Cardiac Emergencies Sharon Brown RN
Jan 04, 2016
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
• 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
• 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
Diastolic MurmursSystolic Murmur
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
Conduction Visually #2Cardiac Conduction #1
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:• Hypovolemia, • Hypoxia, • Hydrogen ion (acidosis), • Hyper-/hypokalemia, Hypoglycemia, • Hypothermia.
• The T’s include:• Toxins, • Tamponade(cardiac),• Tension pneumothorax, • Thrombosis (coronary and pulmonary), • Trauma.
•H’s and T’s
•ACLS/AHA Guidelines
Therapeutic Electrical Interventions
• 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 FibrillationDose: 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 Dose500-100mg 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)
• • 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, pre-existing 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 PostCardiac 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 arrests37% of all cardiac arrests
Discharge12% make it to discharge
Post Resuscitation Deaths10% die due to recurrent dysrhythmias30% die to due to cardiovascular
collapse40% die due to PRE (Post Resuscitation Encephalopathy)
Post Resuscitation Encephalopathy
Initial insult from cardiac arrestPeriod of intense hyperperfusion
Cell injuryOxygen free radical formationInflammatory cascadeGlutamate mediated cell death
Loss of autoregulationSludging and hypoperfusionPerfusion/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 OrdersHYPOTHERMIA
INDUCTION ORDERS
Decrease Patient Temperature to ≤ 34 ۫C
Goal: Achieve patient temperature of 32 – 34◦C within 1-2 hours of resuscitation.
Complications of Hypothermia
No difference in complication rates in normothermic and hypothermic cohorts
• Potassium shiftsIntracellular shift with induction
Extracellular shift with warming• Fluid status
Cooling causes diuresisWarming causes hypovolemia
• Respiratory AlkalosisTemperature 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
• CoagulopathyMay alter clotting cascade, platelet function
• Cardiac dysrhythmiasLittle 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 AnginaCharacteristic 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
• History• OMI/MONA• Frequent monitoring• Percutaneous Coronary Intervention (PCI)• Fibrinolytic Therapy
– Activase, Retavase, TNKase Table 31-13• Heparin, NTG, ACE, B-Blocker
Bradycardia
• HR less than 60• Inferior wall MI• Can be vagal response• Treat the underlying cause
First-Degree AV block
• Can be a normal physiologic variant• PR interval >0.20 seconds• Pt. is usually asymptomatic• Treatment is usually not indicated
Second Degree AV blockMobitz 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
• 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.