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.