1. Cardiovascular: Valvular, Cardiomyopathy, Aneurysm and Cardiac Surgery
Click here- Heart valves at work!
Review of Heart Valve sounds (etc)
A&P Heart Valves- Click here
Use these slide as supplement to Notes and Learning Guide

2. Valvular Heart Disease (Access to Helpful Interactive Sites)
HeartPoint: HeartPoint Gallery (many resources here!)
Valvular Disease (great introductory video!)
Valvular Heart Disease:
Heart Valves at Work *UTube
Flashcards (Test your knowledge!)

3. Pathophysiology Stenosis- Regurgitation (insufficiency)
narrowed valve, sloews forward blood flow
increases afterload, dec. CO
Regurgitation (insufficiency)
increases preload
heart pumps same blood again
blood volume and pressures reduced in front of affected valve; increased behind affected valve
results in heart failure

4. *All valvular diseases have characteristic murmurs (click to hear!)
Damaged valve disrupts blood flow=turbulence & sound!
Caused by
Rheumatic Heart Disease
Acute conditions (infective endocarditis)
Acute MI
Congenital Heart Defects
Aging, etc

5. Mitral Valve Stenosis

6. Mitral Valve Stenosis Etiology/Pathophysiology:
Most cases due to rheumatic fever
Contractures and adhesions of valve leaflets- “fish mouth”
Dec. flow into LV>LA hypertrophy>inc. pulmonary pressures> pulmonary hypertension
Dec. CO-lead to Rt. Heart failure

7. Mitral Valve Stenosis Clinical Manifestations:
Early symptom-dyspnea on exertion (DOE)
Cough, hemopysis, etc.
Late- Signs Rt. Heart failure (dec. CO)
Atrial fib. (enlarged atrium)
Murmur- loud S1, low pitched diastolic murmur
Hoarseness, seizures, stroke (emboli risk)
Management Mitral Valve Stenosis

9. Treatment for Mitral Stenosis (non-surgical) Balloon Valvuloplasty

10. Valvular Surgery Heart Surgery Innovations - (27 min)
Access site to see and hear the newest information!
Heart Surgery Innovations - (27 min)
11:22 valves
20 beating heart
20 aortic valve

11. Mitral Regurgitation Etiology/Pathophysiology/Manfesations
Valve does not close fully
Regurgitation of blood into LA during systole
Dev. LA dilation and hypertrophy > pulmonary congestion > RV failure
LV dilation and hypertropy-accommodate increased preload (from regurgitation)
Dec. CO
Acute and chronic MR
Acute-poorly tolerated-fulminating pulmonary edema
Chronic- Lt. ventricular failure, S3 sound, pansystolic murmur

12. Mitral Regurgitation

13. Treatment of Mitral Valve Regurgitation Innovations (Percutaneous) MitraClip Repair
MitraClip 3D Animation View video -procedure to correct mitral valve regurgitation! Non-invasive

14. Mitral Valve Prolapse Etiology/Pathophysiology/Manifestations
Mitral valve cusps “billow’ into atrium during ventricular systole
Most common form valvular disease, associated with Marfan’s syndrome (Michael Phelps…does he have it?)
Usually benign-complications- MR, infective endocarditis (IE) , SCD
Usually asymptomatic- mid systolic click, and last holosystolic murmur
Chest pain (atypical)-does not respond to antianginals
Dysrhythmia risk
?Need for prophylactic antibiotics (IE risk)

15. Mitral Valve Prolapse
Midsytolic click & late systolic murmur (Click here to hear characteristic sounds of MVP)
UTube- Mitral Valve Prolapse (brief lecture-informative)
UTube- Mitral Valve Prolapse (current research-re prophylactic antibiotics)
Endocarditis and MVP

16. Aortic Stenosis Etiology/Pathophysiology/Manifestations
Congenital or due to rheumatic fever or aging
May be asymptomatic for years
Obstruction LV to aorta > inc afterload > L. ventricular hypertrophy > dec. CO
Eventual pulmonary hypertension, myocardial ischemia and later right heart failure
*DOE, angina, syncopy (SAD)- Classic Symptoms
*Poor prognosis-if symptoms and obstruction not relieved
*Nitroglycerin contraindicated
Normal to soft S1; absent S2; harsh systolic crescendo-decrescendo murmur, loud S4 (click for sound)

18. Classic Symptoms
Syncope
Angina
Dyspnea

19. Aortic Stenosis
*Normal aortic valve has 3 leaflets-not 2 (bicuspid) (Arnold Schwarzenegger- lead to aortic stenosis and require valve replacement)
Aortic valve
Aortic Valve animation

20. Aortic Stenosis Access these sites to learn about procedures to treat/replace damaged aortic valves
Minimally Invasive Aortic Heart Valve Replacement

21. Percutaneous Aortic Valve Replacement
Percutaneous AVR a) Balloon valvuloplasty; b) Balloon catheter with valve in the diseased valve;
c) Balloon inflation to secure the valve; d) Valve in place
Percutaneous aortic valve replacement (AVR)- new treatment being investigated for select patients with severe symptomatic aortic stenosis… Research at Cleveland Clinic is evaluating a percutaneous technique for implanting a prosthetic valve inside diseased calcific aortic valve. The procedure is performed in catheterization lab…a catheter is placed through femoral artery (in the groin) and guided into chambers of the heart. A compressed tissue heart valve is placed on the balloon-mounted catheter and is positioned directly over the diseased aortic valve. Once in position, the balloon is inflated to secure the valve in place. *For patients with severe peripheral vascular disease, surgeons and cardiologists are testing an alternative approach through the left ventricular apex of the heart.

23. Heart Valve replacement
(Aortic valve, patient resource, mechanical, biological)

24. Aortic Regurgitation Etiology/Pathophysiology/Manifestations
Congenital valvular defect
Acute causes- trauma, aortic dissection (life threatening)
Chronic- rheumatic heart disease, bicuspid valvular disease
Retrograde blood flow (inc. preload) from ascending aorta > L ventricle dilation, hypertrophy
Eventual dec. myocardial contractility > dec. CO
Develop pulmonary hypertension, Rt. Ventricular failure (*inc. L. ventricular end diastolic pressure=LVED)
If severe- characteristic “*water hammer pulse” (Corrigan’s pulse), wide pulse pressure, and Musset’s sign
Soft or absent S1, presence of S3, S4; soft, high pitched diastolic murmur, systolic ejection click; Austin Flint murmur

25. Water Hammer pulse
Pulse- “water hammer” -jerky pulse that is full, then collapses due to aortic insufficiency/regurgitation (blood ejected into aorta regurgitates back through aortic valve into L. ventricle ). AKA-called a Corrigan pulse or a cannonball, collapsing, pistol-shot, or trip-hammer pulse. (Click to view video)

26. Aortic Regurgitation
Echocardiography

27. Tricuspid and Pulmonic Valve Disorders
Etiology/Pathophysiology/Manifestations
Tricuspid stenosis (more common than regurgitation)
Result in R. atrial enlargement > inc. systemic venous pressure > atrial fibrillation, peripheral edema, ascites, etc.
Found mostly in rheumatic heart disease, IV drug users
Pulmonic stenosis
Result in R. ventricular hypertension and hypertrophy
Fatigue , loud midsystolic murmur
Uncommon valve disorders

28. Collaborative Care Keys
Prevent recurrent rheumatic fever, infective endocarditis
Identify by characteristic murmur
Aware of effect of stenosis, regurgitation on cardiac hemodynamics (preload, afterload)
Appropriate prophylactic therapy (antibiotics before invasive procedures-at risk patients)
Manage heart failure if present
Manage complications-ie dysrhythmias, risk for emboli (a-fib) etc.
*Treatment depends upon valve involved
Adequate follow-up care.

29. Medications/Diet Manage complications (ie heart failure, dysrhythmias)
ACE,
Dig
Diuretics
Vasodilators
Beta blockers
Anticoagulants *a-fib common
*Prophylactic antibiotics
Treatment specific for disease (ie no *nitroglycerin if aortic stenosis)
Diet
Low sodium-if risk for heart failure

30. Diagnostic Tests Echo- assess valve motion and chamber size CXR EKG
TEE
CXR
EKG
Cardiac cath- measure pressure gradients (hemodynamic function)

31. Transesophageal echocardiogram

32. Surgical Intervention
*Not all types valve disease require surgical intervention
Valvuloplasty-general term valve repair, invasive/non-invasive methods
Percutaneous balloon valvuloplasty (non-invasive)
Surgery
Open commissurotomy- open stenotic valves
Annuloplasty- repair of valve’s outer ring-used for stenosis, regurgitant valve
Valve Replacement
Mechanical-need anticoagulant
Biologic-only last about 15 years
Ross Procedure-transfer pulmonic valve for aortic

33. Valve Replacement Surgery
Patient Teaching-Heart Valve Replacement Surgery (click here)

35. Ross Procedure

37. Important-teaching needs for valve replacement
Excised porcine bioprosthesis; main advantage of bioprosthesis is lack of need for continued anticoagulation-drawback include limited lifespan, on average from 5 to 10 years (sometimes shorter) due to wear and calcification. (No immune suppressive agents required.)
Mechanical valve prosthesis- modern tilting disk variety (for mitral valve); last indefinitely from structural standpoint; patient requires continuing anticoagulation due exposed non-biologic surfaces.
Important-teaching needs for valve replacement

38. Nursing Diagnoses Decreased Cardiac Output Activity Intolerance
Excess Fluid Volume
Ineffective therapeutic regimen
Risk for Infection
Ineffective Protection

39. What Is New?
Heart valve replacement without need for open heart surgery.
Typically, diseased or defective valves replaced with an artificial valve or a tissue valve (from pig or cow).
A new, less invasive procedure, known as percutaneous transcatheter heart valve implantation, involves use of balloon catheters and large stents…
New heart valve transported via stent; stent then expanded to implant the valve.
For patients not able to undergo open-heart surgery… percutaneous heart valve implantation may impact significantly on survival and quality of life. Click for more!

41. New Cont.
New technologies…a tiny metallic clip is being studied for treatment of mitral regurgitation- MitraClip 3D Animation View video -procedure to correct
Valves may last a lifetime for older patients, younger patients may need several replacement procedures over time.
One focus of research-create longer-lasting replacement valves, particularly for patients with congenital heart disease. Research potential toward this goal: stem cell research and the use of endothelial cells.

42. Cardiomyopathy
Condition is which a ventricle has become enlarged, thickened or stiffened.
As a result heart’s ability as pump is reduced
3 Types
Dilated
Hypertropic
Restrictive

43. Cardiomyopathy Primary-idiopathic Secondary Ischemia- from CAD
Infectious/viral disease
Exposure to toxins
Metabolic disorders
Nutritional deficiencies
Genetic

44. Dilated Cardiomyopathy
*Most common type
Diffuse inflammation rapid degeneration myocardial tissue
Heart chambers dilate; impaired systolic function, *atrial enlargement
40% dev. R & L heart failure; dec. EF
*Dysrhythmias are common- SVT, A-fib, VT
Prognosis poor-*need transplant

45. Dilated Cardiomyopathy
Factors Causing:
Genetic predisposition
May follows infectious endocarditis & viral infections
Alcohol related
S&S- (heart failure)
Fatigue, orthopnea, noctural dyspnea
Irregular heart rate, pulmonary crackles, S3, S4
Heart murmurs, sudden cardiac death!

46. Dilated Cardiomyopathy
Collaborative Care
*Focus-control heart failure
Enhance contractility; dec. afterload
Dx Tests (signs heart failure)
Doppler ECHO, EKG, heart cath
Lab (BNP)
Chest X-Ray
Diet/Drugs
Low Na
HF meds

47. Cardiomyopathy- very large heart, circular shape, all chambers are dilated, flabby, myocardium poorly contractile
Normal weight 350 gms –dilated cardiomegaly-700 gms

49. Dilated Cardiomyopathy
Collaborative Care
Surgical/resynchronizationization therapy
VAD or LVAD
CRT (cardiac resynchronization therapy)

50. Dilated Cardiomyopathy
Collaborative Care
Heart transplant

51. Hypertrophic Cardiomyopathy (HCM)
Genetic; IHSS (idiopathic hypertrophic subaortie stenosis), HOCM (hypertrophic obstuctive cardiomyopathy)
Hypertrophy of ventricular mass; impaired ventricular filling (diastole); dec. CO > inc pulmonary & venous pressures
Forceful ventricular contraction
*Obstruction aortic outflow (not all cases)
S&S: syncopy, angina, dyspnea (SAD); S4 develop during or after physical activity
*Sudden cardiac death (dysrhythmia)
Hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy Hypertrophic cardiomyopathy, or HCM, is a disease of the myocardium (the muscle of the heart) in which a portion of the myocardium is hypertrophied (thickened) without any obvious cause.[1][2][3][4][5][6] It is perhaps most famous as a leading cause of sudden cardiac death in young athletes [7] The occurrence of hypertrophic cardiomyopathy is a significant cause of sudden unexpected cardiac death in any age group and as a cause of disabling cardiac symptoms.
A cardiomyopathy is a disease that primarily affects the muscle of the heart. With hypertrophic cardiomyopathy (HCM), the normal alignment of muscle cells is disrupted, a phenomenon known as myocardial disarray. HCM also causes disruptions of the electrical functions of the heart. HCM is believed to be due to a mutation in one of many genes that results in a mutated myosin heavy chain, one of the components of the myocyte (the muscle cell of the heart). Depending on whether the distortion of normal heart anatomy causes an obstruction of the outflow of blood from the left ventricle of the heart, HCM can be defined as obstructive or non-obstructive. The obstructive variant of HCM, Hypertrophic obstructive cardiomyopathy (HOCM) has also historically been known as idiopathic hypertrophic subaortic stenosis (IHSS) and asymmetric septal hypertrophy (ASH). Another, non-obstructive variant of HCM is apical hypertrophic cardiomyopathy [8], first described in individuals of Japanese descent).
While most literature so far focuses on European, American, and Japanese populations, HCM appears in all racial groups. The incidence of HCM is about 0.2% to 0.5% of the general population.

52. Hypertrophic Cardiomyopathy (HCM)
Collaborative Care
Goals
Improve ventricular filling
*Reduce ventricular contractility
Relieve L. ventricular outflow obstruction
Diagnostic Tests
“Forced” apical sound (laterally)
EKG, ECHO (L. ventricular hypertrophy, abnormal wall motion)
Heart cath
Meds
Negative inotropes (Ca channel blockers, beta blockers)
*NO vasodilators, digitalis (usually), nitrates

54. Note obstruction-aortic outflow (HCM)

55. Hypertrophic Cardiomyopathy (HCM)
Collaborative Care
Surgical/Other Interventions
Cardioverter/defibrillator (At risk patients)
AV pacing if outflow obstruction
Ventriculomyotomy and septal myomectomy
Alcohol septal ablation
Live Search Videos: cardiomyopathy

56. Restrictive Cardiomyopathy
Least common
Rigid ventricular walls that impair filling (impaired diastolic)
Contraction (systolic) and EF normal
Prognosis-poor
S & S
Fatigue, dyspnea, exercise intolerance
R. sided heart failure
cardiomyopathy?
Restrictive cardiomyopathy is a serious problem that makes your heart muscle stiff. When your heart muscle is stiff, it can''t stretch to allow enough blood to enter its lower chambers, the ventricles . So blood that would normally enter the heart backs up in your circulatory system.
Most of the time, this leads to heart failure. Heart failure does not mean that your heart stops pumping. It means that your heart can''t pump enough blood to meet your body''s needs.
What causes restrictive cardiomyopathy?
Often the cause is never found. But we do know that there are a number of diseases or problems that can lead to restrictive cardiomyopathy. These include:
Cardiac amyloidosis, a buildup of an abnormal protein in the heart muscle.
Hemochromatosis, a buildup of iron in the heart muscle.
Sarcoidosis, a rare type of heart inflammation.
Radiation therapy and chemotherapy, used to treat cancer.
Carcinoid syndrome, a rare disease that causes certain chemicals to be released into the blood stream. These chemicals can stiffen heart muscle.
Löeffler’s syndrome and endomyocardial fibrosis, conditions that can cause scar tissue in the heart.
Genetic factors. You can inherit diseases, including Gaucher disease and Fabry''s disease, that can lead to restrictive cardiomyopathy. But these diseases can be treated to prevent restrictive cardiomyopathy.
Restrictive cardiomyopathy

57. Restrictive Cardiomyopathy
Collaborative Care
Dx Test
Chest X-ray (cardiomegaly?, show R. and L atrial enlargement)
EKG (tachycardia), supraventricular dysrhythmias, AV block
ECHO wall motion, EMB, CT nuclear imaging
Medications
*No specific treatment
Meds to improve diastolic filling, manage heart failure, dysrhythmia
Surgical/Other Treatment
Poor prognosis
Transplant maybe (depends underlying cause)
The test, endomyocardial biopsy, or EMB, involves inserting a catheter into a vein in the neck and threading it into the heart, so that a tiny amount of the heart muscle can be sampled for analysis. Now, a quick, easy-to-administer blood test is rapidly replacing EMB as the gold standard for diagnosing rejection of the donor heart.

58. Biopsy of heart (EMB)

59. Review-Management Cardiomyopathy
Vad-bridge to transplant
Heart Transplant
Myloplasty
ICD- antiarrhythmics are negative inotropes
Dual chamber pacemaker
*Hypertrophic- excision of ventricular septum-myotomy, inject denatured alcohol in coronary artery that feeds top portion of septum.
*Transplant

60. Heart transplant (slide show)
Virtual transplant (try it!)
Click here-YouTube- Heart-Lung machine

61. A new heart!

62. Cardiomyopathy Nursing Diagnoses
Decreased Cardiac Output
Fatigue
Ineffective Breathing Pattern
Fear
Ineffective Role Performance
Anticipatory grieving

63. Case study 1. What action should you take first?
Ms. C. 81 y/o admitted to CCU with SOB; has a hx of mitral valve regurgitation with left ventricular enlargement. She received 100mg Lasix IV in ER and her dyspnea improved. She has O2 at 3L/min. She has crackles bibasilar and monitor is SR rate with occ. PVC’s. The only med ordered is morphine 2-4mg IV as needed for chest pain or dyspnea.
As you go to assess her, you find her in bed at 60 degree angle. She is pale, has circumoral cyanosis and respirations are rapid and labored.
1. What action should you take first?
A. Listen to breath sounds
B. Ask when the dyspnea started
C. Increase her O2 to 6L minute
D. Raise the HOB to degrees

64. Case study 1. What action should you take first?
Ms. C. 81 y/o admitted to CCU with SOB; has a hx of mitral valve regurgitation with left ventricular enlargement. She received 100mg Lasix IV in ER and her dyspnea improved. She has O2 at 3L/min. She has crackles bibasilar and monitor is SR rate with occ. PVC’s. The only med ordered is morphine 2-4mg IV as needed for chest pain or dyspnea.
As you go to assess her, you find her in bed at 60 degree angle. She is pale, has circumoral cyanosis and respirations are rapid and labored.
1. What action should you take first?
A. Listen to breath sounds
B. Ask when the dyspnea started
C. Increase her O2 to 6L minute (symptoms indicate acute hypoxemia, need to inc O2 flow, HOB already elevated)
D. Raise the HOB to degrees

65. Case Study-Question 2, 3
2. Which of these complications are you most concerned about, based on your assessment?
A. Pulmonary edema
B. Cor pulmonale
C. Myocardial infarction
D. Pulmonary embolus
3. Which action will you take next?
A. Call the physician about client’s condition.
B. Place client on a non-rebreather mask with FiO2 at 95%.
C. Assist client to cough and deep breathe.
D. Administer ordered morphine sulfate 2mg IV.

66. Case Study-Question 2, 3
2. Which of these complications are you most concerned about, based on your assessment?
A. Pulmonary edema- hx of inc SOB, mitral valve regurgitation, and sx hypoxemia, pink frothy sputum indicate L. ventricular failure….prioroity
B. Cor pulmonale
C. Myocardial infarction
D. Pulmonary embolus
3. Which action will you take next?
A. Call the physician about client’s condition.
B. Place client on a non-rebreather mask with FiO2 at 95%. (in this case, priority is still oxygenation, give morphine and call physician still appropriate…)
C. Assist client to cough and deep breathe.
D. Administer ordered morphine sulfate 2mg IV.

67. Case Study questions #4, 5
4. What additional assessment data are most important to obtain at this time?
A. Skin color and capillary refill
B. Orientation and pupil reaction to light
C. Heart sounds and PMI
D. Blood pressure and apical pulse
5. B/P is 98/52, apical is 116, irregular at with frequent multifocal PVC’s. Physician is called and these orders received. Which one should be done first?
A. Obtain serum dig level
B. Give furosemide 100mg. IV
C. Check blood potassium level
D. Insert #16 french foley catheter

68. Case Study questions #4, 5
4. What additional assessment data are most important to obtain at this time?
A. Skin color and capillary refill
B. Orientation and pupil reaction to light
C. Heart sounds and PMI
D. Blood pressure and apical pulse (Need VS to know changes in CO)
5. B/P is 98/52, apical is 116, irregular at with frequent multifocal PVC’s. Physician is called and these orders received. Which one should be done first?
A. Obtain serum dig level
B. Give furosemide 100mg. IV
C. Check blood potassium level (Must know serum K level, low level might be cause of PVC, know prior to Lasix)
D. Insert #16 french foley catheter

69. Question #6, 7, 8 6. Which order could be assigned to an LVN?
A. Obtain serum digoxin level
G. Give furosemide 100mg. IV
C Check blood potassium level
D. Insert #16 french foley catheter
7. While waiting for potassium level, you give morphine sulfate IV to the patient. A new graduate asks why you are giving the morphine. What is the best response? It will:
A. prevent chest pain.
B. decrease respiratory rate.
C. make her comfortable if intubation required.
D. decrease venous return to heart
8. Her K is 3.1; physician orders KCL 20meq. IV. How this be given?
A. Utilize a syringe pump to infuse KCL over 10 minutes.
B. Dilute KCL in 100 ml of D5W and infuse over 1 hour.
C. Use a 5ml syringe and push KCL over at least 5 minutes.
D. Add KCL to 1 liter of D5W and give over 8 hours.

70. Question #6, 7, 8 6. Which order could be assigned to an LVN?
A. Obtain serum digoxin level
G. Give furosemide 100mg. IV
C Check blood potassium level
D. Insert #16 french foley catheter (All LVNs trained to insert Foleys)
7. While waiting for potassium level, you give morphine sulfate IV to the patient. A new graduate asks why you are giving the morphine. What is the best response? It will:
A. prevent chest pain.
B. decrease respiratory rate.
C. make her comfortable if intubation required.
D. decrease venous return to heart (Morphine dec. venous return, dec. ventricular preload)
8. Her K is 3.1; physician orders KCL 20meq. IV. How this be given?
A. Utilize a syringe pump to infuse KCL over 10 minutes.
B. Dilute KCL in 100 ml of D5W and infuse over 1 hour.(only safe way, too fast, > cardiac arrest; too slow may not correct problem rapidly enough)
C. Use a 5ml syringe and push KCL over at least 5 minutes.
D. Add KCL to 1 liter of D5W and give over 8 hours.

71. Questions #9, 10, 11
9. After infusing KCL, you give Lasix. Which of nursing action will be most useful in evaluating if lasix is having desired effect?
A. Obtain the client’s daily weight
B. Measure the hourly urine output
C. Monitor blood pressure
D. Assess the lung sounds
10. The physician orders a natrecor 100mcg IV bolus and an infusion of 0.5 mcg/ min. Which assessment data is most important to monitor during the infusion?
A. Lung sounds
B. Heart rate
C. Blood pressure
D. Peripheral edema
11. Which nurse should be assigned care for this client?
A. Float RN who worked on CCU stepdown for 9 years and floated before to CCU
B. RN from staffing agency, 5 years CCU experience and orienting to CCU today
C. CCU RN, already assigned to a newly admitted client with chest trauma
D. New graduate RN who needs experience in caring for client with left ventricular failure.

72. Questions #9, 10, 11
9. After infusing KCL, you give Lasix. Which of nursing action will be most useful in evaluating if lasix is having desired effect?
A. Obtain the client’s daily weight
B. Measure the hourly urine output
C. Monitor blood pressure
D. Assess the lung sounds (Major problem-pulmonary edema, lung sounds most important)
10. The physician orders a natrecor 100mcg IV bolus and an infusion of 0.5 mcg/ min. Which assessment data is most important to monitor during the infusion?
A. Lung sounds
B. Heart rate
C. Blood pressure (natrecor causes vasodilation, diuresis, ck for hypotension)
D. Peripheral edema
11. Which nurse should be assigned care for this client?
A. Float RN who worked on CCU stepdown for 9 years and floated before to CCU (had experience with this type patient & on unit)
B. RN from staffing agency, 5 years CCU experience and orienting to CCU today
C. CCU RN, already assigned to a newly admitted client with chest trauma
D. New graduate RN who needs experience in caring for client with left ventricular failure.

73. Question #12, 13
12.Which information would be important to report to the physician?
A. Crackles and oxygen saturation
B. Atrial fibrillation and fuzzy vision
C. Apical murmur and pulse rate
D. Peripheral edema and weight
13. All meds are scheduled for 9 AM. Which would you hold until you discuss it with the physician?
A. Furosemide 40mg po bid
B. Ecotrin 81mg po daily
C. KCL 10meq three times a day
D. Captopril 6.25mg po three times a day
E. Lanoxin .125mg po every other day

74. Question #12, 13
12.Which information would be important to report to the physician?
A. Crackles and oxygen saturation
B. Atrial fibrillation and fuzzy vision (dysrhythmias, visual disturbances, common side effects of digoxin toxicity)
C. Apical murmur and pulse rate
D. Peripheral edema and weight
13. All meds are scheduled for 9 AM. Which ones would you hold until you discuss it with the physician?
A. Furosemide 40mg po bid
B. Ecotrin 81mg po daily
C. KCL 10meq three times a day
D. Captopril 6.25mg po three times a day
E. Lanoxin .125mg po every other day
**Hold Furosemide and Lanoxin- low potassium potentiates dig toxicity

75. Abdominal Aortic Aneurysm
Click Here for an excellent lecture on AAA- Abdominal Aortic Aneurysms!! (You Tube)
Quickly tells you all the essentials!

76. Aortic Aneurysms
Aortic Aneurysm – go to page 5
Aneurysms (video)

78. Aneurysms = Time Bombs
Outpouchings or dilations of arterial wall
May involve aortid arch, thoracic aorta and/or abdominal aorta
*1/2 all aneurysms larger than 6 cm rupture within one year.
*Thrombi form on dilated arterial wall lead to emboli
Male and smoking great risk factor,

79. Classifications Aneurysms True- Fusiform, Saccular
False- (a pseudoaneurysm)- have disruption all layers arterial wall, from trauma, etc.
C.Aortic dissection; D. “False” aneurysm

80. Saccular- true aneursym, pouchlike, narrow neck connecting buldge to one side of arterial wall
Fusiform- most are fusiform; 98% are below renal artery, circumferential, relatively unifrom in shape

81. Thoracic Aortic Aneurysm
Frequently asymptomatic
May have substernal, neck or back pain
Coughing, due to pressure placed on the windpipe (trachea)
Hoarseness
Dysphagia
Swelling (edema) in neck or arms
Myocardial infarction, or stroke due to dissection or rupture involving branches of the aorta

82. Abdominal Aortic Aneursysm
Pain intensity correlates to size and severity
Pulsating mass in mid and upper abdomen; bruit over the mass
May have thrombi
Can rupture causing shock and death in 50% of rupture cases
Mimic pain associated with abdominal or back disorders
“Blue toe syndrome” due to emboli
Complications-Rupture!
Anterior
Posterior (better chance for survival)
When a weak area of the abdominal aorta expands or bulges, it is called an abdominal aortic aneurysm (AAA). The pressure from blood flowing through your abdominal aorta can cause a weakened part of the aorta to bulge, much like a balloon. A normal aorta is about 1 inch (or about 2 centimeters) in diameter. However, an AAA can stretch the aorta beyond its safety margin as it expands. Aneurysms are a health risk because they can burst or rupture. A ruptured aneurysm can cause severe internal bleeding, which can lead to shock or even death.
Less commonly, AAA can cause another serious health problem called embolization. Clots or debris can form inside the aneurysm and travel to blood vessels leading to other organs in your body. If one of these blood vessels becomes blocked, it can cause severe pain or even more serious problems, such as limb loss.
Each year, physicians diagnose approximately 200,000 people in the United States with AAA. Of those 200,000, nearly 15,000 may have AAA threatening enough to cause death from its rupture if not treated.

83. Aortic Dissection - blood invades or dissects the layers of the vessel wall (not really an aneurysm)
Dissecting aneurysms-unique and life threatening. A break or tear in tunica intima and media allows blood to invade or dissect layers of vessel wall. Blood is usually contained by adventitia, forming a saccular or longitudinal aneurysm.
Aortic dissection occurs when blood enters the wall of aorta, separating its layers, and creating a blood filled cavity

84. Life threatening emergency
Aortic dissection
Life threatening emergency
Intima tears, causes hemorrhage into media
Hypertension- main cause
With contraction of heart, inc. pressure, further damage
Cause uncertain- hypertension- *primary, Marfan’s syndrome, blunt trauma, inc age symptom- excruciating pain-tearing, ripping sensation
90% mortality if untreated

85. *Symptoms depend upon location

86. Collaborative Care Goal-*identify and prevent rupture Diagnostic Tests
Most dx on routine work-up
If identified, tests specific to determine size, location
CXR, CT or MRI, Abd ultrasound, TEE, ECHO, angiography, Abd. Ultrasound
EKG
Recognize “Terrible Triad” impending rupture
Pulsating hematoma, back pain, hypotension

87. Collaborative Care-Medications
Anti-hypertensives
Beta blockers,
Vasodilators
Calcium channel blockers
Nipride
*Avoid direct arterial vasodilators (as hydralazine)
Sedatives
Niacin, mevocor, statins
Post-op anti-coagulants

88. Collaborative Care/Surgery, Other Options
Usually repaired if >5cm
Open procedure- abd incision, cross clamp aorta,aneuysm opened and plaque removed, then graft sutured in place
Pre-op assess all peripheral pulses
Post-op-check urine output and peripheral pulses hourly for 24 hours- (when to call Dr.)
Endovascular stents- placed through femoral artery

89. Surgical repair of an abdominal aortic aneurysm
Surgical repair of an abdominal aortic aneurysm. A, Incising the aneurysmal sac. B, Insertion of synthetic graft. C, Suturing native aortic wall over synthetic graft.

90. Bifurcated (two branched) endovascular stent grafting of an aneurysm
Bifurcated (two branched) endovascular stent grafting of an aneurysm. A, Insertion of a woven polyester tube (graft) covered by a tubular metal web (stent). B, Stent graft is inserted through large blood vessel (e.g., femoral artery) using a delivery catheter. Catheter is positioned below renal arteries in area of aneurysm. C, Stent graft is slowly released (deployed) into blood vessel. When stent comes in contact with blood vessel, it expands to preset size. D, A second stent graft can be inserted in contralateral (opposite) vessel if necessary. E, Fully deployed bifurcated stent graft

91. Aneurysm repair
Live Search Videos: aneurysm

92. Live Search Videos: aortic aneurysm-percutaneous approach to abdominal aneurysm repair

93. Nursing Diagnoses Risk for Ineffective Tissue Perfusion
Risk for Injury
Anxiety
Pain
Knowledge Deficit

94. Prevention
Ultrasound-extremely effective at detecting AAAs. U.S. Preventive Services Task Force (USPSTF) recommends-anyone aged 65 to 75 who has ever smoked undergo a one-time ultrasound screening for AAA
2.Prevent atherosclerosis
3.Treat and control hypertension
4.Diet- low cholesterol, low sodium and no stimulants
5.Careful follow-up if less than 5cm-can grow 0.5cm/yr

95. Rupture- signs of ecchymosis
Key Complications
Rupture- signs of ecchymosis
Back pain
Hypotension
Pulsating mass
Live Search Videos: aortic aneurysm (See rupture)
Thrombi
Renal Failure

96. Priority Question # 1, #2
1. During initial post-operative assessment of a patient who has just transferred to post-anesthesia care unit after repair of an abdominal aortic aneurysm all of these data are obtained. Which has most immediate implications for client’s care?
A. Arterial line indicates a blood pressure of 190/112.
B. Monitor shows sinus rhythm with frequent PAC’s.
C. Client does not respond to verbal stimulation.
D. Client’s urine output is 100ml of amber urine.
2. It is the manager of a cardiac surgery unit’s job to develop a standardized care plan for post-operative care of client having cardiac surgery. Which of these nursing activities included in care plan must be done by an RN?
A. Remove chest and leg dressings on the second post-operative day and clean the incisions with antibacterial swabs.
B. Reinforce patient and family teaching about the need to deep breathe and cough at least every 2 hours while awake.
C. Develop individual plan for discharge teaching based on discharge medications and needed lifestyle changes.
D. Administer oral analgesic medications as needed prior to assisting patient out of bed on first post-operative day.

97. Priority Question # 1, #2
1. During initial post-operative assessment of a patient who has just transferred to post-anesthesia care unit after repair of an abdominal aortic aneurysm all of these data are obtained. Which has most immediate implications for client’s care?
A. Arterial line indicates a blood pressure of 190/112. (HIGH RISK OF RUPTURE)
B. Monitor shows sinus rhythm with frequent PAC’s.
C. Client does not respond to verbal stimulation.
D. Client’s urine output is 100ml of amber urine.
2. It is the manager of a cardiac surgery unit’s job to develop a standardized care plan for post-operative care of client having cardiac surgery. Which of these nursing activities included in care plan must be done by an RN?
A. Remove chest and leg dressings on the second post-operative day and clean the incisions with antibacterial swabs.
B. Reinforce patient and family teaching about the need to deep breathe and cough at least every 2 hours while awake.
C. Develop individual plan for discharge teaching based on discharge medications and needed lifestyle changes. (RN develops individual teaching plan)
D. Administer oral analgesic medications as needed prior to assisting patient out of bed on first post-operative day.

98. Case study from Hospital

105. OPEN HEART SURGERY

107. Diagnostic Tests EKG exercise stress test CXR cardiac cath-
echocardiogram
thallium scan

108. PRE-OP TEACHING

109. Open Heart Surgery Open Heart Surgery-What to Expect!

110. Intra-op Events hypotension cardioplegia cross clamping aorta
cardiopulmonary bypass
heparinized

111. CP Bypass

112. Heart Lung Machine (video)

113. Post-op Appearance
mechanical ventilator-SIMV mode
hemodynamic monitoring- dec. CO
cardiac monitoring-SVT and Afib common
mediastinal tube-100cc first hour to 500/24
multiple IV sites and lines
pacer wires
foley-hourly output

114. Assessment vital signs PAP PCWP CO urine output bleeding
fluid balance and neuro

115. Complications decreased cardiac output cardiac tamponade hypokalemia
Hemorrhage-replace cc for cc first hr. then 55/24 hours
neuro changes
resp insufficiency
infection and pain-demoral, splint incision. Offer pain med: percoset or vicodin q 4hr.

116. Cardiac tamponade
Paradoxical pulse is a pulse that markedly decreases in amplitude during inspiration. On inspiration, more blood is pooled in the lungs and so decreases the return to the left side of the heart; this affects the consequent stroke volume.

117. Cardiac tamponade (influenced by volume and rate of accumulation)
Beck triad (jugular venous distention, hypotension, and muffled heart sounds)
Pulsus paradoxus is measured by careful auscultation with a blood pressure cuff. The first sphygmomanometer reading is recorded at the point when beats are audible during expiration and disappear with inspiration. The second reading is taken when each beat is audible during the respiratory cycle. A difference of more than 10 mm Hg defines pulsus paradoxus.
Cyanosis
No drainage from mediastinal tube

118. Decreased Cardiac Output
decreased preload-need fluid
inc. afterload- need to dec. B/P (Nipride)
dec. contractility- need dobutamine
Arrhythmias- SVT and Afib common

119. Post-op Care Goals
Promote CV function, tissue perfusion and stablization of VS

120. cont.
Promote respiratory function and sufficient oxygenation by promoting chest drainage and use of IS

121. Goals Promote fluid and electrolyte balance Promote renal function
Promote rest, comfort, and relief of pain
Promote neurological function
Promote psych adjustment
Promote early movement and ambulation