Cardio- Part 2

  1. Angina Pectoris
    • *Constricting, squeezing or suffocating sensation
    • *Precordial or substernal pain or pressure
    • *May radiate to left shoulder, jaw, arm, or other chest areas

    Duration = Less Than 5 Minutes (STABLE)
  2. Stable Angina
    • *Pain when heart's oxygen demands increases
    • *Transient myocardial ishemia
    • *Fixed coronary obstruction
  3. Variant Angina
    Pain due to vasospasm of coronary arteries
  4. Silent Myocardial Ischemia
    Myocardial ischemia without pain

    *Often times diabetics
  5. ACS (Acute Coronary Syndrome)
    • *Unstable angina
    •    -symptoms at rest (minimal exertion) > 20 min.
    •    -new onset, severe angina, less than 1 month
    •    -worsened pattern of angina
    • *Non-ST Elevation Myocardial Infarction (non-stemi)
    • *ST Elevation Myocardial Infarction (STEMI) - all of the layers of myocardium are being effected
  6. ECG Change -- T Wave Inversion
  7. ECG Changes -- ST segment
    • INJURY
    •    *ST depression = subendocardial injury
    •    * ST elevation = Transmural injury
  8. ECG changes -- Abnormal Q Waves
    Transmural Infarct
  9. Serum Cardiac Markers -- Myoglobin
    • Time of Elevation = Within 1 Hour
    • Time of Peak = 4-8hrs
  10. CK-MB serum markers (Creatine, Kinase, MB)
    • Time of Elevation = 4-8 Hours
    • Time of Peak = 24-36hrs
    • Return to Baseline = 2-3 days
  11. Troponin Serum Markers (either "I" or "T")
    Time of Elevation= Within 3 hours

    Return to Baseline = 7-10 days
  12. Ischemic death of myocardial tissue
    Myocardial Infarction
  13. Type of Myocardial Infarctions
    • Sybendocardial (affects inner 1/3 to 1/2 of wall)
    • Trasnmural (affects all 3 layers of the heart wall)
  14. Pathologic process of a Myocardial Infarction
    • *Anaerobic metabolism, reversible injury, necrosis, scar tissue
    • *"Stunned Myocardium"
  15. An Acute MI (AMI) Leaves behind ______
    Yellow area
  16. AMI Chest Pain characteristics
    Severe, crushing, constrictive, OR like Heartburn
  17. Sympathetic Nervous System Responses of AMI
    GI distress, nausea, vomiting, tachycardia, vasoconstriction, anxiety, restelessness, feeling of impending doom
  18. Skin pale, cool, diaphoretic, weakness in arms and legs
    Hyportension and Shock
  19. How/When do women report AMI
    Atypical, Elderly, Shortness of Breath, Fatigued, GI symptoms
  20. Complications of MI
    • Sudden Death
    • Heart Failure
    • Cardiogenic Shock
    • Pericarditis
    • Dressler's syndrome
    • Thromboemboli
    • Cardiac Rupture
    • Ventricular Aneurysm
  21. Inflammation of the pericardium causes:
    • Pain 
    •    -abrupt, sharp, precordial
    •    -worse with deep breathing or swallowing
    •    -better with sitting up and leaning forward
    • Exudate (if an infectious process...)
    •   -Serous --> pericardial effusion
    •        *Cardiac tamponade = rapid accumulation of exudate that compresses the heart
    •   -Fibrous --> friction rub; adhesions
    • ECG changes
    • Fever, Malaise, Dyspnea, Leukocytosis
  22. Fluid level in the Pericardial sac:
    30-55 ml of fluid
  23. Pericarditis may restrict heart's movement due to....
    Serous exudate filling the pericardial cavity (pericardial effusion)

    Fibrous scar tissue making the pericardium stick to the heart (constrictive pericarditis)
  24. Causes of Pericarditis
    Infection, Trauma, Immune/Collagen or Metabolic Disorders, Ischemia, Post-Open Heart Surgery, Radiation
  25. Consequences of Pericardial Effusion
    Fluid in the pericardial cavity ---> Restricts heart expansion ---> Left ventricle cannot accept enough blood ---> decreased cardiac output ---> decreased blood pressure and shock


    Fluid in pericardial cavity ---> Restricts Heart Expansion ---> Right Ventricle cannot accept enough blood ---> Increased venous pressure; jugular distension
  26. Abnormal Pulsus Paradoxus
    On inhaling, the right ventricle fills with extra blood

    Because the heart cannot expand fully when the right ventricle is overfilled, the left ventricle is compressed and cannot accept much blood

    On the next heartbeat the left ventricle does not send out much blood: systolic BP drops

    Abnormal = 10mmHg or > drop in SBP during inspiration.... ((Cardiac Tamponade))
  27. Disorders affecting the Heart Muscle
    Cardiomyopathy (CMP)
  28. Types of Cardiomyopathy
    Primary or Secondary

    • Genetic -- Hypertrophic
    • Mixed -- Dilated, Restrictive
    • Acquired -- Myocarditis, Peripartum & Takotsubo (stress)
  29. Opathy
  30. Hypertrophic Cardiomyopathy is characterized by....
    Ventricular Hypertrophy with Small LV Chamber Size causing decreased stroke volume due to impaired diastolic filling

    Frequent asymmetric septal hypertrophy causing LV outflow obstruction

    Obstruction worsened by increased contraction or decreased filling
  31. If there is a small chamber and thicker muscle....
    diastolic filler problems occur (thickening of the septum)
  32. Most Common Cause of Death in Young Athletes
    Ventricular Dysrhythmias
  33. Myocyte Hypertrophy w/ Myofibril Disarray
    Affects young adults.

    Manifestations: Gradual Symptoms vs. Sudden Death, Chest Pain, Fatigue, Syncope Worse with Exertion
  34. Progressive Dilation of Chambers and Impaired Pumping of Ventricles (Low EF)
    Dilated Cardiomyopathy
  35. Causes of Dilated Cardiomyopathy
    • Idiopathic-- we don't know 100%
    • Alcoholism
    • Mycoardial Infarct/Ischemia
    • Drugs
  36. Manifestations of Dilated Cardiomyopathy
    • Thrombus/Emboli
    • Stretch on Mitral Valve
    • (low ejection)

    ....sudden death
  37. Restrictive Cardiomyopathy
    • Increased Rigidity of LV restricting Filling
    • Contraction relatively normal
    • Heart Muscle is not as Compliant
  38. Causes of Restrictive Cardiomyopathy

    Endocardial Infiltrations (Amyloidosis, Sarcoidosis), radiation ribrosis, metastatic tumors, genetic
  39. Acute Inflammation of Myocardium and Conduction System without evidence of MI caused by VIRAL (coxsackie group B), AIDS, Bacterial/Fungal infections, hypersensitivity reaction, autoimmune diseases
  40. Manifestations of Myocarditis
    None, Flu-Like Syndrome, HF, Emboli, Can mimic ACS, Sudden Death
  41. Dilated CMP develops in last month of pregnancy to 5 months after delivery
    Peripartum Cardiomyopathy
  42. Risk Factors of Peripartum Cardiomyopathy:
    advanced maternal age, black race, multifetal pregnancies, preeclampsia, tocolytic therapy to prevent premature labor/delivery
  43. Takotsubo CMP
    • *Transient, Reversible LV dysfunction caused by profound psychological or emotional stress
    • *Middle-age women w/ acute STEMI,  but normal coronary arteries
    • *Impaired LV contractility with ballooning of apex and basal hypercontractility
  44. Valve will not open all the way; it is harder to force blood through it-- Murmurs
  45. Valve will not close all the way; it leaks when it should be closed
    Regurgitation (insufficiency)
  46. Steps to Identify Defective Valves:
    *the blood going through the valve makes a noise (heart murmurs)

    • Where they are--which valve are they near?
    • How they sound-- high/low pitched
    • When they happen-- systole or diastole
  47. Systolic Murmur
    Between S1 and S2
  48. Diastole Murmur
    Between S2 and next S1
  49. When will you hear murmurs?
    • If a valve is stenotic, you will hear a murmur of
    • blood shooting through the narrow opening when the valve is
    • open

    • If a valve is regurgitant, you will hear a murmur of
    • blood leaking back through when the valve should
    • be closed
    • (mitral regurgitation)
  50. Types of Mitral Valve Disease
    • Mitral Stenosis
    • Mitral Regurgitation
    • Mitral Valve Prolapse (backward balloon)
  51. Acute, recurrent inflammatory disease that follows throat infection with group A (B-Hemolytic) strep
    Rhematic Fever
  52. What causes Rhematic Heart Disease
    Chronic Valvular Heart Disease
  53. What are the S/S of Rhematic Heart Disease
    Carditis, Polyarthritis, Aschoff  body (nodules), Erythema marginatum, subcutaneous nodules, Sydenham chorea (involuntary movements), Fever
  54. Life Threatening Infection of Endocardium and Heart Valves characterized by microbial colonization leading to friable lesions (vegetations) and tissue destruction
    Infective Endocarditis
  55. Organisms that cause Infective Endocarditis
    Staph. Aureus, Strep. Viridans, Gram neg. & positive bacteria, yeasts, & fungi
  56. 2 Predisposing Factors of Infective Endocarditis
    • Damaged Endocardial Surface
    • Portal of Entry
  57. 3 Classifications of Endocarditis
    • Acute
    • Subacute
    • Chronic
  58. Manifestations of Endocarditis
    • Fever & Chills
    • Change in Murmur
    • Anorexia
    • Malaise
    • Lethargy
    • Petechial And Splinter Hemorrhages (Jane Way)
    • Cough
    • Dyspnea
    • Arthritis
    • Diarrhea
    • Abd./Flank pain
  59. Primary Pace Maker
    • SA Node
    • (impulses travel across the atrium through the AV node to go back to the ventricle)
  60. What must you have for Depolarization/Repolarization to occur?
    Sodium Shifts
  61. Types of Refractory Periods
    • Absolute (no stimulus...longest matter how strong the stimulus is, it will not be able to cause depolarization)
    • Relative (stronger stimulus...can depolarize...where abnormal heart rhythms occur)
    • Supernormal Excitatory Period (weaker stimulus...very short segment)
  62. Records electrical activity of the heart
  63. Points within Electrocardiography
    • P = Atrial Depolarization--Mechanical Event
    • QRS = Atrial repolarizing, Ventricular Depolarization-- Ventricle Muscle Contracts

    T = Ventricular Repolarization (back to resting state)
  64. Early Heart Beats
    Ectopic Beats
  65. Mechanisms of Cardiac Electrical Activity
    • Automaticity -- causes of alteration: injury, hypoxia, electrolyte imbalance, enlargement/hypertrophy of atria or ventricles, exposure to certain chemicals or drugs.....Ectopic Foci: extra focus, start from extra point in heart
    • Excitability -- all can receive the stimulus to cause impulse to take route through heart
    • Conductivity
    • Refractoriness -- go back to resting state
  66. What 4 Major Things lead to a dysrrhythmia?
    • Cells firing erratically
    • Injury to Myocardial Tissue (ischemia)
    • Low Oxygen levels in blood (hypoxia)
    • Electrolyte Imbalances (Potassium, Magnesium, Calcium)
  67. Types of Dysrhythmias
    • Bradicardia -- <60
    • Tachycardia -- > 100
    • Ectopy -- Premature Contractions
    • Fibrillation -- disorganized current flow (quivering, no distinct contraction, blood is stagnant and not effective)
    • Supraventricular -- generate from atria or from AV node
    • ***Ventricular -- no forward cardiac output...bp drops to nothing...death very quickly
    • Heart Block -- Occur in AV node
    •     *1st Degree
    •     *2nd Degree
    •     *3rd Degree
  68. Impaired pumping ability of the heart with inability to maintain sufficient CO (inadequate cardiac output)
    Heart Failure
  69. Causes of Heart Failure
    • Ischemia/MI
    • Hypertension
    • Cardiomyopathy (abnormality in the ehart muscle causing it to get bigger but not function properly)
    • Volume Overload (excessive IV's for several days)
    • Excessive Work Demands (severly anemic person struggling to get oxygen to tissues)
    • Arrhythmias
  70. Types of Heart Failure
    • Systolic -- contractility prob; will not send blood forward (low ejection fraction)
    • Diastolic -- filling problem, heart cannot relax, the blood backs up and CO is decreased (low ejection fraction)
    • Left -- lung symptoms, (vast majority)
    • Right -- venous congestion (Emphysema)

  71. RAAS Mechanism
    Increased Renin, Increased Angiotensin 2 (...leads to Vasoconstriction...leads to Growth Factor For Myocardial Cells...leads to hypertrophy), Increased Aldosterone (...leads to Sodium and Water Retention/excretion of Potassium)
  72. Peptides that are released in response to increased atrial (ANP) and ventricular (BNP-- for Btype) stretch and pressure
    Natriuretic Peptides
  73. What do Natriuretic Peptides do?
    • Cause rapid loss of sodium, water, and moderate potassium in urine.
    • Inhibit aldosterone and renin secretion (helps vasodilate).
    • Inhibit release of epinephrine.

    ***Lab test can measure the level of BNP
  74. Class 1 Heart Failure
    Patients are asymptomatic; patients have no limitation of their activities, and they do not have symptoms from ordinary activities
  75. Class 2 Heart Failure
    Patients are Short Of Breath/Fatigued with moderate activity such as climbing two flights of stairs; they are comfortable at rest or with mild exertion and have slight limitation of activity
  76. Class 3 Heart Failure
    Patients are Short of Breath/Fatigued with very mild exertion activity, such as climing one half flight of stairs; are comfortable only with rest and have marked limitation of their activity
  77. Class 4 Heart Failure
    Patients are Exhausted, Short of Breath, and Fatigued at rest; any activity brings on discomfort and symptoms; they have severe limitations on their activity and are confined to bed or chair
  78. Manifestations of Heart Failure
    • Fluid Retention and Edema
    • Respiratory (Left Side)
    •    -Dyspnea
    •    -Paroxysmal Nocturnal Dyspnea (PND)
    •    -Orthopnea (elevated head makes sleep better)
    • Fatigue, Limited Exercise Tolerance
    • Cachexia and Malnutrition
    • Cyanosis
  79. Manifestations of Right Sided Heart Failure
    • Congestion of Peripheral Tissues
    • Dependent Edema
    • Liver Congestion
    • GI tract Congestion
    • Anorexia, GI distress, weight loss
    • Signs related to impaired liver function
  80. Manifestations of Left Heart Failure
    • Decreased CO
    • Pulmonary Congestion
    • Activity intolerance and signs of decreased tissue perfusion
    • Impaired gas exchange
    • Pulmonary Edema
    • Cyanosis and Signs of Hypoxia
    • Cough with Frothy Sputum
    • Orthopnea
    • Paroxysmal nocturnal Dyspnea
  81. Acute Pulmonary Edema
    • Capillary fluid moves into alveoli
    •     -lung becomes stiffer
    •     -harder to inhale
    •     -less gas exchange in alveoli
    •     -crackles
    •     -frothy pink sputum
    • Hemoglobin not completely oxygenated
    • ***EMERGENCY
    • anxious, air hunger, use of accessory muscles, skin cool & clammy, tachycardia, cyanosis
  82. S/S of Pediatric Respiratory Distress
    • Nasal Flaring
    • Sternal Retraction
    • Tripoding
    • Use of Accessory Muscles
    • Tachypnea
    • Cyanotic
  83. Problems of Inadequate Tissue Perfusion
    • Pump Failure- delivery to tissues
    • Circulatory Failure

    • Effects: Decreased Tissue Perfusion
    • Impaired Cell Metabolism
    • Release of Vasoactive Inflammatory Mediators
    • Cell Death
  84. ****TYPES OF SHOCK
    • Cardiogenic -- Pump Failure
    • Hypovolemic -- Decreased Blood Volume (dehydration, traumatic car accident)
    • Distributive -- Loss of Vascular Tone
    •    -Neurogenic
    •    -Anaphylactic
    •    -Sepsis and Septic Shock
  85. Type of Shock in which there is massive vasodilation due to parasympathetic overstimulation
    Neurogenic (Distributive)
  86. Type of Shock in which there is vasodilation and vasuclar permeability causing pooling and edema
    Anaphylactic Shock
  87. Type of Shock from a severe infection, bacteremia, systemic inflammatory response syndrome (SIRS) -- massive vasodilation, chemicals released in blood, hemoglobin is not realeased as regularly
    Sepsis/Septic Shock
  88. Manifestations of Shock
    • ***Change in Skin Temperature (blood is shunted to major organs, autoregulation, cold and clammy)
    • Hypotension <bp
    • Tachycardia >hr
    • Change in LOC- less coherent and sleepy
    • Decreased urine output- kidney is not getting adequate perfusion
    • Thirst
    • MAP (< 70 ) --considered emergency
  89. ****Major Complication of Shock
    MODS -- Multi-System Organ Dysfunction Syndrome
  90. Acute Febrile Illness of Young Childhood that Affects the skin, brain, eyes, joints, liver, lymph nodes, and can cause heart disease and aneurysms of coronary arteries
    Kawasaki's Disease
  91. Acute Phase of Kawasaki's Disease
    (7-14 days) with fever, rash, cervical lymphadenopathy, conjunctivitis, redness, and swelling of hands and feet, oropharyngeal effects
  92. Subacute Phase of Kawasaki's Disease
    (10-24 days) with peeling of the skin on the hands and feet
  93. Convalescent Phase of Kawasaki's Disease
    (8 Weeks) with arthritis, urethritis, pyuria, GI, hepatitis, CNS
  94. Cardiac Manifestations from Kawasaki's Disease
    CORONARY ANEURYSMS-- with s/s of ischemia, pericarditis, myocarditis, heart failure, and dysrhythmias
  95. In Fetal Circulation...Connects RA and LA
    • Foramen Ovale
    • (allows for complete bypass of the baby's lungs)
  96. In Fetal Circulation....Connects PA to Aorta
    • Ductus Arteriosus
    • (allows for complete bypass of the liver and goes straight to the baby's heart)
  97. Circulatory Changes that take place at Birth
    *Placental Oxygenation to pulmonary oxygenation

    • *Hypoxemic state to High Oxygen Tension State
    • (closure of the ductus arteriosus)

    *High pulmonary vascular resistance (PVR) to low PVR

    • *Low resistance placental circulation to increased SVR and left heart pressures 
    • (Closure of foramen ovale)
  98. Opening or connection that lets blood move from one side of the circulation to the other
  99. Most shunts occur in the _____ and move blood either from the left to right or right to left
  100. Because the ____ side of the heart is stronger, blood is usually pushed from the _____ to the _____ side
    • Left;
    • Left; Right
  101. When are shunts NORMAL
  102. What lets blood go from the right atrium to the left atrium to bypass the lungs?
    foramen ovale
  103. What lets blood go from the pulmonary trunk to the aorta to bypass the lungs?
    Ductus arteriosus
  104. What lets blood go from the visceral veins to the vena cava by passing the liver
    Ductus Venosus
  105. Types of Heart Defects
    • Communication b/w heart chambers
    • (atrial and ventricular septal defects)

    • Altered development of heart chambers/valves
    • (pulmonic stenosis, tetralogy of fallot, coarctation of aorta, endocardial cushion defects)

    • Malposition of heart chambers and great vessels
    • (transposition of the great vessels)

    • Altered closure of fetal communication channels
    • (patent ductus arteriosus)
  106. Causes of Congenital Heart Defects
    • Genetic, environmental
    • (ie: mother is exposed to Measles, certain drugs, etc)
  107. Classifications of Congenital Heart Defects
    Anatomic Defects

    • Hemodynamic Alterations
    •    shunting of blood

    • Effect on Tissue Oxygenation
    •    cyanotic defects
    •    acyanotic defects
  108. Left --> Right Shunt...more blood goes to the lungs rather than the body (extra workload on the lungs but tissues are not effected)
    Acyanotic Defects
  109. Right --> left Shunt...Deoxygenated blood goes to the body and less blood goes to the lungs
    Cyanotic Defects
  110. Manifestation of Congenital Heart Defects
    • Cyanosis
    • Respiratory Difficulty
    • Fatigue
    • Heart Failure
    • Difficulty Feeding
    • Failure to Thrive (they don't eat as much or gain weight bc they don't have energy)
Card Set
Cardio- Part 2
part 2