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wvc 2 cardiac lectur
wvc 2 acute cardiac M. wilcott
| Question | Answer |
|---|---|
| Walls of the heart | myocardium |
| Starlings law of the heart | more cardiac muscles are stretched the more forcefully they contract. |
| Infarction | tissue death or necrosis of tissue |
| Cardiac cycle overview | sequence of events in one heart beat; stage 1& 2: ventricle filling and contraction of the atrium; stages 3,4,5: movement of blood from the ventricles into pulmonary artery and aorta. |
| Cardiac output formula | co= hr x sv |
| Stroke volume | the volume ejected out of the left ventricle at each beat |
| Abi | measures PVD, divide ankle systolic BP/ brachial systolic BP; 09. Indicates PVD, 0.8 moderate PVD; 0.5 severe PVD. It is done by measuring the systolic BP at brachial and systolic BP at dorsais pedis and dividing DP/brachial (use a Doppler) |
| S3 | happens right after the s2; ken-tuck-EE; slosh-ing-IN; ventricular gallop; too much fluid on board and pt. is developing heart failure. |
| S4 | happens right before s1; happens with decreased compliance; TEN-i-see; A-stiff-wall; atrial gallop ; pushing blood into a non-compliant ventricle; indicates MI |
| Phases of Cardiac Cycle…Isovolumetric vent. contraction- Depolarization causes tension & pressure to rise in vents. closing the mitral & tricuspid valves; Vent. ejection -Pressure rises to open semilunar valves & vents eject blood into pulm. art. & aorta | Isovolumetric relaxation-Vent. pressure falls closure of semilunar. All valves closed; Vent. filling -Atrial pressure exceeds vent. pressure causing mitral & tricuspid to open. 70% of vent. filling is passive during this part. Atrial kick last 30% ejected |
| Contractility | The inherent ability of the myocardium to stretch and contract normally |
| The more stretch during diastole, the greater the systolic contraction | – Starling’s law (The more volume in the ventricles, the greater the stretch) |
| CO = | HR x SV… Volume of blood ejected by the heart in each minute – 4 to 7 liters |
| Heart Rate = | The number of times the ventricles beat each minute. |
| Stroke volume- | The amount of blood ejected by the left ventricle during each systole (beat) |
| Preload | lThe degree of myocardial muscle fiber stretch at the end of diastole. Preload is determined by the left ventricular end-diastolic volume. Excessive filling of the ventricles results in excessive LVED and a decreased cardiac output |
| Afterload | The pressure the left ventricle must overcome to get blood out of the heart.The higher the pressure in the aorta, the more force the ventricles must use to eject the blood. |
| Systemic Vascular Resistance (SVR) | is the pressure the heart must work against to get the blood out. |
| Postural Vital Signs (Check BP and pulse while patient is lying supine, must be supine for at least 3 minutes prior to measurement..Have patient sit up, check BP & pulse within 1-2 minutes…Have patient stand up, check BP & pulse within 1-2 minutes) | Used to detect change in circulating volume such as dehydration or vasodilation. decrease or more than 20 mm Hg in systolic BP, 10 mm HG in diastolic pressure, as well as an increase of heart rate by 10-20%. |
| PMI – point of maximum impulse | Found midclavicular, 5th intercostal space (the mitral area at the apex) |
| Heart Sounds | The first, loudest sound is the ventricular systole, and represents the closing the tricuspid and mitral valves; The second sound is the closing of the aortic and pulmonary semilunar valves.(Valves not closing properly cause heart murmurs) |
| Rub | Occurs with heart beat; Sign of infection, inflammation or infiltration; Pericarditis, cardiac tamponade |
| Conduction | Mechanical Function of the heart is regulated by electrical activity |
| Inherent conduction rates SA, AV, Bundle of His, Prukinje fibers? | SA- Rate 60 - 100 bpm AV-(Located floor of the right atrium)-Rate 40-60 bpm..Bundle of His-Intrinsic rate 40-60 bpm…Purkinje Fibers- 20-40 |
| Use large boxes to count beats. Memorize numbers | 300, 150, 100, 73, 60, 50, 43, 38, 33, 30… |
| P Wave and PR Interval | Represents atrial depolarization; Smooth, rounded and upright in leads I, II and 1; l0.5-2.5 mV amplitude |
| PR interval is | atrial depolarization and repolarization (Normal length of the PR interval is 0.12 to 0.20 seconds) |
| QRS complex represents | Normal is 0.06-0.10 seconds (Ventricular depolarization) Impulse down the Bundle of His to the Purkinje system; Coincides with mitral and tricuspid closing (S1) |
| ST Segment | Early ventricular repolarization; From the J point to the beginning of the T wave; Length changes with heart rate; Normal not elevated more than 0.5 mm |
| QT Interval | Ventricular depolarization and repolarization; Beginning of the QRS complex to the end of the T wave; Varies with age, sex and heart rate; |
| Approach to EKG Interpretation | Is it regular or irregular? Is it fast or slow? Are there P-waves? Is there a P-wave for every QRS? Measure the PR interval; Measure the QRS; Measure the QT interval |
| Analyze the ekg tracing in this order | Measurements; Rhythm Analysis; Conduction Analysis ; Waveform Description ; Ecg Interpretation ; Comparison with Previous ECG (if any) |
| PR Interval: | 0.12 - 0.20 sec |
| QRS Duration: | 0.06 - 0.10 sec |
| QT Interval | (QTc < 0.40 sec) |
| Ecg analysis: Normal sinus rhythm | The P waves in leads I and II must be upright (positive) if the rhythm is coming from the sinus node. |
| ECG analysis Normal Sino-atrial (SA), Atrio-ventricular (AV), and Intraventricular (IV) conduction | Both the PR interval and QRS duration should be within the limits PR Interval: 0.12 - 0.20 sec ; QRS Duration: 0.06 - 0.10 sec QT Interval :(QTc < 0.40 sec) |
| ST segment depression is always an | abnormal finding, although often nonspecific; ST segment depression is often characterized as "upsloping", "horizontal", or "downsloping". |
| Short PR interval: < 0.12s indicate | AV Junctional Rhythms (inverted P-wave II, III, aVF); Ectopic atrial rhythms origin near AV node (PR int. is short b/c atrial activation origin close to AV node); Preexcitation synd.: electricity bypasses av node or charge goes directly from atrium 2 vent |
| Prolonged PR intervals: >0.20s First degree AV block (PR interval usually constant): | Intra-atrial conduction delay (uncommon); Slowed conduction in AV node (most common site) ; Slowed conduction in His bundle (rare); Slowed conduction in bundle branch (when contralateral bundle is blocked) |
| Convex or straight upward ST segment elevation (e.g., leads II, III, aVF) is | abnormal and suggests transmural injury or infarction: |
| Prolonged QRS Duration (>0.10s) or (> 0.12s): | QRS dur. 0.10-0.12s: Incomplete rt. or lt. BBB; Nonspecific intraventricular conduction delay (IVCD) //QRS dur. > 0.12s : Complete RBBB or LBBB; Nonspecific IVCD; Ectopic rhythms originating in ventricles (e.g., ventricular tachycardia, pacemaker rhythm) |
| During ischemia, cells experience | a temporary shortage of oxygen and downgrade their activity to conserve energy. The continued lack of oxygen eventually causes cellular injury. |
| Ischemia and injury cause changes in repolarization that are reflected on an EKG | as ST segment and T wave abnormalities.3 As the heart attack progresses, infarction causes changes in depolarization, resulting in an abnormal QRS complex. |
| The ST segment is usually flat and on the same level as the isoelectric line. As cellular injury occurs, | EKG may show elevated ST segment. Each 1 mm square on graph paper equals 0.1 millivolts on the vertical axis; an elevation of more than one box might indicate an MI. ST segment elevation is considered to be early evidence of MI |
| T wave inversion may also occur at the same time as | ST segment elevation, or maybe even before it. T wave inversion is a change that's suggestive of ischemia |
| The first sign of tissue death on EKG typically occurs later, with the appearance of | pathologic Q waves. A Q wave that is either 0.04 seconds wide (one small box) or that has a depth of at least 25% of the size of the R wave is considered pathologic—and highly suggestive of an MI.3 |
| Lead V2, V3, and V4 see the (looks at the?) | anterior wall of the left ventricle. |
| Lead V1 is the (looks at the?) | septal lead.1 |
| Leads I, aVL, V5, and V6 look at the | lateral wall. |
| Leads II, III, and aVF see the | inferior wall of the left ventricle. |
| The aVR lead is of limited use for recognizing | an MI.2 |
| MIs occur mostly in the | left ventricle, since it has the greatest oxygen demand and is therefore more affected by occlusion of a coronary artery |
| Bradycardia | A pulse rate of less than 60 bpm; How is the patient tolerating the rhythm? Are there medications causing the rhythm? Is there an underlying medical condition causing the rhythm? WHY are they Bradacardic? |
| Hemodynamics of Bradycardia | Myocardial O2 demand is reduced; Coronary perfusion time is adequate b/c of prolonged diastole; If the rate is too slow, cardiac output & bp may drop and this will decrease coronary perfusion causing sx |
| Causes of Bradycardia | Athlete’s normal rate; Excessive vagal stimulation; Hypoxia; Inferior MI; Beta-adrenergic blockers; Calcium channel blockers; Digitalis |
| Symptoms of bradycardia | Dizziness, syncope, Weakness, Confusion, Hypotension, Dyspnea, Ventricular ectopy, Angina, frequent PVCs |
| Bradycardia Interventions | Treat only if symptomatic; Atropine 0.5 mg – 1.0 mg IV push, end point is 0.04mg/kg; Treat hypotension with fluid replacement or vasopressors; Withhold medications that cause bradycardia; Pacemaker |
| Premature Atrial Complexes (Originate outside SA node in irritated foci) | Rogue foci has a P-wave that is shaped differently from the SA P-wave. It may be seen as a distortion of the T-wave; No hemodynamic consequences, patient is usually asymptomatic…a warning of other rhythms such as a-fib or a-flutter |
| Atropine | 0.5 mg – 1.0 mg IV push |
| Interventions for PACs | Based on patient symptoms and frequency; Type IA antiarrhythmics, quinidine, procainamide, propranolol, digitalis; Reduce stress; Avoid foods that trigger stress – caffeine; Observe for more serious arrhythmias |
| Atrial Fibrillation/Flutter | Rapid firing of SA node in flutter; Disorganized firing of many atrial foci in fibrillation; Flutter is more difficult to convert; Fibrillation has more hemodynamic consequences; Tx for both is aimed at controlling rate and re-establishing sinus rhythm |
| Atrial Flutter | SA rate is rapid; Blocked by AV node; Symptoms related to ventricular rate; Synchronized cardioversion is the tx of choice; Drugs: Digoxin, Ca Channel Blockers, Ibutalide |
| Atrial fibrillation | Disorganized impulses from multiple atrial foci; No atrial contractions, atrial kick is lost; Irregular vent. response; Favors formation of multiple thrombi; Drugs: Heparin or Enoxaprin, Ca Channel blockers, Dig., Quinidine; Cardioversion, Ablation |
| Symptoms of Atrial Fibrillation | Usually dependent on ventricular rate; Can hear and feel irregular pulse; Take an apical-radial pulse for a full minute to determine rate; Monitor shows an irregular-irregularity; No discernible P-waves; QRS complexes are narrow |
| Co-morbidities with A Fib | AMI; Mitral stenosis; Atrial-septal defect; CHF; Cardiomyopathy; Post-surgery CABG; Hyperthyroidism; Pulmonary emboli; WPW syndrome; Congenital heart disease; Chronic obstructive pericarditis |
| Types of Heart Blocks (4) | 1st degree AV block; 2nd degree, Mobitz Type I or Wenckebach; 2nd degree, Mobitz Type II; 3rd degree or complete heart block |
| 1st degree AV block | PR interval 0.20 or greater; Delay in conduction through the AV node; Usually asymptomatic; Can be caused by AV node ischemia, edema, meds or electrolyte imbalances (K+) |
| 2nd degree, Mobitz I(Also called Wenckebach) | A progressive LENGTHENING of PR interval until a beat is dropped; Overall ventricular rate sufficient for cardiac output; Usually asymptomatic |
| 2nd degree, Mobitz II | More ventricular complexes are blocked; PR interval when it occurs, is constant!!!; May progress suddenly to complete block; Symptoms depend on frequency of ventricular beats |
| 3rd degree block | Complete dissociation between the SA node and ventricles; PR interval is not constant; Ventricular contraction is conducted from a junctional or ventricular pacer; Symptoms depend on the overall rate; Intervention is required if the rate is low; |
| Interventions for heart block (Depend on patient symptoms) | Anticipate need for pacemaker based on probability of progressing block; Atropine for bradycardia, may not be effective in 2nd degree, type II and 3rd degree; Isoproterenol should not be used in myocardial ischemia as it will increase damage; Pacemaker |
| Bundle Branch Blocks | conduction delay caused by blockage of branches of Bundle of His; Impulse travels down unblocked branch depolarizing that vent. the other ventricle is depolarized late; Prolongs QRS interval to > 0.12; Underlying rhythm is sinus so P-waves are present |
| Right Bundle Branch Block (RBBB) | Characterized by QRS > 0.12; V1 and MCL shows small R followed by S wave and a taller or prime R wave. Gives it a rabbit ears or letter M appearance; Can occur normally or with CAD, pulmonary embolism or anterior MI. Sometimes in tachycardia, rate-related |
| Left Bundle Branch Block (LBBB) | Blockage of the left branch of the Bundle of His; QRS > 0.12; In V1 or MCL, S wave; Does NOT occur normally. Caused by hypertensive heart disease, aortic stenosis, acute heart failure, MI |
| idioventricular Escape Rhythms | going to be rhythm where there are no p-waves and the rate is between 20 and 40 BPM |
| Junctional Rhythm | is going to be a rhythm where you cannot identify the p-wave and the rate is between 40 and 60 BPM |
| Causes of Junctional Rhythm | Sick sinus syndrome; Vagal stimulation; Digitalis toxicity; Inferior infarction; Rheumatic heart disease |
| Interventions for Junctional Rhythm | Correct the underlying cause; Treat symptomatic patients; Improve cardiac output; Atropine; Pacemaker |
| Idioventricular Rhythm (If you didn’t have this, you’d have nothing) | Regular rate at 20 to 40 bpm; Slow rate, loss of atrial kick reduce cardiac output; Transcutaneous pacing; Also seen in dying heart, just before asystole |
| Causes of Idioventricular Rhythm | Myocardial ischemia; Myocardial infarction; Digitalis toxicity; Pacemaker failure; Metabolic imbalances |
| Pacemaker Placement | Beneath the skin of the chest; Pacer wires to the ventricle; Complexes are wide because generated from the ventricles |
| Pacemakers Can do | transcutaneous or transthoracic pacing using patches on the skin; Transvenous pacing inserts the wires via a peripheral vein; Permanent pacer |
| Types of Pacers | Single-chamber atrial pacers; Single-chamber ventricular pacers; Dual-chamber ventricular pacers; Atrio-ventricular sequential pacers, which pace both atrial and ventricular chambers. |
| Paced Rhythm | Note the spike prior to the QRS; The complexes are wide because they are generated from the ventricles; Note what percentage of beats are paced |
| Pulseless Electrical Activity (PEA) | Electrical conduction system is intact; Mechanical pumping of the heart is not; Disconnect between what you see on the monitor and how the patient looks…..No pulse |
| PEA acronym | Problem- Search for probable cause; Epinephrine – 1 mg IV q 3-5 minutes; Atropine – If rate is slow, up to 0.04 mg/kg |
| Causes of PEA | Hypoxia; Hypovolemia; Hypothermia; Hyper/Hypokalemia or other metabolic disorders; Tension pneumothorax; Tamponade –cardiac; Thromboembolic obstruction; Toxic/ Therapeutic disturbances |
| PATCH MD Mneumonic for PEA | P- Pulmonary embolus/ A- Acidosis/ T – Tension pneumothorax/ C- Cardiac tamponade/ H (4)- Hypovolemia, Hyperkalemia, Hypothermia, Hypoxia (also Hypoglycemia)/ M- Massive MI/ D- Drug overdose |
| Sequence of Interventions for patients with PEA | Establish unresponsiveness; Assess ABC’s; Initiate CPR; IV access; Intubation; Problem Intervention; Drugs |
| Asystole | Absence of electrical and mechanical cardiac response; Not a good sign; Make sure what you see on the monitor reflects what you see with the patient; Check in another lead |
| Asystole interventions | Check in another lead; Transcutaneous pacing; Epinephrine; Atropine; |
| Causes of Asystole | AMI; Severe electrolyte disturbances; Massive pulmonary emboli; Prolonged hypoxemia; Severe acid-base disturbances; Electric shock; Drug intoxication such as cocaine overdose |
| Sequence of Interventions in asystole | Establish unresponsiveness; Assess ABCs; Initiate CPR; IV access; Intubation; Check another lead; Transcutaneous pacing; Drugs |
| Aortic Aneurysm | Dilation or outpouching of the aorta; Can occur in the inferior or superior portions; Superior aortic aneurysms are called thoracic aortic aneurysms; Inferior are called abdominal aortic aneurysms and are more common |
| Risk Factors for aortic aneurysms | Male; Advanced age; Hypertension; Smoking; Athersclerosis; Connective tissue disorders; Diabetes; Trauma |
| Symptoms of AAA | Steady, gnawing pain of the abdomen, flank or back pain; Pulsation in the upper abdomen slightly to the left of midline between the xiphoid process and the umbilicus; Auscultate a bruit; Most are asymptomatic until rupture is imminent |
| Symptoms of Impending AAA Rupture | Sudden, severe pain of the back or lower abdomen that radiates to the groin, buttocks or legs; Hypovolemic hemorrhagic shock; Abdominal distention |
| Aortic Aneurysm Repair | Resection of the affected area; Replace or support with dacron graft; May be necessary to ligate aorta briefly during surgery |
| Symptoms of Thoracic Aortic Dissection and Rupture | Back pain; Shortness of breath, hoarseness; Sudden, excrutiating back or chest pain; Neurologic changes; JVD; New murmur; Hypovolemic, hemorrhagic shock |
| Post-operative Care for aneurysm | Assess for bleeding; Keep BP in normotensive range; Assess urine output; Monitor cardiac; NG tube; Doppler exam of all extremities; Meticulous pulmonary hygiene |
| Arterial Occlusive Disease | Occlusion of the large arteries from atherosclerosis or thrombi; Can emergently occlude blood flow to extremities and be life-threatening; Risk factors: male, smoking, aging, HTN, hyperlipidemia, DM, family history |
| Symptoms of Acute Occlusion in arterial occlusive disease | Pain; Pallor; Pulseless ; Paresthesia; Paralysis; |
| Interventions in arterial occlusive disease | Restore circulation; Embolectomy; Graft; Bypass graft; Balloon angioplasty; Stents |
| CAD Risk Factors | Age;Heredity; Gender; Smoking; Obesity; Sedentary; Stress; Dietary habits; Diabetes; Hypertension; Hyperlipidemia; Smoking; |
| Three Stages of HTN: | Stage I - BP 140/90 to 159/99; Stage II - BP 160/100 to 179/109; Stage III - BP > 180/110 |
| Diuretics for the Management of Hypertension | Loop diuretics- furosemide (lasix), ethacrynic acid (edecrin); Thiazides- HCTZ (Diuril, Hydrodiuril);Potassium sparing- Spironolactone (aldactone), Triamterone (dyrenium) |
| Beta-Blockers for the Management of Hypertension | Block adrenergic impulses in the heart and peripheral vessels; Lower heart rate and contractility; propranolol, Atenolol, Nadolol & Metoprolol |
| Calcium Channel Blockers for the Management of Hypertension | Interfere with the movement of calcium ions; Results in reduced vasoconstriction; Nifedipine, Verapamil, Diltiazem |
| ACE- Inhibitors Management of Hypertension | Inhibits the action of the angiotensin-converting enzyme; ACE is a strong vasoconstrictor; Postural hypotension is common; Captopril, Enalapril and Lisinopril |
| Central Alpha Agonists Management of Hypertension | Prevent reuptake of norepinephrine in the central nervous system; Lower peripheral vascular resistance; Clonidine, Methyldopa |
| Vasodilators for the Management of Hypertension | Relax vascular smooth muscle and reduce total peripheral resistance; Minoxidil, Doxazosin, Terazosin, Nitroglycerin, Nitroprusside |
| Inotropic – | affects the force of contraction |
| Chronotropic – | affects the rate of contraction |
| Unstable Angina | One of the Acute Coronary Syndromes; Occurs with rest or minimal exertion; Increase in intensity, duration and frequency; Plaque rupture, thrombus formation |
| Symptoms of Angina | Substernal chest discomfort; Can radiate to the left arm. Precipitated by exertion or stress; Relieved by NTG or rest; Lasting < 15 minutes; Few associated symptoms |
| Non Q-wave MI is | subendocardial, it does not go through all the myocardial layers |
| Q-wave MI | or transmural goes through the wall of the myocardium. More damage. |
| Blockage of the Left Anterior Descending | Perfuses the anterior wall and most of the septal wall of the left ventricle; 25% of all MIs and highest mortality rate; Left ventricular HF, ventricular arrhythmias; Highest incidence of lethal arrhythmias and sudden death |
| Blockage of the Circumflex | Supplies blood to the lateral wall of the left ventricle and portions of the posterior wall ; Branches off the LAD |
| Obstruction of the Right Coronary Artery | Perfuses the SA and AV nodes, the inferior and diaphragmatic portion of the left ventricle. Inferior MI |
| Assessment & Priority Interventions for AMI | Airway, Breathing,Pulse, BP, Skin; Heart Auscultation; Lung Auscultation; Pain Assessment; History of this episode; Current Medications/ Allergies; O2; Monitor; IV Access; ASA; Nitro; Morphine, if pain unrelieved w/ NTG; Support Circulation |
| Never put ECG leads over… | bone, make sure area is clean and minimal hair. |
| Which leads are Bi-polar leads | 1,2,3 |
| 12 Lead EKG initial Septal injury – | ST elevation in V1, V2 |
| 12 Lead EKG initial Anterior injury – | ST elevation in V2-V4 |
| 12 Lead EKG initial Lateral injury – | ST elevation in V5, V6, I, AVL |
| 12 Lead EKG initial Inferior injury – | ST elevation in II, III, AVF |
| 12 Lead EKG initial Posterior injury – | ST depression in V1-V4 |
| EKG Changes with MI | Initial ST elevation; If no reperfusion takes place, T-wave inversion; T-wave less inverted as injury resolves; Injury to muscle leaves pathologic Q waves |
| CK-MB – rises in | 4-6 hrs after MI, peaks at 12-24 hrs |
| Troponin- | More specific to heart muscle. Rises 4-6 hrs after MI, peaks at 12-14 hrs and returns to normal in 5 to 9 days. Measured on admission, in 6 hrs and 12 hrs after admission. |
| Thrombolytics Best results when administered within first | 6 hours of the coronary occlusion |
| contraindications of thrombolytics | surgery within last 3 months; history of intracranial hemorrhage; neoplasm in the cranial cavity; known cerebralvascular legion; ischemic stroke last 3 months; suspected aortic dissection; active bleeding; significant closed head or face trauma. |
| Cardiac Catheterization | Done to determine where the obstruction is in emergent situations; Done to look at the coronary arteries to determine need for bypass; conscious sedation |
| Right Heart Cath | Rt femoral vein to rt atria via vena cava; Looks at the right side of the heart & pulmonary valve, PAWP; May be used as access to left heart through the rt atrial septum |
| Left Heart Cath | Femoral or brachial artery against blood flow up the aorta OR via the right heart through the atrial septum; Looks at the left heart, aortic, mitral valves; Arteriography visualizes the coronary arteries |
| Stents | Placed during heart cath; Mesh that opens the vessel; Keeps the unstable plaques secured |
| Drug-eluting stents is often infused with | aspirin or plavix |
| Balloon Angioplasty | Balloon is placed in the area of narrowing during cardiac cath; Inflated and pushes the plaque against the vessel wall; Opens the vessel; risk of thrombus |
| Risks of Cardiac Catheterization | Acute myocardial infarction; Stroke; Arterial bleeding; Thromboembolus; Lethal dysrhythmias; Death |
| Post-Catheterization Care | VS per surgical protocol, Sedation might have been used, monitor ABCs; Monitor groin sites for hematoma, bleeding; Monitor pedal pulses, perfusion on the lower extremity used for the procedure. |
| When assessing for a hematoma associated with cardiac catheterization you must | look and palpate the site; if you need to hold direct pressure above the entry site. |
| Stress Tests – | May be done as exercise test or heart is stressed with drugs (Dobutamine, Adenosine)…identify problems that my only be present while the heart is under a load. |
| Nuclear Imagining – | Technetium Pyrophosphate scan or Thallium scan. radionuclide is injected to identify blood flow problem areas. |
| Electro-physiologic Studies – | Similar to heart cath but tests the electrical system of the heart |
| Manifestations of Successful Reperfusion of Heart Muscle | Cessation of chest pain; Onset of ventricular arrhythmias (managed when appear); Resolution of ST depression; A peak of 12 hours for cardiac markers |
| Minimally Invasive Direct Coronary Artery Bypass (MIDCAB) | Sometimes called off-pump CABG; The coronary arteries are repaired without stopping the heart; Advantages are less side effects and less recovery time; Disadvantages are more incisional pain, cannot do multiple grafts |
| Post-op Care CABG | Assisted breathing on ventilator; Monitoring pressures; Monitor rhythm; Assess for bleeding; Pain control; Assess circulation to donor extremity |
| Complications of CABG | Bleeding; Dysrhythmias; Pain; Atrial fibrillation; Pleural effusion; Depression; Mental status changes; Acute respiratory distress syndrome; Multiple Organ Dysfunction Syndrome; Reocclusion of grafts |
| Discharge Instructions for CABG | Medications; Care of incisions; Sternal precautions; Symptoms that require medical attention; What to expect in the recuperative period; When the patient can resume normal activities |
| sternal precautions… Do not lift more than 8 pounds; Do not push or pull w/ your arms when moving in bed & getting out of bed; Do not flex or extend your shoulders over 90°; Avoid reaching too far across your body; Avoid twisting or deep bending . | Don’t vagal; Brace chest when coughing/sneezing (vital during the first 2 weeks at home); No driving until cleared by your cardiac surgeon; Avoid long periods of over the shoulder activity; Report any clicking or popping noise around your chest bone. |
| Systolic murmur- | Aortic stenosis and mitral regurgitation, occur during systole. They can be classified by when the murmur begins and ends, between S1 and S2. |
| Diastolic murmur- | Mitral stenosis and aortic regurgitation occur during diastole. start at or after S2 and end before or at S1. |
| Friction rub- A pericardial friction rub originates from the | pericardial sac & occurs w/ movements of heart during cardiac cycle. Usually transient & a sign of inflammation, infection, or infiltration. in pts w/ pericarditis resulting from MI, cardiac tamponade, or post-thoracotomy. |
| Hemodynamics of Tachycardia | Increased oxygen demand by the heart muscle; Decreased filling time with shorter diastole; Blood is moved through the lungs more rapidly to get oxygen out to the body quickly in stress situations; Can trigger angina pain in CAD |
| Sinus Tachycardia | Rate > 100 bpm; Regular rhythm; P-wave for every QRS; QRS complex is narrow and upright in Lead II |
| Paroxysmal Supraventricular Tachycardia (PSVT) | Brief periods of tachycardia; Narrow complexes; No visible P-wave or P-wave buried in the T; Regular rhythm. Symptoms are related to ventricular rate and whether it is a sustained rhythm |
| Interventions for Narrow Complex Tachycardias | Assess ABCs; Oxygen; Monitor; IV Access; Vagal maneuvers; Adenosine; 12-lead EKG; Cardioversion |
| Premature Ventricular Contractions | Wide complex; Comes early; No P-wave; Usually has compensatory pause; When taking a radial pulse, it feels like a skipped beat |
| Multifocal PVCs | Wide complexes; Come early; No P-wave; Compensatory pause (usually); Different shapes (morphology) |
| Premature Ventricular Complexes | Can occur in a regular pattern; Bigeminy is every other complex, trigeminy is every 3rd complex; Can come as pairs or triplets or short runs of beats (this is really brief ventricular tachycardia) |
| Bigeminey | PVC every other beat |
| Trigeminey | pvc every third beat |
| Sustained tachycardia | goes on longer than 30 seconds |
| Ventricular Tachycardia | Can be a perfusing rhythm; You are treating tachycardia if there is a pulse; You are treating ventricular fibrillation, if there is no pulse. Treat the patient not the monitor |
| Intervention for Ventricular Tachycardia with Pulse | Assess ABCs; Oxygen; Monitor; IV Access; Drugs: Amiodarone or Lidocaine; Cardioversion; Correct underlying problem |
| Defibrillation vs. Cardioversion | Defibrillate ventricular rhythms that have no pulse & more joules… Synchronize cardioversion is for tachycardias that have a pulse or R-wave for capture |
| Cardioversion | Used for SVT, atrial tach, atrial fibrillation, atrial flutter, ventricular tachycardia with a pulse |
| Identifying Ventricular Fibrillation | The patient is unresponsive; No breathing, pulse or blood pressure; Monitor shows a disorganized pattern; No P-wave or QRS. lectrical and mechanical are ineffective; No cardiac output; Without intervention, death will occur |
| Ventricular Fibrillation interventions | Defibrillation; Immediate recognition of problem; Immediate CPR….Early defibrillation=Better Outcomes…Chain of Survival: BLS – Defibrillation - ACLS |
| Automatic External Defibrillator | will only shock v-fib; Lightweight defibrillating device; Designed for easy use; Attach electrode pads; Press the button; Machine gives instructions |
| R on T PVC to Ventricular Fibrillation | A PVC is generated from an ectopic ventricular site; It hits on the T-wave during the absolute refractory period Interruption of electrical conduction with massive disorganization: V-fib |
| Automatic Implanted Cardioverting Defibrillator (AICD) | Can be with or without pacemaker option; Senses ventricular tachyarrythmias; Placed the same as a pacemaker |
| Discharge Instructions for AICD (automatic implanted cardioverting defibrillator) | S/S of infection; Avoid pressure over area or jerking arm upward that may damage unit or displace lead; Wear alert bracelet & carry AICD info with you at all times; Inform doctor of “shocks” received from unit, particularly if they increase in frequency |
| Cardiogenic Shock Definition | “An alteration in tissue perfusion that occurs at a cellular level.”; “The whole-body response to poor tissue oxygenation..a condition rather than a disease.” |
| Cardiogenic Shock - | 0ccurring in 15% of all patients with AMI; Caused by significant left ventricular dysfunction; >40% of left ventricular muscle mass is infarcted or affected; Mortality 85% or greater |
| Pathophysiology of cardiogenic shock-Left ventricle is injured causing dysfunction; Compensatory mechanisms attempt to increase cardiac output; As cardiac output falls, baroreceptors stimulate the sympathetic nervous system; | Increased HR & left vent filling pressure, peripheral resistance (afterload) in an attempt to increase venous return; These compensatory responses increase O2 demand and further compromise the heart |
| Ejection Fraction | Percentage of blood pumped from the heart with each heartbeat…Normal is 55% to 75% (Measured in the left ventricle) (40% to 55% indicates some damage) Normal does not mean there is NO damage in an AMI |
| The Vicious Cycle of cardiogenic shock… | Injured left vent. from MI; low cardiac output; Sympathetic compensation; Increased oxygen demand; Increased cardiac ischemia, oxygen debt; Even lower cardiac output; The result is poor perfusion of major organs like the kidneys & liver |
| Sx of Cardiogenic Shock- Pale, cold, clammy skin; Low systolic BP; Tachycardia; Gallop rhythm, faint heart sounds, possible holosystolic murmur; Rapid, shallow respirations; Oliguria; Restlessness, confusion; Narrowing pulse pressure; Cyanosis; | Diagnostics; PAWP shows increase caused by ineffective pumping & increased PVR; ABG shows mixed metabolic & respiratory acidosis, hypoxia; ECG shows AMI, ischemia, ventricular aneurysm; Echo shows left vent. dysfunction; Increased cardiac enzymes; |
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