Cardiac Flashcards
Which artery on the heart is often called the “widowmaker”?
left anterior descending coronary artery
Where is the point of maximal impulse (PMI)? Why is it significant?
– PMI = 5th intercostal space, midclavicular line, left of the sternum
– where the apical pulse can be located = loudest heart sounds
Which valves make up S1 sounds? Which valves make up S2 sounds?
– atrioventricular valves (mitral/tricuspid) = S1
– semilunar valves (aortic/pulmonic) = S2
Describe the pathway of electrical conduction in the heart.
- sinoatrial (SA) node = natural pacemaker of the heart; where conduction starts
- atrioventricular node
- bundle branches (left and right)
- perkinje fibers
What are the 2 types of cells located in the heart, and what kinds of electrolytes do they require?
– electrical cells
- require
- sodium
- potassium
- calcium
- in order to initiate impulses
– mechanical cells
- require calcium in order to initiate contraction
What is normal mean arterial pressure (MAP) that is required to maintain adequate blood flow?
must be at least 60 mm Hg, but normal is 70 - 110
What is the difference between cardiac output (CO), stroke volume (SV), preload, and afterload?
– cardiac output: amount of blood pumped from the left ventricle each minute
– stroke volume: amount of blood ejected from the left ventricle with each contraction
– preload: volume of blood in the ventricles at the end of diastole
– afterload: resistance the left ventricle must overcome to circulate blood (semilunar valve pressure and peripheral blood vessel pressure)
What kinds of factors could impact preload? Afterload?
– preload:
- hypervolemia
- regurgitation of cardiac valves
- heart failure
– afterload:
- hypertension
- vasoconstriction
– an increase in afterload results in an increase in cardiac workload (the heart has to work that much harder to overcome greater amounts of pressure)
What are 2 types of receptors that are a part of the autonomic nervous system that help to regulate blood pressure?
– baroreceptors: detect pressure in the blood vessels (vena cava, right atrium, and aorta) and regulate BP
– chemoreceptors: detect concentrations of electrolytes in the blood and controls amount of fluid that permeates through blood vessel walls to control BP
What are the different pulse grades?
- 0 = absent pulse
- 1+ = weak and thready
- possibly due to hypovolemia
- 2+ = normal
- 3+ = full
- possibly due to elevated temperature or exercise
- 4+ = full and bounding
- abnormal
- can indicate hypervolemia or elevated BP
What are the different edema grades? What are possible causes of edema?
- 0 = 0 mm = none
- +1 = 2 mm = trace
- +2 = 4 mm = moderate
- +3 = 6 mm = deep/severe
- +4 = 8 mm = very deep/severe
– edema could be the result of cardiac, hepatic, or renal problems
What is the best indicator of fluid balance?
daily weights
What are some common signs and symptoms of cardiovascular problems?
- pain, discomfort
- dyspnea, DOE (dyspnea on exertion), orthopnea, PND (proximal noctural dyspnea)
- fatigue
- palpitations
- edema
- syncope
- N/V
- SOB
- diaphoresis
What are S3 and S4 sounds? What are murmurs, rubs, and clicks?
– S3 sounds are an extra sound after S2 sounds due to rapid filling of left ventricle
- could be caused by CHF, left ventricular failure, or mitral valve regurgitation
– S4 sounds are an extra sound before S1 sounds due to atrial contraction if ventricles are noncompliant
- could indicate left ventricle hypertrophy, hypertension or aortic stenosis
– murmurs: whoosing sounds
– rubs: scratching sounds
– clicks: metallic sounds
What are the lab tests that can indicate cardiac problems?
- sodium
- magnesium
- potassium
- lipid panel
- total cholesterol
- < 170 mg/dL for pts 20 and younger
- 100 - 199 mg/dL for pts 21+
- HDL
- > 45 - 55 mg/dL
- LDL
- < 70 mg/dL for very high risk pts
- < 130 mg/dL for low risk pts
- triglycerides
- < 150 mg/dL
- total cholesterol
- enzymes & protein panel
- highly sensitive CRP (hsCRP)
- indicates inflammation of cardiac tissue
- creatinine kinase (CK)
- 30 - 220 U/L
- enzyme in heart and muscle tissue that increases with damage
- will see this with rhabdo, MI, and laying down for a while
- myoglobin (Mb)
- 30 - 90 ng/mL
- produced during injury to muscle cells
- troponin T (cTNT)
- 0.0 - 0.10 ng/mL
- this is the gold standard lab for cardiac problems
- protein directly related to cardiac damage
- highly sensitive CRP (hsCRP)
- B-type natriuretic peptide (BNP)
- increased production when there is an increase in blood volume in the heart chambers – indicates HF
- < 100 pg/mL = no HF
- 100 - 300 pg/mL = HF present
- 300+ pg/mL = mild HF
- 600+ pg/mL = moderate HF
- 900+ pg/mL = severe HF
What are some diagnostic tests that can identify cardiac problems?
- CXR
- EKG
- Holter monitor
- records EKG continously over long periods
- echocardiography
- measures
- amount of blood flow through chambers (ejection fraction)
- normal = 60 - 70%
- contraction under stress
- tumors and clots
- congenital abnormalities
- amount of blood flow through chambers (ejection fraction)
- measures
- thallium stress test
- thallium injected
- thallium doesn’t enter damaged tissue
- dark spots with no thallium can be visualized
- cardiac catheterization
- coronary angiography
What is the difference between ischemia and infarction?
– ischemia: insufficient oxygen supply to sustain myocardial contraction
- does not always result in permanent damage
– infarction: necrosis due to prolonged severe ischemia
- causes irreversible damage to tissue
What conditions make up coronary artery disease?
- stable angina
- acute coronary syndrome
- unstable angina
- acute myocardial infarction
- new onset angina
- variant (Prinzmetal’s) angina
- pre-infarction angina
What is chronic stable angina pectoris?
- “strangling of the chest”
- temporary imbalance between
- coronary arteries’ ability to supply oxygen
- the cardiac muscles’ demand for oxygen
- limited in duration
- does not cause permanent damage
- usually relieved by
- nitroglycerin
- rest
What is acute coronary syndrome (ACS)?
- pts with either
- unstable angina
- acute myocardial infarction
- new onset angina
- variant (Prinzmetal’s) angina
- pre-infarction angina
- atherosclerotic plaque in coronary arteries ruptures, causing platelet clumping and clot foramtion
Differentiate between the diseases under ACS.
– unstable angina: chest pain during rest; exertion causes severe limitations; chest pains last 15+ minutes
- poorly relieved by nitroglycerin or rest
- exertion can increase the number and severity of attacks
– acute myocardial infarction: heart attack due to blockage of blood flow to heart via coronary arteries
– new onset angina: first few incidences of chest pain; usually occurs with exertion
– variant (Prinzmetal’s) angina: usually result of coronary artery spasms; usually occurs after rest
– pre-infarction angina: days or weeks leading up to MI
What are STEMIs and NSTEMIs?
– STEMI = ST elevation MI
- traditional manifestation of MI where the ST segment is elevated on the EKG
– NSTEMI (non-STEMI) = non-ST elevation MI
- uncommon manifestation of MI where the ST segment appears abnormal but it is not necessarily elevated or the ST segment appears normal but the pt is clearly having cardiac issues
- common presentation in women
- diagnose NSTEMIs with trope labs
What is a myocardial infarction? What are some ways it can result?
– myocardial infarction: most serious acute coronary syndrome; myocardial tissue is abruptly and severly deprived of oxygen
– possible causes:
- occlusion of blood flow
- necrosis – can extend an MI if left untreated
- hypoxia – can extend an MI if left untreated
- ventricular remodeling (scarring of heart tissue; long-term damage to cardiac function)
What can exacerbate damage to the heart during an MI?
catecholamines
released during stress –> causes release of epi and norepi –> increases damage to the heart
Which demographics have a higher risk of MIs?
- Hispanic and African American women have a higher risk of MIs, especially in older age
- men tend to experience MIs in younger age
- women tend to experience MIs in older age
- men experience STEMIs more often
- women experience NSTEMIs more often
- higher risk of death due to MIs because of non-traditional symptoms
What are the 5 descriptors of chest pain? (PQRST)
- Precipitating factors
- Quality
- Region and raditation
- Severity and associated symptoms
- Timing
What are some immediate interventions for pts with MI?
- place on non-rebreather – 10 - 15 L/min
- place on IV immediately
- administer medications
- place on EKG
- diet:
- restrict sodium
- restrict cholesterol
- restrict caffeine
What are serum lab tests that can indicate cardiac problems? Which tests are gold standard?
- creatine kinase of muscle band (CK-MB)
- used when trope tests aren’t available
- aren’t as useful anymore
- cardiac troponin (cTn)
- determine cardiac injury
- any positive amount suggest cardiac injury
- myoglobin (Mb)
- high sensitivity but low specificity for skeletal and muscle issues
- can be used to rule out MI
- lactate dehydrogenase (LDH)
- not specific for cardiac tissue
- hsCRP
- BNP
– gold standard = tropes + EKG
Other than women, what other demographic presents MIs differently?
DM pts – have silent MIs
What are some interventions for acute cardiac pain?
- pain relief
- decrease myocardial oxygen demand
- increase myocardial oxygen supply
- oxygen
- 100% non-rebreather @ 10 - 15 L/min
- ensure pt sats 95+%
- deep breathing exercises
- oxygen
- drugs
- nitroglycerine
- vasodilator –> increases oxygen available to tissues
- contraindicated in pts with erectile dysfunction
- morphine sulfate
- vasodilator
- beta-blockers (lopressor)
- blocks catecholamines
- decreases heart’s oxygen demand
- just keep an eye on BP
- ACE inhibitors (-pril meds)
- given within 48H of MI to prevent scarring
- MONA
- morphine
- oxygen
- nitrogen
- aspirin
- nitroglycerine
- reposition
- comfort
- semi-Fowler’s
- provide quiet and calm environment
What are some interventions for ineffective tissue perfusion?
- drugs
- aspirin
- thrombolytic agents
- restore perfusion to injured area
What are some drug interventions for acute coronary syndrome?
- glycoprotein (IIb and IIIa) inhibitors (RePro, Integrilin, Aggrastat)
- antiplatelet
- prevents fibrinogen from attaching to activated platelets
- heparin
- anticoagulant
- can be used in conjunction with glycoprotein inhibitors
- draw baseline aPTT prior to heparin administration (bolus or infusion)
- after 6H, baseline should be higher than the control
- 1.5 - 2x higher
- indicates therapeutic effect
- fibrinolytics (Reteplase, Tenecteplase)
- clot buster to help reperfuse the tissues
- IV or intracoronary administration
- ensure pt has no hx of injury 90 prior
- could result in bleeding out
- beta-adrenergic blocking agents (carvedilol)
- long-acting vasodilators
- ACE inhibitors
- relaxes BVs
- calcium channel blockers
- increase cardiac perfusion and vasodilation
What are some surgical interventions for acute coronary syndrome?
- percutaneous transluminal coronary angioplasty (PTCA)
- angioplasty = reshape blood vessels by inflating a balloon
- may involve stent placement
- prior to procedure, administer Plavix to prevent platelet/clot formation
- IV heparin after procedure
- other IV meds to use for procedure
- nitroglycerine
- diltiazem – BV relaxer
- glycoprotein inhibitors
- long-term medications
- antiplatelets
- beta blockers
- ACE inhibitors
What are the 3 phases of cardiac rehabilitation?
-
phase 1: D/C from hospital
- pt has limited mobility
- must be careful with activity
-
phase 2: clinic
- routine exercise
- DM checks
- phase 3: long-term adherance to exercise
What are dysrhythmias? What are some interventions?
– dysrhythmias: irregular beating of heart
– interventions:
- identify dysrhythmias
- assess hemodynamic status
- evaluate discomfort
- keep heart monitors and 12-leads on pt
What is cardiogenic shock? What are some signs and symptoms?
– cardiogenic shock (AKA class 4 HF): necrosis of more than 40% of left ventricle
– s/s
- tachycardia
- hypotension
- can lead to renal insufficiency and eventually renal failure
- BP < 90 mm Hg or 30 mm Hg less than pt’s baseline
- urine output < 30 mL/hr
- cold, clammy skin
- poor peripheral pulses
- agitation, restlessness
- confusion
- pulmonary congestion
- tachypnea
- chest discomfort/pain
- pts are typically unresponsive
What are some interventions for cardiogenic shock?
- pain relief
- reduce preload and afterload
- drugs
- vasopressors
- reperfusion therapies
- intra-aortic balloon pump
- last resort
- arthrectomy
- retrieval of clots/plaques
- stent placement
- rheolytic thrombectomy
- saline jets break up clots/plaque
- aspirate out broken clots/plaque
- coronary artery bypass graft (CABG)
- grafts are taken from mammary and saphenous veins
- only use for
- > 70% stenosis
- unstable angina
- CAD in DM pts
What is heart failure? What are some causes? What are some risk factors?
– heart failure (pump failure): inability of the heart to work effectively as a pump, causing the blood to back up, liver congestion, and peripheral edema
– causes:
- coronary artery disease
- HTN
- valvular heart disease
– risk factors:
- aging
- DM
- obesity
- hyperlipidemia
- chemical dependencies
- drugs
- alcohol
- smoking
What are the 2 types of heart failure?
- left-sided (CHF)
- right-sided
Describe left-sided heart failure. What are some signs and symptoms? What are the 2 subtypes of left-sided heart failure?
– stroke volume is reduced
- blood backs up into left side of heart and pulmonary circulation
- pulmonary pressure increases
– s/s:
- fluid overload in pulmonary circulation results in
- dyspnea
- paroxysmal noctural dyspnea
- weakness
- fatigue
- dizziness
- acute confusion
- pulmonary congestion (pink-tinged sputum)
- oliguria
– 2 subtypes:
-
systolic dysfunction (AKA foreward failure): ventricular dilation (dilated myopathy) – left ventricle stretches and dilates
- reduced ejection fraction (<40%) because the heart cannot contract forcefully enough to pump blood into circulation
- preload increases, stroke volume decreases
-
diastolic dysfunction: left ventricular stiffness
- left venticle inadequately relaxes due to hypertrophic/restrictive cardiomyopathy
- ventricular filling during diastole are impaired
- common in women with chronic HTN
Discuss the etiology of left-sided heart failure.
- systemic HTN is the most common cause of heart failure
- structural heart changes (like valvular dysfunction) can cause pressure or volume overload on the heart
- 1/3 of MI pts develop heart failure
Describe right-sided heart failure. What are some signs and symptoms?
– right ventricle cannot empty completely
- usually caused by left ventricular failure
- can also be caused by pulmonary diseases
– s/s:
- peripheral edema
- due to increased volume and pressure in venous system
- jugular vein distention
- increased abdominal girth
- swollen hands/feet
- dependent edema
- hepatomegaly
- ascites
- weight changes
- indicative of fluid gain
What are some lab tests to assess for heart failure? What are some diagnostic tests?
– lab tests:
- electrolytes
- H&H
- determine if the pt is anemic from heart failure
- B-type natriuretic peptide (BNP)
- enzyme in chambers of the heart to detect pressure
- levels increase with HF
- levels decrease when the heart is stable
- urinalysis
- proteinuria
- high specific gravity
- ABGs
– diagnostic tests:
- CXR
- shows enlarged heart
- visualizes PE
- echocardiography = best diagnostic tool
- EKG
- hemodynamic monitoring
- pulmonary artery catheter assesses for cardiac function and fluid volume
- pressures are increased with heart failure
What are the 4 classes of heart failure?
- class 1: no limitation of physical activity
- class 2: slight limitation of physical activity
- class 3: marked limitation of physical activity
- class 4: inability to carry out any physical activity without discomfort
What is the difference between acute and chronic heart failure?
– acute HF: rapid onset; body doesn’t have time to activate compensatory mechanisms to improve cardiac performance
- compensatory mechanisms:
- activation of SNS
- activation of RAS system
- angiotensin causes ventricular remodeling
- ventricular remodeling
- scarring that can occur due to prolonged activation of SNS and RAS
– chronic HF: heart failure that develops more slowly
What are some drugs that can be used to reduce afterload?
-
ACE inhibitors: angiotensin-converting-enzyme inhibitors that cause vasodilation (decreased resistance to ventricular contraction)
- can cause respiratory side effects – dry, nagging cough
- suppress RAS system
- prevent ventricular remodeling
- -pril medications
- enalapril
- fosinopril
-
angiotensin retension blockers (ARB): reduce ventricular ejection
- suppress RAS system
- prevent ventricular remodeling
- -sartan medications
- valsartan
- losartan
-
human B-type natriuretic peptides (hBNP): lower pulmonary wedge pressure (vasodilates) and improves GFR
- nesiritide
What are some interventions to reduce preload?
- diet
- restrict sodium
- restrict fluid
- drugs
- morphine
- for acute HF
- helps with anxiety
- promotes vasodilation
- diuretics
- first choice for older pts with HF
- monitor BP
- examples:
- furosemide (Lasix)
- bumetanide (Bumex)
- thiazide (HCTZ)
- venous vasodilators
- monitor BP
- example:
- isosorbide mononitrate
- morphine
What are some drugs that enhance contractility?
-
digoxin:
- increases contractility
- reduces HR
- slows conduction through AV node
-
inotropic drugs
- improves cardiac output and perfusion
- increases contractility
- used short-term for acute HF
- example:
- dobutamine
-
beta-adrenergic blockers
- reverses sympathetic stimulation
- reduces catecholamine levels
- examples:
- carvedilol
- metoprolol
-
hyperpolarization-activated cyclic nucleotide-gated blocker
- ivabradine
What are some other interventions (other than drugs and preload interventions) for heart failure?
- continuous positive airway pressure (CPAP)
- decreases preload and afterload
- improves cardiac output
- improves ejection fraction
- decreases preload and afterload
- cardiac resynchronization therapy (CRT)
- AKA bi-ventricular pacing
- stabilizes ventricular contraction
- examples:
- pacemakers
- defibrilators
- gene therapy
- injection of growth factors into cardiac cells to help with scarred cardiac cells
- surgery
- heart transplant
- last choice for end stage HF
- ventricular assist device (VADs)
- mechanical pump that works with pt’s own heart
- heart reduction
- heart transplant
What is one type of heart reduction surgery? How does it work? What disease does it treat?
– Batista left ventricular reduction
- removes a piece of myocardium
- sutures together the 2 sides
- decreases ventricular size, causing more effective and more vigorous pumping
– treats Chagas’ disease
What part of the heart is replaced in a heart transplant? What is important to note about pts after heart transplants? What are some medications for heart transplant pts? What are some potential complications for heart transplants?
– all parts of the heart are replaced except for the back wall of the atria
– new hearts:
- beat faster (100 - 110 beats/min)
- slow to respond to increases in activity
- ^these are due to nerves of the heart being cut during transplant
– heart transplant pts have to be on the following meds for life:
- immunosuppressants
- antihypertensives
- diuretics
– complications:
- rejection
- infection
- renal failure
- HTN
- osteoporosis
- lymphoma
- CAD
What are some indications that heart failure is worsening or recurring?
- rapid weight gain
- decrease in exercise tolerance
- cold symptoms
- excessive nocturia
- development of dyspnea/angina at rest
- increased edema in feet, ankles, or hands
What is heart valve disease? What are some risk factors? What are some causes?
– heart valve disease: either stenosis of valves (narrowed valves) or valve insufficiency/regurgitation (widened or scarred valves that cause backflow of blood)
– risk factors:
- aging – 60+
- usually the cause of aortic and mitral valve disease
- big risk factor
- hx of heart valve disease
- pregnancy
- fatigue/overwork of heart
- congenital abnormalities
- drug use
- HTN
– causes:
- rheumatic fever
- strep throat
- atherosclerosis
- high BP
- congenital heart defects
- endocarditis
- IV drug abuse
- increased pressure on left side of heart
- lung disease
- increased pressure in lungs
- can cause right-sided valve disease
What are the 5 types of valvular heart disease?
-
mitral stenosis
- results from rheumatic carditis due to hx of rheumatic fever or strep
-
mitral regurgitation
- mitral valve doesn’t close all the way
- causes backflow of blood in the left atrium
-
mitral valve prolapse
- mitral valve becomes enlarged and prolaspes into the left atrium during systole
- often asymptomatic
-
aortic stenosis
- wear and tear disease – happens a lot with aging
-
aortic regurgitation
- aortic valve doesn’t close completely
What are some diagnostic tests for heart valve disease?
- CXR
- EKG
- stress test
- echocardiogram
- helps evaluate structure and ejection fraction
What are some interventions for heart valve disease?
- rest
- drugs
- diuretics
- beta blockers
- digoxin
- oxygen
- nitrates
- vasodilators
- anticoagulants
- prevents thrombus formation due to valve replacement
- a. fib and a. flutter (and general conduction abnormalities) are common complications of valve replacements
- prevents thrombus formation due to valve replacement
- surgery
- reparative procedures
- valve replacement
- remodeling – removal of scarred tissue
- balloon valvuloplasty
- used for pts at high risk for surgical complications
- benefits are short-term (~6 months)
- transcatheter aortic valve replacement (TAVR)
- for pts who are not surgical candidates and high risk pts
- direct or open commissurotomy
- removing thromboli or damaged leaflets
- debridement of vegetation on valves
- valves do not have their own circulation so WBCs can’t reach them
- mitral valve annuloplasty
- reconstruction of leaflets
- replacement procedures
- prostetic valves
- can be mechanical, cadaver, or bovine tissue
- need to be replaced Q7 - 10 years
- xenographs: tissue that comes from biological origin but not human
- still need to be on anticoagulants
- prostetic valves
- reparative procedures
What is infective endocarditis? What are some risk factors?
– infective endocarditis: microbial infection of the endocardium
- infection by vegetation that grows on the endocardium
-
vegetation: clusters of growing bacteria that commonly develop on heart valves and linings of large arteries
- these can sometimes be seen on echocardiograms
– risk factos:
- IV drug abusers
- valve replacement recipients
- pts with systemic infections
- pts with structural cardiac defects
What are some portals of entry for infective endocarditis? What are common pathogens?
– portals of entry:
- oral cavity
- skin rash
- lesion/abscess
- infection
- surgery/invasive procedure
– pathogens:
- strep
- staph
What are some signs and symptoms of endocarditis?
- murmurs
- heart failure
- arterial embolization
- can be blood emboli or vegetative emboli
- vegetative emboli will not respond to anticoagulants
- can be blood emboli or vegetative emboli
- splenic infarction
- blood flow to spleen is compromised
- can result in ischemia or necrosis
- neurologic changes
- petechiae
- splinter hemorrhages
How is infective endocarditis diagnosed? What are some interventions?
– diagnosis:
- blood cultures
- new regurgitant murmur
- echocardiography
- demonstrates endocardial involvement
– interventions:
- antimicrobials
- IV administration 4 - 6 weeks
- balance activities with rest
- surgery
- repair/removal of infected valve
- repair/removal of congenital shunts
- draining of abscesses in heart or elsewhere
What is pericarditis? What is chronic constrictive pericarditis? What are some causes of pericarditis?
– pericarditis: inflammation of pericardium
- can be bacterial, viral, or fungal
– chronic constrictive pericarditis: thickening of pericardium due to chronic inflammation
- can be caused by infection, cancer, or radiation therapy
– causes:
- post-MI
- Dressler’s syndrome
- post-heart surgery
- post-pericardiotomy syndrome
- can occur 1 - 6 weeks after procedure
What are some signs and symptoms of pericarditis?
- substernal precordial pain
- radiates to left side
- grating, oppressive pain
- aggravated by breathing, coughing, swallowing
- pain when lying supine
- alleviated by sitting up and leaning forward
- percardial friction rub upon auscultation
What are some interventions for percarditis?
- NSAIDs
- antibiotics
- cortiosteroids
- immunosuppressants
- pericardial drainage
What is pericardial effusion (cardiac tamponade)? What are some signs and symptoms? What are some risk factors? What are some interventions?
– pericardial effusion: accumulation of fluid in the space between pericardium and the heart
- results in compressing of the heart
- causes ineffective pumping, HR issues, BP issues, and decreased ejection fraction
– s/s:
- jugular vein distention
- paradoxical pulse
- abnormally large decrease in systolic pressure and pulse during inspiration
- decreased cardiac output
- muffled heart sounds
- circulatory collapse
– risk factors:
- cancer pts
- chemotherapy pts
- hemodialysis pts
- hx of pericarditis
– interventions:
- pericardiocentesis
- pericardial window
- a portion of the pericardium is removed, allowing fluid to drain
- diuretics
- anti-inflammatories
What is rheumatic carditis? Which population experiences it more frequently? What are some signs and symptoms?
– rheumatic carditis: inflammation of all layers of the heart
- sensitivity response from upper respiratory tract infection by group A beta-hemolytic streptococci
- characterized by:
- Aschoff bodies
- nodules in the myocardium which form scar tissue
- impaired contractile function of myocardium
- thickening of pericardium
- valvular damage
- Aschoff bodies
– population = pts with rheumatic fever
- 50% of pts develop
What is cardiomyopathy? What are the 2 types?
– cardiomyopathy: when the heart loses the ability to pump effectively; arrhythmias
- leading reason for heart transplant
– 2 types:
- ischemic: heart muscle damage from coronary artery disease or MI
-
non-ischemic: 3 types
- dilated
- hypertrophic
- restrictive
What is dilated cardiomyopathy? What are some causes? What are some signs and symptoms? How is it diagnosed? What are some interventions?
– dilated cardiomyopathy: when the heart muscles get stretched out, resulting in an inability for the heart to pump effectively
- can affect 1 or all of the heart’s chambers
– causes:
- ETOH
- pregnancy
- viral infection
- toxins
- genetics
– s/s:
- same as HF
- activity intolerance
- fatigue
- SOB
- edema
- arrhythmias
– diagnosis:
- CXR
- EKG
- cath
- echo
– interventions:
- drugs:
- digoxin
- calcium channel blockers
- beta blockers
- diuretics
- vasodilators
- rhythm control
- VAD
- transplant
What is hypertrophic cardiomyopathy? What are some causes? What are some signs and symptoms? How is it diagnosed? What are some interventions?
– hypertrophic cardiomyopathy: thicker arrangement of heart muscle fibers, usually in the left ventricle or septum
- thicker muscles are non-functional
- high risk of sudden death
– causes:
- genetics
– s/s:
- abnormal S3 and S4 sounds
- murmurs
- mitral regurgitation
- activity intolerance
– diagnosis:
- H&P
- EKG
- echo
– interventions:
- decrease activities
- drugs:
- beta blockers
- calcium channel blockers
- antiarrhythmias
- diuretics
- surgery:
- pacemakers
- valve replacement
- thinning of septum
What is restrictive cardiomyopathy? How is it different from other cardiomyopathies? What are some causes? What are some signs and symptoms? How is it diagnosed? What are some interventions?
– restrictive cardiomyopathy: a rare, not very obvious disease in which the walls of the ventricles are very stiff but not necessarily thickened
- different than other cardiomyopathies because the heart doesn’t necessarily present as enlarged – stiff walls make the ventricles non-functional
– causes:
- secondary disease – usually results from another disease
- commonly related to amyloidosis
- amyloids (abnormal protein fibers) accumulate in the heart muscle cells
- cause inflammation
- results in formation of lumps on organs and iron overload
- stiffens the ventricular tissue
– s/s:
- same as CHF
- nausea
- bloating
- fluid retention around liver, stomach, and intestines
– diagnosis:
- H&P
- echo
- heart size is small
- reduced ejection fraction
- MRI
- CT
- cath
- biopsy
– interventions:
- no specific treatments
- palliative care – symptom management
- diuretics may help with fluid accumulation
