Exam 2 Flashcards
atrial flutter is usually associated with
underlying CAD, rheumatic, or other heart diseases
what happens in atrial flutter
ectopic focus in the atria fires at 250-350 bpm
what node is the gatekeeper
AV node
atrial flutter
diff between cause of afib and a flutter
a fib can happen in healthy people
what happens in afib
ectopic focus in the atria stimulates chaotic impulses at 350-500bpm
afib vs aflutter ventricular rate
afib - irregular
aflutter - regular ventricular rate
p waves in atrial flutter
NO P waves
afib
goal for atrial arrhythmias
get back to 60-100 NSR
what is affected by ventricular rate
hemodynamic effects like BP and O2 and perfusion
what greatly affects cardiac output in atrial arrhythmias
loss of atrial kick and ventricular fililng time
3 medications for controlling atrial rate
Ca channel blockers
Beta blockers
digoxin
if patient has afib but is hypotensive what med to use
amiodarone because it doesnt affect BP
digoxin use / moa / problem
heart failure
controls HR and strengthens contractility
takes 2-3 days to go into effect
med for thrombus formation
heparin IV then oral warfarin
cardioversion vs defib 2
cardioversion =
lower energy
SYNCHRONIZED
when is cardioversion used
afib
warfarin onset/antidote
2-4 days (so start is when starting heparin)/vitamin K
apixaban onset of action
1-4 hours
if patient has renal insufficiency but needs warfarin what to order
labs - BMP
warfarin MOA
inhibits clotting factors that depend on vitamin K
cause of hypovolemic shock
decreased circulating volume from - hemorrhage, dehydration, GI or urinary losses, burns, pancreatitis, surgery, trauma
cardiogenic shock is result of
the heart’s inability to deliver adequate circulation to the tissues due to cardiac pump failure
distributive shock cause
Vasodilation and redistribution of blood volume.
Due to sepsis, spinal cord injury, and anaphylaxis.
obstructive shock cause
Occurs from impairment of cardiac ventricular filling or impairment of ventricular emptying.
Causes include cardiac tamponade, tension pneumothorax, and massive pulmonary embolism.
common s.s of ALL shock 10
Hypotension
high RR
high HR (except neurogenic)
Altered LOC
Hypoxia
Increased serum lactase because of low Oxygen switching to anaerobic
Metabolic acidosis
Decreased urine ouput
Pale and cool extremities
Dec bowel sounds
priority nursing diagnosis no matter the type of shock
ineffective tissue perfusion
s/s of hypovolemic shock
hypotension,
orthostatic hypotension,
tachycardia,
delayed capillary refill,
dry mucous membranes,
poor skin turgor,
thirst,
weight loss,
oliguria,
concentrated urine,
altered mental status.
cardiac output values in hypovolemic shock
reduced map, cvp, pawp, preload, stroke volume, cardiac output but elevated SVR
labs for hypovolemic shock
hypernatremia >145
inc hct in dehydration
low hct/hbg if bleeding
priority for hypovolemic shock
identification and correction of the source of blood loss
goal of blood and fluid admin in hypovolemic shock
restore tissue perfusion and oxygen transport
recommended MAP for restoration for shock
> 65
electrolyte complications of hypovolemic shock 2
hypocalcemia
hyperkalemia
6 nursing actions for hypovolemic shock
identification and correction of source of blood loss.
Application of pressure and preparation for surgery.
Establish and maintain large, functioning IV access.
Monitor fluid resuscitation parameters – MAP > 65, urine output > 0.5-1 mL/kg/hour, decreasing lactate level.
Monitor for respiratory compromise and pulmonary congestion.
Monitor for complications of renal insufficiency/failure and cerebral ischemia. (change in LOC)
Maintain patient safety – patients are at a high risk for falls.
types of distributive shock
neurogenic and anaphylaxis
cause of neurogenic shock
Occurs when a spinal cord injury to the cervical and upper thoracic spinal cord causes a temporary interruption in the sympathetic innervation leaving parasympathetic innervation unopposed.
s/s of neurogenic shock 5
parasympathetic!!
immediate loss of autonomic and motor reflexes below the level of injury.
vasodilation
redistribution of blood volume
WARM DRY SKIN
BRADYCARDIA
HYPOTENSION
LOW HR
hemodynamic findings for neurogenic shock
decreased MAP, CVP/RAP, and PAWP,
reduced preload
goal of tx for neurogenic shock
to restore adequate tissue perfusion by correcting vasodilation and bradycardia using fluid, meds(atropine)
5 priorities for patient in neurogenic shock
spine immobilization THEN airway and ventilation
monitor vitals
give atropine for bradycardia
IV fluids and vasopressors for hypotension
assess skin
dopamine
MOA
admin
SE 2
monitor
acts on beta 1, beta 2 and dopaminergic adrenergic receptors to increase cardiac contractility and afterload(increases Bp in high doses due to vasoconstriction).
given through CL
tachycardia (good for neurogenic shock), dysrthyth.
MAP- if not 65, increase dose
Norepinephrine
MOA
admin
monitor
potent alpha-adrenergic agonist. Vasoconstrictive, increases MAP with LITTLE CHANGE IN HR or cardiac output
CL
monitor urine output and kidney function
phenylephrine
moa
admin
assessment prior
SE
alpha receptor drug leading to vasoconstriction without an increase in heart rate. but increases BP, cardiac output and SVR
infusion pump CL
assess HR, BP, RR, O2
bradycardia, dec pulses, temp and paresthesia
anaphylactic results in 5
vasodilation, bronchoconstriction, GI contractions, dec blood volume and smooth muscle contraction,
s/s of anaphylaxis
wheezing,
dyspnea,
flushing,
uticaria,
nausea/vomiting,
diarrhea,
abdominal cramps,
palpitations,
dizziness,
hypotension,
tachycardia,
syncope,
anxiety,
feeling of impending doom.
priority of nursing care for ana 5
maintain airway
O2
monitor BP and HR
Epi without delay
antihistamines
epi moa
bronchodilation and vasoconstriction
obstructive shock cause
impaired ventricular emptying due to pulmonary embolus
s/s of obstructive shock due to PE
hypotension,
tachycardia,
chest pain
O2 <92
resp alkalosis
elevated d- dimer
oliguria
altered LOC
hemodynamic findings of obstructive shock
inc HR, CVP, PAWP, SVR
dec BP, CO
sign of tension pneumothorax
tracheal deviation
cardiac tamponaude tx
periocardiocentesis to remove fluid
tension pneumothorax tx
large needle or chest tube insertionq
pulmonary embolus tx
thrombolytic therapy/surgery
what to do after pericardiocentesis
they will have chest tube so make sure output is flowing good
8 nursing actions for obstructive shock
assist with the pericardiocentesis or chest tube insertion.
Maintain patient safety
Continuously monitor HR, BP, RR, and pulse oximetry.
Administer oxygen as ordered.
Promote patient comfort and provide reassurance.
Perform baseline neurologic assessment
administer thrombolytics without delay for pulmonary embolus,
monitor for signs and symptoms of bleeding and coagulation lab values.
1st degree heart block - prolonged and constant PR
look for drug toxicity because some meds can cause heart block
2nd degree block- wenchebach
progressive lengthenning of PR until QRS id dropped caused by drug toxicity, heart disease, myocarditis, acute rheumatic fever
treat with atropine if asymptomatic
2nd degree mobitz
CONSTANT PR interval
caused by drug toxicity, acute MI, vascular disease
treat with pacemaker
counting atrial rate
p waves
3rd degree block
complete AV dissociation
atrial rate > ventricular rate
caused by acute MI, drug toxicity
treat with pacemaker and maybe epi
temp pacemaker
used in emergency situations,
after open-heart surgery,
acute anterior/inferior MI with heart block
transvenous pacemaker
antecubital or central vein threaded to heart
epicardial pacemaker
after heart surgery , wires out of sternal incision connected to generator
transcutaneous pacemaker
through the skin with pads – least effective so used outside hospital or initially in ED until they can get another option
permenant pacemaker
used in patients with acquired 2nd or 3rd degree heart block, bundle branch block, cardiomyopathy, heart failure, tachydysrhythmias, SA node dysfunction. Can be combined with an ICD (implantable cardioverter-defibrillator).
nursing actions for pacemaker 5
ECG assessment
Assessment of the insertion site for bleeding/swelling/hematoma formation
Assess and address pain
Provide education/information
For temporary pacemakers,
adjust settings as needed
failure to sense
pacemaker set to 70, you see 82 and spikes - inc sensitivity
failure to capture
only see spikes- increase energy delivered
over sensing due to
coughing and pacemaker firing- dec sensitivity
failure to fire
change battery
8 education for pacemakers
Check pulse
Notify hcp of bleeding and infection at insertion site usually happening at day 3
Can shower after 48 hours
Avoid heavy lifting and lifting arm for a month
Report Feeling shocks
No electronics or cell phones in pocket
Avoid metal detectors
Medical alert bracelet
swan ganz/thermodilution catheter is used to
monitor preload (CVP/RAP, PAWP), afterload (SVR) and cardiac output.
and to to obtain cardiac output/index values (svo2) by thermodilution
describe thermodilution
(cold NSS injected and catheter reads the time/temperature as the NSS moves through the heart to provide values).
benefits of swan ganz catheter 4
monitors pressures, preload, give fluids, check CO
pulm wedge pressure is
tells us preload for L side of the heart
right ventricular pressure wave
spikes(contractions)
pulmonary artery pressure wave
systole and diastole and continuous numerical readings
pulmonary artery wedge pressure wave
inflate balloon here , wave dampens and it gives you number for pressure - then deflate baloon - if you see dampened wave and are not in PAWP notify hcp!!
arterial line used for
continous BP monitoring and to draw blood
swan ganz catheter consideration
leveled at phlebostatic aixs when patient is in supine position
arterial catheter consideration
perform allens test prior to insertion in radial artery, and perform NV assessment of extremetities q shift
general care for hemodynamic monitoring devices 9
aseptic
prime and flush with NSS/heparin
remove air bubbles
inflate pressure to 300
prevent kinks
monitor insertion site
connnect to transducer
zero system
perform square wave test
4 steps to allens test
Compress the radial artery, then
Compress the ulnar artery and have the patient open and close their fist.
Release the ulnar compression and observe for blood return to the hand.
If ulnar compression is released and blood does not return to the hand, the radial artery should not be used for arterial line insertion.
preload
volume of blood in the heart (specifically the left ventricle) at the end of diastole.
afterload
force the right ventricle must generate to eject blood into the pulmonary vasculature and the left ventricle must generate to eject blood into the aorta (left ventricular resistance is systemic vascular resistance).
cardiac output
volume of blood pumped by the heart in 1 minute.
cardiac index
cardiac output adjusted for BSA.
svo2
% of O2 bound to Hgb returning to the right side of the heart after the tissues have extracted what they need.
2 measures of preload
CVP and PAWP
CVP
reflects preload of the right side of the heart, normal 2-6 mmHg
PAWP
reflects preload of the left side of the heart, normal 5-12 mmHg
when is preload increased and decreased
Increased in fluid overload, CHF, pulmonary edema and cardiogenic shock
Decreased in hypovolemic shock
measure of afterload
SVR - normal 800-1200 Dynes
when is SVR increased and decreased
SVR may be increased initially in hypovolemic and septic shock as a compensatory mechanism, but then decreases
SVR remains increased in cardiogenic shock as a compensatory mechanism and due to circulating catecholamines
As SVR increases, cardiac output decreases
cardiac output
Determined by Stroke Volume (SV) X Heart Rate (HR)
Normal 4-8 L/min
when is cardiac ouput decreased
shock
cardiac index
divided by BSA (body surface area) of the patient and is a more precise measurement of the pumping action of the heart. Normal 2.2-4 L/min
MAP
Normal MAP is 70-105 mmHg, a minimum of 60 mmHg is needed to maintain perfusion to vital organs, and a MAP of 65 mmHg is usually the goal when vasopressors are administered.
SVO2
Normal is 65-75%. Readings can help determine if the patient’s cardiac output and oxygen delivery are high enough to meet the patient’s needs.
scvo2 and factors that affect it
levels are higher (3-11% higher) because they are not true ‘mixed’ samples.
cardiac output, hemoglobin levels, arterial oxygen saturation, oxygen demand.
acute decompensated HF characterized by
development of dyspnea associated with rapid fluid accumulation in the alveolar and interstitial spaces of the lungs
R ventricular filling causes
peripheral and organ edema
L ventricular filling in HF causes
fluid to build up in the lungs and
What lab study is particularly helpful in assessing heart failure? What are normal values and what other factors can affect this test?
underlying cause of ADHF
either diastolic in nature (failure of the ventricle to relax and fill) or systolic in nature (failure of the ventricle to stretch and contract effectively).
s/s of ADHF
same as cardiogenic shock except not always hypotension
leading cause of mortaility among complications of ACS is
cardiogenic shock
most common cause of cardiogenic shock
left ventricular failure following a MI
s/s of cardiogenic shock
restlessness,
anxiety,
agitation.
Cyanosis,
pallor,
cool/clammy skin,
decreased capillary refill.
Tachypnea,
pulmonary congestion.
Decreased cardiac output (< 2.0 L/min) and cardiac index,
decreased BP < 90 mm Hg,
increased pulmonary artery wedge pressure (PAWP) > 18 mm Hg.
ABG with metabolic acidosis and hypoxia.
Serum lactate level > 4 mmol/L.
Reduced mixed venous oxygen saturation.
Decreased urine output,
Na/H2O retention.
Decreased bowel sounds/peristalsis.
4 ways to improve cardiac output
Controlling heart rate
Decreasing preload
Decreasing afterload
Improving contractility
how to control HR in cardiogenic shock
digoxin, calcium channel blockers, beta adrenergic blockers
how to control dec preload and afterload in cardiogenic shock
nitroglycerin, nitroprusside, morphine and diuretics, and sodium restriction
how to improve contractility in cardiogenic shock
inotropic medications: dopamine, dobutamine, digoxin, milrinone
when are ACE and arbs used
when pt is recovering from HF and has reduced ejection fraction
Nesiritide
use
moa
SE 5
for HF
inhibits ADH production and vasodilates which results in inc urine output, dec PAWP, dec preload and dec dyspnea
hypotension, arryhthm, circulatory collpase, electrolyte imbalance, renal insufficiency
IABP (intra-aortic balloon pump)
improves cardiac output - counter-pulsation device, increases blood flow to the coronary arteries and decreases afterload
impella
designed to propel blood to decrease the work of the heart
ventricular assist device
takes over work of the ventricle to allow time for rest and healing, or as a bridge-to-transplant
How does the nurse know if the mechanical intervention to improve cardiac output is effective?
What assessment findings would indicate improvement?
What assessment findings would indicate a complication?
- urine output, dec swelling, skin color, improved SOB and O2 stat, less crackles, improved LOC, not tachycardic
complications: pale skin/cyanosis/cool and clammy, bleeding, loss of pulses distal to device, altered labs
nursing responsibilities for mechanical devices in cardiogenic shock 7
evaluating arterial pressure values and tracings (balloon inflates at the start of diastole and deflates before onset of systole).
Monitor for alarms indicating a leak or loss of augmentation.
Monitor for blood in the extender tubing.
keeping the head of the bed < 30 degrees and avoiding hip flexion.
Monitor urine output hourly.
Assess for complications – limb ischemia, bleeding, infection, and thrombocytopenia (patients are anticoagulated using heparin infusion).
Monitor hemodynamic status continuously.
stroke volume
The volume of blood pumped out of the left ventricle of the heart during each systolic cardiac contraction.
what affects stroke volume 7
reduced or increased preload
decreased contractility
decreased filling time
heart size
fitness level
gender
contraction duration
normal CO value
4-8
