Hemodynamics Flashcards
risk factors for CAD
high lipid level above 240 over age 65 HTN smoking viral ardiomyopathy
cardiac output
HR x SV
CI =
CO x BMI (includes body mass)
amount of blood pumped out of LV during systole & amount remaining at end of diastole
ejection fraction
normal EF
60-70 %
O2 demand exceeds ability of coronary arteries to supply heart with O2, (usually insufficiant blood flow)
myocardial infarction
what is MI caused by
thrombus or spasm (plaque), you have cyanosis in 10 seconds, after minutes, anaerobic metabolism produces lactic acid, stimulates nerves to send pain messages through thoracic cavity = CP
how long are the cells viable for
20 minutes, after that they have sustained necrosis, that are of the heart stops beating
what is the leading cause of morbidity and mortality
MI
transmural
full thickness
subendocardial
partial thickness
what will show in the EKG for the zone of infarction
develop a Q wave
what will show in the EKG for the zone of injury
ST evaluation
what till show in the EKG for the zone of ischemia
T wave inversion
what leads will be affected if the anterior part of the heart is injured/ischemic
V1-V4
LAD
what leads will be affected if the inferior part of the heart is injured/ischemic
II, III, aVf
RCA
what leads will be affected if the lateral part of the heart is injured /ischemic
V5, V6, I, aVl
left circumflex
where is the worst place to infarct
LAD
*widow maker
when does healing begin after an MI
24 hours, leukocytes start working, macrophages remove damaged (necrotic) tissues, tissues are vulnerable for 10-14 days
what happens after injury to the myocardium
compensated bby thickening, dialating & remodeling (CHF)
abrupt loss of cerebral blood flow, only 20% of survivors leave the hospital
sudden cardiac arrest
Tx for cardiac arrest
ICD surgery, low EF is a sign prior to arrest, most have had MIs in the past
management of MI in acute stage, short term goals
relieve pain*, control lethal arrhythmias, preserve the myocardium (stop progression of MI)
*primary goal
pain is =
cell death
long term goals for management of MI in acute stage
cope effectively with anxiety, compliacne with rehab program, modify/alter risk factors
Dx of acute MI
H&P
serum enzyme levels CK & troponin*
most indicative (a protein not an enzyme)
12 lead EKG 1 mm ST elevation
CXR, CBC, thyroid, lipid, CRP, CT/PET, Echo, stress test, cardiac cath
ST segment elevation
more than 1 mm above or below isoelectric line
why does ST segment elevation occur
myocaridal injury, happens over affected area of the ventricle, they return back to the isoelectric line in about 2 weeks
T wave inversion
ischemia causes symmetrical inversion of T wave,
Q wave development
normal Q wave is 1 mm or less, Q wave develop wen ST segments are elevated, appear several hours/days after MI
what is the greatest sign of ischemia
pain
why is morphine sulfate given
decrease anxiety, O2 demand, and restlessness
why is nitro given
vasodilator used for pain relief, deceases preload & afterload, decreases myocardial O2 demand
side effects of morphine and nitro
watch BP, can drop quickly
*assess VS Q5-10 minutes
what are the most common side effects of MI
arrhythmias
what is given for PVCs and V tach
lidocaine give bolus then follow up with drip administer amiodarone (1st line) O2
what is given to preserve the myocardium
thrombolytics within 30 minutes (if criteria is meet)
O2
stool softeners (decrease risk of straining, decrease the use of valsalva maneuver)
nutrition (low fat diet)
Beta blockers
decrease infarct size, decrease preload and afterload, decrease HR/contractility
ACE inhibitors
decrease remodeling of ventricle, decrease ventricular dilation, decrease CHF & mortality
Anti coag (Heparin)
decrease risk of thrombi, decrease re-occlusion 12-24 hours after thrombolytic therapy
ASA
inhibit platelet aggregation rapid antithrombic
Magnesium
usually only as an antiarrhythmic (Torsods)
what other interventions can be done for MI
HOB elevated, bed rest for 12 hours, reduce stress, rest and comfort, Mild sedative to reduce anxiety, sleeping pills, dietary restrictions (clear liquids to cardiac diet, I & O, daily weights, decrease salt/chol/fat/caffeine, CABG, PTCA, therapeutic hypothermia
PTCA
percutaneous transluminal coronary angioplasty
CABG
emergency measure for revascularization of myocardium
therapeutic hypothermia
proven to improve neurological outcomes following cardiac arrest
what is recommended as first line Tx for MI
PTCA, fibrolytic therapy, CABG
plan of care for MI pt
perform ongoing assessment, limit energy expenditure, maintain hemodynamic stability (increase CO & tissue perfusion, keep BP and HR increased {not hypotensive}), tx complications, provide emotional support, teach
hypothermia protocol
keep temperature between 32-34 degrees, monitor temp with bladder temp probe, keep target temp for 12-24 hours, cooling blankets, ice packs in groin and torso
Signs Sx of possible MI
diaphoretic, increase temp, pallor, N/V, confusion, syncope, stroke, CP, EKG changes, JVD, peripheral edema, abnormal heart sounds, SOB, orthopnea, tachypnea, crackles, frothy sputum, decrease UO, anxiety, agitation, denile
what heart sound is common in MI
S4 (decrease of LV compliance, atrial gallop)
when is a pericardial friction rub develop in MI pt
2-3 days post infarct, inflammation causes loss of function (pericarditis)
what is the most frequent complication of MI
arrhythmias (80%)
V fib after MI
cause sudden death 2 hours post MI
sinus tach after MI
anterior wall MI, need to correct with adenosine to slow the rhythm, need to increase myocardial O2 demand, decrease systemic perfusion
PACs after MI
1/2 of all MI pts will have
a fib after MI
common with anterior MI, decrease CO, formation of clots
PVC after MI
most develop a few hours after MI, need O2, correct any acid imbalance, IV lidocaine, pronestyl, cordarone (amioderone)
2nd degree type 1 after MI
inferior MI, temporary pacer, or atropine if hemodynamically significant
2nd degree type 2 after MI
anterior MI, need pacemaker
accelerated idioventricular rhythm after MI
most common reperfusion rhythm, tolerated well, no Tx
what are the major goals of MI
tx the underlying cause, presume CO and tissue perfusion
MI complications are
thromboemboli, pericarditis, dresslers syndrome, ventricular septal rupture, ventricular aneurysm, cardiac rupture, papillary muscle rupture
have in deep veins of leg or chambers of the heart, can lead to stroke, pulm. emboli, peripheral arterial occlusion
thromboemboli
who is at high risk for emboli
severly ill, hx of valvular heart disease, greater than 60 years old, prolonged bed rest, a-fib/a-flutter
Tx for possible thromboemboli
heparin, Coumadin, OOB quickly, if have edema (bed rest until it clears)
inflammation of visceral/parietal pericardium or both
Pericarditis
causes of pericarditis
cardiac compression, decrease ventricular filling, decrease emptying and failure = result in cardiac tamponade
S/Sx of pericarditits
CP mild to severe, increase with inspiration, coughing, movement in upper body
sitting forward can relieve the pain
excess fluid in the pericardium causes what
tamponade, drained with needle, catheter or surgery
Hallmark sign of pericarditis
fricition rub, heard at left sternal boarder
also have fever, dyspnea, cough, EKG have ST segment elevation
Tx for pericarditis
Tx of Sx: pain, anxiety, decrease CO
give analgesics, anti-inflammatory, NSAIDs
when is pericardiocentesis used
if tamponade develops
look for JVD, listen for rub, assess for CP
Dressler’s syndrome
Post MI syndrome, occurs 10 days to 3 months post MI,
pleuritic type CP, hypersensitivity to products of necrotic myocardium
pericarditis with pleural effusion (called late pericarditis, may be an autoimmune response)
S.sx of dresslers syndrome
pleuritic pain, fever, increase SED rate & WBC, friction rub audible, left pleural effusion, arthralgia (joint pain)
Tx for dresslers syndrome
same as pericarditis, any CP must be Tx as a recurrent ischemic attack
analgesics, anti-inflammatory, NSAIDs
Ventricular septal rupture
develop rapidly, usually end in death, rare, when blood is shunted from LV to RV
S/Sx of ventricular septal rupture
hear new, loud systolic murmur, progressive dyspnea, tachy, pulm. congestion
Tx for ventricular septal rupture
urgent cardiac cath to surgically correct
after load reducers: Nipride
preload reducers: Lasix
non contractile thinned LV wall results in reduction of stroke volume, increase of stress on necrotic portion of LV wall, region bulges out during systole, and a scar forms
ventricular aneurysm
where does ventricular aneurysm commonly occur
in apical area, may develop in hours or weeks
Dx for ventricular aneurysm
palpate ectopic impulses, bulge noted on xray or ECHO
Tx for ventricular aneurysm
manage complications, may need surgery
What does prognosis depend on with ventricular aneurysm
size of aneurysm, LV function, severity of co existing CAD, rupture of aneurysm is rare
cardiac rupture
when you have leukocyte scavenger cells remove necrotic debris causing a thin cardiac wall, important for patients to continue to rest
S/sx of cardiac rupture
see sudden neck vein distension, hypotension (not bradycardia), PEA, happens rapidly, usually 5-6 days post MI
papillary muscle rupture
95% fatality rate, support the mitral valve, rupture causes mitral valve regurgitation
S.sx of papillary muscle rupture
dyspnea, pulmonary edema, decrease CO, increase volume in L atrium, hear systolic murmur
complete rupture of papillary muscle
acute mitral regurgitation, cardiogenic shock, high mortality rate
what does partial rupture cause
mitral regurgitation but can support need emergency surgery to replace the valve
an abnormal accumulation of fluid in alveoli and interstitial spaces, leads to LV failure and is life threatening, interferes with gas exchange between alveoli & pulmonary capillaries
acute pulmonary edema
patho of pulmonary edema
increase hydrostatic pressures or decrease colloid oncotic pressure, fluid leaves the pulmonary capillaries & enters interstitial spaces (edema),
common causes of acute pulmonary edema
left sided CHF (flash edema)
S/sx of acute pulmonary edema
paroxysmal nocturnal dyspnea*, agitation, pale, cyanosis, cool clammy, accessory muscle use, wheezing, coughing with frothy blood tinged sputum, increase of HR, increase or decrease of BP, increase of PaCO2 = acidosis
impaired cardiac function, ventricle is unable to maintain CO sufficient to meet metabolic needs
acute congestive heart failure
most at risk for CHF
HTN
what compensatory mechanisms are activated with CHF
adrenergic system, renin angiotensin aldosterone system, ventricular dilation/ventricular hypertrophy, increase of sympathetic nervous system
adrenergic system
release epi
increase PVR, blood is shunted from non vital organs to heart and brain, increases preload
renin angiotensin aldosterone system
constriction of renal arterioles
decreases GFR, increases reabsorption of Na, fluid retention = increase of CO
ventricular dilation/ventricular hypertrophy
stretches & increases ventricular wall thickness
hypertrophy helps the ventricle overcome the increase of pressure, increases afterload (remodeling)
*give ACE inhibitor
increase of sympathetic nervous system
increase of HR and contractility (increases the need for O2)
what do compensatory mechanisms affect
HR, preload, afterload, stroke volume, contractility
R sided CHF (cor pulmonale)
ineffective RV contractile function
most commonly caused by failure of the left side or blood backing up behind the left ventricle (JVD)
left sided CHF
disturbance of contractile function of LV resulting in pulmonary congestion or edema, decrease of CO, most frequently occurs with LV infarcts
acute vs. chronic
refers to the rapidity with which syndromes develop and the activation of compensatory mechanisms
S.sx of acute CHF & pulmonary edema
resting dyspnea, cachexia (wasting), orthopnea, weight increase, tachy, JVD (with R sided), apical pulse is displaced left and down, hear S3 & S4, crackles, wheeze, edema (symmetrical), cool shiny swollen no hair, brownish color, restless, hepatomegaly (ascities), void @ night increases
Goal of care with CHF
reduce edema and cardiac workload, increase CO, manage HTN, decrease afterload
Dx for CHF and pulmonary edema
H&P, ABGs, CXRay, hemodynamic monitoring, 12 lead EKG, ECHO (EF), cardiac cath, BNP, D Dimer
BNP
b type natriuretic peptide, hormone secreted by ventricular tissue in response to increase of volume and pressure
D Dimer
used to rule out blood clotting problems,
monitor Tx if in DIC
goals of therapy for CHF and pulmonary edema
decrease intravascular volume (Lasix) decrease venous return (preload) decrease after load (nipride, tridil, morphine) improve gas exchange improve cardiac function reduce anxiety (morphine)
Tx for CHF and pulmonary edema
HOB elevated, O2, bed rest, monitor VS, UO, daily weights, possible cardioversion (if hemodynamically unstable tachycardia), intubation, tx underlying cause
Medications for CHF and pulmonary edema
ACE inhibitors (1st lind Rx) Diuretics positive inotropic agents phosphodiesterase inhibitors vasodilators BB morphine natrecor
ACE inhibitors
(1st lind Rx, suppresses renin, increase CO, limits remodeling), SE: cough, if bad enough put on ARB instead
Diuretics
decrease preload and workload of heart, assess lung sounds, strict I & O
*if given too fast can cause hearing loss temporarily
Positive inotropic agents examples
Digoxin and dobutamine and dopamine
Digoxin
cardiac glycoside, decreases HR, increases muscle contractility, good for A fib A flutter, increases CO and SV
SE: N/V, HA, anorexia, double/blurred vision, confusion
Dobutamine and Dopamine
B adrenergic agonists
used short term in ICU, increases contractility, blood flow to renal, mesenteric, coronary and cerebral vascular beds
SE: increases ventricular irritability, increases O2 demand by myocardium
phosphodiesterase inhibitors
Inocar & Primacor
increase CO, promotes vasodilation, decrease SVR and PAWP
SE: arrhythmias, GI and decrease BP, thrombocytopenia
*need frequent assessments of BP
Nipride & Nitrates
increase cardiac performance, decrease after/preload
Nipride: very potent, have rapid decrease in BP, SE: N/V, confusion, tinnitus, *hypotension, long term can have cyanide poisioning
Tridil
relieves pain, arterial and venous vasodilation, relieves pulmonary congestion, decrease cardiac workload, decrease cardiac O2 consumption
SE: hypotension, HA
morphine
drug of choice if anxiety is an issue, causes vasodilation, induces decrease venous return, decreases pain, anxiety, myocardial demand
SE: decrease RR, brady arrhythmias, hypotension
natrecor
for refractory CHF and pulmonary edema (when not responding to other Rx)
relaxes vascular smooth muscle, inhibits Na and water retention, suppresses renin secretion, decreases aldosterone, decreases PCWP
SE: hypotension, arrhythmias, angina, HA, back pain, anxiety, nausea
IV drip depends on weight, frequent VS & I&O
what other therapies can be done for CHF and pulmonary edema
biventricular pacing (increases LV performance)
cardiac transplant
intra-aortic balloon pump (IABP)
VAD (bridge to transplant)
resynchronization
relies on electric leads to correct an arrhythmia, electrically stimulate heart muscle to synchronize contractions of ventricles only when lower chambers beat in harmony can they contract with enough force to push blood caring O2 through the body
what teaching can be done for CHF and pulmonary edema
diet: decrease salt (2 gram) fluid restriction (2000 ml/day) weigh daily (no more than 2 lbs/day) rest follow Tx plan
Pump failure, failure to maintain blood supply to the circulatory system and tissues, due to decrease of CO
cardiogenic shock
Cardiogenic shock is manifested by
decrease perfusion, hypotension, decrease or absent UO, change in LOC, sweating, pallor, initially tachy
etiology of cardiogenic shock
common cause is extensive LV failure with an acute MI, decrease of CO to systemic circulation, blood backs up into the pulmonary vasculature, filing heart tries to pump harder = decrease of CO and BP, decrease of blood to coronary arteries = ischemia (c/o CP, changes on EKG), metabolic acidosis
causes of cardiogenic shock
papillary muscle rupture, LV free wall rupture, end stage cardiomyopathy, cardiac tamponade, massive pulmonary emboli
patho of cardiogenic shock
decrease in perfusion of O2, the compensatory mechanism is exceeded (circulatory failure develops), impaired LV compliance, vasoconstriction, shock
initial management of cardiogenic shock
O2 and inotropic agents (digoxin, dopamine, doubtamine)
S.sx of compensation (cardiogenic shock)
tachy, increase BP(initial) /PAWP, cool, clammy skin, decrease UP, decrease urine Na, rapid deep respirations (resp. alkalosis { increase pH, decrease PaCO2), altered LOC, decrease bowel sounds, hyperglycemia
compensatory mechanisms eventually fail = decrease Bp, narrow pulse pressure, anaerobic metabolism and lactic acid build up (metabolic acidosis)
refractory stage
irreversible, all systems have cellular necrosis, Blood clots from DIC, inadequate cerebral perfusion, hypothermia, death
Dx of cardiogenic shock
H&P
decrease CBC, DIC screen increase, BUN increase, glucose increase, lactate increase, CXR (show ARDS),
nursing management for cardiogenic shock
control HR, ID and Tx cause, maintain airway, IV fluids (NS, LR, Hespan), Tridil, Nipride, correct any arrhythmias, VAD, heart transplant, nutrition (TPN/protein for wound healing), VS, UO, bowel sounds, hygiene (prevent skin breakdown), emotional support
medications for cardiogenic shock
vasopressors (dopamine) (maintain BP, increase contractility/CO)
monitor I&O, BP, HR, tissue sloughing
Dobutamine (preferred when no hypotension)
increases CO and SV with minimal increases in HR and BP
Inocor: decreases afterload and preload, relaxes vascular smooth muscle
Levophed (norepi) dilates coronary arteries, need a PA line, peripheral vasoconstrictor
stabilizes cardiovascular function, increases coronary and cerebral blood flow, does not correct shock, life saving measure after MI, and while waiting for transplant
IABP (intra-aortic balloon pump)
IABP
sausage shaped polyurethane balloon wrapped around a cath, positioned in the descending thoracic aorta, inserted into the femoral artery, inflated during diastole, deflates just before systole (synchronized with EKG)
what are the functions for the IABP
relieves the LV workload
forces blood into coronary arteries
decreases afterload
the inflation/deflation cycle is called
counter pulsation
where does the blood below the balloon go
propelled forward towards the PV system and enhances renal perfusion
what are the hemodynamic effects of IABP
increases diastolic pressure, coronary perfusion, O2 to the myocardium, decreases afterload, decreases HR
Balloon maintenance
catheter in groin must be protected from kinking or dislodgement, assess peripheral pulses, check for infection, HOB elevated 45 degrees or less, log roll, low dose heparin
what is a possible risk of IABP
thrombocytopenia
the longer the IABP is on, mechanical trauma from inflation/deflation destroys platelets
myocardial revascularization, Tx for CAD, use of arteries for bypassing areas of stenosis, done so distal myocardium can receive blood
CABG
what arteries are used for CABG
internal mammery artery (most common)
radial artery and inferior epigastric artery
pre op of CABG
stop smoking, pre cardiac cath, ECHO, stress, labs, teaching, pre op bath
intra op of CABG
large bore IV, EKG, central line, foley, NG, intubation, epicardial pacing for bypass, blood is diverted, CPB (cardiopulmonary bypass), once surgery is complete heparin is reversed with protamine sulfate, bypass is removed and heart is restarted
CPB (cardiopulmonary bypass)
venous cath sits in right atrium, machine oxygenates blood as flows and removes waste, anticoagulated, hypothermic, aorta is clamped, heart is arrested, then surgery is started
what do they use to arrest the heart
potassium
Post op CABG
early extubation, hemodynamic stability, pain management, care of 2 surgical sites (chest and leg)
complications with CABG
loss of appetite, swelling, diff. sleeping, constipation, mood swings/depression, muscle pain in shoulders, temporary muscle loss, fatigue, cardiac tamponade, arrhythmias, emboli, fever, hemorrhage, PE, Stoke, occluded graft, pancreatitis
MIDCAB
minimally invasive bypass direct coronary artery bypass,
done when have single vessel disease, low risk pt, uncomplicated valve repair, no bypass machine needed, several small incisions made between ribs, harvest L internal mammary artery and anastomose to LAD artery, lateral chest tube or mediastinal tube placed, use video assisted thoracic surgery (VATS)
nursing care for MIDCAB
IV nitro (decrease coronary artery ischemia) pain management, LOS 3 days
for pts with inoperable CAD who are not candidate for traditional procedures, create channels between the ventricular cavity and coronary microcirculation, allows for blood flow to ischemic areas, use high energy laser to create 20-40 channels in the myocardial wall
transmyocardial revascularization (TMR)
what do the new channels allow
stimulate new blood vessels to grow or may destroy nerve fibers to the heart
decrease angina
complications of TMR
murmur, arrhythmias, heart failure, perforation of vessels, bleeding, infection, damage to mitral valve, tamponade
most common initial therapy for angina, create or promote blood flow when nitrates cant anymore, cath with balloon inserted in the femoral artery to coronary artery through a sheath, insert cath just past the lesion, balloon is inflated and atherosclerotic plaque is compressed
percutaneous transluminal coronary angioplasty (PTCA)
what does the PTCA cause
angina, bc the vessels are blocked when balloon is inflated, may need to administer nitro
advantages of PTCA
alt to open heart surgery, performed under local anesthesia, eliminates recovery time, normal activity level in 1 week
what can be a complication of PTCA
acute coronary occlusion, coronary spasm, bleeding, re stenosis, psuedoaneurysm of femoral artery, arteriovenous fistula at sheath removal site
anti Xa goal
0.3-0.7
glycoprotein IIb/IIa
used for increased risk pt such as DM, females, angina, recent MI,
similar to PCTA but smaller laser on tip of cath, laser is for plaque ablation/restores blood flow, effective in restenosis of stents, extracting pacer leads and vein graft occulsions
laser angioplasty
expandable mesh like structure used to maintain patency by compressing the artery wall, resists casoconstriction, may be medicated
stents
plaque is shaved off using a rotating blade or high speed rotary device, and is then suctioned to prevent emboli, used to debulk lesions,
arthrectomy
bypasses the affected ventricle and allows the heart to rest, longer term use than IABP, used on left, right or both, battery operated mechanical heart, bridge to transplant
VAD (ventricular assist device)
LVAD
blood is diverted from L atrium, bypasses left ventricle sent to pump and returns via cannulation of ascending aorta
RVAD
blood is diverted from R atrium, bypasses right ventricle, sent to pump and returns via cannulation of pulmonary artery
candidates for VAD include
CHF, unable to wean from heart lung machine, awaiting transplant, an MI with cardiogenic shock
safety issues with VAD
don’t disconnect both cables that connect the controller to its power source at the same time, drink plenty of fluids to maintain blood flow through device
weaning criteria for VAD
intrinsic MAP of 60 or higher, CI greater than 1.8, may not survive
destroys ectopic cells in heart with heat through a cath, used to Tx atrial and ventricular tachycardia, have burning sensation and their heart beating faster after procedure
ablation
what is the standard practice in acute STEMI/MI , goal is to salvage myocardial muscle /open artery, cause lysis of the thrombus and reopen the obstructed artery (restore blood flow to affected tissue)
fibrinolytics
how long does it take for entire thickness (transmural MI) to be necrosed
4-6 hours
criteria for fibrinolytic
no more than 12 hours from onset of CP
ST segment elevation or new onset of LBBB
ischemic CP for 30 minute duration
CP unresponsive to nitro
no condition that would cause a predisposition to hemorrhage
contraindications of fibrinolytic
recent surgery (within 2 weeks) pregnancy or recent delivery Hx of stroke recent major trauma bleeding disorders recent organ biopsy prolonged CPR severe advanced illness severe renal or hepatic disease
what is the EO of fibrinolytic
coronary artery reopens in 30-90 minutes (increase perfusion, myocardial O2 with relief of Sx, zones of myocardial ischemia/size of infarcted area is limited, ST segment returns to baseline, CPK/CPK-MB will return to normal
Nursing management of fibrinolytic
Start IV lines, assess continuously, monitor EKG, bleeding, coag studies, avoid IM injections, monitor neuro, reocclusion may occur (watch EKG for St segment changes and dysrhythmias)
what evidence will you have if you have reperfusion
cessation of CP, reperfusion dysrhythmias (PVC, bradycardia, heart blocks, v tach (rare), ST segment resolution (back to baseline), CPK rises rapidly after reperfusion called washout
CPK
enzyme released by damaged myocardial cells
Ndx for fibrinolytic
ineffective cardiopulmonary…
acute pain
anxiety
deficient knowledge
what fibrinolytic agents are used
TPA (alteplase) RPA (reteplase) TNKase (tenecteplase) SK (streptokinase)* APSAC (anistreplase)* * non clot specific
what is used in conjunction with fibrinolytic therapy
anticoagulants (heparin) and antiplatelets (asa)
battery powered device that provides extrinsic electrical stimuli to cause cardiac contraction when intrinsic cardiac electrical activity is inappropriately slow or absent
artificial pacemaker
when is temporary emergency pacing needed
used for significant/hemodynamically unstable pts, bundle branch blocks, bradycardia with Sx, lyme disease, prolonged PR intervals
what will the QRS in the EKG strip look like with a paced beat
the QRS may be slightly widened, a paced beat is normally shown as a negative deflections
S.sx of a pt that may need a pacemaker
syncope, light headedness, fatigue, SOB, angina, hypotension, signs of decreased CO (biventricular pacemaker is needed)
fixed rate (asynchronous) pacemaker
does not sense, does not see what the heart is doing-fixed rate!, competes with intrinsic rate, used when potential to cardiac arrest
demand (synchronous) pacemaker
has a sensing circuit, will only fire on demand, senses when the heart rate is low
what are the 2 types of demand pacemakers
single chamber: most common, I atrium OR ventricle, it senses and paces
Duel chamber: senses and paces the atrium AND ventricle
unipolar lead wires
loop of conductivity large (larger spike) lead has a negative pole at tip of wire and positive at the generator
bipolar lead wires
conduction look is smaller, smaller spike, less electro-magnetic interference problems, pacers have both negative and positive poles on end of pacer wire
transcutaneous pacer
external pacer, quick and easy to use, not meant for long term use
transvenous pacer
Tx of choice, temporary, used to treat hemodynamically significant bradycardias, not effective in Tx ventricular standstill/PEA
goal for temporary pace controls
have low # for sensitivity (want it to be sensitive), R on T is biggest risk
epicardial pacing
electrode end of wire looped through or loosely sutured to epicardial surface of atria or ventricles/Post op CABG
permanent pacemakers
done with IV conscious sedation under local anesthesia in cath lab, permanent pulse generators powered by lithium batteries life span 10 years
what are the 3 basic functions of permanent pacemaker
sensing-pulse generator sees intrinsic beats
firing-delivers stimulus to heart
capturing-heart has responded to stimulus
pacemaker codes
A-atrium V-ventricles D- both atrium and ventricles I- inhibited R- rate responsive M- mulitiprogram
inhibited pacer
pacer turns off or inhibits output if hearts activity kicked in
triggered pacer
pacer turns on or fires if preset interval expires
VVI codes
commonly used, temporary transvenous pacer, ventricular pacing, ventricular sensing, good for afib
ventricular capture
ventricle responded to pacing stimulus, spike on EKG followed by wide QRS
native beat
also called intrinsic, represents pts own electrical activity
fusion beat
pacer fires at same time as intrinsic heart beat occurs, both forces simultaneously depolarize ventricles
ICD
fires when heart rate increases, has to distinguish if fast rate is sinus tach, SVT, afib, RVR or V tach
has criteria for discharge/shocking
tiered therapy
ability of ICD to deliver different types of therapy, cardioversion, d fib, antibrday pacing, also records and telemetry
active fixation
pacing lead with screw, barb, prong, hock or some device affixed to tip of lead embedded in myocardium to ensure stable placement
passive fixation
a lead not embedded, own tissue will grow around it and keep it in place
if a ICD goes off should the pt go to the hospital
yes!
implanted cardioverter.defibrillator
hx of spontaneous sustained v tach, sudden cardiac death,
pacemaker malfunctions: failure to capture:
ventricles failed to respond to pacing stimulus, EKG shows spike that occurs on time but not followed by QRS, increase stimulation threshold
pacemaker malfunctions: failure to sense
under-sensing, generator doesn’t sense intrinsic beats, EKG shows spike after QRS but earlier than it should
*if pacer is temporary-turn it off
what can happen if pacing occurs at random times
can cause v tach…NOT GOOD
what do pts with ICDs need to avoid
MRIs, TENS, lithotripsy
if you are going to cardiovert a pt with a temporary pacer what needs to be done
pacer must be turned off
forces produced by volume and pressure, which affect circulating blood throughout the body, used for critically ill pts, bedside monitoring
hemodynamics
why is hemodynamics needed
cardiac function, circulating blood volume, physiologic response to Tx
what are the indications for hemodynamics
critical care pts
- decrease CO
- deficient fluid volume or excess fluid volume (CHF)
- ineffective tissue perfusion
invasive catheter with tubing connecting the pt to the transducer, which receives the signal and converts it to electrical energy (monitor), have to flush system to keep patent
fluid filled pressurized tubing system
what needs to be done at the beginning of every shift
must “0” the transducer, the equipment needs to be calibrated to atmospheric pressure
*the transducer is open to air via the 3 way stop cock, and then a “0” will be displaced on the monitor
what needs to be monitored with entering the catheter for hemodynamics
needs to be monitored by waveform analysis bc it is entering the hearts chambers, threaded into the vena cava into the right side of the heart
draw a line from the 4th intercostal space to a midaxillary line on the side of the chest, it is a physical reference point on the patients chest that is used as a baseline for consistent transducer height placement, approximately the level of the atria
phlebostatic axis
where do you want the transducer located
want the air reference stopcock level with the phlebostatic axis, the tip of the catheter should be in line with transducer, to ensure accurate hemodynamic measurements
what position does the pt have to be in during hemodynamics
HOB needs to be elevated (0-60 degrees), make sure measurements are consistently taken at the same angle
what needs to be done with hemodynamics (nursing management)
accurately calibrate the equipment, know normal values, est. safe alarm limits, be able to troubleshoot any problems
damping
distortion of the waveform
a thermo dilution catheter capable of measuring cardiac output
Pulmonary artery (PA) monitoring aka Swan-Ganz catheter
the PA catheter can measure include
- pulmonary artery systolic & diastolic pressures
- pulmonary artery mean pressure
- pulmonary artery occlusion pressure (PAOP)or wedge (PAWP)
- cardiac output
- able to calculate additional measurement
measured through distal port, PA pressure reflects left and right sided heart pressures
PA and PCWP (pulmonary capillary wedge pressure)
the PA systolic pressure is produced b
the right ventricle (normal 15-27 mmHg)
Normal PA systolic/diastolic = 25/10
wen is increased PA pressure seen
atrial or ventricle septal defects, increase pulmonary blood flow as a result of L to R shunt, pulmonary HTN, LF failure, volume over load, ischemia, mitral regurgatatoin
indirect measure of LVEDP (left ventricular end diastolic pressure), balloon of the catheter is inflated, wedging in a small branch of the pulmonary artery for less than 15 seconds
Wedge pressure (PCWP) normal range is 6-12 mmHg
abnormal wedge (elevated)
an elevated wedge is going to cause decrease CO, this NEEDS priority intervention!
LV failure, ischemia, pericarditis, mitral stenosis or mitral regurg., fluid overload
abnormal wedge (decreased)
hypovolemia, venous dilating drugs
the amount of blood pumped out by a ventricle
HR x SV =
when peripheral tissue needs more O2, the normal healthy heart can augment HR and SV to increase cardiac output
cardiac output
what is a method to measure cardiac output
thermodilution
if pt is on PEEP what will happen to your PA pressure
will be increased
cold or room temperature solution is injected into the right atria part of the PT catheter. There is a thermistor near the end of the catheter that countinusouly measures the temperature of blood flowing past it
thermodilution
normal CO
4-8 l/min
normal CI
2.2-4.0 l/min/m2
what is the best indication for cardiac function
CI
normal SVR
900-1400 dynes/second/cm5
normal PVR
37-250 dynes/second/cm5
causes of decreased CO
decrease preload
increase of afterload
MI
complications of hemodynamic monitoring
infection**
thrombi, cardiac perforation, electrical microshocks, complete heart block, pulmonary infarction (balloon left inflated)
what can decrease complications with hemodynamic montioring
balloon needs to be completely deflated after a wedge pressure is obtained (pulmonary infarction),
electrical equipment needs to be grounded, less than 1.5ml of air to inflate balloon, need pressure bag on NS drip to maintain patency
measured through the proximal port in the right atrium, determines volume status and RV function, guide to overall fluid balance
Central venous pressure (CVP)
normal CVP
2-6 mHg
a decrease in CVP is do to
hypovolemia, venodilation, venous obstruction (mass) and decrease venous return
a increase in CVP is do to
increase blood volume, right sided heart failure with vasoconstriction, cardiac tamponade, positive pressure breathing, straining
represents the variation in stroke volume during the respiratory cycle, may be a better indicator of volume responsiveness than with a CVP or PCWP, need an A line waveform,
Stroke volume variation
stroke volume variation is only used in what kind of pt
mechanically ventilated patient
direct measurement of atrial blood pressure, intra arterial cath located in the radial artery, connect to the electronic monitor and a fluid filled pressurized tubing system
intra-arterial monitoring (A-line)
A line assessment
“Allen’s test”
occlude both ulnar and radial artery, pt needs to clench and unclench their fist, release pressure and observe for return of color to hand, if color returns in 5-7 seconds, circulation is adequate, if color returns in 7-15 seconds, circulation is impaired, longer than 15 seconds means inadequate circulation and the radial artery should NOT be cannulated
when is Allen’s test done
prior to insertion of intra arterial monitoring line (A-line)
complications with A-line
infection, accidental blood loss, impaired circulation to the extremity
represents perfusion pressure throughout the cardiac cycle, sensed by baroreceptors in the carotid sinuses and the aortic arch, basis for autoregulation by some organ systems
MAP (mean arterial pressure)
what does the MAP need to be to perfuse the coronary arteries
MAP greater than 60
normal is 70-100
ideal is to be able to maintain MAP between 65-75 mmHg
calculation of MAP
(diastole x 2) + (systole x 1) /3 = MAP
provides continuous assessment of the balance between O2 supply and demand
Central Venous Oxygen Saturation (ScV2)
normal ScVO2
75%
*in a critical pt 60-80% is adequate
this indicates adequate balance of O2 supply and demand
a ScVO2 of less than 60 % indicates
decrease of O2 supply or an increase of demand
a ScVO2 of more than 80% indicates
a decrease in demand or an increase in supply
most people extract 25% of O2 from Hgb, therefore venous return is =
75%
what pts is hemodynamics good for
shock, trauma, pulmonary & cardiac disease or multiple organ dysfunction syndrome (MODS), fluid management, hemodynamically unstable pts
Inferior wall infarction involves
Occlusion in right coronary artery
Anterior wall infarction result from
Occlusion of left anterior descending artery
Lateral or posterior infarction are caused by
Occlusion of left circumflex artery
Cardiac output is
The volume of blood in liters pumped by the heart in 1 minute
Cardiac index is
The measurement of CO adjusted for body surface area
Systemic vascular resistance
Opposition by the left ventricle
Pulmonary vascular resistance
Opposition encountered by the right ventricle
Preload
Volume within the ventricle at the end of diastole
An increase of PAWP and PAD pressure indicates
Heart failure or fluid volume overload
A decrease of PAWP indicated
Volume depletion
Normal cardiac resting output is
4-8 liters per minute
