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Year 3: CardioPulm Rehab > Lecture 9: Medical and Surgical Management > Flashcards

Lecture 9: Medical and Surgical Management Flashcards

1
Q

lifestyle modifications for lowered HTN

A

1kg weight loss = 1mmHg BP reduction

low sodium diet <1500mg

pharmacology to decrease fluid volume and increase vasodilation (combo of diuretics, ACE or ARB, and Ca channel blockers

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2
Q

function of diuretics

A

stops sodium reabsorption by kidneys = more urine

decrease fluid levels = decrease blood volume in circulation = decreases preload (less blood returning to heart so less needs to be ejected)w

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3
Q

what is a loop diuretic

A

most effective/most utilized

inhibits movement of K and Cl across membrane

not 1st line of defense; may want to first try something that doesn’t affect electrolytes so much; can be dangerous/need to replace

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4
Q

function of ACE inhibitors

A

acts on RAAS to reduce intravascular fluid to reduce preload

prevent normal increase in circulating blood volume

prevents normal vasoconstriction and increased SVR that LV has to push against

can’t be used with pts with lung disease due to side effects of smooth mm contraction of all-sized airways

inhibits conversion of And I to II (occurs in lungs)

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5
Q

function of Angiotensin receptor blockers (ARBs)

A

acts on RAAS to prevent normal vasoconstriction used to raise BP

Ang I gets converted to Ang II in lungs but And II is blocked from distal receptors

much safer for pts with lung disease

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6
Q

function of Ca channel blockers

A

stops Ca entrance into myocardium = coronary vasodilation

decreased myocardial contraction strength and O2 demand (LV doesn’t have to work as hard to meet body O2 demand)

acts on peripheral vasculature smooth mm to vasodilate

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7
Q

pharm goals for management of CAD

A

decreased myocardial O2 demand

increase myocardial O2 demand

strengthen LV contractility

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8
Q

sx management goals of CAD

A

reduce/remove atherosclerotic plaque

bypass blocked coronary arteries before progression to MI

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9
Q

Drugs that decrease O2 demand for those with CAD

A

BBs
CCBs
nitrates

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10
Q

Drugs that increase O2 demand for those with CAD

A

thrombolytics
anti-platelets
anticoagulants

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11
Q

drugs that increase LV strength

A

ionotropes

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12
Q

function of beta blockers

A

stops epi and norepi from binding to B1 and B2 receptors

nonselective BBs block both B1 and B2

cardioselective BBs only block B1 receptors to prevent unwanted respiratory involvement

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13
Q

methods of administration of nitrates

A

sublingual tablet
sublingual spray
sublingual powder
paste to spread on skin
transdermal patch
continuous IV drip (abbreviated gtt)

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14
Q

thrombolytics function

A

accelerate clot breakdown

normal clot lysis happens naturally over period of days to weeks

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15
Q

antiplatelets function

A

stops platelet adherence

doesn’t stop RBCs from sticking to one another, just prevents platelets from adding to clot formation

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16
Q

anticoagulant function

A

prevent clot formation

stops normal clothing cascade from occurring

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17
Q

types of inotropic meds

A

cardiac glycosides

sympathomimetics

phosphodiesterase inhibitors

arteriodilators (indirect ionotrope)

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18
Q

how do cardiac glycosides work

A

decrease active transport of Na and K to increase intracellular Na

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19
Q

how do sympathomimetics work

A

mimics action of epi/norepi to increase sympathetic NS drive

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20
Q

how do phosphodiesterase inhibitors work

A

increase myocardial contractility without altering the Na-K pump

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21
Q

how do arteriodilators (indirect ionotrope) work

A

decrease after load by decreasing arterial resistance (decreases SVR)

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22
Q

what is a PCI

A

percutaneous coronary intervention

can be performed electively or emergently

ACS - door to balloon time <90 min

typically used for 1-2 vessel blockage

catheter inserted bia distal artery to access coronary arteries with goal of restoring blood flow to cardiac mm

pts generally on 2 anti-platelets post sx to prevent thrombus (aspirin + plavix)

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23
Q

balloon angioplasty vs angioplasty with stent

A

balloon = Cath used to inflate balloon to open a blocked artery

stent = stent placed in place of inflated balloon to keep artery open; drug eluding stent is most common

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24
Q

indications for a coronary artery bypass graft (CABG)

A

lesions threatening major portions of myocardium

multi-vessel disease, especially L sided blockages

ongoing ischemia following MI

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25
Q

how does a CABG work

A

graft comes from internal mammary artery from internal chest wall or saphenous vein from leg

veins are cauterized, flushed with heparin, and inverted for normal blood flow

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26
Q

what is a sternotomy

A

most commonly used approach to access heart

suprasternal notch to xiphoid process

sternum is wired closed

soft tissue is sutured and glued

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27
Q

what is cardiopulmonary bypass (CPB)

A

heart cannot move during sx but body/brain still need perfusion

CPB initiated via cannulation at aorta and IVC/SVC

blood removed to oxygenator and returned straight to aorta for distribution

once CPB is complete, ice slush is poured into mediastinum to stop heart

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28
Q

what is an off pump CABG

A

heart is accessed from L sided thoracotomy

can only operate on L sided coronary aa

no CPB

less expensive, no sternal precautions, faster recovery

isolated portions of myocardium stopped via electrical “starfish”

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29
Q

describe what typically happens post op with CABG pts

A

straight from OR to CVICU (no normal sx post op)

RT and RN work to wean down ventilator support and wean off drops/sedation over the 1st 6 hours

goal = be extubated within 6 hours

monitoring of urine output, chest tube output, all sx sites, and external pacemaker

goal = pt in chair within 8 hours of arrival and standing within 12 hours (depends on unit and pt stability)

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30
Q

common CABG complications

A

pain

respiratory distress (15-20%)

impaired cognition/delirium (CPG “pump head”)

acute blood loss/cardiac tamponade (bleeding in pericardium/pressure)

increased risk clot burden; difficult to balance risk of CVA with risk of hemorrhage if anti-coagulated too soon post sx

dysthymia/ectopy

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31
Q

when is valve repair/replacement indicated

A

for symptomatic valve dysfunction

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32
Q

what is a valvuloplasty

A

minimally invasive repair (widening) using balloon Cath technology

risk of replacement outweighs repair

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33
Q

how does valve replacement work

A

mechanical or tissue (allograft or xenograft); mechanical required lifelong INR goal adjustment

can replace multiple valves in 1 sx

frequently done in conjunction with CABG

open repair requires sternotomy

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34
Q

what is transcatheter aortic valve replacement (TAVR)

A

minimally invasive prodecure to replace aortic valve

utilizes similar process as cardiac cath via femoral or radial artery access in Cath lab

valve replacement will always be mechanical

sometimes used if pt has high risk of open sx replacement

long term outcomes may not be as strong as open AVR

35
Q

what is an external placemaker

A

set up as backup

typically 60 bpm

procedure of weaning away

36
Q

what are chest tubes/JP drains

A

need to ensure no post op hematoma formation

37
Q

what is a pulmonary artery catheter (PAC) for invasive monitoring of heart function

A

measures R atrial pressures, pulmonary aa pressure, CO, cardiac index, and temperature

inserted in RIJ or R subclavian, “floated down” the SVC, through RA, RV, and into pulmonary aa

held in place my sutures and adhesive dressing at neck

if dislodged, indwelling components can cause potentially fatal ectopy

38
Q

what is an arterial line

A

invasive and instant BP measurement

usually in radial aa but can be femoral or brachial

if pressure in the line is lost, pt can bleed out

39
Q

what is a central venous catheter

A

large IV placed in IJ, subclavian, or femoral vein

allows for meds/fluids to be given directly

40
Q

line considerations

A

no mobility 2-4 hours post extubation to reduce risk of airway edema/stridor

no mobility 2 hours post central line removal to reduce risk of developing hematoma (especially in neck/groin)

femoral lines should not limit mobility but some facilities have restrictions

41
Q

first approach to dysrhythmias

A

pharm management; want to stabilize cell membranes during action potential by controlling movement of electrolytes

42
Q

other approaches to help dysrhythmias if pharm management doesn’t work

A

pacemaker

internal cardiac defibrillator (ICD)

variety of other electrophysiologic procedures or sx that can be dine if less invasive measures are unsuccessful

43
Q

class I dysrhythmia meds

A

Na channel blockers

limits myocardial excitation and contraction

44
Q

class II dysrhythmia meds

A

beta blockers

inhibits sympathetic NS

45
Q

Class III dysrhythmia meds

A

K channel blockers

prolongs refractory period and makes it more difficult for myocytes to respond to stimulation from one another

46
Q

class IV dysrhythmia meds

A

Ca Channel blockers

slows conduction through AV nodes

47
Q

what is a permanent pacemaker (PPM) and how does it work

A

creates action potential in necessary areas

in L chest with leads inserted via cephalic vein through the SVC into R atrium, R ventricle, or L ventricle

can be single chamber, dual chamber, or biventricular

subcutaneous generator functions at a fixed rate, mode, with variety of settings and backup settings

48
Q

indications for pacemaker

A

bradycardia

type II-III heart blocks

other uncontrolled arrhythmias

49
Q

things to keep in mind about placement of permanent pacemaker

A

generator may need to be replaced if batteries run out

can interrogate PPM via external device to change settings, charge battery, turn off, etc

PPM post op precautions

50
Q

complications of PPM

A

infection
lead movement/migration
bleeding, clots
no MRI, TENS, NMES
caution near magnets

51
Q

what is a leadless pacemaker

A

new

does not require leads or L upper chest generator

inserted via femoral vein and IVC into RV

can influence RV or LV electrical activity based on location

52
Q

what is an internal cardiac defibrillator

A

similar to PPM and fires in event of arrhythmia

leads inserted into AV node and ventricles

pts with EF <35% have higher chance of fatal ventricular fibrillation so sometimes ICD placed prophylactically

combination PPM-ICD devices if pt meets indications for both

53
Q

indications for internal cardiac defibrillator

A

VFib

VTach

cardiac arrest

HF/CM with EF <35%

hypertrophic CM

combo heart block with ventricular arrhythmia

54
Q

what is cardiac ablation

A

minimally invasive procedure that controls arrhythmia by creating scar tissue in myocardium

targets ectopic foci

might not permanently fix problem

55
Q

what is a maze procedure

A

type of cryo ablation specifically used for persistent AFib

creates maze of scar tissue to block abnormal signals but allows normal impulse conduction

requires partially open or laparoscopic approach and frequently done in conjunction with other CTS

56
Q

what is an atrial appendage and the clinical indication

A

both atria have extra tissue that can expand if needed

L atrial appendage is larger and can be more problematic

higher pressures on the L can case the LAA to expand and be a reservoir for blood

> 90% of clots that cause CVA originate in LAA

57
Q

what is watchman’s procedure

A

presence of R or L atrial appendage increases risk of clot development in AFib

minimally invasive procedure via femoral or radial artery that “plugs” appendage to prevent clot formation

higher pressures in L side of heart create enlarged LAA

58
Q

what is LAA or RAA surgical closure/when is it indicated

A

if watchman’s wasn’t successful or contraindicated, the atrial bulge can be surgically closed

can be done laparoscopically but also in conjunction with other open heart sx

59
Q

what is cardioversion

A

electrophysiological procedure that restores normal rhythm

needs to be done in a highly monitored environment

can be done electively or emergently if pt is in fatal rhythm during MI or cardiac arrest situation

conscious sedation used for procedure

used frequently for AFib with RVR if meds aren’t controlling adequately

60
Q

goals of pharm management for heart failure

A

maintain CO

fluid reduction to reduce preload

augment LV contractility and decrease after load

limit sympathetic nervous system action

61
Q

HF medication types

A

diuretics
ACE/ARB
BBs
antiarrhythmics
Ionotropes

62
Q

what is mechanical circulatory support

A

if LV isn’t functioning well enough to perfuse tissues, MCS can be used to supplement CO

various devices can be surgically inserted to improve heart function

63
Q

what is an intra-aortic balloon pump

A

MCS device placed into proximal descending aorta via femoral, axillary, or subclavian artery

balloon attached to helium tank that inflates during diastole and deflates before systole

inflation = pushes blood into coronary aa while aortic valve is closed to provide optimal coronary cardiac output

deflation = suction of deflation assists with dropping after load and reducing work load on failing LV

64
Q

what is an impella

A

MCS device placed into LV via femoral, axillary, or subclavian aa

mechanically pimps blood from LV into the aorta at a set rate

unloads the LV work and decreases myocardial O2 demand

65
Q

what is a left ventricular assist device (LVAD)

A

implanted MCS device that replaces the workload of the LV and has a motor that controls blood flow at a set rate to maintain cardiac output

can be used as a bridge to transplant, temporary ventricular rest, or as destination therapy

longest living pt with LVAD = died after 15 years

66
Q

components of LVAD

A

pump
drive line
controller
external power
batteries

machine weighs between 4-6 lbs

must have power source

no pulse

67
Q

LVAD medications (in addition to typical meds for HF)

A

lifelong anti-coagulant (Life of the LVAD)

aspirin or plavix or both

pulmonary HTN meds to reduce R heart workload

supplements

68
Q

LVAD complications

A

bleeding; LVAD cant function correctly if pt isn’t anticoagulated

bloot clots; device mechanism can case clots; prevalence is decreasing

R sided heart failure; device placement on L side can alter normal RV movement/function

drive line infections; soft tissues infections can migrate to heart

69
Q

describe a heart transplant/important statistics

A

more pts on waitlist than will ever receive a heart

extensive medical, physiological, educational, and financial screening process

estimated 1st 5 year expense = $1.6 million

80-90% have 1 year survival rate

60% have 5 year survival rate

average survival is 12 years

70
Q

what does it mean that pts who are candidates for heart transplants are on max medical management protocols

A

severe functional deficits

limited life expectancy

some must remain hospitalized until transplant becomes available

71
Q

indications for OHT

A

end stage heart failure

congenital heart disorder

cardiomyopathy

72
Q

indications for OHT

A

age >75

severe mental/psychological instability

drug, tabacco, ETOH use w/I 6 mo

BMI >35

malnourishment

uncontrolled DM

PVD

severe lung disease

autoimmune disease with multi system involvement

AIDS

current/recent malignant cancer

other systemic illness with shortened life expectancy

73
Q

contra

A
74
Q

process of heart transplant

A
  1. pt placed on waitlist after being deemed candidate
  2. geographic waitlist maintained by United Network of Organ Sharing (UNOS)
  3. when an organ becomes available, is matched to a pt based on various characteristics (age, blood type, size, etc)
  4. oran is preserved and transported to recipient
75
Q

OHT medications

A

immunosuppressants: prevent organ rejection

corticosteroids: reduce inflammation/risk of rejection

antibiotics/antivirals: prevent illness in setting of immunosuppression

insulin: counteracts side effects of OHT meds that cause hyperglycemia

statins: improve long term outcomes, reduce risk of CAD in donor heart

Anticoagulants/anti-platelets: reduce risk of CAD in donor heart

76
Q

OHT complications

A

infection
- highest risk 12 months post op
- opportunistic infections in setting of immunosuppression

rejection
- 50-80% in first 12 months
- symptoms of rejection = fever, fatigue, myalgias

very challenging to balance risk of rejection with infection

77
Q

what is carotid endarterectomy

A

sx procedure to remove plaque build up frequently at CCA-ICA bifurcation

reduces CVA risk drastically

78
Q

what is carotid stenting

A

implanted stent to open artery in area of atherosclerotic block

79
Q

indications for AAA surgical repair/replacement

A

> 5cm or high rate of growth

rupture or + S&S

risk of dissection

80
Q

describe the open sx approach for aortic repair/replacement

A

aorta repaired/replaced via open laparotomy incision

higher blood loss and open complications with open repair

81
Q

describe endovascular aortic repair (EVAR)

A

can be done it pt is too high risk for open repair

vasculature accessed via B femoral aa

faster recovery and lower mortality/morbidity in short term

worse long term outcomes, higher rates of needing re-do sx

82
Q

what is embolectomy/thrombectomy/atherectomy

A

removal of blood clot or atherosclerotic plaque

can be achieved in a variety of ways

83
Q

what is balloon angioplasty and stenting

A

peripheral revascularization

very similar to cardiac PCI

Year 3: CardioPulm Rehab (8 decks)

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