Cardiac Med Surg

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  1. What are some normal age related changes in the heart?
    • left ventricular wall thickening
    • stenosis of valves
    • decreased HR (increased vasovagal tone)
    • Rigid myocardium and decreased flexibility
    • Decreased baroceptor receptivity
    • Increased recovery time
  2. What are some risk factors for heart disease?
    • Age (older)
    • Gender (male)
    • Lifestyle
    • Smoking
    • HTN
    • Hypercholeseremia
    • Family history
  3. Describe aspects of the nursing assessment important for cardiac problems
    • Patient H/P
    • Nutritional History
    • Family History and genetic risk
    • Current health problems: pain or discomfort, dyspnea, DOE, orthopnea, syncope, fatigue, palpitations, edema or extremity pain
  4. What is the BNP?
    • Brain Nitrauretic Peptide: this is labroatory test. An increased BNP is the brain trying to tell the heart (left ventricle) to pump more blood for more oxygen
    • Normal BNO is equal to or less than 100
    • CHF is indicated by BNP of equal to or greater than 300
  5. What would be a reason for increased preload? Increased afterload?
    • Increased Preload: hypervolemia
    • Increased Afterload: pharmacological
  6. What would be a reason for decreased preload? decreased afterload?
    • Decreased Preload: Hypovolemia
    • Decreased Afterload: aortic compliance, blood viscosity, valvular disease
  7. What is systlolic Heart failure?
    • The heart cannot contract strong enough due to weakening of the muscle, such as by an MI
    • EF is less than 40%
    • Preload is increased and pulmonary vascular restriction increases leading to congestion
  8. What is diastolic heart failure?
    • Inadequate Left Ventricular relaxation that leads to a decreased CO
    • As systemic vascular restriction is increased, ventricular compliance decreases and the Left Ventricular wall thickens
    • It is caused almost exclusively by HTN (20-40% of all cases, more common in women)
    • THE EF IS PRESERVED and is equal to or > 40%
  9. What causes right sided heart failure?
    • Number one cause is left sided HF
    • Right Ventricular MI
    • Pulmonary HTN
    • Cor Pulmonale
    • Tricuspid Regurg
  10. What are S/S of Left sided HF?
    • Inadequate tissue perfusion
    • Pulmonary and systemic congestion
    • Image Upload
  11. What are the S/S of right sided HF?
    • Pulmonary and systemic edema
    • Image Upload
  12. What is high output heart failure?
    often seen in sepsis, anemia and is many times a secondary response to a systemic problem
  13. Describe the S/S of and increased afterload
    • Increased:Arterial vasoconstriction
    • cool, clammy skin
    • cap refill >5 sex
    • Narrow pulse pressure
  14. Describe the s/s of a decreased afterload
    • Decreased: Atrial Dilation
    • warm, flushed skin
    • bounding pulses
    • widening pulse pressure
    • hypotension
  15. What is the Frank Sterling law?
    Increased preload= increased CO

    like a rubber band, the further you stretch it the harder it snaps

    In HF, the rubber band has stretched so far it no longer snaps back. (Sterling Law has failed in HF)
  16. What will enhance preload? What will reduce preload?
    • Enhance: fluids, exercise
    • Reduce: nitrates, diuretics
  17. What will enhance afterload? What will reduce afterload?
    • Enhance: exercise, vasoconstrictors
    • Reduce: Vasodilators
  18. What are the s/s of preload maladaptation?
    • tachycardia
    • weak pulses
    • decreases UO
    • dry mucus membranes
    • poor skin turgor

    • Thirst
    • distended neck veins
    • crackles in lungs
    • bounding pulses
  19. What are the s/s of decreased preload?
    • -May be caused by hypovolemia/dehydration
    • -SNS stimulation relseases catecholamine, epinephrine & norepinephrine for compensatory tachycardia
    • -Vasoconstriction occurs to maintain BP
  20. What is the best indicator of fluid balance?

    2.2 lb= 1 kg = 1L of fluid
  21. What are interventions for left sided HF?
    Image Upload
  22. What are interventions for right sided HF?
    Diuretics and ACE inhib, SCDs, I/O & weights, low sodium diet, activity if tolerated, turn to prevent ulcers.
  23. How do baroceptors and peripheral chemoreceptors effect BP differently?
    • Baroceptors in the aortic arch detect HTN and send messages to decrease BP
    • Peripheral chemoceptors in the corotids respond to hypoxia and will increase BP
  24. Describe the difference in prescribing beta blockers, ACE inhib and CC blockers in cardiac problems
    • Beta Blocker: an antiarrythmic used in MI
    • ACE Inhib: prevents cardiac remodeling from the renin-angiotensin system. Used for HF and MI
    • Calcium Channel Blocker: Used to control stable angina. Promotes vasodilation and myocardial perfision
  25. Describe the three types of angina
    • Stable angina (exertional angina): occurs with either emotional or physical stress. Controlled by rest and nitroglycerin
    • Unstable Angina (preinfarction angina): stable angina that increases in intensity over time
    • Variant Angina (Prinzmetals angina): occurs as a result of coronary artery spasm, often during rest
  26. What differentiates angina from an AMI?
    • The pain lasts for more than 15 min and is unrelieved by nitroglycerin or aspirin
    • Both with show changes in the ST segment, but only angina will show myoglobin, CKMB and triponin in labs
  27. Medication information for digoxin
    • increases contractility while reducing HR
    • Slows conduction through the AV
    • node
    • inhibits the sympathetic nervous system (fight or flight response)
    • may hide symptoms of hypoglycemia
    • do not give if HR is less than 60 bpm
    • It is absorbed thru the stomach and antacids will decrease absorption
    • Therapeutic range is 0.5-2 mg/mL
    • Antidote is digibind
  28. What is the time of a small block on a rhythm strip? Big block? How many big blocks in a second?
    • Each small block is .04 sec or 1 mm
    • Each large block is .2 sec or 5mm
    • It takes 5 big blocks to make up 1 sec
  29. What is the normal length of a P wave?
    2.5 mm or 0.1 sec
  30. What is the normal length of the PR segment?
    3-5 mm or 0.12 -0.2 sec
  31. What is the normal length of the Q wave?
    .75-1 mm or .04 sec
  32. What is the pathologic Q?
    Absence of activity due to scar tissue from MI.  Leads to a large R wave
  33. What is the normal length of the QRS complex?
    less than 3 mm or 0.12 sec
  34. What is the normal length of the ST segment?
    1-2 mm or 0.04-0.08 sec
  35. What is the normal length of the T wave?
    2 mm or .08 sec
  36. What are the ESR and C reactive protein indicative of?
    The inflammatory response
  37. What is infective endocarditis?
    • microbial infection of the endocarditis
    • High risks include IV drug users, valve repacements, systemic infections, structural cardiac defects
    • Ports of entry include oral cavities, skin rash, lesions, infection, surgery
  38. What are the s/s of infective endocarditis?
    • Murmurs
    • HF
    • arterial embolism
    • splenic infarction
    • neurologic changes
    • petechiae
    • Splinter hemorrages (in finger nail beds)
  39. What are the interventions and treatments of endocarditis?
    • treated with antimicrobials, adequate nutrition and rest
    • Monitor I/O and weight, HOB elevated and keep airway patent
    • Removal of the infected valve or repair/removal of stents
    • Repair of damaged valves and chordae tendinae
    • Draining the abscesses in heart or elsewhere
  40. What is pericarditis?
    • Inflammation of the pericardium
    • Dressler's syndrome (from heart injury)
    • Postpericardiotomy syndrome (post surgery)
    • Chronic constructive pericarditis (Results in thickening of the pericardium)
  41. What are the s/s of pericarditis?
    • substernal, pericordial pain radiating to shoulder
    • Grating paid aggravated by breathing or coughing
    • Pain worsened in supine position
    • Pericardial friction rub sounds
  42. What are the interventions and treatments of pericarditis?
    • Pain management
    • NSAIDS
    • Antibiotics
    • Pericardectomy
  43. What is rheumatic carditis?
    • Inflammation of all layers of the heart after an upper respiratory tract infection with group 1 beta-hemolytic streptococci
    • Formation of aschoff bodies lead to scarring of the heart tissue
    • Leads to impaired contraction, thickening of the pericardium and valvular damage
  44. What are the s/s of rheumatic carditis?
    • Tachycardia
    • Cardiomegaly
    • New or changed murmur
    • Pericardial friction rub
    • Precordial pain
    • Changes in ECG
    • HF
    • Existing strep infection
  45. What are the interventions and treatments for rheumatic carditis?
    • Treat infection
    • Manage symptoms
    • Treat valvular damage
  46. What is pericardial effusion?
    • Fluid in the pericardial sac.
    • Puts the patient at risk for cardiac tamponade
    • Listen for pericardial friction rub
  47. What are the interventions and treatments of pericardial effusion?
    • Pericardiocentesis to remove fluid
    • Cutting a window in the pericardial sac to relieve fluid and pressure
  48. What is cardiac tamponade?
    • This is a life threatening condition
    • S/S include JVD, paradoxical pulses,
    • decreased CO, muffled heart sounds, circulatory collapse
  49. What are the interventions and treatments for cardiac tamponade?
    • Hemodynamic monitoring
    • Pericardiocentesis
    • Pericardial window
    • Pericardectomy
  50. What is cardiomyopathy?
    • Subacute or chronic disease of cardiac muscle
    • Dilated: thinning of the heart muscle to allow more blood in chamber. weakens muscle
    • Hypertrophic: enlargement of the heart tissue that leads to stiffening.
    • Restrictive: Enlargement of the heart tissue without stiffening. There is limited space in the chamber.
  51. What are the interventions and treatments for cardiomyopathy?
    • Drug therapy (diuretics, vasodilating agents, cardiac glycosides)
    • Implantavle cardiac defibrillations
    • Avoid toxin exposure
    • Alcohol cessation
    • Heart transplant
    • Percutaneous alcohol septal ablation
    • Ventriculomyomectomy
  52. How are blood cultures taken?
    • They are taken from 2 different vascular sites prior to beginning antibiotics
    • The samples should be taken 15-30 min apart, as per protocol
    • One aerobic tube and one anaerobic tube
    • Do not take sample from an access line
  53. What is mitral stenosis (diastolic)?
    • A thickening or calcification of the mitral valve, usually from rheumatic carditis
    • Can be caused by tumors, calcium or thrombus
    • It narrows the opening and prevents normal blood flow from the LA to LV during diastole
    • LA pressure increases, left atrium dilates, PAP increases, and the RV hypertrophies
    • Pulmonary congestion and right sided HF occurs
  54. What are the s/s of mitral stenosis?
    • May be asymptomatic
    • Dyspnea, orthopneas, dry cough, hemoptysis, pulmonary edema
    • Murmur heart at apical during diastole
    • Right sided HF symptoms as it worsens
  55. What is mitral regurg (systolic)?
    • During systole, the mitral valve does not close all the way, allowing a backflow
    • This backflow goes back into the LV during diastole, leading to an increased volume
    • May be caused by rheumatic heart disease, papillary muscle rupture or rupture of the cordae tendinae
    • May have afib and signs of LV failure, may also lead to RSHF as cor pulmonale
  56. What is mitral valve prolapse?
    • More common in women, may be congenital defect
    • Valvular leaflets enlarge and prolapse into LA during systole
    • Creates a click between S1 and S2
    • Most cases are asymptomatic, but patient may express chest pain and DOE as well as dissiness or syncope
  57. What is aortic stenosis (systolic)?
    • Atherosclerosis and calcification of the aortic valve (often in the elderly). Occurs during systole.
    • may be caused by rheumatic fever, congenial or trauma, endocarditis
    • It is the most common valvular disease from wear and tear.
    • Results in LV hypertrophy, increaed O2 demands
    • Causes right sided HF by pulmonary edema and afib
  58. What are the s/s of aortic stenosis?
    • Early: dyspnea, angina, syncope
    • Late: marked fatigue, debilitation and peripheral cyanosis, crescendo murmur is heart
  59. What is aortic regurg (diastolic)?
    • Aortic leaflets to do not close during diastole, causing regurg from the aorta in the LV
    • The ventricle hypertrophies to accommodate increasing fluids volume
    • Caused by infective endocarditis, hypertension, congenital, marfans
    • May remain asymptomatic for years
    • S/S include dyspnea, orthopnea, palpitations and angina, increased systolic HTN and bounding pulses
  60. What are the s/s of valve dysfunction?
    • fatigue
    • weakness
    • general malaise
    • DOE
    • dizziness and syncope
    • chest pain or discomfort
    • weight gain
    • prior history of rheumatic heart disease
  61. What is the significance of cardiac murmurs?
    • Often the first sign of underlying valvular disease
    • Systolic murmurs may be do to physiological increases in blood viscosity or might indicate asymptomatic cardiac disease
    • Diastolic murmurs are almost always pathological and need the attention of a cardiologist
  62. What constitutes Acute Coronary Syndromes (ACS)?
    • Unstable Angina
    • Acute Myocardial infarction
  63. What is Sequelae?
    • Rupture of atherosclerotic plaque which leads to platelet aggregation
    •  and a thrombus
    • Vasocontriction occurs, blocking blood flow and oxygen
    • 40% plaque accumulation will block blood flow
  64. How are AMIs classified?
    • ST elevation (STEMI): is a traditional presentation
    • Non-ST elevation (NSTEMI): is common in women
    • Unstable Angina: most commonly used terminology
  65. What are the zones of an MI?
    • Transmural MI involves all 3 layers of the heart
    • The subendocardial muscle layer has the longest myobrils, the greatest 02 demand and the poorest blood supply
    • The three layers are: ischemia, injury, necrotic tissue
    • Image Upload
  66. What changes in the body does an MI cause over time?
    • Hypoxia from ischemia leads to vasodilation and acidosis
    • Potassium, Calcium & Magnesium imbalances cause further changes in conduction and contration
    • Catecholamines (Epi/norepi) lead to increased HR, contractility and afterload causeing ventricular dysrhythmias
  67. How does the ECG change over time after an AMI?
    • Within Minutes: The T wave peaks
    • Minutes to hours: ST elevation
    • Days: Q wave formation and loss of R wave. T wave may invert
    • Weeks to Months: T wave will normalize, but pathologic q wave may persist
    • Image Upload
  68. What are the acute treatments for AMI?
    • Get IV access and give morphine for pain
    • Oxygen
    • Nitroglycerin
    • Antiplatelet or Aspirin (have them chew the aspirin 325mg)
    • Put into semi fowlers position
    • Image Upload
  69. What medications are used in long term therapy for AMI?
    • Glycoprotein inhibitors: prevent fibrinogen from attaching to platelets at thrombus
    • Abciximad (ReoPro)
    • Eptifibatide (Integrillin)
    • Tirofiban (Aggrastat)
    • Beta Blockers: taken daily, decrease size of infarct by prolonging diastole and increasing perfusion
    • Metoprolol XL (Toprol XL)
    • Carvedilol CR (Coreg CR)
    • ACE inhib: prevent ventricular remodeling
    • Fibrinolytics: for reperfusion
    • t-PA
    • Alteplase (Activase)
    • reteplase (Retevase)
    • Tenecteplase (TNK)
  70. What is the definition of shock?
    When oxygenation and tissue perfusion needs are not met and cell function cannot be maintained
  71. What are the different types of shock?
    • Hypovolemic: too little blood, decreased O2 and decreased MAP
    • Cardiogenic: heart muscle pumping is impaired and O2 decreased. Stage IV HF.
    • Distributive: third spacing shock, not enough fluids to oxygenate cells
    • Obstructive Shock: HF caused by an obstruction.
    • Septic Shock: Whole body inflammation
  72. What are the stages of shock?
    • Initial Stage (Early Stage): MAP is decreased by 10 mm Hg.  The body is compensating well and symptoms are limited.
    • Nonprogressive stage (Compensatory Stage):MAP continures to decrease 10-15mm Hg. The body begins to try and compensate by vasoconstrition to divert the blood to the essential organs.  Hypoxemia occurs of these nonessential cells.  The kidneys hold onto water to increase BP.  Acidosis and hyperkalemia occur.
    • Progressive Stage (Intermediate stage): MAP decreases beyong 20 mm Hg.  The body is no longer to oxygenate even essential organs.  This is a life threatening emergency and progresses quickly.  Vitals and s/s will worsen drastically.  Needs to be reversed within an hour
    • Refractory Stage (Irreversible stage): Cell death is drastic due to hypoxemia, even of the major organs.  Multiple organ failure occurs. Interventions do not slow progression towards death.
  73. What is the treatment for shock?
    • Oxygenation
    • IV therapy: crystalloids maintain fluid and electrolyte imbalances (NSS, LR)
    • Colloids restore osmotic pressure and fluid volume (blood and blood products)
    • Drug therapy is no response to fluid replacement
  74. What is the drug therapy for shock?
    • Vasoconstrictors: stimulate venous return by blood vessel constriction.  
    • Dopamine (Intropin, Revimine)
    • Norepinephrine (Levophed)
    • Inotropic agents: stimulate adrenergic receptors in the heart to improve muscle contraction
    • Docunatmine (Dobutrex)
    • Milrinone (Primacor)
    • Myocardial Dilators: sodium 
    • Nitroprusside (Nitropress, Nipride)
  75. What is the CABG surgery?
    • It is the most common type of cardiac surgery and the most common procedure for the older adult
    • Occluded coronary artery is bypassed by venous (from leg) or arterial (often mammary (IMA) which remains paten 90% of the time for 12 yrs) blood vessels for by synthetic grafts
Card Set:
Cardiac Med Surg
2014-03-24 00:18:36
LCCC Nursing Cardiac Medsurg

For Exam 2
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