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 ID: 784723
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Slide1
Cardiac Emergencies
Sharon Brown RN
Slide2Numbers
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.
Slide3Risk factors for CHD
Elevated cholesterol levels
Untreated HTN
Tobacco use
Diabetes
Obesity
Lack of regular physical activity
Poor dietary intake
Slide4CMS
Centers for Medicare and Medicaid (CMS)
Core measures that are identified to ensure that patients with ACS receive appropriate evidence based standards of care.
Slide5Anatomy and Physiology
Slide6ASSESSMENT
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
Slide7Cardiac 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
Slide8Cardiac 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
Slide9Cardiac 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
Slide10Cardiac 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
Slide11Cardiac 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 Murmurs
Systolic Murmur
Slide12Cardiac Valves – Murmur Characteristics
Slide13Pericardial 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
Slide14Cardiac Structure
Cardiac Conduction – Putting It Together
Conduction Visually #2
Cardiac Conduction #1
Slide15Cardiac Structure
Cardiac Contraction Cycles
Slide16Cardiac 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.
Slide17Cardiac Structure
Cardiac Coronary Circulation
Slide18Cardiac 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
Slide19Therapeutic Electrical Interventions
Defibrillation
Cardioversion
Pacemakers
Implantable cardioverter-Defibrillator
Slide20Resuscitation Interventions
Fluids
Pharmacologic Therapy
Post-Cardiac Arrest Therapeutic Hypothermia
Slide21Adenosine
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
)
Slide22Amiodarone
: 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.
Slide23Atropine
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)
Slide24Calcium Chloride
Indication: Magnesium Toxicity or Calcium Channel blocker Over Dose
500-100mg IV
Be
careful with patients on Digitalis
Slide25Diltiazem
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
Slide26Dopamine
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))
Slide27Epinephrine
↑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)
Slide28Lidocaine
Alternative therapy for refractory VF/
pulseless
VT
Dose
:
1-1.5mg/ KG IV followed by
1-4mg/min infusion
Slide29Magnesium
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
Slide30Morphine
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
Slide31Nitroglycerin
Indication: Chest Pain
relaxes vascular smooth
mucscle
.
Can be given topical, spray, sublingually,
IV
Contraindicated in patients taking some medications for erectile dysfunction
Slide32Sodium 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
Slide33Vasopressin
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
Slide34Therapeutic Hypothermia
Slide35Improving Post
Cardiac Arrest Outcomes
Facts: After cardiac arrest,
brain injury
is a major source of morbidity and mortality!
Slide36Current 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)
Slide37Post 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
Slide38Beneficial Effects of Hypothermia
Decrease in cerebral metabolism
Maintains integrity of membranes
Preserves ion homeostasis
Decrease Ca influx
Decrease free radical formation
Decrease vascular damage
Slide39Hypothermia Induction Orders
HYPOTHERMIA 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 shifts
Intracellular shift with induction
Extracellular shift with warming
Fluid status
Cooling causes diuresis
Warming causes hypovolemia
Respiratory Alkalosis
Temperature corrected ABG allows changes in minute ventilation to support normal PaCO2
Hyperglycemia
Slide41Complications 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
Slide42Shifting 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
Slide43Acute 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
Slide44Assessment
PQRST-What are the elements?
12 lead EKG
Cardiac Markers
Slide45Differential 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
Slide46Patient Management
History
OMI/MONA
Frequent monitoring
Percutaneous Coronary Intervention (PCI)
Fibrinolytic Therapy
Activase, Retavase, TNKase Table 31-13
Heparin, NTG, ACE, B-Blocker
Slide47Bradycardia
HR less than 60
Inferior wall MI
Can be vagal response
Treat the underlying cause
Slide48First-Degree AV block
Can be a normal physiologic variant
PR interval >0.20 seconds
Pt. is usually asymptomatic
Treatment is usually not indicated
Slide49Second 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
Slide50Second 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
Slide51Third 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
Slide52Pericarditis
Inflammation of pericardial sac
S/S~ fever, chills, severe chest pain, friction rub
Pain increases when patient lies down and decreases when sitting up
Slide53Cardiac Tamponade
Fluid accumulation in pericardial sac
Beck’s Triad~JVD, hypotension, distant heart sounds
Pericardiocentesis
Slide54Aortic 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
Slide55IMPLANTED 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.