Final Flashcards
Dysrhythmias are caused by
Hypoxia, Ishemia, Sypathetic stimulation, drugs, Electrolyte imbalance, rate, stretch
1 reason adult cardiac arrest
underlyning heart problem. Kids- resp failure/ sepsis
Heart blood path
Superior Vena Cava, Inlet of the superior vena cava, right atrium, inlet of the inferior vena cava, Coronary sinus, Inferior vena cava, Coronary sinus, Inferior vena cava, Tricuspid valve, Right Ventricle, Interatrial septum, Interventricular Septum, Left atrium, Mitral valve, Left ventricle
Heart conduction
- SA Node
- AV node
- Bundle of His
- Bundle branches
- Purkinje fibers
AV node
- Conduction is delayed at the AV node to allow the ventricles to fill with blood
- Also limits the rate of ventricular stimulation during excessive atrial firings
Purkinje fibers
Finger like branches that penetrate the cardiac muscle
Properties of cardiac muscle
- Contractile muscle fibers
2. Auto-rhythmic cells
Contractile muscle fibers
Responsible for pumping activity of the heart, Make up bulk of musculature of myocardium
AutoRhythmic cells
Make up 1% of cardiac cells, most found in SA node, cause myocardial fibers to contract, stimulate and create action potential
Four properties of cardiac muscle
- Automaticity
- Excitability
- Conductivity
- Contractility
Excitability
Response to stimulation or irritation, Ischemia and hypoxia cause myocardial cells to become more excitable (irritated)
Conductivity
Unique ability of the heart cells to transmit electrical current from cell to cell throughout the entire conductive system
Contractility
Is the ability of cardiac muscle fibers to shorten and contract in response to an electrical stimulus
Electrolytes responsible for electricity
- Potassium (K+)
- Sodium (Na+)
- Calcium (Ca2+
Nervous system role
plays important role in the rate of impulse formation, conduction, and contraction strength
Sympathetic stimulation role
- Cause increase in HR
- Increase in AV conduction
- Increase in heart contractility
- increase in excitability
Parasympathetic stimulation role
- Decrease in HR
- Decrease in AV conduction
- Decrease in contractility
- Decrease in excitability
5 leads
White in the clouds over grass (green), with crap in the middle, then smoke (black) over fire (red)
Ectopic beat
any beat outside of SA node
foci/focus
where the ectopic beat originates
dysrhythmia
abnormal cardiac conduction, also termed arrhythmia
Escape Beat
a heart beat that originates outside the sinus node after a period of SA node inactivity
Myocardial Ischemia
partial or complete obstruction of blood flow, reducing oxygen supply to the heart
Angina
chest pain associated with reduced coronary blood flow
Stable-persistent, with excertion. Unstable-unexpected, at rest, more intense and longer
Myocardial infarction
death of muscle tissue
Atrial Kick
Responsible for cardiac output (10-30% ventricular filling)
Heart block
Conduction stopped or insignificantly delayed
Automaticity
ability of heart to beat on own
Normal rates: SA Node, AV junction, Bundle Branches, Purkinje Network
SA- 50-100
AV- 40-60
Bundle-30-40
Purkinji- 30-40
Steps to reading ECG
- HR
- Heart rhythm (reg/ irreg) R-R interval
- Presence of P wave
- Is there a QRS following each P wave
- PR interal (is it less than 0.20)
- QRS complex (Is it less than 0.12 seconds)
- ST segment (baseline)
PVC
Wide ectopic beat from ventricles
ECG run at same speed of
25mm/sec
Large ECG square
0.20, containing 5 small squares (0.04s)
1 minute= 5 large boxes
Ventricle rhythm, comparing the R-R ratio with the longest/ shortest… how many seconds to make irregular
> 0.12
Pwave
Represent atrial conduction originated in the SA node, Paces the heart.
- Less than 2.5 mm in height
- more than 0.10 seconds in length
PR Interval
Normal 0.12-0.20 seconds
-Longer= delay in conduction through the AV node (AV block)
Complete heart block=
third degree heart block
QRS Complex
-Normal is less than 0.12 seconds long,
Represents ventricular depolarization
Rules of QRS
- If the first deflection is downward than it is a Q wave
- The initial upward deflection is an R wave
- The first neg. deflection following R is an S wave
- QS is a negative deflection with no positive deflection at all
- regardless of missing waves it is still called QRS complex and represents ventricular depolarization
Twave
reflects ventricular repolarization, inverted T waves suggest ischemia
ST segment
Normally baseline, A depressed ST segment suggests myocardial ischemia
-an elevated segment suggests myocardial infarction
Sinus Dysrhthmias
Sinus bradycardia- Regular rhythm, HR < 60bpm,
Sinus tachycardia- Regular rhythm, HR 100-160bpm
Supraventricular tachycardia
Ventricular rate: 150-250bpm
- Regular rhythm
- P waves may be hard to see
- Narrow QRS
- Connect SVT to adenosine as first line drug
- Cardioversion
Complications of A. Flutter
-Diminishes atrial filling: results in minimal atrial assistance in filling the ventricles (10-30% CO)
-Development of thrombi in atrial walls: need for blood thinners
(blood in atrial for too long)
Tx of A. Fib
Reduce the heart rate with cardioversion,
Medication to maintain normal rhythm:amiodarone,
medication to control ventricular rate: calcium channel blockers, beta blockers,
Medication to reduce atrial thrombus: coumadin, Pradaxa, Xarelto, Eliquis,
Cardiac ablaton: burn places in heart
Associated causes of A. Flutter/ A. Fib
COPD, CHF, Valvular heart disease, Chronic hypertension, Ischemic heart disease, MI
First Degree AV block
Normal rate, regular rhythm, one p wave before each QRS,
- PR prolonged and constant (longer than 0.20)
- usually no tx needed
Second Degree AV block- Wenkebach type 1
- Progressive prolongation of the PR interval until a Pwave is not conducted
- Patterns repeats itself
- it occurs when an abnormality in the AV junction delays or blocks conduction of some of the impulses through the AV node
Second Degree AV block- Mobitz type II
PR intervals: for conducted p waves, P-R intervals is consistent (normal or can have a 1st degree block), muliple p waves not followed by QRS wave
Mobitz type II result from
serious problem such as MI or ischemia, requires tx to improve cardiac output, pacemaker is indicated
3rd degree (complete) AV block
Normal everything, but no measurable PR intervals, heart must pace to maintain acceptable cardiac output
List one major complication/ risk of having Atrial fib.
Thrombi= must be on blood thinners, and emboli= stroke
H’s and T’s
Hypovalemia Hypoxia Hydrogen Ion (acidosis) Hyper/Hypokalemia Hypothermia
Tablets Tamponade Tension Pneumothorax Thrombosis-coronary (MI) Thrombosis-Pulmonary (PE)
Hydrogen Ion
Check if its acidosis/ or metabolic… fix with bicarb when acidosis
Hyper/Hypokalemia fix
Hyperkalemia-fixed with albuterol
Hypokalemia- fixed with potassium
Tamponade
Cardiac, Relieve pressure around heart (squeeze)
Thrombosis- coronary
MI- clut buster
PCI-Stent-relieve block, angioplasty-open up, see block
Thrombosis - pulmonary
PE- Clot buster
Remove clot
Run of 3
Run of v. tach: loses C.O.
Happens every 2? Bigemity
Every 3? Trigemity
Ventricular Tachycardia
-Three Consecutive PVC’s is considered a “run” of ventricular tachycardia
-Ventricular Rate= 100-250 bpm
-Ventricular rhythm essentially regular
-QRS > 0.12 seconds
-Ventricular tach without a pulse is an emergent situation. BLS should be initiated as soon as possible and the pt defibrillated
DONT DELAY SHOCKING
Ventricular tachycardia shocking?
Can have with or without pulse
With pulse-Can cardiovert
Without pulse- Defib/ CPR 2 min then check/ push meds= restore CO
Polymorphic V. Tach
Twisting of points
V. tach common causes
- MI
- Myocardial Ischemia
- Pt may become severely hypotensive to the point of syncope
- Cardiac output may deteriorate significantly causing the pt to become unresponsive
- Serious arrhythmia, often leading to ventricle fibrillation
Torsade De Pointes
THINK MAGNESIUM-important in muscle contraction
Polymorphic Ventricular Tachycardia (PVC)
“twisting of points”
Caused by multiple things
-Drugs including: antidepressants, antidysrhythmics, eating disorders, and electrolyte imbalances
-Treated with mg sulfate (in crash cart)
V. fib tx
Follow pulseless ventricular tachycardia/ ventricular fibrillation ACLS algorithm
Compare asystole and PEA, SHOCK ASAP
Asystole
- Complete absense of electrical and mech activity
- no cardiac output
- Flatline: used to determine clinical death
- must confirm in two leads
Tx: Follow asystole/ PEA ACLS algorithm
Remove monitors
Can only do CPR and EPI
PEA
Pulseless Electrical Activity
Connected to Asystole
-Electrical Pattern that is seen on EKG or rhythm strip, bud does not produce a pulse
CAB
Circulation- most important
Airway
Breathing
check PETCO
External defibrillator
Can also perform cardioversion, external heart pacing-transcutaneously shocking or pacing(capture to see NRG is strong enough), synchronizing
Defibrillation
Delivery of a uniform current of sufficient intensity to depolarize ventricular cells and terminate the abnormal heart rhythm
- Momentary asystole provides opportunity for SA node to regain control
- Also called unsynchronized counter shock
- Monophasic 360 or biphasic 200
Rhythms that we Defibrillate
Pulseless V. tach and V. fib
Cardioversion Rhythms
SVT! Unstable tachycardia, Unstable A. flutter or A. Fib, High ventricular rate= 150bpm or more
- No CPR , patient is awake and having symptoms
goal: restore ventricular rate
Routes of delivery
IV= Intravenous
IO= Intra-osseous
Endotracheal
Approved ETT drugs
NAVEL N: Naloxone/ narcan- reverse opiates A: Atropine- Symptomatic Brady V: Vasopressing- Potent vasoconstrictor E: Epinephrine- Given Q 2-3 min, PRN L: Lidocaine- Antiarrythmia
(plus mycomyst, combivent, duo, ect)
Drugs that have dose changes as increased
Amiodarone and Adenosine
RES Q-POD
Improves cardiac output by improving venous return during chest recoil- creates a vacuum like effect in chest
- also has a light that flashes to guide ventilation: keeps from hyperventilating
- If pt is resuscitated successful, the Res Q POD must be removed (immediately after ROSC)
- Aka impedence threshhold device
- Can be used with ETT and BVM
PETCO
End Tidal CO2
- Reflects perfusion efforts during CPR- circulation not ventilation
- If end tidal CO2 drops below 10mmhg, improve compressions or switch compressors
- At 40mmhg; ROSC
- Keep at 10-20 during CPR atleast
- Measured during exhalation
STEMI
ST elevated myocardial infarction
- PROTOCOL; EKG within 10 minutes of ED admission
- TX: Fibrolytics or percutaneous coronary intervention (PCI) (angioplasty, stenting): 90 minutes
- MONA
TX for suspected MI
MONA
M: Morphine- Helps pain, reduces stress
O: Oxygen- Treat hypoxemia, low dose 1-4lpm, maintain SpO2 (too much=coronary vasoconstriction)
N: Nitroglycerin- tx angina (chest pain), cause vaso coronary dilation be careful of low BP
A: Aspirin- doesnt bust clots, helps stop continue of formation
Cardiovert at
50Joules- any tach
Adenosin
SVT IV Access 6mg followed by rapid flush of saline 12 mg rapid flush No compressions
Epinephrine
1mg every 3-5 minutes followed by CPR
PEA, Pulseless vtach,
Amiodarone
300mg
150mg ETT
Pulseless Vtach
Continue CPR
Norm Pleural fluid in a healthy adult is
approx 8ml hemi-thorax
Mediastinum
Portion of the thoracic cavity lying in the middle of the thorax between the two cavities. It extends from the vertebral column to the sternum and contains the trachea, esophagus, heart, and great vessels of the circulatory system
Apex of lung
Rises 2-3 cm above the medial third of clavicle into neck
Lung Pleuras
serous membrane forming closed sacs
Two layers:
-Visceral pleura: adheres to lung; continuous with parietal pleura at root of lung
-Parietal pleural- lines the thoracic cavity
Stomata
Normally pleural fluid is drained through small holes in the parietal pleura
- Connected to intercostal lymphatic vessels and drain to mediastinal lymph system (creating and draining pleural fluid
- Eventually emptying into left subclavian vein
Pleural Effusions results when
the capacity of pleural lymphatic drainage is overcome with transudative or exudative occurance
Pleural effusion: Transudative
Occurs when the integrity of the pleural space is undamaged
- “train” fluid has to come from something else
- CHF
Pleural Effusion: exudative
Caused by inflammation in the lung or pleura
- “Devil” comes from something nasty
- Pleural lung cancer: Mesothelioma
- Infection
Airbronchograms
Airways stick out , tissue around it has increase densities
-CHF
Causes of transudative
CHF, Cirrhosis of the liver, Atelectasis, CVP line in pleural space, Lymphatic obstruction, Renal Failure, Urinothorax
Causes of exudative
Carcinoma, lymphoma, Mesothelioma, TB, Pneumonia, Drug induced (amiodarone), Yellow nail syndrome??
Etiology of pneumothorax
- Air passes through the vessels pleura through the lungs and into the pleural space
- Perforation of chest wall and parietal pleura
- Gas forming microorganisms (empyema) in the pleural space
Empyema
Pus
Bleb
Small collection of air between the lung and outer surgace of lung (visceral pleural) usually found in the upper lobe of the lung
- When bleb ruptures= pneumothorax
- Small subpleural 1-2cm
Bullae
no discernible wall more than 1cm
Open Pneumothorax
opening in chest wall
- Stab wound, surgery, gunshot, impalement
- with or without lung puncture (usually always lung puncture)
- Exposes pleural space to atmospheric pressure
- sucking chest wound
Closed Pneumothorax
Rupture inside
- Chest wall intact
- leak through lung and visceral pleura
Pleural Pressures
-5 (exp/ resting lung)
-8 (inspired)
Vented-> if paralyzed= positive pressure on inspiration
Pneumothorax types
- Spontaneous
- Traumatic
- Iatrogenic- due to med. procedure
Spontaneous pneumothorax
Primary
-No underlying lung disease (blebs in 80%)
-Young patients 20’s: rapid growth spirts, not all required cx tube, tall thin males
Secondary
-Underlying lung disease, COPD/CF/Asthma
chest pain is seen in nearly every patient with a pneumo. Palpation of the chest wall does not worsen the pain
Traumatic Pneumothorax
Penetrating - gunshot, knife puncture, auto or industrial accident -Pleural space is in direct contact with atmosphere Blunt -bat, airbag -rib fracture, non piercing chest trauma -Piercing into lung parenchyma -alveolar rupture
Tension Pneumothorax
- Occurs when air pressure in pleural space is greater than atmospheric pressure
- lung depressed toward mediastinum
50% are diagnosed at bedside, clinical sings of tension pneumo are:
- Diminished BS on effected
- Hyper-resonance to percussion (tap)
- Tachycardia
- Hypotension
Chest tube catheter size
Adult: 36-40 fr
Teens/ small adults: 28-32 fr
Children/ infants: 12-18 fr
For pneumothoraces size 16-20 may be used for adults
Pleurodesis
Fuse visceral and periodal pleura- tx chronic pleural effusions
Decortication
scrape out lung infection
Chest tube placement
Draining air (pneumothorax) -2nd or 3rd intercostal space midclavicular or midaxilary line Draining fluid -4th through 6th, away from diaphragm hemo-towards front -all chest tubes
Pleural effusion vs. Pulmonary edema
Effusion-surrounding lung pushing up lung
Edema- In lung, from heart (L), in pulmonary sacs/ alveolar space
Tx ARDS on mech vent
Use high peep and low FiO2 or Low PEEP and High FiO2
Three bottle concept, chest tube
A. Suction control- attached to suction, filled 20cmH2O which draws in RA, and controls suction
B/C. Waterseal: set to -2cmH20, air cant return, see’s bubbles during pneumothorax
D. Collection Chamber: pneumo=dry, otherwise pulls in pleural fluid
Desired suction applied to pleura space
-10 to -20cmH2O
Intrapleural pressures
-8cmH2O
Resting pressures
-4 cmH2O
Ejection Fraction
Percent of the end diastolic vol that is rejected with each beat
Norm 50-70
?measure directly echo
EDV
amount of blood in the ventricle at the end of filling
Measure indirectly with end diastolic pressure
Norm 120-180
ESV
Norm 50-60ml
Amount of blood in ventricle at the end of emptying
Ventricular Volume
End systolic volume and EDV
Stroke Volume
Measure by echo or indirectly
Amount of blood ejected by left ventricle with each contraction
Norm 60-130
Composed of.. preload, contractility, afterloadMeasure by echo or indirectly
Amount of blood ejected by left ventricle with each contraction
Norm 60-130
Composed of.. preload, contractility, afterload
Venous Return
All the blood coming back to heart
Venous system holds 64% of total blood vol for emergencies
10 in arteries
75 in pulmonary capillary bed
Body surface area
Calc using pts weight and height
Found on monogram
Norm2.5-4.0
Universal
Cardiac index
Varies with body size
CI= CO/ BsA
Why do we worry about left side of heart
Provides blood flow/ pulse to body
Satisfies the bodies o2 demand
Removes waste
Transports hormones and nutrients
Normal systemic BP, pulmonary, MAP
Systemic= 120/80 Pulmonary= 25/8 MAP= sBP + (2xdBP) / 3, keep above 60
Transition
Tricuspid valve closes (lub) when the ventricular pressure exceeds that of the attia
Atrial Contraction
Sa mode causes atrial contraction filling the ventricles another 10-30% ( increases the volume of blood into the ventricles)
Blood flow [right side of heart]: diastole
Blow flows into the atria and ventricle [85% of blood in the heart is received)
- tricuspid valve remains open
- ventricle is in a relaxed state (pressure below that of vena cava)
Hemodynamic medications
Inotropes: Contraction
Chronotropes: Time, increase or decrease HR
-ex atropine: increase HR, Beta blockers Decrease HR
Dromotropic Effect: conduction
-Speed of conduction, Amiodorone
Systolic heart failure
Heart muscle isnt strong enough to pump blood
Diastolic heart failure
Heart cant relax
Most common cause of an increase in PCWP is
left heart failure
Placement of PA catheter
When it reaches the superior vena cava or the rt atrium the balloon is inflated
- waveforms change as it advances into the pulmonary artery
- Eventually a wedge pressure will be obtained
Critical conditions where PA catheters are considered
- Severe cardiogenic pulmonary edema, unstable angina, ventricular pathology
- ARDS pts who are hemodynamically unstable
- Major coronary bypass surgery with MI and poor ventricular function
- Pts with cardiogenic (fix pump) or septic shock (fix underlying cause)
Risks of Swan-Ganz catheter
- Invasion of the catheter may cause dysrhythmias
- Chance of pulmonary infarction with balloon occlusion
- Air embolism
Who gets swan ganz catheter
- Benefits outweigh the risks
- Recent studies (20years worth) suggest no significant change in improvement or mortality of pts
- must be individualized
Risk with balloon inflation
Pulmonary Infarction
what can the swan ganz/ PA catheter do
- Pace heart: temp internal pacing
- Measure CO
- Measure PCWP
- Measure CVP
- Measure PA
=While placing swan: Possible disrythmias
Respiration and CVP
- CVP decreases with inspiration (neg pressure)
- CVP increases with positive pressure vent
- CVP increases with PEEP
- Respiratory factors skew CVP readings
- CVP are used to trend
Decrease in CVP
- Decreased venous return
- Decreased intra-thoracic pressure
- Increased ability of the heart to move blood forward
Increase in CVP
- Increased venous return
- Increased Intra-thoracic pressure
- Decreased ability of the right heart to move blood
CVP Measures, and reflects
right heart function and reflects:
- Preload and end diastolic filling pressure
- Ability of the right heart to pump blood into the pulmonary system into the left side of the heart
PICC is less likely for
pneumothorax
Types of Centrally located catheter lines: Central Venous lines
PICC (pick)-ICU pts
Porta Catheter-Chemo pts
Swan-Ganz- Cardiogenic shock pts
Tunneled catheter- Long term use
Complications from arterial line
-Ischemia: Embolism, thrombus, arterial spasm
Prevented by irrigating with diluted heparin solution
-Hemorrhage: if arterial line becomes disconnected
-Infection: incidence increases over time
Arterial line inserts
only catheter going against stream 1. Radial (most common): easy access 2. Brachial 3. Femoral RISK CAN BLEED OUT EVERY BEAT
