Cardiac A&P CAD week 1 Flashcards
Perfusion: Priority assessment
BP MAP Pulses Cap Refill LOC Bowel Sounds Urine Output Pain Skin Color Temperature
Perfusion: how do we know perfusion is adequate?
A/O MAP > 65 UOP > 30 mL/hr Pulses wnl Warm to touch Tissue color wnl
What are priority labs for perfusion?
Priority Labs Hgb/Hct, RBC Protein/Albumin BUN/Creat Cardiac & Liver Enzymes BNP
What are signs of inadequate perfusion?
Light headed Confused Sensation loss Decreased organ function Ischemic pain Cell & Tissue necrosis
Describe the blood flow through the heart
Blood comes from periphery, RA, RV, pulmonary vasc., LA, LV, out thru aorta to rest of body
Preload
volume of blood in ventricles at end of diastole (end diastolic pressure)
What might preload be increased?
hypervolemia
regurgitation of valvse
HF
Afterload
Resistance left ventricle must overcome to circulate blood
the pressure the heart is pressing against
When might afterload be increased?
hypertension
vasoconstriction
What should a nurse do if patient has low CVP?
fluid replacement
What should a nurse do if patient is hypervolemic?
adminster diuretic
What should right atrial pressure be?
2-8 mmHg
What should systolic pulmonary pressure be?
15-25 mmHg
What should diastolic pulmonary pressure be?
8-15mmHg
What is the SA node?
Pace maker of heart; initiates heart beat for atrium
What is AV node?
AV node = gate keeper; decides how many beats get to go through to ventricle
What is s3 heart sound
Extra heart sound - indicates that patient has extra volume on boared; however, this can be normal in children and pregnant women
What is s4 heart sound
Abnormal, heart is resistant to volume coming in
Describe the 5 areas for listening to the heart and where they are?
a. Aortic: R 2nd intercostal space
2. Pulmonic = L 2nd intercostal space
3. Erb’s point = S1 and S2, L 3rd intercostal space
4. Tricuspid = Lower left sternal border, 4th intercostal
5. Mitral = L 5th intercostal, medial to midclavicular line
Geriatric considerations: mycocardium
Thicker and stiffer valves (calcified)
SNS does not respond as well
Baroreceptors do not respond as fast to pressure changes
Aorta and arteries calcify
Geratric considerations: women
Heart and it’s vessels are smaller; harder to work on; more effort
geriatric considerations:
Onset of heart disease sooner than females
CAD patho
Lipids deposit leading to endothelial injury and inflammation of the artery
- progressive disease
- fatty streaks
- fibrous plaques
- complicated lesions with thrombus formation
CAD assessment
family hx
non-modifiable risk factors
s/s occlusion (angina and poor perfusion)
risk factors / lifestyle
CAD labs and diagnostics
- C Reactive Protein
- Serum Cholesterol Levels
- Fasting Glucose > 100 mg/dL increases the risk
What is C reactive protein
measures inflammation
CAD interventions
Promote PA and nutrition
Stop smoking, drinking too much and using substances
Monitor blood levels with risk assessment
CAD Complications
ACS / unstable angina
MI
Sudden cardiac event that can be fatal
CAD medications
Simvastatin and Niacin (for cholesterol)
Low dose aspirin
Ezetimbe (lowers cholesterol)
CAD education
diet decreased in saturated fat and increase in plan based - polyunsaturated
exercise 30 minutes a day most days
What to obtain from health hx
family hx hx s/s common complications medications nutrition elimination activity sleeo
What do we evaluate with the lungs
Hemoptysis
Cough
Crackles
Wheezes
What do we evaluate with the abdomen
Distension Hepatojugular reflux - Patients reclining and as you push on liver Pulsatile mass - Anuerism in abd
What are common skin findings with CAD
Clubbing Cool skin & diaphoresis Cold, pain or pallor of toes or fingertips Peripheral cyanosis Ecchymosis or bruising Edema Hematoma Pallor Rubor Feet and ankle ulcer Thinning of skin around a pacemaker or defibrillator Xanthelasma (yellow plaques observed along nasal portion of eyelids)
Why would an angioplasty be used and how does it work?
USE: Build up of cholesterol partially blocking bloodflow through artery
a. stent with balloon inserted into partially blocked artery
b. balloon inflated to expand stent
c. balloon removed from expanded stent
d. the expanded stent now allows for adequate blood flow
Cardiac markers: Troponin
Should be less than 0.4
Peak in 10-12 hours, normalize in 10-14 days
Cardiac markets: Ck with MB
38-174 u/L
MB< 5% increase 4 hours peak 24 normal 48
Cardiac markers: myoglobin
(5-70 mcg/mL, increase 1-3 hour peak 12 hour)
What values should the 4 different types of lipids be at?
Cholesterol < 200
Triglycerides < 150
LDL 100-129
HDL 60
Brain naturetic peptide range
< 100
C reactive protein value
< 3.0
Homocysteine value
4-15
Holter monitor
ECG someone wears for couple of weeks to evaluate heart
Implantable loop recorders
only record when patient has s/s
used for infrequent s/s of patients
Trans telephonic monitoring
Transmit ECG via telephone
Diagnose arrhthmias and pacemaker evaluation
Wireless moblie cardiac monitoring systems
Transmits arrythmias via telephone for early intervention; can be challenging for elderly
What is an electrocardiogram?
Shows the electrical impulses thru the heart
- each phase of the cardiac cycle is reflected by specific wave forms
What are the different waves of ecg and what do they represent?
P wave - atrial depolarization (atrial contraction)
QRS complex - ventricular depolarization (ventricle contraction)
T wave - ventricular repolarization (ventricle relaxing)
U wave - relaxing of purkinje fibers
Where does atrial contraction (P wave) take place?
SA node
- atrium in heart contracting (depolarization)
what is a U wave?
not common in clinical setting - believed to be produced by the resting of the purkinje fibers
PR interval
starts at the P wave (atrial contraction), ends right before ventricle contraction
ends essential at the AV node (gatekeeper)
ST segment
starts at end of QRS complex (ventricular contraction), and ends right before T wave
important when diagnosing MI
What are arrhythmias / dysrhythmia?
disorder of the formation or conduction (or both) of the electrical impulse within the heart, altering the heart rate, heart rhythm, or both and potentially causing altered blood flow
What people are at risk for arrhythmias?
Aging population, heart disease, polypharmacy, drug interactions with drug users
What is a condition in which you would see a U wave
hypokalemia
How are readings of ecg categorized
sinus
atrial
ventricular
How do you tell the heart rate on ECG
count each QRS segment (1 segment = 1 heart beat)
What is a sinus arrhythmia?
Sinus nose creates an impulse at an irregular rhythm; clinically insignificant
When might we see sinus arrhythmia?
sometimes associated with respiratory cycle
occurs frequently in young and decreases frequently with age
Describe sinus arrhythmias in comparison with respirations
Rate is the arrhythmia increases with inspiration and decreases with expiration
What is sinus rhythm?
the normal rhythm of the heart where electrical stimuli are initiated in the SA node, and are then conducted through the AV node and bundle of His, bundle branches and Purkinje fibres. Depolarisation and repolarisation of the atria and ventricles show up as 3 distinct waves on ECG.
Sinus bradycardia: patho
Sinus nose creates a slower than normal rate
What may cause sinus bradycardia?
lower metabolic needs vagal stimulation medications increased ICP MI
What are clinical manifestations of sinus bradycardia?
Rate less than 60 BPM; all other measurements on ECG are normal
Serious: confusion, chest pain, hypotension
Sinus bradycardia: medical and nursing management
Only treated is serious s/s present
- confusion, chest pain, hypotension
hypotension –> trancutaneous pacing, atropine, dopamine or epinephrine (atropine first)
Sinus tachycardia: patho
Sinus nose creases an impulse that is faster than normal
Sinus tachycardia: cause
Physiologic (compensating for o2 demands), stress, medications that stimulate SNS
Sinus tachycardia: clinical manifestations and assessment
Rate greater than 100 BPM
All other measures are normal
Sinus tachycardia: medical and nursing management
ID and treat cause
Fluid replacement if patient is hypovolemic
Atrial flutter: patho
atrium impulses at regular but rapid rate (between 220-350 times per minute)
SA node letting out many impulses and the ”gate keeper” (AV node) says no no no no no (stays closed)…OKAY you can go thru (opens) and this is all the fluttering you see on the ECG
What do you see on ECG with atrial flutter
No P wave - flutter wave
What might cause atrial flutter?
emboli
Atrial flutter: clinical manifestations and assessment
may or may not be symptomatic
Atrial flutter: clinical and nursing management
Cardioversion
Ablation
Atrial flutter: medical management
DIG BB Calcium channel blockers Amiodarone Anticoagulant
Atrial fibrillation: patho
Atria is fibrillating – not even a controlled attempt at contraction
– think of wiggling a bowl of jello
20-30% of blood in that chamber going to ventricle – loss of volume
Who is at risk for a fib
Age, valvular heart disease, CAD, hypertension, heart failure, cardiomyopathy, DM, OSA, obesity, pulmonary disease, hyperthyroidism, surgery (open heart)
5 time increase risk for CVA r/t emboli
Atrial fibrillation: clinical manifestations and assessment
may or may not be symptomatic
decrease cardiac output r/t decrease filling time
Atrial fibrillation: medical and nursing management
Control ventricular rate
Prevent thromboembolism
Cardioversion (rhythm control)
Atrial fibrilation: medications
Dig BB Ca2+ channel blockers Amiodarone Anticoagulants
Premature ventricular complex: patho
Starts in the ventricle and conducted before the next normal sinus impulse
Premature ventricular complex: causes
Caffeine, nicotine, alcohol
acidosis, hypokalemia, hypoxia
increased occurance with aging and considered a marker in CHF
What can premature ventricular complex lead to?
cardiac ischemia and infarction
Premature ventricular complex: clinical manifestations and assessment
Bigeminy, trigeminy, couplet, triplet
Multifocal, unifocal
Premature ventricular complex: medical and nursing management
treat cause (hypokalemia
Ventricular tachycardia: patho
Three or more ventricular beats at a rate of 100bpm
Ventricular tachycardia: causes
MI, hypokalemia hypomagnesemia, CMP, long QT
Ventricular Tachycardia: clinical manifestations and assessment
Monomorphic or polymorphic (torsades)
Decreased cardiac output, pulselessness
Ventricular Tachycardia: management
Amiodarone
Lidocaine
BB
Cardioversion or defibrillation
Ventricular fibrillation: patho
Rapid, disorganized ventricular rhythm
Unsuccessful treatment of VT
Ventricular fibrillation: manifestations
irregular
pulseless
cardiac arrest and death are imminent
Ventricular fibrillation: management
CPR Defibrillation Epinephrine Amiodarone Lidocaine Magnesium
Ventricular asystole: patho
No cardiac activity
Ventricular asystole: manifestations
no pulse, death is imminent
Ventricular asystole: management
CPR
Poor prognosis
Hypothermia is really only good change for recovery
What are signs and symptoms of low blood pressure?
Dizzy/light headed Blurred vision Rapid HR Fatigue Lack of concentration Cold, clammy skin
Pulseless electrical rhythm: patho
may have organized electrical rhythm on the monitor but not breathing and pulseless
Pulseless electrical rhythm: causes
Temperature, tamponade, toxins, hypovolemia, electrolytes (K+), acidosis
Pulseless electrical rhythm: management
CPR
Heart blocks
Occur when there is damage to the conduction system of the heart OR ischemia
Heart block - new onset
new onset is a sign of worsening symptoms or can be precursor to further blocks rhythm changes
What are the types of heart blocks
First degree AV block
Second degree type II
3rd degree
total
go look at the ECG of these slide 48
What are the types of pacemaker therapy
transcutaneous
endocardial leads
transvenous
dual chambers
What should you see on ECG when someone has a pacemaker
Pacemaker spike, ECG complex should follow
P wave should follow an atrial pacer
QRS should follow a ventricular pacer
- capturing
Pacemaker therapy: complications
bleeding infection displacement of leads restrictions following placement patient should know rate
Electrical cardioversion
Delivery of a timed electrical current to terminate a tachyarrythmia
The defibrillator is set to synchronize and discharge during the ventricular depolarization
Synchronize prevents the delivery on the T wave, which could result in V fib
What are nursing assessments for someone who is receiving cardioversion?
DIG held 48 hours prior
NPO at least 4 hours
Monitor airwar
Assess for signs of embolism
What do electrical cardioversion joules depend on?
type of technology and arrhythmia: 50-200
What is defibrillation?
Used on patient WITHOUT pulse - not used with patient has pulse
200-360 joules
not synchronized
CPR immidiately following defibrillation of there is not a return of pulse
Implantable cardiac defibrillator: use
terminates life threatening episodes of tachycardia or fibrillation
Deactivation of subcutaneous implantable cardioverter defibrillator (S-ICD) at end of life
will allow the natural death to occur instead of the shocks with arrhythmia at the end of life
Cardiac arrest: patho
ventricular fibrillation OR ventricular tachy; profound bradycardia
- asystole
- PEA
Cardiac arrest: manifestations
Consciousness BP pulse are lost, eyes begin dilating within 45 seconds, seizures may or may not occur
Cardiac arrest: emergency management
CPR
CAB (Compression, airway, breathing)
How long does a normal PR interval last
0.12-0.20 seconds
how long is each small box on the EKG?
0.4 seconds
What are the 5 steps to interpreting ECG?
- P waves presents? How many in 6 seconds
- P waves regular?
- R waves regular?
- How many R waves in 6 seconds
- Length or PR interval and length of QRS complex
