Download 7 - Cardiac Emergencies

Cardiac Emergencies
Sharon Brown RN
Numbers
• AHA states that every 26 seconds, an
American will suffer from a cardiac event and
every minute someone dies as a result of a
cardiac event.
Risk factors for CHD
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Elevated cholesterol levels
Untreated HTN
Tobacco use
Diabetes
Obesity
Lack of regular physical activity
Poor dietary intake
CMS
• Centers for Medicare and Medicaid (CMS)
• Core measures that are identified to ensure
that patients with ACS receive appropriate
evidence based standards of care.
Anatomy and Physiology
ASSESSMENT
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PQRST
Could be pain, discomfort, pressure, tightness
R/O most threatening first
Newer studies show that many young MI
patients are positive for cocaine yet drug use
is rarely questioned in MI
Cardiac Structure
• Cardiac Anatomy
•Two parallel pumps
•Right heart – Low pressure
system
•Left heart –
High pressure
system
•Atria -- receive blood
and ventricles pump
into circulation
•Systole refers to
contraction.
•Diastole to filling.
•Pumps work in a
coordinated rhythm
Cardiac Structure
• Cardiac Valves -Atrioventricular (Tricuspid and
Mitral)
– Leaflets attached to a valve annulus between the
chambers
– Chordae tendinea strong fibrous cords attached to valve
leaflet on one end and papillary muscle on other
– Papillary muscle projects into ventricular wall
– Systole pulls the chordae tendinea using the papillary
muscle to control valve operation
– Valves form a parachute to prevent prolapse during
contraction
Cardiac Structure
• Cardiac Valves -Atrioventricular (Tricuspid and Mitral)
•Heart Sounds-S1
•S1 produced by closure of
Mitral and tricuspid valves
•Best heard with diaphragm
of stethoscope at apex
•Mitral valve closes slightly
before tricuspid and may
produce an audible split
•May also be heard in PVCs,
RBBB, and ASD
Cardiac Structure
• Cardiac Valves - Semilunar Valves
(Pulmonic and Aortic)
•Heart Sounds-S2
•S2 produced by closure of
both valves
•Best heard at the base of the
heart -- 2nd ICS at the sternal
border
•Aortic valve close slightly
ahead of pulmonic and may
produce split S2 (heard on
inspiration)
•Systolic murmurs produced
by stenosis
•Diastolic murmurs produced
by incompetent or regurgitant
valves
Cardiac Structure
• Cardiac Valves - Murmurs
Systolic Murmurs
•Systolic murmurs result from
papillary muscle dysfunction
•May result from myocardial
ischemia causing death of papillary
muscle
•Results in regurgitant murmur
(Most common murmur heard)
Diastolic Murmurs
•Diastolic murmurs result from
stenotic valves
•Valve tight as blood tries to fill
during diastole
Systolic Murmur
Diastolic Murmurs
Cardiac Valves – Murmur
Characteristics
Pericardial Friction Rub
• Described as rough, scratching, squeaky sound
• Caused by inflammation of pericardium
– Occurs in 15% of MI, Not uncommon after cardiac
surgery
• Heard best with patient leaning forward, holding
breath in full expiration
Pericardial Friction Rub
Cardiac Structure
• Cardiac Conduction – Putting It Together
Cardiac Conduction #1
Conduction Visually #2
Cardiac Structure
• Cardiac Contraction Cycles
Cardiac Contraction Cycles
• Atrial Excitation
– This occurs when the SA node sends out an electrical impulse through the right and left atria.
– This action creates the “P” wave on an EKG Rhythm.
• Atrial Systole
– As the atria contract, the blood pressure in each atrium increases, forcing additional blood into
the ventricles.
– This action creates the “Q” wave on an EKG Rhythm.
• Atrial diastole
– As the signal passes through the AV node the atria and ventricles are both at rest
• Ventricular Excitation
– Occurs as the electrical impulse travels from the AV node through the bundle branches and
Purkinje fibers.
– This action creates the “RS” wave on an EKG Rhythm.
• Ventricular Systole
– Occurs as the right and left ventricles contract and push blood out.
– This action creates the “T” wave on an EKG Rhythm.
• Ventricular Diastole
– During this phase the ventricles are at rest.
– This action creates the “U” wave on an EKG Rhythm.
Cardiac Structure
• Cardiac Coronary Circulation
Cardiac
Arrest
• The H’s include:
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•H’s and T’s
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•ACLS/AHA Guidelines •
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Hypovolemia,
Hypoxia,
Hydrogen ion (acidosis),
Hyper-/hypokalemia, Hypoglycemia,
Hypothermia.
• The T’s include:
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Toxins,
Tamponade(cardiac),
Tension pneumothorax,
Thrombosis (coronary and pulmonary),
Trauma.
Therapeutic Electrical Interventions
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Defibrillation
Cardioversion
Pacemakers
Implantable cardioverter-Defibrillator
Resuscitation Interventions
•Fluids
•Pharmacologic
Therapy
•Post-Cardiac
Arrest
Therapeutic
Hypothermia
Adenosine
• Re-Entry SVT
• Dose: 6mg IV/IO push followed by 20ml
saline
• 1-2min later 12mg IV/IO Then move on to
other therapy(ie Cardioversion)
Amiodarone
• : Shock Resistant Ventricular Fibrillation
Dose: 300mg IV/IO,
• Second does of 150mg if VF recurs
• 24hr maximum is 2.2gm
• Half-life lasts up to 40 days?
• Remember …300 without a pulse, 150 with a
pulse.
Atropine
• Indication: Sympomatic Bradycardia
• Dose: .5 mg IV, can be given up to 3 ms
• Sequence for Bradycardia is: Atropine, TCP,
Epinephrine, Dopamine. If no IV access go
straight to TCP.
• Can be given for organophosphate poisoing
(extremely large dose needed: 2-4 mg)
Calcium Chloride
• Indication: Magnesium Toxicity or Calcium
Channel blocker Over Dose
500-100mg IV
• Be careful with patients on Digitalis
Diltiazem
• Indication: Slow Rapid Ventricular Response
associated with A. Fib/A. Fluter
Dose: 0.25mg/kg
• After 15 min 0.35mg/kg,
• Infusion: 5-15mg/hr titrated to heart rate
• Avoid in patients with WPW
Dopamine
• Function: Cardio Genic Shock(Increases Cardiac
Output and BP)
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• Dose:
• 1-5mcg/kg/min(Renal and Splanchnic Dilation)
• 5-10mcg/kg/min(Beta Effects(inotropy))
• 10-20mcg/kg/min(Alpha
Effects(vasoconstriction))
Epinephrine
• ↑Myocardial and CNS blood Flow d/t α
effects
• Dose: 1mg IV push Q3-5 min
• 2-2.5mg down the ET tube
• May need higher doses with ß blockers or
Calcium channel blockers
• Given in anaphylaxis (0.3 mg 1:1000, SQ)
Lidocaine
• Alternative therapy for refractory
VF/pulseless VT
• Dose:
• 1-1.5mg/ KG IV followed by
• 1-4mg/min infusion
Magnesium
• Torsade De Pointe VT
• Hypomagnesmia hinders the cellular movement
of K+ and thereby makes the heart
proarrhythmic.
• Dose: 1-2gm IV push over 1-2 minutes.
• Torsade with pulse = 1-26mg in 100ml D5W over
• 5-60 minutes
Morphine
• Analgesic of Choice for ischemic pain w/ ACS
that is not relieved by Nitroglycerin.
• Also good for treating pulmonary edema as it
decreases venous return to the heart and has
a mild bronchodilatory effect.
• 2-4mg IV push
Nitroglycerin
• Indication: Chest Pain
• relaxes vascular smooth mucscle.
• Can be given topical, spray, sublingually, IV
• Contraindicated in patients taking some
medications for erectile dysfunction
Sodium Bicarb
• Indication: Acidosis reversal.
• Initial dose without a blood gas: 1meq/kg IV
push
• w/ half dose administered q10min
• Mainly used for TCA OD, Hyperkalemia, preexisting metabolic acidosis
Vasopressin
• Shock refractory VF or pulesless VT &
Asystole in place of initial or second dose of
epinephrine. Has powerful vasoconstrictive
effects.
• Dose: 40u IV one time then return to
epinephrine
Therapeutic Hypothermia
Improving Post
Cardiac Arrest Outcomes
Facts: After cardiac arrest, brain
injury is a major source of
morbidity and mortality!
Current Cardiac Arrest
Outcomes
Pre-hospital ROSC (Response of
Spontaneous Circulation)
45% of v-fib arrests
37% of all cardiac arrests
Discharge
12% make it to discharge
Post Resuscitation Deaths
10% die due to recurrent dysrhythmias
30% die to due to cardiovascular collapse
40% die due to PRE
(Post Resuscitation Encephalopathy)
Post Resuscitation
Encephalopathy
Initial insult from cardiac arrest
Period of intense hyperperfusion
Cell injury
Oxygen free radical formation
Inflammatory cascade
Glutamate mediated cell death
Loss of autoregulation
Sludging and hypoperfusion
Perfusion/demand mismatch
Beneficial Effects of
Hypothermia
•Decrease in cerebral metabolism
•Maintains integrity of membranes
•Preserves ion homeostasis
•Decrease Ca influx
•Decrease free radical formation
•Decrease vascular damage
Hypothermia Induction Orders
HYPOTHERMIA
INDUCTION
ORDERS
Decrease Patient
Temperature to ≤ 34
۫C
Goal: Achieve patient
temperature of 32 –
34◦C within 1-2 hours
Complications of
Hypothermia
No difference in complication rates in normothermic
and hypothermic cohorts
• Potassium shifts
Intracellular shift with induction
Extracellular shift with warming
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Fluid status
Cooling causes diuresis
Warming causes hypovolemia
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Respiratory Alkalosis
Temperature corrected ABG allows changes in
minute ventilation to support normal PaCO2
Hyperglycemia
Complications of
Hypothermia (Con’t)
• Neutropenia
Neutropenia and increased incidence of pneumonia
seen in patients exposed to prolonged hypothermia
(>24hrs) in other applications
• Coagulopathy
May alter clotting cascade, platelet function
• Cardiac dysrhythmias
Little risk for clinically significant dysrhythmias if
temperatures are maintained >30°C
Shifting of Potassium
Hypothermia
Serum Potassium
“Hypokalemia is expected with hypothermia
as potassium moves into the cell, as the
patient is re-warmed there will be a rebound
effect, therefore aggressive supplement of K +
is not recommended.”
Do not provide supplement unless K+ < 3.0
mmol/l or cardiac instability
Target K+ 3.5/cardiac stability
Acute Coronary Syndrome
• General term used to describe a group of
coronary artery diseases and their symptoms.
– Unsable Angina
– STEMI
– Non-STEMI
• Assessment is key
• Differential diagnosis
Assessment
• PQRST-What are the elements?
• 12 lead EKG
• Cardiac Markers
Differential diagnosis of Angina
Characteristic
Stable Angina
Unstable Angina
Location of pain
Substernal, may radiate to
jaw, neck,arms, back
Substernal, may radiate to
jaw, neck,arms, back
Duration of Pain
1-5 minutes
5min, occurring more
frequently
Characteristic of pain
Aching, squeezing,
choking, heavy burning
Same as stable, but more
intense
Other symptoms
Usually none
Diaphoresis, weakness
Pain worsened by
Exercise, activity, eating,
cold weather, reclining
Exercise, activity, eating,
cold weather, reclining
Pain relieved by
Rest, NTG
NTG may only give partial
relief
EKG findings
Transient ST-segment
depression, disappears
with pain relief
ST-segment depression,
often T-wave inversion,
EKG may be normal
Patient Management
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History
OMI/MONA
Frequent monitoring
Percutaneous Coronary Intervention (PCI)
Fibrinolytic Therapy
– Activase, Retavase, TNKase Table 31-13
• Heparin, NTG, ACE, B-Blocker
Bradycardia
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HR less than 60
Inferior wall MI
Can be vagal response
Treat the underlying cause
First-Degree AV block
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Can be a normal physiologic variant
PR interval >0.20 seconds
Pt. is usually asymptomatic
Treatment is usually not indicated
Second Degree AV block
Mobitz I/Wenckebach
• Atrial rhythm is regular.
• PR interval gradually lengthens and then one P wave is not
followed by a QRS
• S/S ~CP, SOB, ALOC
• Most frequently caused by drugs (Beta-Blockers, Calcium
channel blockers and Digoxin. Also can be Vagal.
• Treat the underlying cause
Second Degree Block type 2
• PR interval is constant until ans atrial impule is
blocked. No QRS after a p wave
• S/S Chest discomfort, SOB, ALOC
• Treatment usually requires pacemaker and
Atropine
Third Degree AV block
• Atrial and Ventricle disassociation
• Both rates are usually regular, but do not
correlate
• S/S CP, SOB, ALOC, syncope
• Tx includes pacemaker
• Do not use lidocaine/amiodarone
Pericarditis
• Inflammation of pericardial sac
• S/S~ fever, chills, severe chest pain, friction
rub
• Pain increases when patient lies down and
decreases when sitting up
Cardiac Tamponade
• Fluid accumulation in pericardial sac
• Beck’s Triad~JVD, hypotension, distant heart
sounds
• Pericardiocentesis
Aortic Aneurysm
• Abdominal are 4 times more likely than
thoracic
• S/S-usually sudden. Pulsating mass in
abdomen, back pain radiating to abd,
“Ripping” chest pain
IMPLANTED CARDIOVERTER DEFIBRILLATOR
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ICDs are becoming more common
ER visits related to miss-firing are common.
Treat CP in these patients are you would normally.
Patient will usually have a card describing what type
of device is being used.
• Placing a magnet over device will disable shocking,
but not pacing.
• If override defibrillation is necessary, make sure pads
are at least 10 cm away.