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  1. Can think of volume, afterload as pressure how?
    • Lot of volume, lot of pressure
    • Low volume, low pressure (afterload)
  2. Systole
    LUB
    DUB

    Diastole
    • Systole- moment after End Diastole.
    • AV valves slam shut (LUB)
    • Pressure builds, contraction starts
    • Semilunar valves open.
    • Aortic valves open, pushing blood into aorta, aortic valves slam shut (DUB). Pressure in ventricle low, all pressure or volume went to aorta.

    'Resting,' filling up the gas tank. Filling with blood, mitral valve will open, blood will go into ventrical (provides only 20% of blood flow/kick), so atria not necessary to survive, but it sure helps.
  3. MTAP
    • Timing of valves closing.
    • Mitral/tricuspid
    • aortic/pulmonic
  4. Aorta
    How many times does heart beat per minute? How big is it? How many sections does it have? How does it compare to other vessels in pressure?
    • 100,000x/day
    • 2/5cm in diameter. Aorta has 4 sections
    • Highest pressure vessel
  5. Where is aorta attached?
    Ascending
    Aortic arch
    Descending aorta
    -thoracic
    -abdominal
    • Aorta basically attached to aortic valve of heart.
    • Ascending
    • -1st branch: coronary arteries branch off first
    • -2nd branch: (aortic arch) brachiocephalic artery (innominate)
    • - supplies rt carotid artery, rt subclavian.
    • -3rd branch: left carotid artery
    • -4th branch: left subclavian artery
    • Descending aorta
    • -thoracic
    • ---visceral branches: Lungs, pericardium esophagus, lymph nodes
    • ---parietal branches: chest muscles, diaphragm, spinal chord
    • -abdominal-
    • ---celiac artery-gastric, liver, spleen
    • mesenteric arteries
    • ---intestines, renal, ovatries, testicular
    • (feeds kidneys (1st ones to bail, so important to monitor for heart), gut)
  6. Why would rt sided heart attack create risk of arrythmias?
    SA node on that side
  7. How much avail O2 does body use vs heart?
    25% vs 50%
  8. when do coronary veins dump into coronary sinus (rt atrium)
    Coronary veins dump into coronary sinus (rt atrium) fill and deliver during diastole
  9. P wave
    atria contract in unison (ish). Tech term for contraction is depolarization.
  10. QRS
    • Impulse trav from AV node to purkinje fib as it passes through ventricles. Think percolate the ventricles
    • Ventricles contract
    • doesn't just tell ventricles contracting, but that atria are chilling out (just can't see it cuz ventricles overshadow). Big upspike is R wave. Ventricles have to contract harder, take longer so R spike is higher and longer.
  11. T wave
    smoke break. repolarization of ventricles.
  12. EKG
    10 leads how many views?
    purpose?
    • 12 views (you can see coming and going, like walking across the room).
    • to estab baseline before surgery, or suspected heart attack
  13. EKG
    Smoke over fire, clouds over grass
    white is the right
    • White lead goes on rt shoulder
    • clouds are white (white on right), grass is green (lower right),
    • smoke (black on left upper) goes on left over fire (red on left lower) goes below
  14. telemetry
    generally ___ to ___ leads
    Holter monitor?
    Dr's order to shower?
    What should you place over?
    implications if sweaty?
    what if hairy?
    • 3 to 5
    • smoke over fire clouds over grass + one on chest
    • portable transmitter with telemetry
    • not bones. Subcut tissue below stickers.
    • yes
    • watch for asystole because they'll come off. shave the hairy guys.
  15. Stress tests
    Radioisotopes?
    -Angiograms
    Why use dye? Angiogram, can have heart, renal
    • EKG monitoring during exercise
    • Don't do radioisotope as often anymore.
    • -More common now
    • If dye on normal person, see black. If you inject dye, you see blank areas. Tells us where blockage is.
  16. Left heart cath
    • Inject dye into left ventricle, you can see how much blood is backing up into L atrium, mitral valve isn't working
    • *could do for rt side, venogram.
  17. Cardiac output normal about _______ L/min
    Stroke volume measured in_____, normal is roughly ______
    When HR^, BP ____
    • CO=HRXSV
    • 4-8 L/min
    • mL/beat, 50

    btw, 1L=1kg, don't forget to convert; SV in mL, CO in L
  18. Cardiac cath, how do access coronary arteries?
    • Sheath inserted into femoral artery
    • to coronary art then Lventricle
    • inject dye
  19. After, monitor...
    • flat for 4-6 h
    • for hematoma, will be what internal bleeding looks like
    • tachypnea (body is needing more O2)
    • hold press at least 30m
    • *pedal pulses- emergency
    • kidneys (get baseline 1st) because dye hard-BUN, creatnine on them, 1st ones to bone out.
  20. seafood, kiwi eggs
    Allergies that might complicate, use weaker dye, use antihistamines
  21. Mucomist in relavance to this
    protects kidneys from dye.
  22. Labs:
    WBC 4-11 X 10^3/uL
    Hgb F 12-16, M 13.5-18 g/dL
    Crit F 38-47% M 40-54 %
    PLT 140-450 X 10^3/uL
    ESR F <20mm/hr M <30mm/hr
    • WBC+ infection -gen prob w bone marr
    • Hgb + COPD? maybe over blood tranf -anemia
    • Crit (%) + dehyd (not for sure) - maybe bleed, ", overhydrated
    • PLT heparin can make PLT go down.
    • Doesn't assess is they are sticky just how many there are
  23. Total cholesterol: Desirable level?Borderline
    High
    HDL v. LDL
    • 200
    • 200-239
    • 240 or more
    • Happy v. Lousy
    • HDL binds to LDL,
    • takes from tissue to take to liver
  24. Risk factors for
    heart disease
    0.Normal Sinus
    rhythm
ST (sinus tachy)
SB (sinus brady) 
AFib
Heart blocks 
PVC


    0.NSR more than just bpm


    0.must be 60-100,
    regular R to R interval, must have P wave for every QRS T


    0.only way to tell is EKG


    0.*when HR gets to 160, hard to
    see P wave. Can't call it sinus tach unless you see a P wave


    0.Normal (more than 100)


    0.Normal (less than 60)


    0.AFib


    0.Heart blocks


    0.Premature ventricular
    contraction


    0.


    0.


    0.
    Normal aging, phys may affectheart pump, 50% of MI occur to people over 650.Fam hx0.Parent or skibling with CB diseaseprior to 50 places pt at higher risk0.Sex (men) classic sx-arm pain0.(women) may get classic sx,GI, more heartburn0.Race (african american ^errisk), nicotine is vasoconstrictor, hyperlipidemia, DM0.
  25. Normal Sinus rhythm
    ST (sinus tachy)
SB (sinus brady) 
AFib
Heart blocks 
PVC.NSR more than just bpm.must be 60-100,regular R to R interval, must have P wave for every QRS T.only way to tell is EKG*when HR gets to 160, hard to see P wave. Can't call it sinus tach unless you see a P waveNormal (more than 100)Normal (less than 60)AFib0.Heart blocks
  26. Sinus Tach
    • reg HR greater than 100,
    • greater than 100bpm
    • myo consumption increase d/t increased demands on heart
    • watch for hypotension or hyper, dec sats, chest pain in patients w poor CV disease
  27. Sinus Bradycardia
    reg HR, less than 60. watch for hypotension, syncope, lt headed. May need a pacemaker.
  28. AFib
    • irreg HR
    • Disorganized electrical activity in atrium. Chaos
    • common, serious. disorg electrical activity in atrium (quivering atria 150-600bpm), no reg p wave. ventricles respond 100-200 bpm. HR variable, irreg, deadly clots can form in atria, pt must be anticoaged warfarin, HR needs to be controlled, people can live w Afib
  29. Where would AFib clot go?
    might cause MI, clot travels to brachiocephalic, carotid, or other carotid, risk for stroke. Usually doesn't end up in arms.
  30. Afib: affect on ventricles?
    • Atria are quivering 150-600bpm
    • Ventricles trying to respond, periodically responding, in uncontrolled AFib can do 100-200 tops. HR variable, irregular
  31. AFib causes
    • -Heart doesn't like to be touched-
    • bypass surgery (Afib common after)
    • severe HTN
    • inc demand (like COPD)
  32. Rhythm/ blocks
    • problem w SA-AV node conduction
    • HR may be slow, irregular, hypotension
    • Caused by MI, CHF, Med tox, hypokalemia
  33. -SA node fed by
    -What takes over?
    • -right coronary artery
    • -AV node, slows things down, so makes it bradycardic
  34. PVCs can be caused by______?
    (normal) stress, anxiety, stress and fatigue, cigs, ETOH w/d, can be precurs of lethal dysrhythmias
  35. PVC
    Multifocal PVC
    Vtach
    • Abnormal hb generated from spot on ventricle
    • orig from different spots on the ventrical, the "party guy" trying to get everyone else. Just one OK
    • Vtach- everyone's partying together, still marching, but still together just in wrong place
  36. Vtach
    • (code blue; no pulse or not breathing. No A or B and no C- all combined or any one, rapid response)
    • 3PVCs in a row (not per minute, in a row is Vtach)
    • HR 140-240bpm
    • May not have a pulse
    • Pulseless Vtach
    • CPR, defibrillate (stop all activity, hope all partiers get in line)
  37. Vtach causes?
    • Disorganized electrical impulses in the ventricles
    • ventricles are quivering, NO pulse, CPR, needs Dfibrillation.
    • hypoxemia, hypokalemia, low mg, OD,
  38. Pacemakers
    Transcutaneous
    Transvenous
    Permenant
    • Intitiate controls HR
    • Del electrical impulses
    • via electrodes to myocardium, atria, ventricles, or both. Most set on demand mode (watches and fires PRN)
    • Transcutaneous (difibrillator, set at pacemaker style, deliver electricity through skin. 2 leads, one on arm, one on chest). painful, so don't leave on too long)
    • *figure out why hr is slow?
    • If can't figure out why or fix, put in transvenous, still asking why? PC straped on, lead into IVC or subclavian.
    • If still no answer or permenant issue, then put a permenant one
    • Pacemaker lead enters ex jug vein. Lead tunneled sunbcut between pacemaker and external jug vein, generator placed beneath skin in pect region. Tip of lead (electrode) lodged in apex of right ventricle.
  39. Cardiac arrest
    causes?
    s/sx
    • heart's stopped.
    • ventricular tach, ventricular fib, ventricular asystole
    • *no pulse! abrupt loss of consciousness with no resp to sim, gasping respirations followed by apnea; absence of pulse and bp pupil dilation; pallor and cyanosis
  40. What to do for cardiac arrest?
    CPR even more important than difibrillation
  41. Antidysrhythmias

    How many have strokes w A Fib
    • abnormalities of E conduction in the heart
    • could be harmless or not, must have EKG to be sure

    15%
  42. coronary artery
    • atherosclerosis
    • severity measured by blockage size
    • little or no O2 to CA
    • most common cause (sclerotic means plaque/hard)
    • usually by cholesterol. Sticks at first, sticky and
    • fibrous. If stuck there
    • awhile. Backs up pools clots
    • blockage- MI
    • >75% risk of MI may do surgery
    • Angina- body crying out for blood and oxygen
    • when demand = greater than supply ischemia results
    • Rt side SA node
  43. Atherosclerosis
    • Tear in artery
    • Platelets stick
    • Cholesterol sticks
    • Dev of fatty streak, fibrous plaque
    • Dev of complicated lesion
    • Angina
  44. Ischemia to heart/Chest pain not necc MI
    • Myo not getting enough oxygen
    • Unstable
    • (ie, when sleeping) Unpredictable, transient, can be red
    • flag for MI
    • If true MI, pain is persistant. Try taking deep breaths, etc
    • Huge heaviness, tightness, squeezing on chest. May or may not radiate
    • Vital sx
    • Sweaty?
    • SOB? Subjective stuff
  45. Diagnostic tests/angina
    • Freq made on pt hist
    • ECG chg (ischemia will show on ECG)
    • Stress test can det ischemic changes
    • Thallium scan and PET scan
    • Coronary angiogram
    • Giving Nitroglycerin
    • Opens coronary arteries
    • (vasodilates, venodilates, also works on arterial/coronary arteries). Can drop bp
    • If pain relieved by Nitro, angina
    • highly suspected
  46. Angina

    Med Management
    • Open arteries, stop platelets for being so sticky,
    • decrease heart’s workload to need less O2
    • Controlling sx that cause angina
    • Prev and corr of poss risk factors
    • Antiplatelet agg
    • (aspirin)
    • Meds given to vasodilate workload of heart
    • Give beta blockers
    • Slowing of HR
    • Reduce contractility
    • Lower BP
  47. Med mgmt acute angina
    • O2 (nonrebreather)
    • *Nitro q5min X3 of pain doesn’t subside
    • *Notify MD
    • Beta blocker
    • Pt having MI
    • Coronary
    • intervention
    • Angioplasty,
    • stent, CABG?
    • *stable angina, do these, will see order like that for
    • Nitro, check in 5 minutes. Vitals
    • every 5 m
  48. MI
    • Version:1.0
    • StartHTML:0000000162
    • Occlusion of coronary artery -> ischemia -> cell death
    • 35-45 min of ischemia leads to cellular dam
    • necrosis across myocardium, abil of cardiac muscle to pump
    • caused by artherosclerosis or embolus (air, gas, tissue,
    • thrombus)
    • Necrotic debris after MI
    • Tissue not very stable, 6 weeks post MI, necrotic tissue
    • turns to scar tissue
  49. MI
    • Serum cardiac markers
    • CKMB myoglobin, troponin I
    • Remember Troponin 1 gold stand
    • EKG
    • Pain may occur suddently or build over a few minutes
    • Assessment
    • Similar subj or obj data as angina
  50. MI
    • Med mgmt
    • Morphine- inc coronary perfusion, helps w pain, happy juice
    • Anticoags
    • Antiplatelet aggs
    • Heparin therapy
    • Beta blockers
    • Stool softeners (no straining)
    • Top priority to open blockage
    • Dec amount of damage
    • Dec workload of heart
    • O2 meds treat anxiety
    • PVCs or irreg HB
    • Thrombolytic
    • Myocardial cells take approx 4-5 h for entire thickness of
    • muscle to die
    • Reperfus most effective 30-60 min
    • Door to balloon time
    • National standard 90 min. Swedish 45
  51. Coronary angioplasty- reconstruction
    Massive MI- take it easy for 6 weeks

    • Mild MI- Restrict activity for 1st day or two,
    • then can slowly increase



    Pt teaching

    If chest pain NO DRIVING

    Lifestyle changes

    Mod vs non mod

    Smoking cess

    Diet and exercise



    Will be on meds for rest of life.

    Usually in ICU for at least 12 hours
  52. Cardiac rehab
    • Most pts return to work, life
    • Sex after can climb 2 flights of stairs no problem
  53. Meds given
    • Anicoags
    • Antilpt
    • Tissue plasminogen
    • Nitrates
    • Bnete-ad blockers/Ca++ channel blockers
    • Salicylates
    • Antidystrhythmics
    • Stool softener
    • Diuretics
    • Elyte replacement
  54. PCTA
    • Percutaneous transluminal coronary angioplasty (angio means
    • arteries plasty means reconstruction)
    • Get to coronary arteries through aorta, femoral artery
    • Receiving pt from cath lab make sure antiplatelet has been
    • given ASAP
  55. CABG
  56. Coronary Artery bypass graph
    • Sew on piece of other artery, diverting it aroundthe block
    • Just bypasses problem doesn’t fix it
  57. Antidote for narcotics
    narcan (heroin)
  58. Morphine
    resp arrest
  59. Valve problems
    obj
    subj
    -aortic?
    -mitral
    • when valves are compromised or do not open close properly. Stenosis= thickening of valve tiss. narrowed passage.
    • -sim to dec CO
    • -hx rheumatic fever, inab to perform ADLs, palpitations, chest pain, ltheadedness, dizziness, dyspnea (exertional and or at night)
    • -low bp, tired
    • -in the lungs
  60. Med mang interventions
    • antidysrhythmics
    • surg ints
    • repair: ring around weakened leaflets
    • commissuotomy- a surg splitting of a stenosed mitral valve
    • Replacement
    • bioprosthetic or mech
    • porcine
  61. Aortic valve replacement: what do they have to take?
    anticoagulants, coumadin or aspirin
  62. Pericarditis
    clinical manifestation
    subj
    obj
    • inflammation of the membrane surrounding the heart common after MI
    • can mimic an MI, pericarditis increases/decreases w movement, DB&C
    • subj muscle aches dysp
    • obj tachypnea, friction rub, shallow breathing, BP-narrowing pulse pressure
  63. tx pericarditis
    if lots of fluid, what do you do?
    • corticosteroids, antibiotics, pain control, surgical interventions (pericardial window), vitals, decrease dysp (O2, elevate HOB) (pericardiocentesis)
    • pericardiocentesis
  64. Endocarditis
    how does infection get in
    • -more serious than peri, because inside
    • infection of infl of inner membrane
    • -heart valves, vegetative growth scars tissue.
    • cure bact growth first
    • heart surgery, IV surgery dental minor surgery, gyne exams
  65. Endocarditis, signs
    • same as pericarditis
    • same as peri
    • joint pain
    • elevated sedimentation rare (ESR)
    • med management
    • long term antibiotics will cure 90%
    • valve replacement 25%
  66. coronary myopathy
    primary?
    hypertrophic cardiomyopathy?
    • big & floppy
    • unknown cause
    • ventricular walls are stiff
  67. cardiomyopathy
    diagnostic tests
    how long till many die?

    tx of underlying cause
    tx sx, symptoms, slow progression, meds, tx heart failure, cardiac xplant, CM is 50% of heart transplant. dilated cardiomyopathy most common, immunosuppressed.
    • infective, metabolic, ntr, etoh, peripardum, drugs, radiation therapy
    • clin manifestations, see slide

    w in 2 years
  68. PV
    -diagnostic tests
    -angiography/venography
    -D-Dimer
    • -treadmill, doppler ultrasound, bf into arteries and/or veins. eval for clots, obstructions, intermittent claudication (muscle pain during exercise). Duplex study, use ultrasound to loc DVT & is most common DVT test
    • contrast tye
    • D-Dimer, if clots pres, will be elevated
  69. PV
    insufficiency
    ischemia
    • assessment
    • insufficiency
    • cap refill
  70. HTN
    • 120 80
    • Sustained BP 140 90
    • sustained.

Card Set Information

Author:
 Anonymous
ID:
 85459
Filename:
 silverollbars
Updated:
2011-05-19 18:44:30
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DFill
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