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N316 Heart
| Question | Answer |
|---|---|
| Normal pacemaker (bpm) | sinoatrial node – 60-100 bpm |
| What mechanical piece corresponds to the electrical P-wave? | The depolarization of the atria |
| What mechanical piece corresponds to the electrical QRS complex? | The depolarization of the ventricles (repolarization of the atria occurs here but not seen on the ECG) |
| What mechanical piece corresponds to the electrical T-wave? | The repolarization of the ventricles |
| What does the ECG help determine (6)? | Heart rate, rhythm, axis, infarction, electrolyte disturbances and effects of drugs |
| What does a significant Q-wave (1/3 of total QRS) indicate? | Past heart attack |
| How long should the PR interval be? | Less than or equal to 0.20 seconds (5 boxes) |
| How long should the QRS interval be? | Less than or equal to 0.12 seconds (3 boxes) |
| How much does one box on an ECG equal? | 0.04 seconds |
| What are the numbers used to denote bpm on an ECG? | 300, 150, 100, 75, 60, 50 |
| Normal sinus rhythm/Treatment | 60-100 bpm with one P wave before each normal appearing QRS complex./None |
| Sinus bradycardia rhythm/Treatment | Less than 60 bpm with one P wave before each normal appearing QRS complex./If symptomatic, Atropine or Epinephrine via IV – able to give every 5 mins. Long term: external pacemaker. |
| Sinus tachycardia rhythm/Treatment | Faster than 100 bpm with one P wave before each normal appearing QRS complex./Carotid massage (in young, in older can dislodge clot), vagal stimulation, Beta-blocker, Ca+ channel blocker. |
| Sinus arrythmia rhythm/Treatment | Irregular pattern with normal waves and complex./None. |
| Sinus arrest/Treatment | Pause in heart rate with no P waves./CPR, Epinephrine, Vasopressin (can only give once). |
| What is the major problem with Beta-blockers? | There are also beta receptors in the lungs that can be activated so it shouldn’t be given to COPD/asthma patients as it can also slow RR. |
| What does digoxin do? | Slows HR and makes each beat more efficient, uses more effort and thus it makes contraction more forceful. |
| Describe 1st degree heart block. | A PR interval of greater than 0.2 seconds meaning the heart is taking longer to depolarize the atria. Common among elderly and those with arthrosclerosis. No treatment. |
| Atrial flutter | Like a sawtooth. Doesn’t empty completely and blood stagnates. Can cause clots. Greater risk of stroke/pulmonary emboli depending on atria with clot. |
| Atrial flutter or atrial fibrillation treatment | If constant, can be on Coumadin for life. If symptomatic<48 hrs, cardioversion. If symptomatic>48 hrs, TEE (transesophageal echocardiogram). |
| Atrial fibrillation | Random, always irregular. Like keno ball bouncing around, depolarizes over and over until one finally gets through. |
| What is a premature ventricular contraction (PVC) and what are it’s characteristics? | An early beat that is faster than the pacemaker and skips to the ventricle. ST in opposite direction of QRS. Wide, bizarre QRS’s, compensatory. |
| What is given for frequent PVC’s? | Amiodarone – slows HR |
| What is bigeminy? | A PVC every other beat. |
| What is trigeminy? | A PVC every third beat. |
| What is a unifocal PVC? | A PVC occurring from the same stimulus. |
| What is a multifocal PVC? | A PVC occurring from different stimuli. |
| Ventricular tachycardia | PVC after PVC. Individual, wide QRS complexes are seen while P waves are often buried. Treatment: Amiodarone and if unconscious, defibrillation. |
| Ventricular fibrillation | Random, QRS are seen as coarse waves or are unseen. Gonna go! Shock works better than meds. CPR provides time. Call code. |
| What are the 1st line meds provided on a crash cart (3)? | Epinephrine, Atropine and Vasopressin. |
| What are the 2nd line meds provided on a crash cart (2)? | Amiodarone, Dilantin (anti-seizure drug) |
| What do you do if patient in asystole (3)? | Give CPR and epinephrine, call code. |
| Why don’t you want a patient with bradycardia or other heart issues to bear down? | Bearing down can stimulate the vagus nerve causing slowing of the heart rate. |
| What is the normal range for Potassium (K+)? | 3.5 – 5.0 meq/L |
| What is the normal range for Calcium (Ca+)? | 8 – 10 mg/dL |
| What is indicated with an elevated ST segment? | Could be having a heart attack or be undergoing chest pain. |
| What are the risk factors for Coronary Artery Disease (CAD) (11)? | Hypertension, Diabetes Mellitus, high cholesterol, cigarettes, male, family history and age. Less risky: personality traits, obesity, fasting triglycerides, sedentary lifestyle. |
| End diastolic volume (EDV) | Volume of blood in the ventricles just before contraction. |
| End diastolic pressure (EDP) | pressure exerted on the ventricle walls before contraction. |
| Preload (EDV or EDP) | degree of myocardial stretch at the end of diastole (right before the ventricles contract) |
| Afterload | force opposing ventricular ejection (pressure) |
| Stroke volume (SV) | volume of blood ejected by the ventricles with each contraction (influenced by preload, afterload and contractility) |
| Cardiac output (CO) | volume of blood ejected by the ventricles in a minute (CO=SVxHR) – usually 3.5 – 6 liters a minute |
| Ejection fraction | % of blood ejected out after systole |
| Cardiac index | cardiac output adjusted for body size. Probably better than CO – takes into account cardiac output, and pt’s ht and wt. |
| Diagnose: Ejection fraction-40%, confusion, cyanosis, semi-comatosa/comatose, chest pain, arrythmias, SOB and decreased output | Congestive Heart Failure |
| What is the best way to see Congestive Heart Failure? | Echocardiogram |
| Acute Heart Failure | Sudden onset-rapid myocardial failure, causes: MI-arrythmias-decreased contractility, pericardial hemorrhage/tamponade, pulmonary embolism. |
| Chronic Heart Failure | Slowly progressive. Causes: artheroscleritic CAD, myocardial changes d/t HTN and valvular disease, ischemic heart disease, rheumatic heart disease. Compensatory/De-compensatory: Starling’s Law, hypertrophy. |
| What are the tell tale signs of left and right heart failure? | Left – lungs, right – systemic. |
| Left heart failure | Large volume of blood remains in dilated left ventricle – backs up to lungs – pulmonary congestion. Occurs with MI, HTN, aortic stenosis, mitral regurgitation, coarctation of aorta. |
| Signs and symptoms of left heart failure (9) | dyspnea, coughing, rales, orthopnea, paroxysmal nocturnal dyspnea, frothy sputum, S3 and S4, PMI shifted, murmurs. |
| Right heart failure | weakness of right ventricle to circulate blood to lungs, venous blood backs up into systemic circulation. Occurs with pulmonary stenosis, COPD, septal defect, right ventricular infarction. |
| Signs and symptoms of right heart failure (5) | distended neck vein, liver enlargement, jaundice, abdominal pain, hepato-jugular reflux. |
| Medical management of left heart failure (7+meds) | Decrease preload-decrease sodium, restrict fluids, rotate tourniquets, meds (diuretics, morphine, nitrates, Nipride, Minipress, ACE inhibitors) Decrease HR-bed rest, meds (Digoxin, Ca+ channel blockers, B block Decrease afterload-meds (antihypertensives) |
| Medical management of right heart failure | Same as left heart failure, may encourage fluid to raise right ventricle filling pressure. |
| Which LDL apolipoprotein is worse, A or B? | Apolipoprotein B is worse because it is smaller and can get lodged in the coronary arteries. |
| When are the coronary arteries filled? | During diastole, right and left coronary arteries and left circumflex. |
| What is happening when the S1 sound is heard? | The mitral and tricuspid valves are closing. |
| What is happening when the S2 sound is heard? | The aortic and pulmonic valves are closing. |
| Coarctation of aorta | Narrowing of aorta – increases afterload. |
| Starling’s Law | Example: if a rubber band is stretched, it will snap back, the further it is stretched, the harder it snaps back, Over time however, it wears out. |
| In heart failure, an S3 sound can be heard. What causes that sound? | Blood rushing into the ventricle and hits the flabby muscle (strong in a healthy person). Sounds like “Kentucky.” |
| In heart failure, an S4 sound can be heard. What causes that sound? | The atrial kick which forces blood into the flabby ventricle wall. |
| What is PACWP and what does it tell you? | It is Pulmonary Artery Capillary Wedge Pressure. The balloon lodges into the pulmonary artery capillary and gives the pressure ahead of the balloon. It shows the pressure in the L ventricle. (Blocks blood behind balloon so can’t leave inflated long) |
| What controls blood pressure in the body (5)? | Vasomotor center in the brain, baroreceptors in aortic arch, renin-angiotensin system, anti-diuretic hormone, atrial natriuretic factor. |
| What is the vasomotor center? | A center in the brain that can raise and lower blood pressure and heart rate via hormone release. |
| What are baroreceptors? | Receptors in the aorta, heart and lungs that indicate stretch. When overstimulated (HTN), loses ability to alert body to compensate. (Accepts as normal) |
| How does the rennin-angiotensin system work? | Renin converts angiotensin I to angiotensin II in the lungs. This then stimulates the release of aldosterone in the kidney: results in vasoconstriction. |
| How does the anti-diuretic hormone or Vasopressin control blood pressure? | It works by keeping fluid in and maintaining a higher volume and thus raising blood pressure. |
| What are the non-modifiable risk factors of hypertension? (4) | Family history, ethnicity, advanced age, gender. |
| What are the modifiable risk factors of hypertension? (8) | Obesity, Diabetes Mellitus, sedentary lifestyle, increased sodium intake, increased alcohol intake, stress, smoking, increased serum lipids. |
| What are the signs and symptoms of hypertension? (7) | Often asymptomatic, fatigue, reduced activity tolerance, dizziness, palpitations, angina and/or dyspnea. |
| What diagnostic exams are used to diagnose hypertension? (7) | History and physical exam, urinalysis, basic metabolic panel (BMP), liver function test, 24 creatinine clearance, echocardiogram, thyroid stimulating hormone. |
| What drug groups are used to manage hypertension? (5) | Diuretics, adrenergic inhibitors, beta-adrenergic blockers, direct vasodilators, and angiotensin inhibitors. |
| What diuretics are used to manage hypertension? (4+meds) | Thiazide – Cholorhiazide (Diuril), Loop – Furosemide (Lasix), Bumetanide (Bumex), Potassium-Sparing – Amiloride (Midamor) (watch for hyperkalemia), Aldosterone Receptor Blockers – Spirinolactone (Aldactone) |
| What adrenergic inhibitors are used to manage hypertension? (5+meds) | Central Acting Alpha Adrenergic Antagonists (ex: Clonidine), Adrenergic Blockers (ex: Cardura), Beta-Adrenergic blockers (-olol), Direct vasodilators (ex: Hydralazine), Angiotensin Inhibitors (ACE Inhibitor –pril, AII Receptor blockers –tan) |
| When are and aren’t diuretics indicated for use in hypertensive patients? (3 and 2) | USE: Heart failure, Diabetes and Stroke. DON’T USE: Myocardial Infarction and with kidney problems. |
| When are and aren’t Beta blockers indicated for use in hypertensive patients? (3 and 2) | USE: Heart failure, myocardial infarction, diabetes. DON’T USE: Kidney issues, stroke. |
| When are and aren’t ACE Inhibitors indicated for use in hypertensive patients? (5 and 1) | USE: Heart failure, myocardial infarction, diabetes, kidney issues and stroke. DON’T USE: None. |
| When are and aren’t Angiotensin receptor blockers indicated for use in hypertensive patients? (3 and 2) | USE: Heart failure, diabetes and kidney issues. DON’T USE: Myocardial infarction and stroke. |
| How can nurses help manage a patients hypertension? (9)_ | Health promotion, lifestyle changes, DASH diet, exercise, weight loss, BP measurement, no smoking, alcohol moderation, complying with treatment plan. |
| What are the complications associated with hypertension? (7) | Coronary artery disease (CAD), left ventricular hypertrophy (LVH), heart failure (expands to fill more and pumps slower), cerebrovascular disease (CVD), peripheral vascular disease, renal disease, retinal damage. |
| What is coronary artery disease? | A blood vessel disorder called atherosclerosis made of soft deposits that harden with age. Can happen to any artery but it has a preference for coronary arteries. |
| What are the markers of cardiovascular disease? (4) | A high C-reactive protein (1-3 mg/L = average risk, 3+ mg/L = high risk), high leukocyte count (>6.71x109 cells/L), a brain natriuretic peptide > 100 pg/mL, elevated homocysteine > 10 u mol/L. |
| What are the non-modifiable risk factors for coronary artery disease? (4) | Age, genetics, gender and ethnicity. |
| What are the modifiable risk factors for coronary artery disease? (7) | Smoking, exercise, obesity, diet, blood pressure, diabetes, and high cholesterol. |
| What are the types of coronary artery disease? (4) | Chronic stable angina, unstable angina, Prinzmetal’s angina and acute coronary syndrome. |
| Describe chronic stable angina. | Intermittent pain over a long time with the same pattern each time (onset, duration, location), pain usually lasts 3-5 minutes. Management includes: Nitrates, Ca+ channel blockers, beta blockers, lipid reduction, aspirin and stool softener. |
| Describe unstable angina. | New onset that occurs at rest with an unpredictable, worsening pattern. This represents an emergency. |
| Describe Prinzmetal’s angina. | Variant angina that occurs at rest in response to a spasm. Commonly happens in patients with migraines. May not always have CAD. |
| Describe acute coronary syndrome. | Happens when ischemia is prolonged and is not immediately reversible. Encompasses: unstable angina, NSTEMI and STEMI. Angina can lead to myocardial ischemia when O2 demand is greater than supply. |
| How is acute coronary syndrome assessed? | Ischemia results in an inverted or flat T-wave, Injury results in an increased or depressed ST and Infarction results in a change in Q wave. |
| What are the steps that lead to acute coronary syndrome? | Deterioration of stable plaque – rupture – platelet aggregation – thrombus – partial (NSTEMI) or total (STEMI) of coronary artery |
| How do patients usually describe the pain? (4) | Heavy (elephant sitting on chest), Constriction (tightness), Burning (GERD), Pressure (constant pushing), Crushing (squeezing) |
| What are the cardiac markers of acute coronary syndrome? (3) | Myoglobin – detected within 1-4 hours, non-specific. *Troponin* - best indicator. Detected 3-12 hrs and may last 21 days. CK-MB – detected 2-12 hrs, peak at 24 and last for 72. |
| What medications are used to manage acute coronary syndrome? (4, OANM) | Oxygen, Aspirin, Nitrates, Morphine. |
| What are the coronary angiogram treatments for acute coronary syndrome? | Percutaneous Coronary Intervention (balloon), Angioplasty or Percutaneous transluminal angioplasty, stent (keep arteries open at all times, must stay on aspirin/Plavix for life) or atherectomy (plaque removal). |
| What are the surgical treatments for acute coronary syndrome? | Coronary artery bypass graft (through sternum to use arteries to bypass clot), Mid CABG (minimally invasive, more painful, only for one blocked vein), Trans myocardial revascularization (burning a hole in the heart). |
| What are the types of nursing care used for acute coronary syndrome? | Bedrest, monitoring vitals, monitoring EKG, provide support, monitor labs, activity and position, monitor weight, maintain patent IV line. |
| What will an acute coronary syndrome patient undergo once discharged? | Cardiac rehabilitation, follow-up care. |
| What medications are taken for acute coronary syndrome? | Fibrinolytics-Tenecteplase,Streptokinase,Altapase,Reteplase, Aspirin/Clopidogrel(Plavix),Heparin,GP IIB/3A receptor antagonists Abciximal(Reopro)(anti-coag),Nitro (vasodilate), B blockers (lower HP, BP), Statins–Simvastatin (lower choles), Stool softener |
Created by:
jouelle
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