Cardiovascular Function 1 PDF

Cardiovascular Function 1 Dysrhythmias Notes: Why do people get dysrhythmias? ○ Diseases but the natural way is bc we age The heart wall gets thicker Cardiac muscle cells tend to lose density and become less...

Cardiovascular Function 1 Dysrhythmias Notes: Why do people get dysrhythmias? ○ Diseases but the natural way is bc we age The heart wall gets thicker Cardiac muscle cells tend to lose density and become less functional and we develop collagen deposits Pneumonic for reasons people get dysrhythmias: H: ○ hypoxia (heart becomes irritable from lack of oxygen) I: ○ Ischemia: In cardiac infarction, part of the heart is damaged and the electricity can not pass through so it needs to find a new passage around it and can cause dysrhythmias ○ Angina: decreased blood supply getting to the myocardial muscle ○ Myocarditis ○ Viral infection S: ○ sympathetic stimulation: enhance stimulation from any source, diseases that can do that are: hypothyroidism, congested heart failure, fever, nervousness, and exercise  D: ○ Drugs: antidysrhythmics can cause dysrhythmias, antibiotics (aminoglycosides can cause prolonged QT segment), antipsychotics, digoxin (adjunction arrhythmia) ○ As we age, our ability to metabolize drugs decreases E: ○ electrolyte ○ potassium: when possible use the digestive track when giving potassium (every 10mu, it raises their levels by 0.1) Oral is preferred ○ magnesium (it is cardioprotective) given in a code situation, given IV push in a code situation ○ Calcium: heart muscles use and need calcium, uses to beat ALWAYS GIVE MAGNESIUM FIRST and then potassium because it helps stabilize potassium levels B: ○ bradycardia (too slow) S: ○ sympathetic stretch When we look at EKGs Rate Rhythm P waves PRI +QRS are they consistent  ST segment T wave ○ St segment elevated: infarction ○ St segment depressed: ischemic ○ The problem with the T wave Peak is inverted: it is important to think of myocardial infarction until we know otherwise Management of the Patient with Dysrhythmias and Conduction Problems : Old material (not being tested on this until the FINAL EXAM) ○ Normal electrical conduction (SA node fires create the P wave and then get down to the AV node which is the PR segment and initiates QRS and then sends it down to the bundle of his and then terminates in the binges of fibers) Normal readings: PR interval: 0.12 - 0.20 secs QRS: 0.6 - 0.12 secs ○ NSR ○ Sinus tachycardia What causes it? Someone had a heart attack, exercise, pain, fever, dehydration, and hypovolemic Maximum heart rate: 220- (your age) and it should equal the high heart rate your heart should go ○ Sinus arrhythmia Usually not a problem, common in pediatrics Sinus rhythm is irregularly associated with the breathing pattern ○ PAC ○ Atrial flutter  ○ Atrial fibrillation There is a big chance of developing a clot ***Concept to keep in mind Formula of cardiac output ○ The amount of blood the heart puts out in one minute 4-8L Hr Stroke volume Preload: the amount of stretch on the heart at the end of diastole (resting period) aka the amount of blood that is in the heart ○ If measuring it can be anywhere from 2-6 Afterload: the resistance of the left ventricle to pumping the blood past the aortic valve into the aorta and feeding the body ○ Measured in dynes: 800-1200 ○ Simular vascular resistance Contractility: how strong the heart is, the force of the heartbeat ○ Measured by an ejection fraction: 50-75% Done by an echocardiogram Management of the Patient with Dysrhythmias and Conduction Problems : New Material Drugs we can use to help: ○ Beta-blockers therapy (MAIN LINE OF THERAPY FOR PEOPLE THAT HAVE HAD A MYOCARDIAL INFARCTION) Amiodarone *** emergency dose for vtach or vfib: 300mg direct IV push, alternated dosage (pt is stable aka not suffering from any cardiovascular inadequacy): 150mg in a 100 d5w over 15 minutes and then will be started on an amiodarone drip (dosage: 1mg/min for 6hrs and then 0.5mg/min for 18hrs) Lidocaine (numbs the heart and the brain** and causes confusion in the elderly) ○ Junctional Dysrhythmias (middle of the heart) PJC Premature beat (same thing as a PAC which is more common than PJC) but this one comes out of the junction the whole key is the P wave You will see the P wave but the PR interval will appear differently, it will be short ○ The normal PR interval is: 0.12 - 0.20 While in PJC the PR interval will be basically right up against the QRS complex making it shorter or it can not visible at all (most common) but make sure it is not a premature atrial beat that didn’t affect the T wave or it can also be inverted or appear afterward in the ST segment Junctional rhythm It has a rate between 40 - 60 bpm  The key to diagnosing this is: what is going on with the P wave ○ Almost always it is absent or inverted or it appears afterwards They can usually treat junctional rhythm with: ○ Pacemaker as soon as possible ○ Ventricular Dysrhythmias (bottom of the heart) PVC Fairly common after open heart surgery Common is cardiovascular disease Premature beat Wide and bizarre ○ Count it anyways I would want to see more than one PVC Ventricular tachycardia rate : >100 bpm “Pt. can be sitting there reading a newspaper” Ventricular fibrillation Definite code situation No cardiac output No spontaneous circulation You need to defibrillate this person asap(shock them asap), start CPR, put a board under the pt to put firmness on the bed Give epinephrine every 3-5min in a code situation Idioventricular rhythm Wide bizarre rhythm  Rate: 20-40 Accelerated idioventricular rhythm (3rd ventricular arrhythmia) ○ Wide bizarre QRSs, regular ○ Rate: 40 -100 Ventricular asystole It can be coarse or fine P waves give you 25% cardiac output, this is a code You do NOT defibrillate bc you can lock the heart out Do CPR, give epi q 3-5 min ○ Important to think about: There gets a point where if we get this person back, they have already been withOUT a heartbeat for 15 minutes now, what exactly are we bringing back since so much damage has been done to their body already ***Before we shut the code down, we need to check asystole and ventricle in 2 leads ○ Conduction Abnormalities AV blocks (1st, 2nd, 1 and ii, 3rd degree) 1st: ○ Not really a block but a prolongation (PR interval 0.28-0.32) ○ Do a 12-lead EKG ○ If new then bring attention to the provider ○ More like a delay 2nd type 1: (pick one name)  ○ AKA: Mobitz one ○ Or AKA: Wenckebach's AV block Diagnostic for wenckebach See the PR interval getting long, long, long, and then drop All about P waves are the P waves getting further from the QRS Referred to as a group beating bc you will see a pattern like sometimes there's 3 and then it’ll drop beat and 4, drop beat, 3 drop beat 4 Not as dangerous 2nd type 1 As pt get better, the block will disappear, they develop a normal rhythm or go into 1st degree AV block, AND THEN a normal rhythm Measure the PR interval ○ Ex he says: One is 0.20 and then the next one is 0.24 and the next one is 0.28 and then you have a P wave without a QRS cashing MORE P WAVES THAN QRS (think heart block) 2nd type 2: ○ AKA: Mobitz type 2  PR interval remains consistent in every QRS except there comes a time when there is a P wave and a dropped QRS This is dangerous: No cardiac perfusion No cardiac output NEEDS A PACEMAKER 3rd degree: ○ Known as AV dissociation No coordination between the P wave and QRS Can be multiple P waves and less QRS Do not give atropine bc it will just speed up the atrial and ventricular rate and not help with the coordination Ex he says: ○ When measuring the PR interval, on the first one it is 0.28, then next it is 0.12, then next it is Needs permanent pacemaker Cardiac Conduction System SA node: 60 -100 AV node: 40-60 Ventricle: 20-40 Juntional Dysrhyhtmias PJC ○ An impulse that starts in the AV nodal area before the next normal sinus impulse reaches the AV node ○ Less common than PACs ○ CAUSES: Digoxin toxicity, heart failure, coronary heart disease ○ P Wave may be absent, before or after the QRS Junctional Rhythm ( junctional escape rhythm) AV node becomes the pacemaker of the heart Sinus nodes become slow, impulses cannot be conducted, and the AV takes over Ventricular rate 40-60 Regular QRS is normal If P wave is present, PRI is < 0.12 seconds S& S reduces cardiac output Treatment like bradycardia Ventricular dysrhythmia You can have vtach where it is unifocal (very even around the whole strip) and then multifocal aka bunny ears (the premature ventricular beat is coming out of 2 different parts of the lower heart Can also have torsades ○ Large QRS and then shrinks and then enlarges again ○ *** Torsade is a vtach that you can convert if ordered and give MAGNESIUM IV PUSH PVC Impulse starts in the ventricle and is conducted through the ventricles before the normal sinus impulse VT Three or more PVCs in a row Rate exceeding 100 bpm Regular Wide bizarre QRS Emergency Take bp as soon as you get in the room, 12 lead EKG If pt is awake and alert then Amiodarone will be given If pt is symptomatic then they will do a cardiovert VF The most common dysrhythmias with cardiac arrest Rapid rate (greater than 300bpm), disorganized Quivering Idioventricular Rhythm Ventricular escape rhythm Rate 20-40 bpm Regular wide, bizarre QRS Ventricular Asystole Flatline Absent QRS Conduction Abnormalities First-degree AV block Second-degree AV block ○ Type 1 ○ Type 2 Third-degree heart block First Degree All impulses are conducted through the AV node slower than normal PR interval greater than 0.20 seconds ○ Prolonged PR interval Second Degree Type 1 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 drops Second Degree Type 2 Some of the atrial impulses are conducted through the AV node into the ventricles The PR interval is constant More P waves than QRS complexes Third Degree No atrial impulses are conducted through the AV node into the ventricles Two impulses stimulate the heart (pacemaker) ○ Atria: P waves may be seen ○ Ventricles: QRS complexes Seem to be together, but not connected