablation: ethanol injected through tube into small artery supplying blood to thickened area, killing cells to shrink tissue to normal size

surgical

• septal myectomy: open heart surgery to remove thickened septum + repairation/replacement of mitral valve

  • in young patients where meds are ineffecrive

What is restrictive cardiomyopathy (RCM)?

myocardium becomes stiff and non-compliant, inhibiting ventricular relaxation and filling = diastolic failure

contractile function and wall thickness is maintained

rare, idopathic RCM has 10-15y expectancy, amyloidosis RCM <1y

What is the etiology of RCM?

• amyloidosis: protein builds up in organs

• sarcoidosis: granuloma accumulation in organs, typically lungs (females)

• hemochromatosis: iron build-up in body

• loffler endocarditis: form of cardiac fibrosis (sub-saharan africans)

• idopathic or hypereosiniphililc fibrosis

• radiation therapy

• drugs: anthracycline, busulfan, ergotamines

What is the pathophysiology of RCM?

• presence of abnormal substances within cardiac cells

• storage of metabolic substances within cardiac cells

• fibrotic injury

• stiff, non compliant ventricles = low preload + high filling = dilated atria, elevated MAP

  • increased RA pressure = systemic venous congestion

  • increased LA pressure = pulmonary congestion

What is the clinical presentation of RCM?

very wide range of symptoms

• poor exercise tolerance

• a fib, arrhythmias

• syncope

How may RCM be diagnosed?

• serology: elevated BNP

• CXR: pulmonary congestion, mild cardiomegaly

• ECG: low voltage ARS, arrhythmias

• echo: bi-atrial enlargement

• biopsy

How may RCM be managed?

• treat underlyin cause(s)

• diuretics

• beta-blockers

• pacemakers, ICDs

• anticoagulants

• heart transplant

What is Arrhythmogenic Rigth Ventricular Cardiomyopathy (ARVC)?

myocardium of RV is replaced with scar tissue or fat, disturbing electrical impulses of the heart

progessive RV myocardium loss leads to weakness + impairs contractility = systolic failure

most common in young patients, especially athletes - early identification and reduced exercise leads to good outcomes

What is the etiology of ARVC?

• genetics: familial background in 50%

• heart muscle infection

What is the pathophysiology of ARVC?

• disruption of disk movement in cardiac monocytes = structural abnormalities in cardiac cells

• impacts Na and K channels = changes in cardiac AP

myocyte dysfunction/death = heart inflammation + replacement of cells with scar tissue and fate = replacement interferes with conduction (arrhythmias occur) = RV wall weakness impairs contraction = progression to LV involvement mimicing DCM

What is the clinical presentation of ARVC?

• arrhythmias

  • Afib

  • premature V beaths

  • Vtach

  • Vfib

• dyspnea

• palpations

• light-headedness, syncope

• periperal edema

How may ARVC be diagnosed?

• ECG: t-wave inversion, right BBB, V arrhythmias

• echo: RV dilation with or without EF reduction and LV involvement, wall motion abnormalities

• MRI: fibrofatty infiltration and thinning of RV myocardium, RV aneurysm, RV dilation