Question Answer
What is Hemodynamic Monitoring – line insertion? Catheter is guided through a large vein, through the right atrium and ventricle into the pulmonary artery. This catheter is called a balloon-tipped, flow-directed, pulmonary artery.
what are the 4 insertions in Hemodynamic monitoring? 1. Internal jugular vein 2. subclavian artery. 3. Anti-cubital vein. 4. femoral vein.
In a Hemodynamics Monitoring where do we Locate the Catheter? Location of Catheter:RA/Just prior- 2-6mmHg. RV:2-25mmHg. PA-12:25mmHg.
what are the procedures for the insertion in Hemodynamic monitoring? Insert the ballon deflated. Advance &watch the pressure waveform on the monitor.Once in RA ballon is inflated &act as a sail, guiding catheter into RV &finally into PA.Once there ballon is deflated & Remain that way except when PCWP measurement is needed
In hemodynamic monitoring what are 4 types of data collected? 1. CVP- central venous pressure. 2. PAP – Pulmonary artery pressure. 3. PCWP – pulmonary capillary wedge pressure. 4. CO- cardiac output.
What are the goals of Hemodynamic monitoring? to Determine conditions of 1)Right & Left heart 2)Vascular system of the lungs 3)Systemic Vascular system. Also the methdology of CVP,PAP,PCWP& Cardiac Output.
What is the methodology of Hemodynamic monitoring – CVP (BEFORE THE Right Heart) Start by [email protected] the CVP before the right heart- If high make a note. It could be fluid overload.
What is the methodology of Hemodynamic monitoring – PAP (AFTER the Right Heart) Start by [email protected] the PAP AFTER the right heart- If high then the right must be OK because both CVP and PAP are high. If low, there must be a problem with the right heart.
What is the methodology of Hemodynamic monitoring – PCWP If high, then there is a problem w/the lung. If PAP and PCWP is high then no problem w/the lung. If PAP is high and PCWP is low then problem is in the lung.
What is the methodology of Hemodynamic monitoring – CO If PCWP is high and CO is high then left heart is not the problem. If PCWP is hihg and CO is low then left heart is the problem.
What is Cardioversion & Defibrillation? Both are methods of changing cardiac rhythms through electrical stimuli. Cardioversion is a form of defibrillation only w/ the synchronization On. This involves the placement of paddles on the chest & applying shcok to the pt.
What type of heart problems does a Cardioversion treat? For treating: NON-lethal arrhythmias 1)Atrial Fibrillation 2)Atrial Flutter 3) Ventricular Tachycardia (with pulse)
What voltage does a cardioversion start? Start @ low voltage around 50-100 joules.
How do you prepare a Cardioversion procedure? 1. Setup O2. 2. have a bag-valve-mask ready @bedside. 3. Prepare for Oropharyngeal suctioning.
What should be done in a synchornization in a Cardioversion? Synchronization must be ON. Synchronize cardioversion to the R Wave on ECG. It causes pt. to slip into a deadly rhythm like pulseless V-tach/V-fib. If so start defibrillation. It should be done w/ resuscitation equipment on-hand. Pt. sedation is helpful
What type of heart problems does a Defibrillation treat? For treating: Lethal arrhythmias 1)Ventricular Fibrillation 2)Ventricular Flutter 3) Ventricular Tachycardia (with pulseless only)
What voltage does Defibrillation starts with? 360 joules.
What should be done in synchronization in a Defibrillation? Synchronization must be set to OFF. Start at 360 joules, continue till successful. In emergency situation 100% O2 is appropriate. Must have resuscitation, equipment on-hand.
What is Basic cardiac life support (BCLS)? 1. Chest compression produce only about 30% of normal cardiac output. 2. Mouth-to-mouth ventilations will deliver no more than 17% O2 (FIO2)
What is the effectiveness of CPR in Basic cardiac life support (BCLS)? 1. Color of face & extremities. 2. Pulse can be felt during compressions. 3. If carotid artery is not accessible, use femoral artery
Basic cardiac life support (BCLS): What should we do when there is no pulse ? 1. No matter what the rhythm continue compressions if there is no pulse. 1)maybe pulseless electrical activity (PEA), 2) Formerly called electro-mechanical dysfunction(EMD)
Basic cardiac life support (BCLS): what are the hazards of CPR? 1. Pneumothorax (from broken ribs) 2. Gastric Distension or rupture 3. Liver laceration 4. Aspiration 5. Cross-contamination 6. Cardiac Contusion (bruising of the cardiac muscle) 7. Continue CPR regardless of above hazards.
Basic cardiac life support (BCLS): What are the key procedural consideration? 1. look, listen, & feel for breathing for @least 10 seconds. Use Carotid pulse. Use current BLS compression /breath ratio. Continue CPR if no pulse.
Basic cardiac life support (BCLS): What are the ventilation rates? 1. Neonates upto 1 month – 40-60/min 2. infants&children upto 8 yrs old – 12-20/min 3. Adult above 8 yrs old : 10-12/min
Basic cardiac life support (BCLS): What are the compression ratio(to breath)? 1.Neonate – 3 compressions then 1 ventilation (3:1), 2. Infant &child= 15:2 3. Adult 30:2
Advance cardiac Life support (ACLS)? it is an exact Algorithm like BCLS it changes from time to time.
Advance cardiac Life support (ACLS): What are the 4 types of Ventricular Arrhythmias? 1. Ventricular Tachycardia(pulseless), 2. Ventricular Fibrillation 3. Bardycardia 4. Asystole.
Advance cardiac Life support (ACLS): What is ventricular tachycardia(pulseless)? 1. Defibrilliate @ 360 joules – check pulse in between 2. if unsuccessful, administer epinephrine, Lidocaine, Amioderone.
Advance cardiac Life support (ACLS): What is ventricular fibrillation? 1. Defibrilliate @ 360 joules – check pulse in between 2. if unsuccessful, administer epinephrine, Lidocaine, Amioderone.3.If pt. has metabolic acidosis by a reasoned ABG – gives sodium bicarbonate.
Advance cardiac Life support (ACLS): ventricular fibrillation-What is precordial thumb? It gives the pt. transitions to v-fib or pulseless v-tach – the transition witnessed as it happened.
Advance cardiac Life support (ACLS): What is Bardycardia? Treat with Atropine, Epinephrine & may use an external pacemaker
Advance cardiac Life support (ACLS): What is Asystole? Must be confirmed in 2 leads – rules out lead dysfunction. Treat w/ Epinephrine, Atropine
Advance cardiac Life support (ACLS): What causes Hypotension? 1. Poor Contractility of the heart 2. Vasodilation 3. Dehydration – most common.
Advance cardiac Life support (ACLS): In Hypotension How do you treat poor cardiac contractility related problems? 1. Digitalis (Crystodigin) 2. Digoxin ( Lanoxin)
Advance cardiac Life support (ACLS): In Hypotension How do you treat Vasodilation related problems? 1. Norepinephrine. 2. Dopamine
Advance cardiac Life support (ACLS): In Hypotension How do you treat dehydration? 1. Administer Fluids 2. Normal saline & other saline concentration


Question Answer
HOW MANY AMERICANS DIE FROM CARDIOVASCULAR DISEASE EACH YEAR? 950,000
WHAT IS THE LEADING CAUSE OF PREMATURE, PERMANENT DISABILITY AMONG WORKING ADULTS? CORONARY HEART DISEASE
NONMODIFIABLE FACTORS OF CARDIOVASCULAR DISEASE HEREDITY, RACE, GENDER, AGE
MODIFIABLE FACTORS OF CARDIOVASCULAR DISEASE HIGH BP, ELEVATED SERUM CHOLESTEROL LEVELS, TOBACCO USE, DIABETES, PHYSICAL INACTIVITY, OBESITY, METABOLIC SYNDROME
NORMAL BP 120/80
PREHYPERTENSION 120-139/80-89
STAGE 1 HIGH BP 140-159/90-99
STAGE 2 HIGH BP GREATER THAN OR = TO 160/100
QUITTING SMOKING REDUCES THE RISK OF HEART DISEASE BY WHAT % AFTER 1 YEAR 50%
STUDIES HAVE SHOWN THAT EVEN WHAT % REDUCTION IN BODY WEIGHT REDUCES THE RISKS ASSOCIATED WITH OBESITY 10%
WHAT IS THE BODY MAX INDEX FORMULA WEIGHT IN LBS / HEIGHT IN INCHES * 704.4
CARDIAC CAUSES OF CARDIAC ARREST CORONARY ARTERY DISEASE (MOST COMMON), DYSRHYTHMIAS, ACUTE MI, VALVULAR HEART DISEASE, CHD, INTRACARDIAC TUMOR
NON-CARDIAC CAUSES OF CARDIAC ARREST PULMONARY EMBOLISM, CHOKING, ASPHYXIA, DRUGS, STROKE, HYPOXIA, ALCOHOLISM
CHAIN OF SURVIVAL FOR CARDIAC EARLY ACCESS, EARLY CPR, EARLY DEFIB, EARLY ACLS
COMPONENTS OF BASIC LIFE SUPPORT RECOGNITION OF SIGNS OF HEART ATTACK, CARDIAC ARREST, STROKE, FBAO, RELIEF OF FBAO, CPR, DEFIB
SHOCKABLE RHYTHMS V-TACH, V-FIB
NON-SHOCKABLE RHYTHMS ASYSTOLE, NO PULSE
COMPONENTS OF ADVANCED CARDIAC CARE BASIC LIFE SUPPORT, ADVANCED AIRWAY MNG, VENTILATION SUPPORT, ECG RECOGNITION, ECG INTERPRETATION, VASCULAR ACCESS AND FLUID RESUSCITATION, DEFIB, SYNCHRONIZED CARDIOVERSION, PACING, MEDS, CORONARY ARTERY BYPASS, STENT INSERTION, ANGIOPLASTY
PHASES OF CPR ELECTRICAL PHASE (FIRST 5 MIN), CIRCULATORY PHASE (5 MIN TO 10-15 MINS), METABOLIC PHASE (AFTER 10-15MIN)
WHEN DO YOU REPEAT THE PRIMARY SURVEY CHANGE IN PT’S CONDITION, INTERVENTIONS NOT WORKING, VITALS UNSTABLE, BEFORE ANY PROCEDURES, CHANGE IN RHYTHM
WHAT IS SECONDARY SURVEY ADANCED AIRWAY, BREATHING, CIRCULATION, DIAGNOSIS, EVALUATE, FACILITATE
TYPES OF ADVANCE DIRECTIVES LIVING WILL, PATIENT SELF DETERMINATION ACT, DURABLE POWER OF ATTORNEY FOR HEALTHCARE
DEFINE CARDIAC ARREST ABSENCE OF CARDIAC MECHANICAL ACTIVITY, NO PULSE, UNRESPONSIVE, ABNEA OR AGONAL BREATHING
WHAT DOES THE UPPER AIRWAY CONSIST OF NASOPHARYNX, OROPHARYNX, LARYNGOPHARYNX
NASAL CANULA LITERS AND FIO2 1L=24%2L=28%3L=32%4L=36%5L=40%6L=44%
SIMPLE MASK LITERS AND FIO2 8-10L & 40%-60%
THE RIGHT CORONARY ARTERY ORIGINATES FROM RIGHT SIDE OF THE AORTA
LEFT CORONARY ARTERY ORIGINATES FROM LEFT SIDE OF THE AORTA
WHAT IS DEPOLARIZATION BEFORE A CONTRACTION, GETTING READY TO CONTRACT, PULSELESS ELECTRICAL ACTIVITY
POLARIZATION IS READY STATE
DEPOLARIZATION STIMULATION
REPOLARIZATION RECOVERY
THE POSITION OF THE __ ELECTRODE ON THE BODY DETERMINES THE PORTION OF THE HEART “SEEN” BY EACH LEAD POSITIVE
3 LEADS THAT LOOK AT THE INFERIOR WALL OF THE LEFT VENTRICLE LEADS 2, 3 AND AVF
2 LEADS THAT LOOK AT THE ANTERIOR WALL OF THE LEFT VENTRICLE V3 & V4
4 LEADS THAT LOOK AT THE LATERAL WALL OF THE LEFT VENTRICLE LEAD 1, AVL, V5, V6
___ PLANE LEADS VIEW THE HEART AS IF THE BODY WERE SLICED IN HALF HORIZONTAL/TRANSVERSE
ECG PAPER… WHAT SIZE ARE SMALL BOXES 1MM WIDE AND 1MM HIGH
ECG PAPER RECORDS AT A SPEED OF 25MM/SEC
EACH HORIZONTAL UNIT REPRESENTS HOW MANY SEC .04 SEC OR 1MM
A LARGE BOX REPRESENTS .20 SEC
DEFINE WAVEFORM A MOVEMENT AWAY FROM BASELINE EITHER POS OR NEG
DEFINE SEGMENT A LINE BETWEEN WAVEFORMS
DEFINE INTERVAL A WAVEFORM AND A SEGMENT
DEFINE COMPLEX SEVERAL WAVEFORMS
WHAT IS A P WAVE FIRST WAVE IN CARDIAC CYCLE, ATRIAL DEPOLARIZATION, SMOOTH, ROUNDED AND ABOUT 0.11 SEC
WHAT IS QRS COMPLEX Q IS FIRST AND ALWAYS NEG, R IS POS, S IS NEG, VENTRICULAR DEPOLARIZATION
WHAT IS T WAVE VENTRICULAR REPOLARIZATION, UPRIGHT EXCEPT IN LEAD AVR
NEGATIVE (INVERTED) T WAVE = MYOCARDIAL ISCHEMIA
PEAKED T WAVE = HYPERKALEMIA
LOW AMPLITUDE T WAVES = HYPOKALEMIA
PR INTERVAL MEASURES 0.12-0.20 SEC
ST SEGMENT REPRESENTS EARLY PART OF REPOLARIZATION OF THE RIGHT AND LEFT VENTRICLES
QT INTERVALS REPRESENTS TOTAL VENTRICULAR ACTIVITY
QT MEASURES 0.36-0.44 SEC
PROLONGED QT = LENGTHENED RELATIVE REFRACTORY PERIOD
3 STEPS TO ASSESS THE RATE ON STRIPS 6 SEC METHOD, LARGE BOXES, SMALL BOXES
STEPS TO ANALYZE A RHYTHM STRIP ASSESS THE RATE, ASSESS RHYTHM, EXAMINE P WAVES, ASSESS INTERVALS, OVERALL APPEARANCE, INTERPRET
CHARACTERISTICS OF SINUS ARRHYTHMIA RATE= 60-100RHYTHM= IRREGULARP WAVES= UNIFORMPR INTERVAL= CONSTANTQRS DURATION= 0.10 SEC OR LESS
CHARACTERISTICS OF SINUS TACHY RATE= 101-180RHYTHM= REGULARP WAVES= UNIFORMPR INTERVAL= CONSTANTQRS DURATION= 0.10 SEC OR LESS
CAUSES OF SINUS TACH EXERCISE, FEVER, PAIN, FEAR, HYPOXIA, INFECTION, SHOCK, CAFFEINE, NICOTINE
HOW IS ATRIAL TACH DIFFERENT FROM SINUS TACH ATRIAL P WAVES DIFFER IN SHAPE
CHARACTERISTICS OF ATRIAL TACHY RATE=150-250; RHYTHM=REG; P WAVES= DIFFER IN SHAPE; PR INTERVAL=SHORTER OR LONGER, P WAVE MAY BE HIDDEN IN T WAVE; QRS DURATION=0.10 SEC
WHAT IS AVNRT ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA
CHARACTERISTICS OF AVNRT RATE=150-250; RHYTHM=NORM; P WAVES=HIDDEN IN QRS; PR INTERV=NOT MEASURED; QRS DUR=0.10 SEC
CHARACTERISTICS OF WOLFF-PARKINSON-WHITE SYNDROME RATE=60-100;
HOW DO YOU RECOGNIZE WPW SHORT PR INTERVAL, DELTA WAVE, WIDENING OF THE QRS
WHAT ARE VAGAL MANEUVERS METHODS USED TO STIMULATE BARORECEPTORS LOCATED IN THE INTERNAL CAROTID ARTERIES AND THE AORTIC ARCH
MAT IS MOST OFTEN SEEN IN SEVERE COPD, HYPOXIA, ACUTE CORONARY SYNDROME, DIGOXIN TOXICITY, RHEUMATIC HEART DISEASE, THEOPHYLLINE TOXICITY, ELECTROLYTE IMBALANCES
ATRIAL FLUTTER IS ECTOPIC, SAW TOOTH
CONDITIONS ASSOCIATED WITH A-FLUTTER HYPOXIA, PULMONARY EMBOLISM, CHRONIC LUNG DISEASE, PNEUMONIA, CARDIAC SURGERY
FIRST DEGREE AV BLOCK P WAVES CONDUCTED BUT DELAYED
SECOND DEGREE AV BLOCK SOME P WAVES CONDUCTED
THIRD DEGREE AV BLOCK NO P WAVES CONDUCTED
DEFIB INDICATIONS PULSELESS VT, VF, SUSTAINED POLYMORPHIC VT
WHAT ARE THE MOST IMPORTANT TREATMENTS FOR THE PTS IN CARDIAC ARREST DUE TO PULSELESS VT OR VE DEFIB AND CPR
ENERGY (JOULES)= AMPS * VOLTS * TIME
TRANSTHORACIC RESISTANCE IS ALSO KNOWN AS IMPEDANCE
WHAT FACTORS AFFECT IMPEDANCE PADDLE SIZE, POSITION, USE OF CONDUCTIVE MATERIAL, PHASE OF PT’S RESPIRATION, PRESSURE, ENERGY
INCREASED RESISTANCE = DECREASED CURRENT DELIVERY
CRITICAL RESUSCITATION TASKS AIRWAY MNG, CHEST COMPRESSIONS, MONITORING AND DEFIB, VASCULAR ACCESS AND MEDS
WHAT DO U DO WHEN A “FLAT LINE” IS OBSERVED ON A CARDIAC MONITOR MAKE SURE POWER IS ON, CHECK CONNECTIONS, MAKE SURE CORRECT LEAD IS SELECTED, TURN UP ECG SIZE ON MONITOR
AED OPERATION TURN ON, ATTACH, ANALYZE, DELIVER
SYNCHRONIZED CARDIOVERSION INDICATIONS UNSTABLE SUPRAVENTRICULAR TACHY, UNSTABLE ATRIAL FIB WITH RAPID VENT RESPONSE, UNSTABLE A FLUTTER WITH A RAPID VENT RESPONSE, UNSTABLE WIDE-COMPLEX TACHY, UNSTABLE VT WITH A PULSE
DEFIB AND CARDIOVERSION COMPLICATIONS SKIN BURNS, RISK OF FIRE, MYOCARDIAL DAMAGE, EMBOLIC EPISODES, DYSRHYTHMIAS, INJURY TO OPERATOR
DEFIB AND CARDIOVERSWION POSSIBLE ERRORS TREATING THE MONITOR, NOT THE PATIENT, OPERATOR UNFAMILIAR WITH EQUIPMENT, FAILURE TO PROPERLY MAINTAIN EQUIPMENT
TRANSCUTANEOUS PACING INDICATIONS SYMPTOMATIC BRADY, NARROW QRS THAT DOES NOT RESPOND TO ATROPINE, WIDE QRS BRADY
PACEMAKER COMPLICATIONS COUGHING, SKIN BURNS, PAIN, TISSUE DAMAGE,
FAILURE TO PACE FAILS TO DELIVER AN ELECTRICAL STIMULUS OR WHEN IT FAILS TO DELIVER THE CORRECT NUMB OF ELECTRICAL STIMULATIONS PER MIN.
FRAILURE TO CAPTURE (PACE) INABILITY OF A PACEMAKER STIMULUS TO DEPOLARIZE THE MYOCARDIUM.
WHAT FACTORS DO YOU CONSIDER WHEN SELECTING IV SITES PURPOSE, AMOUNT AND TYPE OF FLUIDS, DURATION, ACCESSIBILITY, SIVE OF VEIN, EXPERIENCE

ACLS Study Guide Spreadsheet:

Medicine Dosage Indications
Oxygen Dosage 100% BVM &ETT
Epinephrine (Adrenalin)

Stimulates Alpha and beta 1 and beta 2 receptors

 

1 mg of 1:10,000 solution IVP every 3-5 minutes

There is also a 1:1000 concentration- this is considered “High dose Epi”

NO maximum dose 2- 10 mcg/min/bradycardia

Epi drip for ROSC

0.1-0.5 mcg/kg/min

Can cause or worsen myocardial ischemia

Can cause ventricular ectopy

Patient cannot be allergic to Epi because the body produces it naturally

Amiodarone ( cordarone) VF/PVT

300 mg in 20-30 mL NS or D5W IVP

May repeat dose of 150 mg in 3-5 minutes

Stable tachycardias (with a pulse):

150 mg/100 mL D5W over 10 minutes

Maximum dose: 2.2 Gm/24 hours

 

If patient is successfully resuscitated using an antiarrhythmic, hang a drip to prevent them from going back into lethal rhythm

 

 

Must be mixed with 20-30 mL saline or dextrose before administration

 

Antiarrhythmic

Blocks Sodium channels, inhibits sympathetic stimulation, and blocks potassium  and calcium channels

How does it work

Slows conduction through the His-Purkinje system

Inhibits alpha and beta receptors

Creates coronary and peripheral vasodilation

Decreases myocardial contractility but increases CO by decreasing afterload

Refractory V-fib/ PV-Tach

Tachycardia’s in pts. with impaired heart functions

Narrow complex tachycardia that fail to respond to vagal stimulation and Adenosine

Stable monomorphic VT with poor cardiac function

DO NOT GIVE IN PTS WITH 2nd Degree heart block

Lidocaine Ventricular antidysrhythmic ( specific for ventricular ectopy)

Dosage: 1.0-1.5 mg/kg IV bolus

May be give down ETT if no IV access

Max dose: 3 mg/kg

Can only give one antiarrhythmic- if you use Lidocaine, stick with it..

Decrease dose by 50% in patients with

Hepatic disease

> 70 years old ( reduce volume distribution)

Atropine sulfate (atropine) 0.5- 1mg every 3-5 minutes

Maximum dosage: 3 mg

Atropine is not effective in patients with a heart transplant.

Precautions-

Use with caution in MI or ischemia

Can cause ventricular tachydysrhythmias

Action

Increases heart rate ( positive chronotrope)

Indications- if symptomatic

Sinus bradycardia ( symptomatic)

Junctional

2nd degree Mobitz I block

Adenosine (adenocard) Action-

1st line drug for stable SVT  and narrow complex tachycardia after O2 and vagal maneuvers

Dosage-

6 mg IVP very rapidly (SLAM IT)

May repeat 12 mg dose if not successful

Reassess after each dose!

Antiarhythmic

Slows sinus rate and conduction through the AV node

Precautions

Flushing, dyspnea, chest pain

Usually resolves in 1-2 minutes.

Lightheadedness; hypotension

Be prepared to resuscitate if necessary

Can cause a brief period of Asystole

DO NOT GIVE TO ASTHMATIC PATIENT

Causes bronchospasm and can induce a full blown asthma attack and even death

2nd Degree Type II or 3rd Degree CHB

Sick Sinus Syndrome

 

Calcium Channel Blockers Used for narrow complex rhythms

Stable atrial flutter, atrial tach, junctional tach

Verapamil

Diltiazem ( Cardizem)

Dosage depends on patient and MD

Usually IVP bolus and then a drip

Beta Blockers Contraindications

Moderate to severe LV failure and pulmonary edema

Heart rate < 60 bpm

Hypotension ( SBP < 100 mmHg)

Signs of poor peripheral perfusion

2nd Degree or 3rd Degree CHB

Reactive airway disease

Decreases everything Indications

Angina

Hypertension

Atrial fibrillation (with rapid ventricular rate)

Atrial flutter ( with rapid ventricular rate)

Recurrent SVTrything

 

Magnesium Sulfate VT- 1-2 Gm in 10 mL D5W over 1-2 min

VF- give same dose IVP

Indications

Torsades de Pointes

May reduce incidence of post-infarction dysrhythmias

Sodium Bicarbonate Dosage- 1 meq/kg IV

May repeat with 0.5 meq/kg every 10 minutes

Corrects metabolic acidosis

Should not be given in first 10 minutes of a code unless you have a documented acidosis prior to code.

Recommended in

Tricyclic antidepressant overdose

Hyperkalemia

Pre-existing metabolic acidosis

Formula

0.3 x(weight in kg) x BE/2

Divide answer by 50 to get # of amps

Morphine Sulfate (MgSO4)

Duramorph, Infumorph, MS Contin, Roxanol

 

Narcotic ( opioid) analgesic

Dosage

1-3 mg IVP over 1-5 minutes; titrate until pain relief; relief usually in 20 minutes; duration 2-4 hours

Actions

Reduces vascular resistance

Decreases myocardial O2 requirements

Indications

Ischemic chest pain, pulmonary edema, relief of anxiety

Has properties of smooth muscle dilation- dilates the airways; mild bronchodilator effects

Precautions

SEVERE respiratory depressant( reverse with Narcan)

Hypotension; Bradycardia; CNS depression

Nausea/vomiting

Contraindication

Allergy to opioids

CNS depression due to overdose, poisoning, or head injury

Increased ICP

Hypovolemia; hypotension

 

Naloxone Hydrochloride (narcan) 0.4- 2 mg IVP, IM, or SubQ; immediate results

May repeat dose after 2-3 minutes

Attaches and binds to same receptors preventing the absorption of the opiate
Calcium Chloride Dosage varies usually only 1 amp Only indicated in Cardiac Arrest when:

Hyperkalemia

Hypocalcaemia

Calcium channel blocker overdose

Digitalis or Digoxin (Lanoxin) Slows conduction through the AV node prolonging the PR interval

In A flutter and A fib, it decreases the number of atrial impulses reaching the ventricles

Increases force and velocity of myocardial contraction

Increases cardiac output

Actions

Increases contractility

Decreases rate (positive inotrope & negative chronotrope)

Indications

A fib and A flutter with RVR

Dopamine Should be used at lowest dose that adequately perfuses the vital organs

2-10 mcg/kg/min

“cardiac doses” usually  begin at 5 mcg/kg/min

Increases cardiac output, heart rate, & BP

Indicated for symptomatic bradycardia after max dose of Atropine.

Indications

Hemodynamically significant hypotension in the absence of hypovolemia

Hemodynamically significant hypotension= systolic < 90 with poor perfusion, oliguria, or changes in mental status

Infused as a drip only

Precautions

Increases heart rate, therefore may result in myocardial ischemia

Increases myocardial work without increasing coronary blood flow

May induce or worsen ventricular dysrhythmias

If patient is already tachycardic, dopamine is not recommended

Norepinephrine ( levophed) 0.5- 1.0 mcg/min by IV infusion titrated to maintain BP

Usual dose range is 8-12 mcg/min

Very necrotic to peripheral veins- administration through a Central line is preferred.

Can use double or quad strength concentration

How it works

Peripheral vasoconstrictor and as an inotropic stimulator of the heart and dilator of coronary arteries

Increases myocardial oxygen demand

Increases BP

Indications

Severe hypotension (SBP < 70 mmHg)

Cardiogenic shock

Nitroprusside  (Nipride)

 

Indications

Hypertensive emergencies

Actions

Reduces BP rapidly

Easily titratable

Well tolerated by patient

Can be rapidly reversed just by turning it off

Nitro  Nitrostat, Nitro-Bid, Tridil (IV) Angina 1 tab SL q 5 minutes x 3

Unstable angina- IV dosage titrated

CHF- IV dose ( Rx of choice for CHF patients with ischemic heart disease)

Relief is usually immediate if cardiac related

Other drugs such as Viagra, Cialis, etc.

Suspected inferior wall MI with possible right ventricular MI

Hypotension ( SBP < 90 mmHg); Extreme bradycardia ( < 50 bpm);Tachycardia ( >100 bpm)

Increased ICP

Uncorrected hypovolemia

Inadequate cerebral circulation

Constrictive pericarditis and pericardial tamponade

Furosemide (Lasix) 20-40 mg IVP Indications

Pulmonary edema, CHF associated with LV dysfunction

Action

Loop diuretic; vasodilation just prior to diuresis

Can cause hypotension

Thrombolytics Action

Dissolve clots aka “clot busters”

Use of thrombolytics should be initiated ASAP after onset of pain.

Indications

Pain of AMI within time frame (6-12 hours) with no contraindications

Aspirin (Bufferin, Anacin, APC) Classification

Nonnarcotic analgesic; antipyretic; anti-inflammatory

How does it work

Blocks synthesis of thromboxane A2, inhibiting platelet aggregation

ASA 81 and  325 mg tablets Precautions

Asthma

Ulcers

Contraindications

Bleeding disorders. Clotting disorders; allergy Now one of our most important immediate interventions!!!

ASA alone started within 24 hours of onset of AMI reduces overall mortality to almost the same degree as thrombolytics

Patient exhibiting signs of ACS symptoms should be introduced to MONA