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Cardiac Emergencies Sharon Brown RN Cardiac Emergencies Sharon Brown RN

Cardiac Emergencies Sharon Brown RN - PowerPoint Presentation

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Cardiac Emergencies Sharon Brown RN - PPT Presentation

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

dose cardiac valves pain cardiac dose pain valves hypothermia heart wave ekg structure murmurs patient blood rhythm patients heard

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Slide1

Cardiac Emergencies

Sharon Brown RN

Slide2

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.

Slide3

Risk factors for CHD

Elevated cholesterol levels

Untreated HTN

Tobacco use

Diabetes

Obesity

Lack of regular physical activity

Poor dietary intake

Slide4

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.

Slide5

Anatomy and Physiology

Slide6

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

Slide7

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

Slide8

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

Slide9

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

Slide10

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

Slide11

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 Murmurs

Systolic Murmur

Slide12

Cardiac Valves – Murmur Characteristics

Slide13

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

Slide14

Cardiac Structure

Cardiac Conduction – Putting It Together

Conduction Visually #2

Cardiac Conduction #1

Slide15

Cardiac Structure

Cardiac Contraction Cycles

Slide16

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.

Slide17

Cardiac Structure

Cardiac Coronary Circulation

Slide18

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

Slide19

Therapeutic Electrical Interventions

Defibrillation

Cardioversion

Pacemakers

Implantable cardioverter-Defibrillator

Slide20

Resuscitation Interventions

Fluids

Pharmacologic Therapy

Post-Cardiac Arrest Therapeutic Hypothermia

Slide21

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

)

Slide22

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.

Slide23

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)

Slide24

Calcium Chloride

Indication: Magnesium Toxicity or Calcium Channel blocker Over Dose

500-100mg IV

Be

careful with patients on Digitalis

Slide25

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

Slide26

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))

Slide27

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)

Slide28

Lidocaine

Alternative therapy for refractory VF/

pulseless

VT

Dose

:

1-1.5mg/ KG IV followed by

1-4mg/min infusion

Slide29

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

Slide30

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

Slide31

Nitroglycerin

Indication: Chest Pain

relaxes vascular smooth

mucscle

.

Can be given topical, spray, sublingually,

IV

Contraindicated in patients taking some medications for erectile dysfunction

Slide32

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

Slide33

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

Slide34

Therapeutic Hypothermia

Slide35

Improving Post

Cardiac Arrest Outcomes

Facts: After cardiac arrest,

brain injury

is a major source of morbidity and mortality!

Slide36

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)

Slide37

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

Slide38

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

Slide39

Hypothermia 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.

Slide40

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

Slide41

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

Slide42

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

Slide43

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

Slide44

Assessment

PQRST-What are the elements?

12 lead EKG

Cardiac Markers

Slide45

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

Slide46

Patient Management

History

OMI/MONA

Frequent monitoring

Percutaneous Coronary Intervention (PCI)

Fibrinolytic Therapy

Activase, Retavase, TNKase Table 31-13

Heparin, NTG, ACE, B-Blocker

Slide47

Bradycardia

HR less than 60

Inferior wall MI

Can be vagal response

Treat the underlying cause

Slide48

First-Degree AV block

Can be a normal physiologic variant

PR interval >0.20 seconds

Pt. is usually asymptomatic

Treatment is usually not indicated

Slide49

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

Slide50

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

Slide51

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

Slide52

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

Slide53

Cardiac Tamponade

Fluid accumulation in pericardial sac

Beck’s Triad~JVD, hypotension, distant heart sounds

Pericardiocentesis

Slide54

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

Slide55

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.