CC HOLY GRAIL (CARDIAC).pdf

Nur 409 Exam #2 Review Sheet Tuesday March 16th Topics: Cardiovascular 1, 2, 3, 4 Cardiovascular Function 1: Dysrhythmias Management of the Patient with Dysrhythmias and Conduction Problems: Old Material Normal Electrical Conduction: Comes from SA node→ Atria→ AV node→ Bundle of His→ L & R Bundle Br...

Nur 409 Exam #2 Review Sheet Tuesday March 16th Topics: Cardiovascular 1, 2, 3, 4 Cardiovascular Function 1: Dysrhythmias Management of the Patient with Dysrhythmias and Conduction Problems: Old Material Normal Electrical Conduction: Comes from SA node→ Atria→ AV node→ Bundle of His→ L & R Bundle Branches→ Terminating the Purkinge Fibers and causing a contraction Normal SA Node: 60-100 Normal AV Node: 40-60 Normal Ventricle Pace: 20-40 Every cell in the heart can function as a pacemaker (Beneficial) If the SA node becomes damaged or impaired from illness or injury, there are cells in the atria that can take over the pacing If the AV node or secondary pacemaker becomes damaged, there are cells in the ventricle that can take over for pacing Concept of automaticity is very important NSR: Typically a rate of 60-100. Most of us have a HR between this. Sinus Tachycardia: Rate of 100 or greater Predicted MAX HR= 220-AGE. The heart can take at that age ○ An 80 year old man cannot tolerate a HR as fast as a 20 year old boy ○ 70 year old: 220-70= 150 MAX HR You can also find a predicted max zone they are in. 150 HR x 50% (.50)= 75 pretty tight. t ○ Then take 80% = 128 ○ 75-128 = Zone!!! ○ Just pay attention to this If you have a patient just lying there in bed, it’s important to investigate why If they just had a heart attack and after are tachycardic, what med might you need as an intervention? Core treatment for MI- Nitroglycerin, BB (Try to get HR below 100) Causes: Pain, infection, anxiety, dehydration, recent MI If HR is greater than 100= NOT being controlled Realways check k it Sinus Arrhythmia: Irregular rhythm from sinus node (with P waves), typical in peds. Almost always a benign rhythm. HR will increase when pt breathes in and decrease when pt breathes out (Pattern: 83, 76, 83, 76) PAC: Premature beat. Differentiate from JVC→ If you can see a P wave. If you see a P wave, determine it is coming from atria. Atrial Flutter: Arrhythmias of the atria, more organized rhythm, saw tooth pattern (Saw blade upside down), can be irregular sometimes, also flutter and fib sometimes go back & fourth, upper case F waves. Atrial Fibrillation: Arrhythmias of the atria, completely unorganized, no P waves, fibrilatory waves= lower case “f waves”, can actually count them (3:1 atria to ventricular contractions), typically irregular rhythm What Causes Arrhythmias? Any CV Disease, like hypertension, CAD, valve problems Smoking, Age, Anxiety, too much caffeine Caused by those diseases: HISDEBS Hypoxia = Causes Cardiac Arrthymias (myocardium deprived of O2, MI, blockage, muscular death below the blockage) ○ COPD causes strain on right side of the heart (Bc R ventricle has to pump to pulmonary vasculature, increased pressure in R ventricle) ○ Pulmonary Embolism does the same thing Ischemia= Can cause ischemic heart disease, arrthymias, MI, viral infections of myocardium, angina = Lead to arrhythmias Sympathetic stimulation = Hyperthyroidism, exercise, anything that causes heart to beat faster to meet metabolic disease of the body Drugs = All meds used to treat arrhythmias can also cause it, abx can cause elongation of QT segment as well = Lead to arrhythmias Electrolytes = Lead to arrhythmias (Three electrolytes for cardiac: Calcium, potassium, magnesium) Bradycardia = Slow enough can cause arrhythmias Sympathetic Stretch = Enlargement of the atria or ventricles, pt that hasn’t taken care of hypertension develops an enlarged heart can lead to arrhythmias Diseased heart can do anything!!! Can have a whole bunch of different things like AFib and randomly P Waves show up. When you don’t know what you are looking at, best thing is to go to a 12 lead EKG and go to the provider to reflect what you are seeing together Cardiac Conduction System SA node → Atria → go over to left side by bachman’s bundle → SA node picks up the impulse carries it to the bundle of his to the L & R bundle branches I SA node Atria GO 100 2 AV node ventricle 40 60 20 40 Management of the Patient with Dysrhythmias and Conduction Problems: New material Junctional Dysrhythmias PJC: Premature Junctional Contractions Premature beats Causes: Digoxin toxicity (often! Reversal= Digibind) heart failure, CAD ○ Arrthymias in the junction are probably due to this! Less common than PACs Impulse starts in the AV nodal area before the next sinus impulse reaches the AV node NORMAL P QRS T (repeated), then all of a sudden you see a premature beat come in, looks like other tight QRSs You are looking for a p wave or some kind of morph in the preceding T wave of the complex in front of it (higher, dimpled, weird looking like something is in there electrically) ○ If you don’t see the T wave morphed and don’t see any P waves= PJC P wave may be absent, before, or after the QRS 0 PJC Criteria: Premature Inverted P Wave (Sometimes just a short PRI, no inversion). Usually absent P wave most of the time. sinus rhythm w 2 PICS Junctional Rhythm: Sinus nodes becomes slow, impulse cannot be conducted, the AV takes over Ventricle rate 40-60 (Diagnosed by slow rate!) Regular QRS is normal ○ Nice and tight Different looking P waves→ Very close to the QRS ○ Almost always appears behind it ○ No P waves before the segment ○ Retrograde (backwards) or hidden in here behind it If P wave present, PRI is less than 0.12 seconds (Very short) S&S reduces cardiac output Treatment like bradycardia ○ Emergency atropine IV push if symptomatic and put pacemaker on, dopamine drip (vasopressor, increases BP) 0 invertedp Pacemaker shifted from SA node → AV node (New dominant pacemaker of the heart) Site is now shifted very low in the atria Anytime the heart beats too fast or too slow, have to worry about CO Have to make sure perfusing rest of body and brain May need a transcutaneous or venous pacemaker if not working If too fast, not feeding myocardium→ Chest pain or MI Junctional Escaped Beat/Rhythm: Normal rhythm (PQRST), beat is DELAYED (not premature). Heart is sending out impulse but there’s a delay; heart notices SA node isn’t firing so it goes from the AV node Ventricular Dysrhythmias PVC Premature Ventricular Complex: Impulse starts in the ventricle and is conducted through the ventricles before the next normal sinus impulse (Starts in ventricle and stays in the ventricle for as long as the heart can react) Normal rhythm Premature beat Wide and bizzare QRS (.12 or greater!) Inverted wave following the QRS (conduction abnormality) Couplet= 2 PVCs back to back Three in a row= 3 PVCs back to back 3 or more= VTach ○ Monomorphic/all coming from same folci or can be multifoci from multiple places in the heart Ventricular Tachycardia: V TACH 3 or more PVCs in a row (coming from same ectopic point in ventricle) Rate exceeding 100 bpm (100-200 bpm) Regular Wide bizarre QRS Treatment: Make sure pt is ok and then treat them ○ Some pts just sit there with v tach ○ Ask them about symptoms/how they are feeling ○ Get the person to cough to try to break the rhythm ○ Always check K & Mg!! ○ May try amiodirone (chemical conversion) over 10 mins. Hopefully this will convert them V tach can be stable or CODE situation!!! ○ Can have ppl in cardiac arrest with v tach as well ○ Code board under, get thers in the room to help, CPR, defib, Epi 7no SIDE NOTE: Pt’s K is slightly low 3.5 (norm: 3.7-5.3) and mg is slightly low 1.5 (norm: 1.7-2.2). What do you give first?? Mag FIRST! Stabilizing the heart. If K was SUPER low (2) with VTach and PVCs all over, of course give K first! But if you have a choice, give mag first (stabilizing k in the system) Also, K is 3.3 and you give 40 mEq klor by mouth, what do you expect the K to be? For every 10 mEq of k you give, you can expect their serum to raise by.1 ○ You should see 3.7! Do NG tube or orally ideally. Hospitals usually restrict the amount of K going in at once via IV. Keep in mind most of these ppl are very unstable so extra fluid is not a good idea D Ventricular Fibrillation: Most common dysrhythmia with cardiac arrest Rapid rate (greater than 300 bpm) V FIB Disorganized Quivering of the heart Heart is quivering in the chest= NO CO Treatment: CODE!!! Start CPR, defibrillate ASAP, 2 rounds of Epi, may order vasopressin Idioventricular Rhythm: Ventricular escape rhythm VERY SLOW rate. 20-40 bpm Wide & bizarre QRS Regular rhythm Often occurs before people die, not ok with it. Precode or code situation. About Treatment: Would NOT want to give anyone in this situation lidocaine or amiodirone because they have one little tiny pacemaker in their heart. If the provider wants to treat that, it could be very bad for the patient. Give atropine or epi to speed it up Canaan There are subdivisions: Accelerated Idioventricular Rhythm: 40-100. Same principle (Anything over 100 is Vtach) *Not sure if need to know this* Ventricular Asystole: Flatline, absent QRS (ventricular standstill and atria-top of heart doesn’t contribute much to CO) r.D0 I Treatment: CODE SITUATION!!! Start CPR and administer epi ○ Change out providers Q2M to keep strong compressions going Make sure the board is under them for strong compressions as well Should be differentiated from fine VFib: Can mimmick but diff rhythm Let’s say you are in a code for 20 mins and they are getting ready to call it. After 6-8 mins questionable brain activity, before they say he or she is expired, they should check And 2 leads. Fine ventricular fib: Can defibrillate or do something with *With aystole, you should NOT defibrillate. ○ Every time you shock the chest, you raise the level of transthoracical resistance in the chest so if you shock asystole, you can be doing more harm and blocking later efforts Conduction Abnormalities AV Blocks (1st, 2nd I and II, 3rd degree): Relationship of P wave to QRS would distinguish the diff types of heart block 1st Degree AV Block: delay1pause P wave, prolongation (PRI needs to be measured and is longer than normalGreater than.20)= Delayed and slower than normal More of a pause than a block When naming: SR/SB with first degree AV block Cause: Can happen after an MI ○ If new occurence, bring to the provider’s attention ASAP 2nd Degree AV Block Type 1: Mobits 1, winkybok, type 1 (three names) longer PRI then drop Repeating pattern in which all but one atrial impulses are conducted through the AV node into the ventricles Progressive lengthening of the PR interval, until one QRS is dropped WHY is this happening: QRS not being conducted (Bottom of the heart/ ventricle is not contracting from the electrical impulse), which delays the P even more. Then, extra P waves form because it is taking more and more time to get down to the ventricles ○ ANYTIME MORE Ps THAN QRSs= THINK HEART BLOCK!!! Example: PRI:.16,.28,.32. Then, T wave with a P then nothing=drops. Repeats over again in a cycle More dangerous than 1st degree because randomly droppping the CO Look and measure PRI- Will get progressively longer and then result in dropped QRS (PRI=.20 where QRS follows. PRI=.24 where QRS follows, PRI=.28 where QRS follows, Then just P wave with NO QRS bc it drops off 2nd Degree AV Block Type 2: Called mobits two PB constant then drop 2 P: 1 QRS PRI is consistent P wave, QRST (repeated over & over) then….Randomly NO MORE QRS= SUDDEN drop. Random P waves without QRS. Some of the atrial impulses are conducted through the AV node into the ventricles More dangerous→ Decreased CO ○ ANYTIME MORE Ps THAN QRSs= THINK HEART BLOCK!!! ○ Remember there’s injury/illness in an area of the heart causing issues like heart block 3rd Degree Heart Block: Complete dissociation between atria and ventricle. Atria beating at one rate and ventricle beating at another rate, not working together at all No atrial impulses are conducted through the AV node into the ventricles Two impulses stimulate the heart (two pacemakers) ○ Atria: P waves may be seen ○ Ventricle: QRS complexes Seems to be together, but not connected ○ Caliper will show equally spread out P waves *No coordination between the P waves and QRS!* ○ Top part of heart is beating faster than the bottom part Treatment: Needs a pacemaker Cardiovascular Function 2: Adjunctive Modalities & Management of Dysrhythmias Adjunctive Modalities and Management External Electrical Therapy: Things outside of the body Cardioversion: Done while the patient is awake, amount of electricity used, timed therapy Defibrillation: Board→ CPR→ Defib ASAP. Cardiac arrest, code situation Pacemakers: ○ Transcuteanous- Most common ○ Transvenous- Early 80s-90s until transcutaneous ○ Permanent pacemaker ○ Epicardial pacing- Electrodes go right to the heart, like in open heart surgery ○ monomowoommarmommonmamama Swangas catheter?? Swan ICD 9am Diagnostic Testing Ecocardiogram ○ TTE: Transthoracic echo, using sound waves, noninvasive, easy to do. Spot on site check. Just to give an idea on how the heart is functioning, how valves are working and walls are moving Through chest wall, skin, fat tissues, muscles, bone, more abstract ○ TEE Transesophageal Echocardiogram: More invasive, requires consent, moderate sedation or heavier if on ICU on vent Superior to TTE Tube is inserted into the esophagus like an EGD (endoscopy). Layers of tissue between the heart and esophagus are very thin, so they get a good picture with it. Percutaneous Coronary Intervention (PCI) ○ PTCA ○ Coronary Artery Stent Interventions Angioplasty Stent placement ○ Types of stents: Drug-elluding and non-drug elluding Dysrhytmia Treatments Acute or Chronic Medications Depends on dysrhythmia and duration Presence of heart disease Response to previous treatment Depends on the provider Use treatment guidelines LT Medication Examples: Sodium channel blockers (Lidacaine and norpace) Beta blockers (Metoprolol) Potassium blocking agents (Amiodorone, burtilim) Calcium channel blockers (Cardizem, nifedipine/procardia) ○ Know a little bit about how the docs pick them External Electrical Therapy Cardioversion Defibrillation Pacemakers ICD V TACH if When someone is in ventricular tachycardia, what do you do…… See if person is awake and sitting there, ask them how they are doing and do VS OR opposite- Eyes rolled in back of head, CODE, cardiac arrest If awake, ask them to cough or bare down to break the rhythm ○ If it doesn’t, get provider and stop the arrhythmia ASAP Amiodirone (EMERGENCY, cardiac arrest dosing= 300 mg direct IV push) If in Vtach but NOT out/cardiac arrest, put 150 mg in 100 cc of d5w IV piggyback Also use lidocaine (For numbing and vtach and arrhythmias) ○ But can cause confusion in the elderly I Just admitted to the hospital for a heart attack (naive to BP meds), going on rounds and going to give someone lopressor (Hold for systolic BP less than 100, hold for HR less than 60)- Can be kind of strong for them in the beginning. On a low dose (25mq Q12). Check BP at end of shift and BP is 98 systolic. It is possible their BP is lower just bc they are waking up Because new to this type of therapy, come back in 10-15 mins and check BP If you check again then and it’s still in 90s, hold it If it goes up, give it ○ Essential treatment for CAD, heart disease (VITAL) If there’s a problem with medication, it’s better to find out this in the hospital than at home!! Vfib, Vtach (PVCs particularly): Check mg & K!!!! For every 10 mEq of K given: The serum level should go up by 0.1 Remember if both levels are moderately low: Give mg first bc it will stabilize k Also avoid giving cardiac patients extra NS: Just going to hold onto that extra water!! Give it by mouth (tablet) whenever you can 2 Old Fashion Defibrillator Every shift, a nurse checks the defibrillator in the beginning. Run a strip, set energy level to 30 Jewels, charge it, and press the button to see if it works Write on strip: Date, time, initials Now-a-days they usually use pads with pics on them. Make sure pads aren’t expired because they dry out If using paddles, make sure you use approved defibrillator gel!!* NOTHING ELSE Make sure you put around 20-25 lbs of pressure on the chest= Get a good seal on there!!! Need good defibillation effort to patient Everytime you cardiovert/defibrillate somebody, you raise the amount of transthoracic electrical resistance in their chest. You need more energy to get things done. Don’t want to use too much by accident and then the next time have to increase it even more if you have to rescue them again Shocks are sequential: Increasing levels of energy when you cardiovert/defibrillate Could get paddle burns if defibrillate a lot ○ Could hurt, ask pt if they want tylenol or something for pain Monophasic and Biphasic Defibrillators Mono: Sent energy to only one paddle, other paddle is a ground. That paddle required a lot more energy. 200-360 jewels. Older one Bi: Energy distributed between two pads, use less energy. 100-150. 200 is max. AED Most important thing: #1 TURN IT ON!!! Always know where it is If someone is in cardiac arrest (not breathing, not perfusing, no pulse) send a friend to get AED and call 911. Start CPR, start AED- just follow directions 1: Apply pads and turn on One pad on upper right pectoral region And other is over the heart 2: CPR and macchine will tell you when to stop CPR to analyze rhythm 3: Will say shock is needed and deliver shock. Or say no shock indicated- continue CPR 4: This will continue every 2 mins Correct Pad Placement Preconditioned pad: Saline impregnated. Come in a package, open them up, and they come right out and go on the chest Placement is different depending what using it for: If cardioversion/defibrillation: This placement If in cardiac arrest, may come with the pads on Remove any med patches so don’t get burned Make sure they don’t have any metals or wet clothing (conduct electricity accidentally) If pacing: One over heart and other one on back like a sandwich If person is awake tell them to roll so you can put on Cardioversion & Defibrillation Used to treat tachyarrythimias Electrical current that depolarizes a critical mass of myocardial cells After repolarization occurs the sinus node is able to restart as the heart’s pacemaker IMPORTANT: Difference is the timing of delivery of the electric current D Cardioversion: Synched with the heart’s electrical activity…patient MUST have a pulse MUST click the sync button l Want it on R wave You and provider will say ok, going to cardiovert at 50 jewels. If using paddles, you are holding it to the person’s chest and push the button If cardioverting, can have a delay for macchine to find the right timing to deliver energy Don’t want to have R on T phenomenon = DANGEROUS ○ T Wave: Absolute refractory period of the ventricle of the heart (vulnerable, about to repolarize). ○ If the energy delivers at this moment, can precipitate vtach or vfib ○ VERY dangerous Will try to do a cardioversion on these things IF the person is not hemodynamically compromised and not symptomatic ! ○ When the heart goes too fast The heart can’t feed itself on diastole It cannot fill or perfuse properly Can become hemodynamically unstable and decrease in CO Cardioversion > Defibrillation If new arrhythmia and not sure of the status of it exactly, you don’t want to defibrillate them because there’s a chance the patient can have a clot sitting in their heart Don’t want to do this unless sure this isn’t the case ○ May try to coagulate first before doing so There could be something sitting in the left atrium (Small appendage on the left atria that is like a little half tunnel and can form clots there)= Watchman procedure (Little umbrella they deploy that builds up epithelial cells over time so it becomes smooth and takes this out of the equation) ○ Could easily have a stroke on left!!! ○ On right, could easily have PE Just don’t want to cardiovert pts without knowing status Unless emergent They will usually put a big bolus of heparin beforehand to prevent anything from happening Cardioversion is timed and want to make sure they don’t have a blood clot sitting in the atria, and if the arrhythmia is more than 48 hrs, they will try to sit on the person a little bit and manage them as long as not hemodynamically compromised But if they become compromised, inject with heparin and try to save their life Hold dig with Cardioversion: Want SA node to kick in. Dig blocks AV node from kicking in. Want to make sure dig is on hold.. want impulse to get through F If cardioverted: Fully cared for IV for meds Administer some sedation (A little versed- Fast acting, out of system quick) Lidocaine: Numbs the heart and the brain Make sure respiratory and anesthesia is there incase if planned ○ Advocate!!! ○ It is like getting kicked in the chest: Cruel if you don’t give something!! AFTER: If lucky and get normal sinus rhythm, get EKG done to be sure Might be changes in their meds after this Defibrillation: Immediate, unsynchronized…patient has no pulse, no BP (EMERGENCY) Delivery of Electric Current Paddles: Old fashion Conductor pads, multifunction pads: ○ More common, make sure not expired, come with pictures, multifunctional ○ Can use for cardioversion, defibrillation, or pacing ○ Hands free Automatic External Defibrillator (AED): Uses pads Implanted device Internal Cardiac Defibrillator (ICD): Can come with pacemaker too, not always though Example: Pt of his had a pacemaker with ICD and was going down to comfort care. Had to tell them to turn off the defibrillator portion. When people are starting to die, they can have arrthymias (VTach), you don’t want the defibrillator to randomly fire. NEVER shut off the pacemaker= Still treating them. Don’t want them to be moving toward dying and then the device shoots them back up. KEEP this in mind!! Tell the provider if they transfer care Role is essential: Advocating for patient Placement Standard: Anterior chest Safety Measures Good contact ○ Pads to skin (20-25 lbs against chest with paddles) ○ Conductive median ○ Prevent arching on discharge Leaking of electrical current through air (Don’t want to shock yourself) Clear patient ○ Three clear check: Make sure you yell out I’m clear, your clear, all clear Or someone else can accidentally defibrillate themselves ○ Prevent contact with patient or anything touching the patient when the defibrillator is discharged Use correct conductive gel A female with large chest= Might have to go underneath or on the side IF Cardiac Arrest Occurs: Start CPR immediately Five cycles then do pulse check Rotate out providers Q2M Give Epi Q3-5M IV Push If someone is in VTach/VFib= Defibrillation is PRIMARY treatment ASAP!! Cardioversion: Delivery of a timed electrical current SYNCHs with the EKG (Synch button) ○ Patient needs to be connected to a cardiac monitoring on the defibrillator ○ R wave will be “marked”= Timed! ○ Discharges energy on ventricular depolarization (In the QRS) ○ Prevents discharge during repolarization (T wave)= BAD! Delay in discharge ○ Discharge buttons must be held down until shock is delivered ○ Expect when press shock button or press the tabs on the paddles= there can be a delay as the macchine finds the right time to send the shock Type of Cardioversion: Elective ○ Dysrhythmia has lasted longer than 48 hours Anticoagulation may be indicated ○ Digoxin is held ○ NPO (Incase emergency intubation is needed) ○ Pads placed anteroposteriorly (Back & front) ○ Sedation, analgesic, anesthesia To make the patient more comfortable Advocate for the patient! ○ Voltage varies (50-360 joules) If it goes higher than 90, no longer cardioversion. Now, defib ○ If elected cardioversion or at all possible, do a TEE. Much more accurate than TTE when diagnosing clot in atria Urgent: Emergency! Slap it on the chest ○ Unstable SVT, afib, rapid aflutter, or vtach with pulse Make sure no clot= Heparin IV push If Vtach or have a pulse with SVT: Try to get them to cough, bare down, vagal manuever, carotid massage (ONLY PROVIDER- can break off a piece of plaque in carotid and cause a stroke) f Drugs for SVT: Adenosine (Dose of 6mg IV push, can be repeated twice 12mg 2x) Before you give the drug, warn the patient they may feel a little lightheaded Stopping heart for a few seconds, so kind of scary (Don’t tell patient this) Push this med FAST then follow with 10 cc of normal saline fast A Post Cardioversion Rhythm conversion Peripheral pulses* BP* Airway patency, LOC Monitor ○ VS ○ SpO2 ○ EKG* *EKG, pulses, BP= Watch closely over next several hours and make sure it does not repeat again, make sure electrolytes are good (mg, k), LOC, airway, VS, pulse ox D Treatment: Persistent tachyarrthymia (with a pulse) causing: Hypotension Altered mental status Signs of shock: Hypotension, tachycardia, cold clammy skin Ischemic chest pain: Heart going too fast→ HF Acute heart failure Causes hemodynamic compromise Uncontrolled Afib: HR over 100 (Can go up to 180) Cardizem for afib D SVT: Fast rate, 130 or more, one bump Typically give adenosine Try to slow down to get an idea what’s under there so they can better treat it (Distinguish between SVT and afib) VT: Amiodorine (go to drug), lidocaine (caution with elderly), pronestel/procanamide D Defibrillation Emergency ○ VFib, Pulseless Vtach ○ Early defibrillation=better survival rate!! ○ AEDs Depolarizes a critical mass of myocardial cells all at once Higher voltage than cardioversion ○ 120-360 joules (monophasic defibrillator) ○ 100/150-200 joules (biphasic) ○ Cause more damage the higher you go If unsuccessful ○ CPR and ACLS protocols: Board under them, defibrillated (try to stop vtach, vfib from occurring), epi Q3-5M, rotate out providers with CPR Q2M, make sure CPR is fast and deep (100-120) If within a min, 90% survival rate. If delayed up to 12 mins, 2- 5% survival rate Quicker you shock them, the better you are!! Tyes of Defibrillators Monophasic Deliver current in one direction Requires increased energy selection VERY OLD, not really used anymore Biphasic Delivers energy from positive paddle/pad , then reverse back to the original paddle/pad Allows for lower energy usage, non progressive Communication between two pads (one is +) ○ More efficient and cardioprotective Meds During CPR Epinephrine Full strength Epi IV push Convert to NSR Increase cerebral and coronary artery blood flow Amiodorone, Magnesium If ventricular rhythm persists for Vtach Amiodorone: NOT benign drug Treats atrial and ventricular arrhythmias Usually after 24 hours on drip dose, start to transition them to oral dose Complications: Blue man’s syndrome Bradycardia Interstitial lung disease (major problem→ High degree of pulmonary toxicity) Hypo/hyper-thyroidism Cornea problems (discolored), cutaneous probs (skin rashes) even with oral form IV form: Hepatic problems, hypotension skin rashes Remember: If grandma comes in with recurring VT, should be fine. If mom starts getting this drug at 50, they should think about this again Dangerous drug!! But good drug VFib CODE!, defib, CPR, Epi Q3-5M Vtach If nonperfusing: CODE!, Defibrillation, CPR, Epi Q3-5M Check mg, k, treated with amiodorone, lidocaine If with a pulse, sitting in bed: Will try to cardiovert with drugs. If that doesn’t work, they will try with defibrillator (less energy) IscaE eky Asystole Start CPR, Epi Q3-5M DO NOT defibrillate ○ Can prevent further resusitative efforts with defibrillator Ensure it is NOT fine Afib ○ If it is, then you would shock because could get a rhythm back Check this in how many leads? 2!! ○ EMERGENCY SITUATION T mega D D PEA pouts BP Looks like sinus arrhythmia. What if pt has no BP, no pulse, no HR? PEA!!! Heart has electrical and pump parts- Possible the electrical part is working great but the pump isn’t working Causes: Five H’s Five T’s Hydrogen Ions (Acidosis) Hypo/hyper-kalemia ○ If renal failure pt, could have high K ○ Blood gas will show! May decide to treat with regular insulin IV push followed by D50. Force K into cells. Also give calcium bc renal pts run low Hypothermia ○ If found out in the cold, try to warm them up Hypovolemia ○ Ringer’s lactate, NS, type & screen, try to get O- blood as fast as possible Hypoxia Thrombosis (coronary)- heart Cardiac taponade (Bec’s Triad- lowering systolic BP, narrowing pulse pressure, JVD, muffled heart sounds)- heart Tension pneumothorax- lungs PE- lungs Toxins (Overdose on drugs) ○ If they have done a bunch of cycles and this is the turn out, will look at a bunch of factors to determine if PEA infeagin Dso t ca POINT IS = TREAT UNDERLYING CAUSE!!! renalfailure Sire Profound Bradycardia Slow HR & symptomatic Treatment: Give atropine ○ To raise the HR temporarily ○ SE: Can also dilate the pupils= BEWARE when look at eyes. Not neuro Can also order dopamine on IV drip Put external pacemaker pads on patient as well incase need them D Second Degree Heart Block Type 2 Check relationship by counting PRI to see if they are the same. This one has communication between the two ○ Different from 3rd degree, which has no communication between top & bottom parts of heart HR is also VERY slow (35 bpm) 3:1 conduction deficit Treatment: Need pacemaker Third degree heart block No relationship with P waves and QRS. All different PRIs or can’t calculate Pacemaker Therapy Device that will deliver an electrical stimuli to the heart Permanent or temporary Can be combined with AICDs Indicated for: Slow pulse formation (Bradycardia) ○ NOT all people with bradycardia- not the 20 year old track athlete with HR of 54. People who have bradycardia→ Hemodynamic compromise AV or ventricular conduction disturbance ○ Conduction problem → Inferior wall MI- Right side In about 60% of people, the right coronary artery feeds the SA node In 90% it feeds the AV node? If someone has a right sided infarct, watch for heart block!! Can also be used in bad cases of CHF to resynchronize the left and right ventricles to work together better (resynchronization therapy) Pacemaker Design Two components: Generator Circulatory to detect intracardiac electricity and cause a response (sensitivity), measured in millivolts (mV) ○ Milivolts: Sensitivity, how much does the pacemaker see ○ If the sensitivity is very high, the pacemaker can’t see anything. If it can’t see anything and the heart has an intrinsic native beat, it won’t see it and may try to initiate a complex ○ If the sensitivity is too low, the pacemaker can see everything. Every sort of artifact it will interpret as a heartbeat. Then it doesn’t initiate the shock and stimulate the myocardium. Sends the person in the opposite direction Batteries Determine rate in bpm Determines output (strength) in milliamps (mA) ○ Miliamps: Amount of energy required to stimulate the myocardium Rate, milivolts, miliamps= Set by physician Electrodes Leads carry the impulse created by the generator to the heart So, typically put the pacemaker in the pocket of the upper left chest wall and send electrode wires down in through the superior vena cava and down into the heart ○ One inserted into the ventricle (Ventricular pacing) ○ Wire in the atrium and ventricle (AV pacing) ○ Pace the left side of the heart (AV Sequential pacing) ○ Both sides of the heart (Biventricular pacing) Pretty good longevity on the batteries (8-10 years) Pt must alert the provider when the batteries are dying and will have to come back to the hospital when they have to be changed. Pocket developed. Sometimes they will take the wires and swap out those too Any device in the body (pacemaker) is a possibility of a source of infection When removing the pacemaker, hook the person up a temporary wire (transvenous pacemaker), 5 days of abx, down to the lab to replace permanent Maintenace for Pacemakers: Companies will help by using a magnetic over the pacemaker. Can look back weeks to see what has been going on: Failure to Capture: When a pacing stimulus is generated, but fails to trigger myocardial depolarization Failure to Sense: Pacemaker fails to sense or detect native cardiac activity Pacemaker Syndrome: Complication when putting a pacemaker in that causes hemodynamic instability Wire going into tricuspic valve and implanting in the right ventricle. Can cause problems: Monitor these patients Put on anticoagulation Have them take ASA To avoid any complications that will come up Types of Pacemakers Permanent: They keep this Implanted generator Implanted leads Types of Pacemakers Temporary Wire: Watch older people with confusion touching the dials. Lock out system on transvenous temporary pacemaker. Be careful to not dislodge it even by accident Transvenous: ○ Usually use an external jugular (most now) ○ Can use subclavian and femoral (far away and dirty site) ○ If in more than a couple of days can become an infection issue O Epicardial: ○ Typical in open heart surgery ○ Typically people have bradycardia afterwards ○ Attach wires directly to the heart and thread them out through the skin ○ Still attached after closed, wrap wire outside and if they need them they can pace with it ○ Maybe 24 hrs or so after surgery they just pull them out if don’t need them Ventricular probe (via Swan Ganz catheter): ○ Most don’t have this capability, but some have a probe so they can do pacing ○ Becomes a little dicy- When doing hemodynamic parameters and inflating the balloon of the swan it goes up into the pulmonary vasculature and gives you a wedge pressure ○ Catheter is moving a little bit, so don’t want that pacemaker site/activation point to be moving a lot Pads Transcutaneous: You will see most in the hospital today. Sandwich the pads Sometimes need sedation onboard because it can be uncomfortable Should see a pacing spike and then capture immediately after; if it doesn’t, not doing it’s job p s Pacemaker Function Universal Code: *KNOW THE FIRST THREE SETTINGS/WHAT THEY ARE FOR!! 1. Chamber being paced (A, V, D)* Paced. If wire is in atria, ventricle, or both= Can pace this Atrial, Ventricle, Dual (both) ○ If have a pacemaker spike and P wave= The atria is getting paced ○ If have a P wave without a spike, spike, then ventricular wave= Ventricular pace ○ If have a pacemaker spike, P wave, pacemaker spike, QRS= Dual 2. Chamber being sensed (A, V, D, O)* Sensed. It is LOOKING, not doing anything, gathering data Could be set in atria and looking in ventricle or be set in atria & ventricle and looking in both 3. Type of response from pacemaker (I, T, D, O)* What is the response to that looking? Inhibited (sees a native beat coming, holds it back and inhibits) Triggered (makes the heart contract) Dual Off (not used too much) 4. Rate responsiveness ability (O, R) 5. Multisite capability (A, V, D, O) or Antitachycardia function _R f * Only the first three letters are used for pacing codes * The first 3 codes are VERY important 4 & 5 used by physicians (don’t really have to know these) Example: The lab will say we have a DDD (Dual paced, dual sensed, dual pacemaker) Practice Code DVI: Dual: Both the atrium and ventricle have pacing electrode Ventricle: Only the ventricle is being sensed (Camera only here) Inhibited: The pacemaker’s stimulating effect is inhibited by the ventricle activity. It will NOT create an impulse when it senses the ventricle is active Probably will have a problem with sinus node, need to have pacing in atria. Sometimes it works, sometimes it does not Capture: Used to denote that the appropriate complex followed by a pacing spike Down arrow→ Pacemaker spike Following that is a capture Failure to Capture: Pacemaker fires and you don’t get anything (NOT working) Look at those beats alone (That’s what he circled) They are going to tell you to do a 12 lead which isn’t useful Failure to Sense: Native beat and pacemaker spike in the middle of the beat; not sensing what is going on DDD A= Atrial pacing spike with capture B= Ventricle pacing spike with capture C= Pacemaker senses atrial activity and does not fire (inhibits atrial delivery) but after appropriate delay firs ventricle spike (no ventricle activity sensed) D= PVC noted, pacemaker notes endogenous activity, therefore no spike, appropriate inhibition Fixed Vs Demand Fixed Pacemaker is set to pace but not to sense (No matter what) Paces at a constant rate, independent of the patient’s intrinsic rhythm Dangerous because it can hit the T wave Don’t see this too often, old fashion Demand Pacemaker is set to to sense and respond to intrinsic activity Fires only when the patient needs it All pacemakers we discussed before are this type Pacemaker Complications Local site infection Pneumothorax/Hemothorax Bleeding, hematoma ○ Observing the dressing, chest wall for bleeding= If starts bleeding, apply pressure and call provider asap Ectopy from irritation of electrode Dislodgement of electrodes ○ Twidler’s Syndrome: Patient touching the pacemaker a lot overtime and it messes with the wires (Can cause complications) Pacemaker Syndrome: Hemodynamic instability due to problems with insertion AdAVOID With Pacemaker: High voltage electrical lines Strong magnetic fields (Like MRIs)= HAVE to tell them that they have metal in their body with pacemaker so they can work around it ○ Should not go near MRI lab with metal ○ Try to have catscan instead Chain saws, welding equipment If the pacemaker is in the left chest wall, cell phone should not be kept in the pocket right next to it Microwaves used to be a problem but not so much anymore Implanable Cardioverter Defibrillator (ICD) Criteria: Class 3 or 4 HF OR cardiac arrest Protocol docs have to worry about for this Can be used with a pacemaker Electronic device that will detect and terminate life threatening episodes of tachycardia or fibrillation Indicated for patients surviving VT/VF arrest, cardiomyopathy, R or L ventricular dysfunction Responds to two criteria: Rate exceeding a predetermined level ○ Pacemakers can be used to override rapid rates but ICD is designed to Change in the isoelectric line segment Have vests used for patients while they wait for ICD (EXTERNAL): Wear at all times except when taking a bath or shower!* Will send a patient an alarm before it activates (Vibrates beforehand)* Fits into a shirt Will download information to physician Activation of an ICD tach p v Rate sensor activated pmfires Requires a set duration of time to identify the arrhythmia ○ If you have 4-5 beats of Vtach, not going to fire. Prob 10 beats of Vtach Device charges Takes a second look to confirm…and fires ○ You see the pacemaker actually firing toward the end to correct the beat Nursing Management of the Patient with an ICD/Pacemaker Incision site assessment and care Clean ○ Make sure no swelling and no bleeding AdaCXR to confirm lead placement! (Pneumothorax) ○ Should have a 12 lead EKG done after as well Medication evaluation for changes in regimen ○ Maybe a change in meds because now have a permanent pacemaker Diagnostic Testing Echocardiogram Transthoracic (traditional- TTE): Easy to do, noninvasive ultrasound, pretty good at measuring injection fraction, valves, and shape and size of cardiac structures Done by technician, person placed on left side, use a probe and gel, about 20 mins to, visualize the heart using sound waves Also, do bubble test: Inject medication-like substance into person and it works it’s way into myocardial circulation. Will help to determine if there’s a problem with atrial or ventricular septal defect when bubbles passing from one to the other side Transesophogeal (TEE): More invasive, needs consent Can be done on outside at cardiologist’s office Will need someone to come with them because they use enough medication to sedate them but not enough so. Will give more sedation if in hospital and on ventilator to keep them quieter Need resp therapist, nurse, anesthesiologist, attending Better at detecting clots in atria (Before electricardioversion) me 2 Non-Invasive Ultrasound Measure EF% Size, shape and motion of the cardiac structures 6 Cardiac Catheterization Invasive procedure Diagnostic for CAD Assess coronary patency Determine extent of atherosclerosis Determine if revascularization procedures will benefit patient ○ Percutaneous intervention (PCI): Stent deployment ○ Coronary Artery Bypass Grafting (CABG) If left main is involved, 3 vessel disease, lesion greater than 50%= Requires surgery Will always try to put a stent in first if possible !! Sometimes go stenting and staging Transthoracic Echocardiogram TTE: Exact position they are in is shown above. Technician usually behind the pt Going through chest wall, skin, layer of fat, muscle, rib cage= Limited, visually distorted, but painless Takes about 30-45 mins Best to take a deep breathe and hold their breath Use bubble test to see if there’s a patent parametial valley Explain to the person why they are getting this test, time frame of test, position Good at visualizing wall motion function of left ventricle, valves of the heart and determining the ejection fraction (around 50-70) ○ When the left ventricle contracts, it doesn’t eject all of the blood, have a little bit left behind ○ If lower than 40- Get more symptomatic Transesophageal Echocardiogram TEE: Outpatient setting High quality imaging Topical anesthetic Moderate sedation NPO ○ Remain NPO for a couple hours afterwards, given a bedtime speech and swallow after to see if any problems IV patency Monitor BP, HR, Sp02 Complications: Esophageal perforation, sore throat (warn patient about this- if it is REALLY sore they should tell provider for follow up) Monitor during the procedure: If they receive too much sedation Suppression of respiratory system Lowering of BP (Sometimes sedation too heavy for them) ○ Legs up to head ○ A little IV ○ Some puffs with bag valve mask Cardiac Catheterization Gold standard for diagnosing CAD IV insertion: Sedatives, fluids, heparin ○ Can give sedatives but try to avoid bc want to see if the pt is symptomatic BP, ECG, continuous monitoring Resuscitation equipment Radiopaque contract agents are used Monitor BUN, PT/aPTT, INR, H&H, plts, electrolytes Arterial hemostatis Can be done with PTCA (Percutaneous translumunal coronary angioplasty) ○ Can also go through radial artery NPO for at least 8 hours prior to procedure Before Procedure: Have bloodwork done: Don’t want any problems with kidneys and dye (Nephthropathy- damage to the kidney) Give IV hydration: NS 60ml/hr just to hydrate the kidneys Nursing Care: People have allergic reactions to the dye (shellfish) ○ Treated with benedryl and steroids before procedure to avoid problems When come back: Decannulated down in the cath lab Some of the devices have got really good at closure and they can move a bit **But for the most part you have to keep them flat for 6 hours ○ CANNOT turn them too much. Can put small pillow under them *Check both lower extremities and check pulses → Sensitivity, changes in color, warmth, posterior tibial pulse ○ After cath Q15M before and Q30M for 2, Q1H for 4 Visualize the groin too- Going through the femoral artery and sometimes femoral vein, typically do both. Can bleed VERY quickly!!* ○ *If you feel any bleeding or see any bleeding (warn pt about this)= IMMEDIATELY intervene. Can be lifethreatening!! Put pressure on it. ○ If horrible, put whole body weight into holding pressure onto this Can have significant amount of blood loss and significant hematoma formation in groin (compromise blood supply in leg)= Can be significant *HORRIBLE back pain: Underlying warning of bleeding in groin! CHECK! Listen to site with stethoscope to see if hear bruit 6 hours after procedure, get bloodwork again to check amount of hg! Cardiovascular Function 3: Complications from Heart Disease Things that can happen to a patient with HD or heart problems Risk Factors and Hypertension Non-modifable: Age, gender, genetics, race Modifable: Smoking, activity level, nutrition/diet, obesity, DM, harmful use of alcohol Factors: Elevated cholesterol & BP ○ Good cholesterol= Less than 200 ○ LDL: Under 100 ○ HDL= 40-60 and above ○ Explain to pt going home on therapy the difference between good HDL and bad LDL, what normal numbers are and why taking these drugs Teach a patient who had heart attack and had stenting or surgery and is going home on hyperlipidemic therapy trio Hypertension is a silent killer + Diabetes = Worse (Adding high sugar state which tends to damage the arteries) Endothelial Dysfunction: Shrinking of the blood vessels usually due to metabolic process or age, does not involve coronary atherosclerosis (Can do certain changes like diet, exercise to relieve this) Atherosclerosis: Hardening of arteries, accumulation of fat plaque or calcium deposit Ischemic Heart Disease: Atherosclerotic build up with ischemia Angina Pectoris: Unstable and stable Unstable: Doing nothing, can occur anytime. Precursor to having a heart attack Stable: Know when they go up flight of stairs→ Triggers chest pain (So take nitroglycerin before doing so) Myocardial Ischemia: Lack of blood supply/O2 to heart muscle Coronary Thrombosis: Clot or blocking of blood in coronary artery, which turns into MI (Myocardial Infarction) After MI, can have: Arrhythmia & loss of muscle tone (Heart is very irritable) Remodeling: Heart gets better ACE & ARBS can prevent Ventricle can dilate and head toward CHF→ End stage MI Presentation: Women present differently than men! Extreme fatigue, irregular lower/ upper back pain, discomfort in neck, jaw or one or both arms, flu like symptoms, legit headedness, only 50% report chest pain Heart disease= Significant health problem Woman have as many heart attacks as men do Diabetics also present very differently Admitted for non-stemi/rule out of MI If they say they are having a GI upset in the middle of the night and ask for Mylanta. They don’t necessarily present with chest pain either, usually Gi symptoms GATS Divid into two categories: EKG Changes → STMI! No EKG Changes→ Look to see if cardiac markers are raised (Troponin is up, CK Isoenzyme is up= YES)→ Non-STMI No EKG Changes→ Cardiac markers are NOT raised→ Unstable Angina Heart attacks can be classified also as new and old Monitor these patients for the complications of the various types of infarct 12 Lead EKG= VERY important for measuring changes Lead AVR: Complex should always be negative (inverted). IMPORTANT! ○ If limb leads are not on right, the AVR will be positive. Have to do it over again correctly! In reference to location (MI), Inferior Wall: Fed by the right coronary artery ○ Right CA feds the SA node in about 60% of the population Feeds the AV node in about 90% of the population ○ So, if someone has an inferior wall MI, that blood supply to the AV node may be compromised and they can have different degrees of heart block ○ Make sure AV node is working properly Can be a right sided infarct→ Treated totally differently, don’t give nitrates Give volume ○ Right ventricle is really not very strong, volume dependent situation, may wind up giving IV fluids Anterior Wall: From left coronary artery ○ Feeds the left ventricle- Work horse of the heart, responsible for cardiac output Lateral Wall Posterior Wall block What Blood Work is Appropriate for MI? Troponins (First to rise, VERY cardiac specific) ○ Can stay elevated for several days ○ If someone puts off going in post-chest pain days later, they can still see the elevation in the blood work afterwards ○ *Diagnostic criteria* Creatine Kinase ○ Specific enzyme for cardiac function ○ But tends to decrease after 24 hours ○ Someone comes in with full chest pain, draws blood and the troponin and CK are both up. After 24 hours, if the CK starts to trend downwards, the MI is getting better (Past its peak) ○ *CK levels downward= Infarction process has stopped* When patients come in and docs are trying to figure out if they had a heart attack will put in for serial bloodwork and EKGs (Q8H) o ACS Treatment: Medical Management Goals Minimize myocardial damage Preserve myocardial function Prevent complications How… Reperfusion the occluded area ○ Thrombolytic therapy ○ Percutaneous Coronary Intervention (PCI) Reduce myocardial O2 demand Increase O2 delivery Bed rest Chest pain, EKG changes, + blood work in the ER. Where are they going first? Cath lab If they can they will try to put in a stent If not, use thrombolytic therapy ○ Want to know if they are on blood thinners, recent bout of GI bleeding, recent stroke, etc. Specific criteria in hospital for TPA 0 MI MEDS Meds to Manage- Waiting to go to cath lab & stabilize pt: *ASA: Very important ○ If ASA is administered asap in the field or when getting to the hospital, mortality is decreased by 25%. Helps keep the platelets very slippery Morphine: ○ Decreases anxiety and apprehension, vasodilates coronary arteries Nitroglycerin: t 911 ○ Important drug in ER, stabilize before cath lab ○ If they don't get relief after 3 or more nitros 5 mins apart= Red flag that they are actually having a heart attack ○ Beware: Middle age or older man having chest pain, ask if he has had sildenafil, viagra (within 24 hours), silace (longer acting drug- 3 days) These are vasodilators Can’t give nitroglycerin within these time periods with these drugs because can cause a significant drop in their BP BB: ○ Main line therapy for heart disease. Not in ER. ACE Inhibitors: ○ Hold back on these usually for 72 hours ○ Used cautiously with renal impairment pts ○ Can cause angioedema as well (High propensity to slow allergic reactions) Arnies: ?? Combination drugs. If ACE and ARBS don’t work over 3 15mins can Patient with ACS: Nursing Process Assessment Establish baseline*, identify needs, determine priorities ○ Get EKG done a ○ Get on cardiac monitor ○ Get on pulse ox (want 95% and above) ○ Put on 2L nasal cannula to support them if needed Less than 95% ALWAYS or just for the time being than wean off Initially deff give O2 for support Focused physical assessment (system) ○ Listen to heart, feel pulses, making sure not developing increasing symptoms in terms of chest pain IV access Always put 02 for Chest pain is a big thing: A lot of people involved Somone getting EKG Someone starting IV & getting bloodwork Someone getting nasal cannula Someone else getting nitro drip ready Diagnosis Nursing Diagnosis: Based on clinical manifestations, history and diagnostic assessment data (troponin levels) Once have a heart attack, heart is very irritable→ Collaborative problems/potential complication ○ Acute pulmonary edema ○ Heart failure ○ Cardiogenic shock ○ Dysrhythmias/cardiac arrest* ○ Pericardial effusion, cardiac tamponade* Planning Goals Relief of pain and symptoms Prevent myocardial damage Maintain effective respiratory function Maintain adequate tissue perfusion Reduce anxiety on support Nursing Interventions Pain: Administer morphine, nitro, nitro drip Resp: Quick assessment, listen to lungs, pulse ox Tissue perfusion: Secondary to MI can be compromised Reduce anxiety: Morphine can help. Don’t give xanax or anything like that. Worry about symptomatology first. WANT: Pulse ox about 95% HR below 100 ○ Over 100: Bring to provider’s attention and prescribe a BB to keep it down MAP always to be kept over 65 Complications from Heart Disease: Heart Failure: Can be systolic or diastolic format Pulmonary Edema Cardiogenic Shock: Due to myocardial damage or damage to the valves Thromboembolism: Predisposed to having a blood clot or due to heart damage so there’s areas of the heart that have decreased blood flow so can develop embolism Pericardial Effusion Cardiac Tamponade Cardiac Arrest Heart has been damaged→ Musculature has been damaged→ A couple complications Thrombus develop in ventricle bc not contracting well so blood is stagnant Hypotension from impaired contractility ○ Heart doesn’t beat effectively enough, doesn’t feed itself, and decreases in perfusion from coronary arteries and the heart muscle ○ Can result in increasing ischemia Tissue necrosis→ Rupture of ventricle→ Cardiac tamponade OR paillary muscle infarction→ floppy valve → mitral regurgitation →→ CHF Electrically unstable → Arrhythmias (Prevent this: Lidocaine, Na channel blockers, BB, K channel blockers, amiodorone, Ca channel blockers) ○ If having arrhythmias in acute phase, start amiodorone or lidocaine drip Pericardial inflammation → Pericarditis (Can run a low grade fever after MI) Heart Failure Often referred to as CHF Clinical syndrome; S&S of fluid overload or inadequate tissue perfusion Cannot generate a CO sufficient to meet the body demands Once diagnosed, progressive, lifelong condition ○ Medications and lifestyle changes overtime To Diagnose: Echocardiogram ○ Transthoracic TTE: To look at heart, wall motions, and valves ○ Transesophogeal Echocardiogram (TEE) Aap ○ Ejection fraction (< 40%): Normal Ejection Fraction: 55-65% Anything less than 40, patients will be showing significant symptomatology, even at rest. As the number gets lower, the symptoms get worse Systolic or Diastolic Dysfunction Heart failure can be systolic or diastolic dysfunction P can't squeeze Systolic: Inability of the heart to pump effectively Heart becomes very big/enlarged→ Cardiomegaly & muscles don’t squeeze well→ Less blood being squeezed out of the heart Example: Pt had a ejection fraction of 40%. But have a blood volume of 150 mL. 40% of 150 mL = 60% (Pretty good amount) relax stiff cant volume Diastolic: The heart cannot relax, becomes stiff The walls do not contract well and the volume into the ventricle is much reduced Example in diastolic: 60% of 70 mL volume is only 42 mL *Much less blood coming into the system with a diastolic dysfunction vs systolic!!!!! (Preserved EF) ○ *Diastolic dysfunction might be sicker bc not putting out as much volume and the chamber is smaller Pathophysiology of HF Heart and kidneys are interconnected Decreased blood flow from the heart leads to renal insufficiency and renal damage Decrease in renal perfusion triggers off the renin-angiotension-aldosterone system. Aldosterone is released, which means increase in Na, which leads to increase in osmotic pressure, increase to ADH, increase in water reabsorption, leads to fluid overload and edema, damage to the heart Heart damage→ Increasing amounts of fluid retention, aldosterone system as well as activation of the sympathetic NS Renal doc will say to the cardiologist you need to cut down on lasix dose bc it’s affecting the kidneys (Rising BUN and Cr)An But the cardiologist will say back we have to offload the heart to better supply blood to the kidney bc the heart will be more efficient Clinical Manifestations of HF S&S Related to congestion and poor perfusion Etiology CAD, cardiomyopathy, HTN, valvular disorders ○ Cardiomyopathy→ Heart is big & unmanageable (Can be restrictive- rare or hypertrophic types) Chagas: Occurs in southern hemisphere, but can occur in the US as well. Vector borne illness. Building their homes with local materials like wood, mud, etc and these insects live in the rotting timbers and it bites around the lip and then deficates. The victim will take their hand and touch what is on their face and contaminate themselves ○ HTN (If someone doesn’t take their meds overtime)→ Left ventricle gets tired of pushing against a high BP→ Starts to dilate and change Renal dysfunction with fluid overload ○ Cardiorenal Syndrome: Lack of bf to the heart affects the kidneys (retains fluid) and that affects the heart DM: Attacks every system (NS neuropathies, vascular system)→Effects organs Clinical Manifestations of HF Manifestations Manfestation depends on what side is affected ○ Left sided HF: Pulmonary symptoms ○ Right sided HF: Swelling in extremities, liver and abdominal distention A lot of fluid to the viscera Biggest cause of right sided HF is left sided HF. If you have left sided HF, the right side will also start to fail and get both S&S Right side sided HF (Right ventricle): Cor Pulmonale Similar to right sided infarcts or CHF (Right is hard to treat) ○ Do a right sided EKG. Right ventricle is volume dependent. ○ If you are giving people lasix for HF, you are taking away the amount of volume that they have ○ Don’t have a good treatment for right sided infarct or HF so they treat like left sided (with lasix) bc odds are if you have right sided, you have left sided as well ○ Have to be VERY careful to not dehydrate the person/take away too much volume. Otherwise, you will create symptomatology from inability of the right ventricle to beat Manifestations L T HF SS Body righthander Orthopnea: Have to keep pillows to keep them up when sleeping Paroxysmal nocturnal: SOB in middle of the night Oliguria: UO of less than 400/500 cc in 24 hr period Right: Body symptomatology CHF is classified in 2 ways 1, 2, 3, 4 A, B, C, D Mild→ Severe Assessment & Diagnostic Findings Presentation: S&S of pulmonary/peripheral edema Assessment of Ventricular Function: Echocardiogram: Assess the ventricular function. Will confirm the presence of CHF. Also identifying left wall motion function and identifying the underlying cause. Can also get an idea of the ejection fraction. ○ Confirms, Identify underlying cause, Determine EF CXR: White patchy in the lung fields 12 Lead ECG: Diagnosing ischemic changes and arrhythmias. In cases of CHF, may show some changes in the interior wall bc that is measuring the amount of voltage coming out of the heart looking at the lung fields. right CHF LABS If Labs: CBC, Electrolytes, BUN/Cr, LFTs, TSH ○ Watch electrolytes bc most likely giving lasix, so watch that K level!! ○ Diuretic therapy also affects the kidneys as well as a weak heart can affect the kidneys. If right side problem, can have problems with liver function, enzymes being up, thyroid functioning, as well as CBC BNP: B-type Natriuretic Peptide Blood Test ○ Substance secreted from the ventricles in response to changes in pressure that occur when heart failure develops and worsens ○ Bc of fluid overload, presses on myocardial muscle, then muscle releases this chemical called BNP ○ High levels are a sign of high cardiac filling ○ GOLD STANDARD FOR CHF: BNP!!! 2 Medical Management Relieve patient symptoms* Improve functional status and quality of life Extend survival Patients who suffer from CHF have to follow a diet Bags○ 2 g sodium diet ○ Be mindful of fluid intake ○ Diuretics + fluid restrictions= Makes them thirsty Becomes a little bit of a problem. Always the pt in the hospital asking for water or ice chips Treatment ○ Based on type, severity and cause of HF Doctors are looking to maximize the cardiac output with these patients ○ HR x Stroke Volume= CO ○ Stroke Volume= Preload (blood coming into the heart), afterload (amount of resistance the left ventricle faces when it pumps), contractility (ability for the heart to contract/move) Certain meds used to tweek these When looking to get people back to a certain state of reasonable health, looking to help one of these three things or HR GOAL of therapy with HF: Pee it, Pump it, or Pool it Need to expect diuretic therapy (lasix or K sparing diuretic) pump Giving digoxin or doputamine (helps the heart pump better) Hide excess volume in vasculature (giving pt’s vasodilators like nitro drips) Pee pool Pharmacologic Therapy ACE inhibitors (angiotensin-converting enzyme) ○ “pril” ○ Block the conversion of angiotensin I to II ○ Decrease BP, afterload (resistance of left ventricle is much easier) ○ Slows progression of HF ○ Promotes vasodilation and diuresis ○ Good at preventing left ventricular remodulation (FIRST CHOICE) Stop left ventricle from becoming all dilated Complications: ○ Watch renal pts= Can have elevation of BUN and Cr! ○ If can’t tolerate ACE inhibitors (dry cough), will switch them to ARBS ARBs (angiotensin II receptor blocker) ○ “tan” ○ Similar hemodynamic effects ○ Block the effects of angiotensin II at the receptor site ○ Prescribed as an alternative to ACE inhibitors (cough) after load Another class of drugs is called ARNIES: Angiotensinogen receptor inhibitors (combo drugs) Will not test on these!!!* If people cannot tolerate ACE or reach max benefits from either of these drugs, provider may try them on these Pharmacologic Therapy If not getting a good response from ACE & ARBS, may transition to these: Preload afterload Hydralazine & Isosorbide: Antihypertensive & Nitrate For patient who cannot take ACE inhibitor Venous dilation (reduces venous return, lowers preload) Lowers SVR, LV afterload Isosorbide: POOL IT, Vasodilation Decreasing blood supply back to the heart (preload) Lowers afterload (amount of resistance ventricle has to go up against)- GOOD Beta-Blockers “Lol” Reduce the effects of the constant stimulation of the SNS Some patients are on these with heart disease anyways Helps with anxiety as well Diuretics it Remove excess extracellular fluid by increasing the rate of urine produced Loop (Lasix), thiazide (HCTZ), aldosterone blocking Digitalis Increases the force of myocardial contraction Slows conduction through the AV node Decreases HR! Help pumping (inotropes) Digitalis toxicity to 4 Afterload Pee IV Infusions: Inotropes Increase force of contraction Acute decompensated HF Severe ventricular dysfunction Used in hospitals PUMP IT PORTION!!! afterload IV Infusions: Inotropes Milrinone (Primacor) Phospodiesterase inhibitor that delays release of calcium from intracellular reserves and prevents extracellular calcium uptake by the cells Vasodilation, decrease preload and afterload, reduce cardiac workload Reduces the amount of effort the heart has to extend by decreasing amount of O2 that it needs preload Tcontractility DOButamine Catecholamine Increase cardiac contractility Precipitates ectopy and tachydysrhythmias, increases AV conduction When people first come into the hospital with brand new CHF, they often send them to the ICU for a “dobutamine tuneup”. Heart has gotten so weak that they need to try to help them a little bit. Put them on this drip. They will come and stay for a couple days to get the heart beating and pumping more effectively and diuresis them a little bit Initially come to the ICU bc native to the drug (Hypotension or arrthymias) Once been exposed to that once and prove they won’t have a bad response, they will put them on the step down units ○ Maybe home for 2-3 mos and come back again for this IV Infusions: Vasodilators POOL IT PORTION!!! Nitroprusside (Nipride): Very powerful drug and potentially very dangerous Will use for hypertensive crisis or emergency as well as for CHF Excellent arterial vasodilator as well as the venous side (POTENT) Breaks down to cyanide in the body ○ Q24 hours, you have to draw theocyanide levels because you don’t want your patient to become poisoned Wftfanhidelevels ○ Will come in a green bag to protect from the light Main point: Closely monitor for toxicity!!!!! Do a very frequent check on VS (Q15M) ○ Hopefully patient has line to just get continously Nitroglycerin: Potent venous dilator Multipurpose function drug. Used in CHF to pool things, vasodilate the venous side, promote blood flow back to the heart. Also, can use for MI. No max dose. But when you get between 20-50 mcg, it usually gets to an effective level. Nitro drip SE: Headache (Common) ○ Give fiorcet or tylenol for this Nesiritide (Natrecor): Another vasodilator. Less used now-a-days so you don’t have to worry about this too much. A synthetic BNP for acute decompensated HF causing arterial and venous dilation Acute exacerbation of CHF ○ Felt it wasn’t really effective ○ Not prescribed anymore X no lounged Other Meds for HF Anticoagulants: Heparin drip Keep in mind difference of: ○ Therapeutic use of IV heparin: Afib, HF, VTE ○ DVT prophylaxis: Heparin SQ or lovenox (long acting heparin) Antidote for heparin overdose: Protamine sulfate Antiarrhytmic: Amiodorone Bradycardia or blue mans syndrome are big problems with this Causes lung problems (idiopathic lung disease) ○ Not the best idea for someone with CHF to be on that too long Thyroid problems (Hypo and hyper) Cutaneous lesion problems ○ Breakdown of the skin and rashes ○ Corneal lesions in eye Hepatic and hypotension IV form ICD: Internal cardiodefibrillator If have stage 4 HF, may do resynchronization therapy ○ Try to coordinate left and right side of the heart better ○ Does not improve mortality but improves symptoms and better quality of life. But does not help long term Statins: For hyperlipidemia Lipitor is like top in US Take at the same time Better taken at night (Works better!!) ○ Long term maintenance Other statins: Better to take with a meal Normal cholesterol: Less than 200 Normal LDL: Less than 100 Normal HDL: 40 or higher Triglycerides: Less than 150 40 60 Patient with HF: Nursing Process Assessment: Health history: S&S Physical exam ○ Lung, heart sounds ○ JVD week ○ Edema: Teach pts if they put on more tha 2 lbs a day, they may need a change in their meds. OR 5 lbs in a week = LET PROVIDER KNOW Instead of lasix 40, may need lasix 60-80 to get extra fluid off ○ I&O ○ Daily weights Diagnosis: Based on assessment data Collaborative problems/potential complications ○ Hypotension, poor perfusion, cardiogenic shock Cardiogenic shock: Think heart is NOT pumping effectively (Left and right sides) ○ Dysrhythmias ○ Thromboembolism ○ Pericardial perfusion, cardiac tamponade Planning and Goals: Promote activity, reduce fatigue ○ Promote doing activities in the morning and take frequent rest periods Reduce fluid overload symptoms ○ SOB or dyspnea: Call provider! Reduce anxiety ○ Teach breathing and meditation techniques ○ Last resort can use some kind of antianxiety meds Nursing Interventions: Teach pts to read food labels= Be aware of sodium content and avoid fast foods 2lbs Iday 5lbSI Want to try to keep people out of the hospital when have CHF Hospitals are being held by this by the federal gov ○ If someone comes back within 30 days, the hospital won’t get reimbursed (Does not even matter if unrelated events) ○ Set up protocols to ensure this does not happen Appt for pt to see provider within 2 weeks of discharge BIG ISSUE. Call doc ASAP if having any symptoms HF is one of the more expensive diagnoses in the country PREVENTION AND INTERVENTION!!! Pulmonary Edema Acute LV failure ○ MI or chronic HF ○ Flash pulmonary edema Restless, anxious ○ Restless and anxious bc hypoxic and feel they are drowning in own fluid Prevention Can be a new onset (MI) or secondary to chronic HF Treatment: In some cases, BIPAP can treat PE (not flash) by forcing air into the alveoli and pushing fluid out Sometimes the providers will opt for this instead of intubation Good thing for people with CHF and PE, they usually respond very quickly and can get off the treatment pretty fast ○ Maybe on and off within 24 hrs when they are diaphoresized and get all fluid off so they can extubate them. As opposed to someone with pneumonia or ARDS who will stay on the ventilator for a long period Limit sodium in diet Limit intake of processed foods High in veggies, low in animal meats O Flash PE: Specific type that once you see it you will never forget it. You can hear this from the patient’s door, don’t even have to do an exam. Crackling, SOB, diaphoretic, pale, anxious bc not getting O2, hypoxic Comes on very rapidly and has to be treated aggressively Pt’s often get intubated bc they get too acutely ill and rapid an onset Pulmonary Edema Management Medical: Oxygen ○ O2 can mean ventilator support or can just be BIPAP if early enough ○ Can also try nonrebreather mask and diuretics Diuretics: Lasix Vasodilators: Nitroglycerin (monitor BP) PEE it, PUMP it, POOL it NRB Nursing: Positioning ○ Optimizing resp effort (more comfortable sitting up then lying down) ○ Some people are so unstable they need to sit up Psychological support ○ Pts with PE do not do well with restraints bc they increase cardiac workload Monitor medications ○ Before giving lasix, look at K ○ Before give BB or meds that affect BP, check BP Cardiogenic Shock Life threatening condition when decreased CO leads to inadequate tissue perfusion and shock state CO= HR x Stroke Volume (preload, afterload, contractility) ○ Going to try to optimize these ○ Going to try to get people out of cardiogenic shock Heart is not pumping effectively at all ○ Neither the left or right side ○ Not moving blood Insufficiency: Floppy valve Regurgitation: Stiff valve Causes: Ischemic disease (LV or RV damage) Mitral insufficiency or regurgitation End stage HF, cardiac tamponade, pulmonary embolism, cardiomyopathy and dysrhythmias S&S: Low BP, elevated HR & RR, increased work of breathing, cold clammy skin, decreased bf to the kidney (oliguria- 400/500 cc of urine in 24hrs), weak rapid pulse Treatment: Often times they will be on a ventilator Almost always on an assistive device (balloon pump or inpello device, Lvads?) LIFE THREATENING, treat aggressively!!! warp Need open heart surgery, emergency stenting, or heart replacement Usually have a swanganz catheter ○ Get a CDP reading (Will be elevated)= Can be anywhere from 2-8 If CDP is 10= Fluid volume overload problem Will need somekind of reduction in that Usually lasix to reduce CDP (pressure in right atrium) CVP CVP Cvp If CDP is 0 or 1= Fluid volume deficit May need a bolus May be needing blood (volume back) ○ If wedge pressure (normal is 10-12) If it is 18: Volume overload (left side of the heart)= Lasix *DON’T memorize values, just know what it means!!* pressure wedge MVP ICO What is Cardiogenic Shock? PUMP FAILURE Decreased CO and hypoperfusion with adequate intravascular volume ○ Normal CO= 4-8 L/min (Typically the heart will pump this) Different than amount of blood in percentage coming out of the left ventricle= Ejection fraction If L or R sides of heart isn’t pumping correctly will have increased CBP, wedged pressure, and decreased CO Think decreased forward flow Interventions are aimed at restoration of forward flow volume We lose of we don’t perfuse If not moving blood. S&S: SOB, pulmonary congestion, JVD, angina (chest pain from lack of oxygenation), oliguria (no flow to the kidney), organ failure, cold and clammy skin Treatment: All are to restore blood volume going forward!! Initially the body will respond with elevating the BP but it fails Then it starts to cycle over again Treatment Goals for Cardiogenic Shock Correct underlying problem Reduce cardiac workload (preload and afterload): Usually using various meds Improve oxygenation Restore tissue perfusion Some lab values to monitor: Troponins (the heart), serum lactate (indicate the degree of shock), EKG, CXR Typically open heart surgery Massive infarction. Put on ventilator, sedate them, put on balloon device, then take them to surgery or take them to cath lab to put stent in to re-establish BF Want: MAP = 65 and above Serum Lactate= Don’t want above 2 Reduce LV pressure & volume: Nitro or balloon pump If wedge pressure is up: Sign of LV HF (Typically use lasix) Maximize coronary perfusion: Balloon pump The Spiral of Cardiogenic Shock Profound depression of contractility ○ Decreased CO ○ Hypotension Compensatory mechanisms ○ Tachycardia Narrow pulse pressure (r/t low SV) And vascular resistance is increased ○ Increased SVR LV failure ○ Pulmonary edema, dyspnea, S3, murmur, chest pain RV failure ○ Clear lungs, hypotension, elevated RA pressure (CVP), JVD ○ NO pulmonary problems on right side, only left! Cardiac Output= SV x HR Contractility: Ability for LV to pump Dobutamine Pramacore Oral Dig Preload: Amount of stretch in the heart, volume coming into right atrium Afterload: Amount of resistance LV has to meet to pump blood CO= HR x SR Stroke volume Preload The amount of volume in the ventricle at end diastolic filling (stretch) Right atrium→ Ventricle Starling’s Law: Amount of stretch required to give maximum contraction Afterload Resistance to ventricular ejection (resistance) Translates into increased work for the myocardium Contractility Velocity of myocardial fiber shortening (strength) Actual pumping of the heart Hemodynamics of Cardiogenic Shock BeComponents of Cardiac Output Contractility w ionotropes ○ Manage contractility Rate ○ Keep rate