Cardiac Disorders and Management
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Coronary Vascular Disorders
o CAD
o Angina
o Myocardial Infarction (MI)
o Acute Coronary Syndrome (ACS)-describe an array of clinical presentations of CAD that ranges from unstable
angina to acute MI
Coronary Artery Disease (CAD)
o Cardiovascular (CV) disease is the leading cause of death in the US
o CAD is most prevalent type of CV disease in adults
o Coronary atherosclerosis is most common cause of CV
o What’s the Problem With CAD?
 Narrowing of the arterial lumen
 Thrombus formation
 Obstruction of blood flow to myocardium
 AHA CAD progression
o Risk factors
 High lipids
 Smoking
 HTN
 DM
 Obesity
 Family history
 Inactive lifestyle
 Age
 Gender/race
 Which ones are modifiable?
 What can be done to prevent CAD?
o What problems can CAD lead to?
 Ischemia
 Angina
 MI
o How is CAD diagnoses?
 Health history
 Physical exam
 ECG
 Stress testing
 Angiography
Angina Pectoris
o info
 Chest pain caused by myocardial ischemia
 Can occur anywhere in chest, neck, arms, or back
 Most common is behind sternum
 Lack of Oxygen in Tissue=Pain (in ANY tissue)
o Types of Angina Pectoris
 Stable angina
 Unstable angina
 Intractable or refractory
 Variant Angina (AKA Prinzmetal’s)
 Silent Ischemia
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What is the problem?
 oxygen demand > oxygen supply
 Myocardium uses a large amount of oxygen from coronary circulation. Obstruction of a major
coronary artery (commonly from atherosclerosis) causes ischemia and results in episodes of pain
or pressure in the chest.
o Medical Management
 Objective: to decrease oxygen demand of the myocardium and to increase O2 supply
 Pharmacological therapy
 Nitrates, ASA, BB, CCB, antiplatelets, O2
 Reperfusion procedures
 Percutaneous transluminal coronary angioplasty
 Intracoronary stents
 CABG
 Nitroglycerin
 Vasodilator used to ↓ myocardial O2 consumption→decreased ischemia→pain
 Sublingual, tablet, or spray, oral capsule, topical agent of IV
 SL placed under tongue or in buccal pouch
 May be taken 3x in 5-minute intervals for unrelieved CP
 Patient Teaching on Nitroglycerin
 Moisten mouth before taking
 Carry with them at all times
 Keep in original (dark) bottle-very unstable
 Renew supply every 6 months
 Take note of how long it takes for nitro to relieve pain
 Anticipated side effects: headache, hypotension, tachycardia and flushing
 Sit down when taking
o Nursing Management
 PQRST to gather information about CP
 Reduce anxiety
 Prevent/reduce pain (stop all activity, semi-Fowler’s position)
 Patient and family education
o PQRST Assessment of CP
 P: position/location (where? And provocation (what makes it worse?)
 Q: quality (describe the pain)
 R: radiate? Relief?
 S: severity (pain scale); other symptoms
 T: timing (when did it start?)
Myocardial Infarction (MI)
o info
 Sustained ischemia → injury → death of heart muscle cells
 Immediate recognition of signals is crucial
 Time is muscle
 CPR is essential! Basics! ABCD
o Signs and Symptoms
 Sudden and continued CP despite rest and medication
 Shortness of breath
 Diaphoresis
 Indigestion
 Nausea
 Anxiety
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 Cool, pale, clammy skin
Assessment and Diagnostic findings
 Diagnosis usually made based on S/S, ECG, and lab tests
 Goal: ECG within 10 minutes of reported CP or arrival to ED
 Review of cardiac labs
 Troponin: elevates in 3-4 hrs, peak 4-24, stay up for 1-3 weeks
 CK-MB: predominately cardiac specific, first enzyme to increase, elevated short time
 Myoglobin: not very cardiac specific, increases 1-3 hrs after MI, peaks 4-12 hrs, normal within 24
hrs.
Diagnosis?
 Unstable angina: symptoms of ischemia without evidence of acute MI on ECG or cardiac labs
 ST-segment elevation MI (STEMI): ECG changes in two leads; indicates significant damage to myocardium
 Non-ST elevation MI (NSTEMI): elevated cardiac markers without definitive ECG evidence
Medical Management for MI
 Goal: minimize myocardial damage, preserve myocardial function, and prevent complications
 Thrombolytics (stretokinase, tPA) within 3 hours of symptoms
 Inotropic support (dobutamine)- ↓ SVR
 Preload/afterload reduction to decrease O2 demand, diuretics, vasodilators (nitro)
 Emergent PCI
 CABG
Pharmacological Management of MI’s
 Thrombolytics (stretokinase, tPA) within 3 hours of symptoms
 Inotropic support (dobutamine)- ↓ SVR
 Preload/afterload reduction to decrease O2 demand, diuretics, vasodilators (nitro)
 Anticoagulants
Early Treatment of MI’s
 Aspirin
 Nitro
 VS
 12-lead ECG
 Morphine for pain
 Oxygen
 Beta Blocker (metoprolol)
MONA
 M-morphine
 O-oxygen
 N-nitroglycerine
 A-aspirin (have them chew it so it gets into their system faster)
Cardiac Rehabilitation
 Active program started once symptoms are resolved
 Reduces risk through education and physical activity
 Goal: to extend life and improve quality of life
Nursing Process
 Assessment: important to assess baseline symptoms and identify changes in these
 Nursing Diagnoses:
 Ineffective cardiac perfusion
 Risk for imbalanced fluid volume
 Risk for ineffective peripheral tissue perfusion
 Collaborative problems/potential complications
 Acute pulmonary edema
 Acute pulmonary edema
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Heart failure
Cardiogenic shock
Dysrhythmia’s and cardiac arrest
Pericardial effusion and cardiac tamponade
Cardiogenic Shock
o Info
 ↓ CO → inadequate tissue perfusion and initiation of shock syndrome
 May occur after MI (due to areas of ischemia and necrosis)
 Also can occur with end-stage HF, cardiac tamponade, PE, cardiomyopathy, and dysrhythmia
 Life-threatening/high mortality rate
o Who is at risk?
 Elderly (>65 yrs)
 Females
 Diabetics
 Pre-existing CAD
 Anterior wall MI
o Signs and symptoms
 Cerebral hypoxia (restlessness, confusion, agitation), decreased BP, rapid & weak pulse, cold clammy skin,
tachypnea
o Assessment findings
 ↓CO , ↓SV, ↑ SVR , ↓BP, ↓ tissue perfusion
o Management/Treatment
 Medications: diuretics, vasodilators, vasopressors
 Circulatory assist devices (IABP)
 Hemodynamic monitoring
Intra-aortic Balloon Pump (IABP)
o Primary goal: decrease workload and maintain adequate perfusion
o A catheter with an inflatable balloon at the tip is inserted through the femoral artery and the balloon is placed in
the descending thoracic aorta.
o Balloon inflates during diastole and aortic valve closure to augment the pumping action of the heart and decrease
afterload
o Inflation and deflation synchronized to ECG
o Indications: cardiogenic shock, LV failure, post-op open heart, unstable angine, post MI
o Contraindications: aortic valve incompetence, Peripheral vascular occlusive disease, aorto-femoral/ or illiac bypass
grafts, aortic aneurysm
o Complications: ↓circulation to leg, left arm or balloon rupture
o Wean by decreasing ratio 1:1, 2:1, 4:1
Cardiac Arrest
o Info
 Heart ceases to produce an effective pulse and circulate blood
 Most reliable sign of this is by absence of a pulse… check carotids
 Loss of consciousness, pulse and BP
 ineffective or absent breathing.
o Emergency management
 ABCD
 Maintain open airway
 Provide artificial ventilation
 Promote artificial circulation
 Defibrillate (*defibrillate for pulseless Vtach and Vfib)
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Invasive Coronary Artery Procedures
o Percutanous Coronary Interventions (PCI’s)
 Variety of procedures used to treat diseases of the arteries of the heart
 Previously known as angioplasty, PTCA, and balloon angioplasty
 Balloon-tipped catheter threaded from groin artery to blocked/diseased area of the heart. When inflated
it widens the narrowed artery →increased blood flow.
o Randoms
 Anti-clotting meds are used before, during, and after PCI
 Plavix, Lovenox
 Time is muscle
 Goal: restore blood flow to heart muscle within 90 minutes of arrival in ED
 “door to balloon time of 90 minutes”
o Complications
 Bleeding, swelling at insertion site, CP
o Post-procedure care
 Assess for back pain (retroperitoneal bleeding)
 Check pulses (15 min x 2 hrs, then Q1-2 hrs)
 HOB <30 degrees while sheath in place
 Leg straight for several hours
 Direct pressure for 15-30 minutes after removal of sheath
o Stent Placement
 mesh wire tubes inserted during PCI to keep vessel open
 “permanent scaffolding”
o Cardiac Catheterization
 Guidewire, then sheath, threaded into artery or chamber of heart
 Opaque dye injected; fluoroscopy
 Helps determine whether an intervention is needed
 http://upload.wikimedia.org/wikipedia/commons/6/63/Hk_lv_big_bionerd.gif
 Coronary Artery Bypass Surgery
o info
 Surgical revasculization (of areas that have been blocked off)
 Can be used when several arteries have significant blockage
 Blood vessel grafted distal to coronary artery lesion, bypassing the area of obstruction
 Saphenous vein or LIMA (left internal mammary artery) vessels most commonly used
 Off-pump vs on-pump
o Immediate Post-Op Period
 Recovered in critical care unit or PACU
 Very critical period of time
 Focus: achieving hemodynamic stability
 Issues: managing pain, cardiopulmonary status, wound care
 Assessment for complications
 ↓ CO, fluid volume and electrolyte imbalances, impaired gas exchange, impaired cerebral
circulation
Structural Disorders
 Mitral Valve Prolapse
o Info
 Leaflets papillary muscle of mitral valve do not work correctly leading to prolapse of leaflets, allowing
them to go back into the atrium
 Regurgitation?
 Cause is unknown
 Most common form of vavular heart disease
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2x women over men
S/S
 Often patient is asymptomatic
 Palpitations
 Dyspnea
 CP
 Activity intolerance
 Mitral Regurgitation
o Patho
 Caused by defect in mitral valve allowing blood to flow back from LV to LA during systole
 Acute:
o causes: rupture of papillary muscle following an acute MI and rupture or one or more
chordae teninae
o Forceful jet of blood sent retrograde into lt. atrium →sudden increase atrial
pressure→acute pulmonary edema, ↓CO and possibly cardiogenic shock
 Chronic
o Elderly most common as structures sag and stretch over time
 Mitral Stenosis
o Obstruction of blood flow from LA to LV due to narrowing of mitral valve orifice
o Low-pitched murmur
o Occurs during diastole
o Best heard in mitral area
o Can lead to a-fib and atrial thrombi
o ↑ left atrial pressure creates pulmonary congestion, breathlessness, moist cough, and rt. sided heart failure
 Aortic Regurgitation
o Aka aortic insufficiency
o Incompetent aortic valve “leaking valve”
o High-pitched blowing murmur
o Early diastolic
o Heard best at aortic area
 Aortic Stenosis
o Narrowing of aortic valve orifice
o LV has ↑ difficult ejecting blood into aorta → increased intraventricular pressure→LV hypertrophy (↑ muscle
mass)→loss of contractile force in LV
o Leads to ↓ decreased blood flow to aorta means less efficient filling of coronary arteries→Chest Pain
o Two yrs of symptoms→Survival rate of <50% without valve replacement
o Low-pitched, systolic murmur, heard in aortic area
Treatment of Valvular Disorders
 Valvuloplasty-repair of the valve
o Commissurotomy
o Annuloplasty
o Leaflet repair
 Valve replacemento Mechanical valves
o Biologic valves
 Xenografts
 Homografts
 Autografts
Infectious Diseases of the Heart
o Any of 3 layers can be affected by infections
o Named by layer of heart most involved
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o Rheumatic Endocarditis (endocardium)
o Infective Endocarditis
o Myocarditis (myocardium)
o Pericarditis (pericardium)
Infective Endocarditis
o info
 An infectious process which leads to vegetation in heart, usually the leaflets or endocardium
 Usually caused by strep or staph
 Portals of entry: dental procedures, tonsillectomy, burns, rheumatic heart disease, IV drug abuse,
prosthetic valves
 Prevention: oral antibiotics for dental procedures
o Signs and Symptoms
 Systemic signs: mild fever, malaise, murmur, chills, abd. pain, dypsnea
 Petechiae
 Osler nodes: small, red, raised nodules on fingers or toes
 Janeway lesions: hemorrhages, flat, red, nontender macules on palms and soles
 Clubbing
 Anemia, ↑ WBC’s, + blood cultures
 Infective Endocarditis cont’d
o Treatment: antibiotics, may need valve replacement
o Complications: HF, myocardial abscess (from staph), pericarditis, myocarditis, emboli
Myocarditis
o Causes: infectious agent invading myocardium
o S/S: may be asymptomatic or have s/s of HF, ST-T changes, fatigue, dypsnea, temp, CP
o Treatment: tx for dysrhythmia’s and HF, O2, steroids, interferon
Pericarditis
o Causes: MI, viruses, bacteria,trauma, lupus, post-open heart
o S/S: Positional CP (worse when lying down, improved when sitting up/leaning forward), friction rub (heard best at
lower sternal border)
o Complications: pericardial effusion, pericardial tamponade
o Treatment: NSAIDS, steroids
Pericardial Effusion & Cardiac Tamponade
o Pericardial sac normally contains <50 mL of fluid needed to decrease friction of beating heart
o Increase in the fluid raises pressure within the sac and compress the heart
o Cardinal signs: falling SBP, narrowing pulse pressure, rising venous pressure (inc. JVD) and distant (muffled) heart
sounds
Cardiomyopathy
o Info
 Disease of the heart muscle associated with cardiac dysfunction
 Different classifications according to the structural and functional abnormalities of the heart muscle
o Patho: decreased stroke volume→ sympathetic nervous system stimulation and the renin-angiotensin-aldosterone
resonse→ ↑SVR and ↑ Na and fluid retention →workload on the heart
o Known Causes
 Cardiotoxic agents: alcohol, cocaine, Adriamycin
 Aortic stenosis
 HTN
 Ischemia
 Can occur acutely or over time.
o Types
 Dilated cardiomyopathy (DCM)
 Info
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Most common type (~90%)
Significant dilation of ventricles without simultaneous hypertrophy (increased muscle
wall thickness) and systolic dysfunction
Diminished ability of the heart to contract
↑ stystolic and diastolic volumes and ↓ ejection fraction
S/S
o Tachycardia
o Fatigue
o S3, S4 heart sounds
o Murmurs
o S/S HF
o Echo-easy observation of structure and function of ventricles
o ECG may show dysrhythmia’s
o Cardiac catheterization may be used to r/o CAD for the cause of the symptoms
 Management
o Treating underlying causes
o Treatment similar to that for HF
 Enhance contractility of heart
 Decrease afterload
Hypertrophic Cardiomyopathy (HCM)
Restrictive Cardiomyopathy
Arrhythmogenic RV Cardiomyopathy
Unclassified Cardiomyopathies
Heart Failure (HF)
 Info
o Previously referred to as Congestive Heart Failure (CHF)
o HF is a clinical syndrome with s/s of fluid overload or inadequate tissue perfusion
o Problem is with either contraction (systolic dysfunction) or filling (diastolic dysfunction)
o Number of patients with HF is increasing in the U.S. Over 5 million in US have HF, 550,000 new cases each year;
300,000 die each year from HF
o Heart failure is a response to cardiac dysfunction
o Any condition which impedes the ability of the heart to pump blood at a volume required to meet the body’s
needs can lead to HF
 CAD→necrotic damage to LV, Valvular dysfunction, Cardiomyopathy, Infection (myocarditis or
endocarditis)
 Types
o Systolic (more common) is characterized by a weakened heart muscle
o Diastolic is characterized by a stiff and non-compliant heart muscle, making ventricular filling difficult
o Ejection fraction is used to help determine the type of dysfunction nl=55%-65%
 EF is severely ↓ in systolic HF and nl in diastolic
 Signs of Left vs. Right Heart Failure
LEFT
RIGHT
 tachypnea
 Peripheral edema
 Tachycardia
 Hepatomegaly
 cough
 Splenomegaly
 Bibasilar crackles
 Hepatojugular reflex
 S3 and S4
 Ascites
 Increase PA pressures
 JVD
 Hemoptysis
 Increased CVP
 Cyanosis
 Pulmonary HTN
 Pulmonary Edema
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Symptoms of Left vs. Right HF
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RIGHT
Weakness
Anorexia
Indigestion
Weight gain
Mental Changes
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CHRONIC
ongoing
hypervolemic
Na and H2O retention
Structural changes in chambers of the heart
Acute vs. Chronic HF
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LEFT
fatigue
dyspnea
orthopnea
Paroxysmal nocturnal dyspnea
Nocturia
ACUTE
Rapid onset
Pulmonary Edema
Low CO
Cardiogenic shock
Chronic Heart Failure
o Info
 Diagnosis usually made with echocardiogram (ultrasound)
 Ejection fraction (EJ) is determined through echo
 CXR is also helpful
 BNP is key diagnostic indicator of HF
 Exercise testing or cardiac catheterization can be used to determine whether CAD or cardiac ischemia is
the cause
o Medical Management
 Pharmacological therapy
 ACE inhibitors
 BB
 Diuretics
 Digitalis
 Nutritional therapy
 Additional therapy
 O2
 ICD
o Nursing Management
 Careful assessment and monitoring
 Fluid balance, I/O’s
 Daily weight
 Monitoring JVD, VS
 Monitor for complications r/t diuretic therapy
 Hypokalemia, hyponatremia, hyperuricemmia
o Nursing Diagnosis
 Activity intolerance
 Excess fluid volume
 Powerlessness
Acute Heart Failure (Pulmonary Edema)
o Info
 Acute event related to HF
 May occur with MI
 Exacerbation of chronic HF
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Clinical manifestations
 Pulmonary edema: abnormal accumulation of fluid in the lungs
 Rapid onset
 Patient becomes restless and listless
 Sense of suffocation
 Cold hands, cyanotic nail beds, ashen skin
 Weak, rapid pulse
 JVD
 Productive cough
Medical Management
 O2 therapy
 Morphine
 Diuretics
 IV medications
 Dobutamine
 Nesiritide
 milrinone
Nursing management
 Position patient to promote circulation and reduce venous return to the heart (upright and feet dangling)
 Provide emotional support
 Monitor effects of medications