Exam 2 Flashcards

Question

5 lead ecg

Answer 1

White on top right Green on bottom right Brown on tummy Black on top left (smoke) Red on bottom left (fire)

Answer 2

60-100 BPM Primary pacemaker If SA node fails to send out signals—Caused by cardiac arrest/infarction, muscles die and SA node is killed so it can’t send signal

Answer 3

secondary pacemaker 40-60 BPM

Answer 4

30-40 BPM Too slow to provide cardiac output, get them a pacemaker!

Answer 5

1500/number of small boxes

Answer 6

Positive in lead I and II in NSR (points up) Negative in lead aVR in NSR Biphasic in lead V1

Answer 7

Indicates AV conduction time Beginning of the P wave to the QRS complex Measures 0.12-0.20 seconds (3-5 small boxes) Prolonged PR interval=1st degree heart block

Answer 8

Q wave: the first negative deflection after the P wave R wave: the first positive deflection after the P wave S wave: first negative deflection after the R wave

Answer 9

0.04 seconds

Answer 10

small rounded wave follows T wave. Less prominent than the P, QRS, and T waves. Only sometimes present.

Answer 11

lower metabolic rate: sleep, athletic training, hypothyroidism Vagal stimulation: vomiting, suctioning, severe pain, bearing down TAKE COLACE STOOL SOFTENER Idiopathic sinus node dysfunction Increased intracranial pressure Coronary artery disease (e.g. MI of the interior wall) Women’s cycle Resolving the causative factors might be the only treatment needed.

Answer 12

calcium channel blockers, amiodarone, beta-blockers

Answer 13

If the bradycardia produces signs and symptoms of clinical instability (e.g., acute alternative of mental status, chest discomfort, syncope, or hypotension): Atropine: 0.5 mg given rapidly as an IV bolus every 3-5 minutes to a max dose of 3 mg

Answer 14

Physiologic or psychological stress Varies depending on menstrual cycle Medications that stimulate the sympathetic response; stimulants; and illicit drugs ALCOHOL INCREASES HR BECAUSE BP GOES DOWN Enhanced automaticity of the SA node/or excessive sympathetic tone with reduced parasympathetic tone (to improve stress level and increase influence of parasympathetic, deep breathing, meditation Autonomic dysfunction: POTS-increase in heart rate greater than 30 bpm without hypotension when moving to a standing position

Answer 15

Tired heart Low myocardial supply → myocardial ischemia → possible heart attack

Answer 16

synchronized cardioversion is the treatment of choice (reset the heart) Vagal maneuvers: carotid sinus massage, gagging, bearing down, forceful and sustained coughing, and applying a cold stimulus to the face. Administration of adenosine (narrows the QRS) Wide QRS: procainamide, amiodarone, and sotalol Catheter ablation (done in EP lab)

Answer 17

HR changes based on respirations (faster on inspiration, slower on expiration) Does not cause any significant hemodynamic effect and not typically treated Pattern! Irregular but there’s a pattern Defined as regularly irregular

Answer 18

caffeine, alcohol, nicotine, stretched atrial myocardium, anxiety, hypokalemia, hypermetabolic states, or atrial ischemia, injury, or infarction QRS comes earlier than it's supposed to

Answer 19

treat the underlying cause (potassium levels, anxiety, etc)

Answer 20

vagal maneuvers, adenosine. Treated with antithrombotic therapy, rate control, and rhythm control in the same manner as afib

Answer 21

Described with atrial to ventricular ratio (how many p waves per r wave)

Answer 22

Most common heart dysrhythmias uncoordinated atrial electrical activation: rapid, disorganized, and uncoordinated twitching of atrial musculature. Irregular

Answer 23

Older people with structural heart disease, inflammatory or infiltrative disease, coronary artery disease, hypertension, congenital disorder, and heart failure. DM, obesity, hyperthyroidism, pheochromocytoma (a rare, usually non cancerous (benign) tumor that develops in cells in the center of an adrenal gland.), pulmonary hypertension and embolism, obstructive sleep apnea, and acute moderate to heavy ingestion of alcohol

Answer 24

Symptoms of heart failure Hemodynamic collapse Pulse deficit (hard to find) Myocardial ischemia Thrombi

Answer 25

Antithrombotic: aspirin, warfarin (not given as much, new ones given so they don’t have to get levels checked so much), Pradaxa, Xarelto, Eliquis, Savaysa. Heart rate control medications: goal→ resting heart rate is less than 80 bpm. Beta-blocker or verapamil, diltiazem Pharmacologic cardioversion: amiodarone.

Answer 26

Electrical cardioversion: for those hemodynamically unstable (e.g., acute alteration in mental status, chest discomfort, hypotension) and does not respond to medications Old people have small brains so be careful when they fall

Answer 27

40-60 beats/min (above is junctional tachycardia) AV node as the pacemaker

Answer 28

Location of P wave varies P waves may be: Inverted and before, during, or after QRS Absent (hiding in QRS) PR interval: short QRS: normal

Answer 29

May produce s/s of reduced cardiac output Treatment same as sinus bradycardia (Atropine, dopamine, epi)

Answer 30

Treat underlying conditions (CAD or other abnormalities) Catheter ablation Meds and lifestyle mods

Answer 31

beta-blockers, calcium channel blockers, and other antiarrhythmics

Answer 32

reducing or eliminating triggers (avoiding caffeine, alcohol, and nicotine, as well as managing stress and getting adequate sleep)

Answer 33

60-120 BPM

Answer 34

P waves not clear Afib, a flutter, or junctional tachycardia can all be called SVT QRS: normal (tight and narrow, once it’s wide, that means something is wrong with the ventricles)

Answer 35

Adenosine--6mg rapidly: always follow with NS bolus Warn patient: chest pressure, feeling faint

Answer 36

Initiated by Purkinje fibers--"skipped beat" and felt as palpitations in the chest (irregular pulsations) Bigeminy: every other complex Trigeminy: every third complex

Answer 37

Amiodarone

Answer 38

three or more PVCs in a row, occurring at a rate exceeding 100 bpm. Assess the patient!! Emergency: unresponsive and pulseless Patients with larger MIs and lower ejection fractions are at higher risk of lethal VT.

Answer 39

stable monomorphic VT (do not have acute MI or severe HF): continuing assessment Symptomatic monomorphic VT: cardioversion Pulseless VT: defibrillation

Answer 40

ejection fraction <35%: implantable cardioverter defibrillator ejection fraction>35%: amiodarone

Answer 41

most common dysrhythmia in patients with cardiac arrest rapid disorganized ventricular rhythm>300/min

Answer 42

no atrial activity is seen absence of an audible heartbeat, a palpable pulse, and respirations cardiac arrest and death are imminent if not corrected early defibrillation is critical to survival

Answer 43

high quality CPR with minimal interruptions and identifying underlying and contributing factor (do not shock the patient)

Answer 44

AV block delayed or failed conduction of supraventricular impulses through the AV node (atrium) to the ventricles (atrium contracts, ventricles don’t contract appropriately) PR interval is a measure of conduction between the initial stimulation of the atria and the initial stimulation of the ventricles PR interval is used to identifying the degree (type) of block present

Answer 45

Long PR interval >0.2 seconds (5 small boxes) PR interval measurement is constant (all same length!) Not so serious, you can get by

Answer 46

Wenckebach Atrial contractions but no ventricular, can’t stimulate the QRS contraction PR interval becomes longer with each succeeding ECG complex until there is a P wave not followed by a QRS. The changes in the PR interval are repeated between each "dropped" QRS Atrium takes longer and longer to communicate, eventually the ventricle doesn’t receive a signal (QRS drops) This pattern repeats itself Regularly irregular!

Answer 47

Second degree type II: PR interval constant (length varies can be less than 0.2 or longer than that)) for those P waves just before QRS complexes

Answer 48

Complete Two impulses (pacemakers!!) stimulate the heart. PR interval: very irregular More P waves Than QRS complexes Ps and Rs on their own, no coordination PP is the same, and so is RR P wave to R wave ratio is off: More p waves Pacemaker for ventricles is intrinsically much slower, which is why there’s fewer R waves

Answer 49

increase HR and maintain CO Stable, no symptoms: no treatment (usually 1st degree, treatment in third degree) The initial treatment of choice is an IV bolus of atropine, although it is not effective in second-degree AV block, type II, or third-degree AV block. Acute dysrhythmias may be treated with medications or with external electrical therapy (emergency defibrillation, cardioversion, or pacing).

Answer 50

pacemaker for bradycardias and ICDs for chronic tachydysrhythmias [vtach or vfib])

Answer 51

cardioversion and defibrillation: to depolarizes myocardial cells (to terminate a tachydysrhythmia) Indications of a successful response are conversion to sinus rhythm with adequate perfusion

Answer 52

cardioversion: deliver SYNCHRONIZED current (50 jules, aligns with patient’s rhythm, meaning they need to have a rhythm) defibrillation: the delivery of the current is immediate and UNSYNCHRONIZED (VT/VF, irregular rhythms)

Answer 53

Used in emergency treatment of choice for v fib and pulseless VT not for those who are conscious or have a pulse use more voltage than used in cardioversion give epinephrine or vasopressin after defibrillation

Answer 54

a shock is timed to delivered during ventricular depolarization (QRS complex, when ventricles contract) not to delivery the shock during vulnerable period of the T wave repolarization (when heart is relaxed) is used to treat rhythms that have a clearly identifiable QRS complex and a rapid ventricular rate (SVT, monomorphic VT) not for disorganized rhythms (polymorphic VT, VF)

Answer 55

May need to take anticoagulants for a few weeks before the procedure. Digoxin withheld for 48 hours before the procedure (to ensure the resumption of sinus rhythm with normal conduction) No food or drinks at least 4 hours before the procedure Can be chosen to be done to correct afib

Answer 56

use electrical stimulation through pacing pads positioned on a patient's torso to stimulate contraction of the heart =temporary external pacing or noninvasive pacing indication: symptomatic bradycardia unresponsive to atropine therapy or atropine is not available painful, skin burns, tissue damage Get put on a sedative because it’s painful

Answer 57

Symptomatic bradycardia (slow ventricular rate) Symptomatic heart block (also slow rate)

Answer 58

Electronic pulse generator (intrinsic/house pacemaker) Pacemaker electrodes (conduction pathway) Pacemaker is externally programmable

Answer 59

One lead placed in atrium or ventricle Produce large spic on the ECG Sensing and pacing in the chamber where the lead is located More likely to be affected by electromechanical interference

Answer 60

One lead located in the atrium and one in the ventricle Sensing and pacing in both chambers mimicking the normal heart function Less affected by electromechanical interference This is the one we see more

Answer 61

Paced A: atrium V: ventricle D: dual

Answer 62

Sensed A: atrium V: ventricle D: dual

Answer 63

Response to pt's HR I: inhibited (when heart beats normally, the pacemaker does not function) T: triggered D: dual

Answer 64

sinus node dysfunction--no conduction disturbance in the AV node, atrium to ventricle is fine so we can only use one lead since this conduction is fine

Answer 65

AV conduction disturbance With complete heart block, we use DDD because it needs to sense both chambers

Answer 66

Stimulation of the chamber--mimic normal heart conduction Produce a spic on ECG

Answer 67

response of the pacemaker is controlled by the activity of the patient's heart. only function when pt's heart not beat up to programmed rate (usually below 60)

Answer 68

response when it sense intrinsic heart activity (triggered by each p wave)

Answer 69

the heart has responded to the stimulus by producing an appropriate complex

Answer 70

may occur with a low battery or poor connection, doesn’t send out impulse strong enough for contraction. The pacemaker is discharging the impulse; however, there is no responding cardiac contraction Pacemaker says hey heart! Contract! And heart says nope

Answer 71

Check pt has a patent IV, and that the defibrillator, emergency cart and appropriate medications are available Obtain consent–make sure patient is capable to make decision and witness the signature, doctor’s job to educate and answer questions Obtain vital signs and ECG rhythm strips prior to insertion. connect to 12 lead ECG and continuously monitor before, during, and after Anesthetize the area locally Portable chest x-ray is required to confirm placement

Answer 72

monitor the insertion site for bleeding, hematoma, and infection

Answer 73

Movement and dislocation of the lead (don’t lift arms or heavy objects for a while) Bleeding and hematoma Ventricular ectopy or VT from wall stimulation Infection leading to cardiac tamponade Hemothorax, pneumothorax Hiccups: may indicate that the generator is pacing the diaphragm Pacemaker syndrome

Answer 74

most common in VVI–pacemaker is only in ventricle Fatigue, chest discomfort, SOB, activity intolerance, and postural hypotension, they feel worse than before. Teach pt to report this to the doctor

Answer 75

Never exposed to MRI because it may alter and erase the program memory At security gates at airports, government buildings, or other secured areas request a hand search (no wand detection device directly over the pacemaker) Household appliances (eg, microwave ovens) should not cause any concern

Answer 76

Detects and terminates life-threatening episodes of tachycardia or fibrillation, especially those that are ventricular in origin, so vtach and vfib

Answer 77

Dilated cardiomyopathy Hypertrophic cardiomyopathy Arrhythmogenic right ventricular dysfunction Idiopathic prolonged QT syndrome Vtach and vfib are huge risks in these so get an AICD!

Answer 78

Normal to feel tingling if you are touching patient when AICD delivers a shock Not to place defibrillator paddles directly over the device Patient with a permanent pacemaker with defibrillator or AICD should have the device checked after defibrillation (check battery or if rate changed, needs to be replaced if so)

Answer 79

invasive cardiac catheterization Evaluates and treats dysrhythmias Includes cardiac cath and catheter ablation Take fluid out and bring it to lab to check for bacteria, treats bc we're removing fluid and also diagnoses Patient is conscious but lightly sedated

Answer 80

performed in a specially equipped cardiac catheterization lab by an electrophysiologist

Answer 81

destruction of the causative cells Radiofrequency--thermal injury and cellular changes Extremely cold temperature

Answer 82

Similar to those associated with cardiac catheterization: Restriction of activity Duration 2-6 hours (if treatment is indicated) Procedure is not painful but can be tiring. It may also cause feelings that were experienced when the dysrhythmia occurred in the past

Answer 83

Tricuspid and mitral are similar in terms of location (in between atrium and ventricles Aortic and pulmonic are also similar because they both send blood out of the heart

Answer 84

fibrous tissue that anchor valve leaflets to papillary muscles of the ventricles, white stringy thingies Holds onto the valves Heart muscle can die or chordae tendineae can rupture

Answer 85

when valves do not close completely when they are supposed to close.

Answer 86

when valves do not open completely when they are supposed to open (something is stuck)

Answer 87

anterior leaflet: longer posterior leaflet: shorter

Answer 88

Enlargement of one or both of the leaflets of mitral valve. When leaflet is too long it can buckle onto ventricle itself, can’t close completely (regurgitation issue) annulus often dilates; chordae tendineae and papillary muscles may elongate or rupture. A portion of one or both mitral valve leaflets balloons back into the atrium during systole--blood regurgitates from the left ventricle back into the left atrium Needs to close during systole (systolic murmur)

Answer 89

Most never have symptoms A few have fatigue, SOB, lightheadedness, dizziness, syncope, palpitations, chest pain, or anxiety

Answer 90

Extra heart sound--mitral click A murmur of mitral regurgitation may be heard if the valve opens during systole (systolic murmur) and blood flows back into the left atrium. Echocardiography for structure problems is used to diagnose and monitor progression of MVP

Answer 91

Eliminate caffeine and alcohol, stop using tobacco products. Antiarrhythmic medications Chest pain: nitrates or calcium channel blockers or beta-blockers HF management Severe: mitral valve repair or replacement

Answer 92

At risk for endocarditis because of the extra long tissue (bacteria on it) Women diagnosed with mitral valve prolapse without mitral regurgitation or other complications may complete pregnancies with vaginal deliveries Antibiotic prophylaxis is recommended for high-risk patients before and after dental procedures--Amoxicillin, not everyone needs it, just depends on condition

Answer 93

By itself, this is a pathology Blood flowing back from the left ventricle into the left atrium during systole. Due to the thickness and fibrosis of the chordae tendineae pulls on to leaflets so they can’t close tightly systolic murmur

Answer 94

Developing countries: rheumatic heart disease Developed countries: degenerative changes of the mitral valve as people get older

Answer 95

Often asymptomatic Acute mitral regurgitation: usually from a MI--manifests as severe CHF (heart failure management can be used here as well as with MVP) Most common: Dyspnea, fatigue, and weakness, not enough blood pumped to body because it flows back into the left atrium S/s are similar to MVP Big risk for clots!!

Answer 96

Systolic murmur: high-pitched, blowing sound at the apex that may radiate to the left axilla May have irregular pulses Echocardiography is used to DX and monitor

Answer 97

medical management: same as for HF (goal: reduce afterload) surgical management: mitral valvuloplasty (trim and fix) and valve replacement

Answer 98

DIASTOLIC murmur Valve is supposed to open but doesn’t Obstruction of blood flowing from the left atrium to the left ventricle due to the narrowing of the mitral valve orifice/opening

Answer 99

Mitral stenosis blood can’t move so it gets stuck in left atrium and then backs up into the lungs, right side heart failure, reduced cardiac output

Answer 100

Dyspnea on exertion (DOE) Enlarged left atrium (due to thin atrial walls)--create pressure on the left bronchial tree, resulting in a dry cough or wheezing. (also leads to afib) May have hemoptysis from congested lungs, palpitations, orthopnea, paroxysmal nocturnal dyspnea, repeated respiratory infections

Answer 101

Weak and irregular pulse in the presence of afib Low-pitched rumbling diastolic murmur May have s/s of HF

Answer 102

Anticoagulants, beta-blockers, digoxin, or CCB. Avoid strenuous activities, competitive sports, and pregnancy Usually old age so these aren’t issues Also seen in child bearing age!! Fibrosis can cause mitral valve to stick together, not related to age. Fibrotic changes of mitral valve. Can’t take anticoagulants during pregnancy

Answer 103

percutaneous transluminal balloon valvuloplasty great outcome Good for child-bearing age women Catheter goes into right atrium, then needs to locate mitral valve, wire needs to poke a hole between left and right atrium and move down to find stenotic mitral valve. Balloon stretches and opens the mitral valve, remains open and is a cure Problem is that the wall may not heal properly Not as good for elderly because it’s usually due to calcification and this will not prevent recalcification Also mitral valve replacement

Answer 104

Diastolic murmur This valve needs to close during diastole so blood stays in ventricle Flow of blood back into the left ventricle from the aorta during diastole. The left ventricle dilates in an attempt to accommodate the increased volume of blood. Usually asymptomatic

Answer 105

During diastole, mitral valve opens and aortic closes Opposite for systole

Answer 106

Some may be aware of a forceful heartbeat especially in the head or neck. Marked arterial pulsations visible or palpable at carotid or temporal arteries High-pitched, blowing diastolic murmur at the third or fourth intercostal space at the left sternal border. Widened pulse pressure

Answer 107

Avoid physical exertion, competitive sports, and isometric exercise Sodium and fluid restriction

Answer 108

Afterload reduction Valve replacement or valvuloplasty Surgery is recommended for any patient with left ventricular dilation, regardless of the presence of absence of symptoms. Keeps dilating and leads to dilated cardiomyopathy. Diagnosed with echocardiogram

Answer 109

Very commonly seen and easy to hear in little old ladies with calcified aortic valves Aortic valve doesn’t open

Answer 110

loud, harsh systolic murmur heard over the aortic area and may radiate to the carotid arteries and apex of the left ventricle. Low pitched, crescendo-decrescendo, rough, rasping, and vibrating.

Answer 111

focused on controlling risk factors for proliferative and inflammatory responses: diabetes, HTN, HL, avoid tobacco products. Surgical replacement

Answer 112

procedure performed to separate the fused leaflets. (surgeon puts their finger in the stenotic valve to open it up)

Answer 113

Closed: balloon valvuloplasty (can be used for mitral stenosis or aortic stenosis [Usually due to calcification so it'll become stenotic in a few months again]) Open: open commissurotomy

Answer 114

Beneficial for mitral valve stenosis in younger patients with complex medical conditions

Answer 115

Those with left atrial or ventricular thrombus (Wire can dislodge clots) Severe valvular calcifications Thoracolumbar scoliosis (Hard to move wire around when everything is not straight) Rotation of the great vessels Cardiac conditions that require open heart surgery

Answer 116

Mitral regurgitation Bleeding from the catheter insertion sites Emboli Atrial septal defect (wire poking a hole in atrial-septum wall, healing may not happen and lead to this)

Answer 117

Aortic regurgitation Bleeding from the catheter insertion sites Emboli Ventricular perforation, rupture of the aortic valve annulus, ventricular dysrhythmia, mitral valve damage Not as effective as mitral valve procedure because rate of stenosis is high

Answer 118

Repair of a cardiac valve No need for anticoagulation Only mitral valve can be repaired well; other valves are better to be replaced

Answer 119

When valvuloplasty is not a viable alternative: when the annulus or leaflets of the valve are immobilized by calcifications (elderly), severe fibrosis, or fusion of leaflets, chordae tendineae, or papillary muscles

Answer 120

repair of the valve annulus. If chordae tendineae rupture, you can suture them together

Answer 121

More durable Less likely to be infected Need anticoagulants

Answer 122

Less likely to generate thromboemboli and long term anticoagulation is not required

Answer 123

Bioprosthesis: from pigs, cows, or horses. Homografts: human valves Autografts: patient’s own pulmonic valve

Answer 124

dilated cardiomyopathy (DCM) most common hypertrophic cardiomyopathy (HCM) restrictive or constrictive cardiomyopathy (RCM) arrhythmogenic right ventricular cardiomyopathy (ARVC)

Answer 125

Regardless of type and cause, cardiomyopathy may lead to severe heart failure, lethal dysrhythmias, and death. The mortality rate is highest for African Americans and older adults

Answer 126

Most common form Dilated left ventricle without hypertrophy (thin and dilated, floppy and large, can’t pump as well, clots can occur and low cardiac output from diminished contractility) Low EF

Answer 127

pregnancy ischemia heavy alcohol intake (damaging to heart muscle) viral infection chemotherapeutic medications Chagas disease (parasite) 20-30% idiopathic Genetic factors may be involved: first degree blood relatives screening

Answer 128

Dilation of the ventricles without simultaneous hypertrophy and systolic dysfunction Complete recovery is rare Diminished contractile elements (can’t pump the blood out) Diffuse necrosis of myocardial cells (fatal)

Answer 129

Poor systolic function: low EF Increasing end-diastolic pressure Increasing pulmonary and systemic venous pressures Altered valve function (usually regurgitation, when the wall stretches, the chordae tendineae can’t close the leaflet tightly) Thrombi formation

Answer 130

Limited activity based on functional status Salt and fluid restriction Meds Heart transplant LV reduction surgery

Answer 131

Ace inhibitors, diuretics Digoxin to help with contractility hydralazine/nitrate combination Anticoargulation PRN (EF<30%, hx of embolic event) Implantable defibrillators AVOID CA CHANNEL BLOCKERS LIKE VERAPAMIL (pulmonary edema from vasodilation)

Answer 132

Good EF but low CO Rare, with family history: 12-18 years of age: echocardiograms every year 18-70: echocardiograms every 5 years

Answer 133

Thickening begins during early adolescence and stops when growth has finished Heart muscle increases in size and mass: especially along the septum Reduced size of the ventricular cavities Takes longer for the ventricles to relax after systole Cardiac muscle cells disorganized, oblique, and perpendicular to each other, decreasing the effectiveness of contractions and possibly increasing the risk of dysrhythmias

Answer 134

Cardiac arrest (high demand of blood, not enough supply, cardiac arrest) Sustained V-tach and V-fib: most likely mechanism of syncope/sudden death Angina, syncope, palpitations, and left heart failure

Answer 135

No treatment unless there's symptoms Avoid dehydration (avoid diuretics, teach teens about hydration) BB Limited physical activity to avoid dysrhythmia Implanted pacemaker (biventricular) Nonsurgical septal reduction therapy (alcohol ablation)

Answer 136

Diastolic dysfunction caused by rigid ventricular walls that impair diastolic filling and ventricular stretch Systolic function is usually normal (can contract but can’t dilate/stretch to accomodate blood)

Answer 137

Venous congestion, jugular venous distention, hepatomegaly, ascites (signs of right sided heart failure) Due to rigid myocardium: decreased ventricular filling, decreased CO→ weakness and fatigue

Answer 138

May be associated with amyloidosis, sarcoidosis, hemochromatosis Avoid: nifedipine to maintain contractility

Answer 139

Right ventricle replaced with chaotic mix of heart muscle, fibrous tissue, and fat Right ventricle dilates and develops poor contractility Arrhythmia: palpitations or syncope Ventricular tachycardia originating in the right ventricle Sudden death among young athletes

Answer 140

first-degree blood relatives should be screened with 12 lead ECG, Holter monitor and echocardiography

Answer 141

mechanical assist devices and total artificial hearts: Left ventricular assist devices (LVAD) (battery and controls are outside and everything else is inside)

Answer 142

a "bridge to recovery" for patients who require temporary assistance for reversible ventricular failure a "bridge to transplant" for patients with end-stage heart failure until a donor organ becomes available "destination therapy" for patients with end-stage heart failure who are not candidates for or decline heart transplantation

Answer 143

temporarily (1 week or so) (waiting for the heart transplant) deflated during systole; inflated during diastole reduces afterload increases myocardial perfusion/function

Answer 144

Heart transplant balancing rejection and infection postoperative function depends on the heart being implanted within 4 hours of harvest from the donor

Answer 145

Cardiomyopathy ischemic heart disease valvular disease rejection of previously transplanted hearts congenital heart disease

Answer 146

Immunosuppressants: tacrolimus (Prograf) cyclosporine mycophenolate mofetil (CellCept) azathioprine (Imuran) corticosteroids (prednisone)

Answer 147

increase arterial injury and inflammation osteoporosis weight gain, obesity, diabetes, dyslipidemias, hypotension, renal failure, and CNS, resp, and GI disturbance

Answer 148

1 year survival rate: 81-95% 10 year survival rate: 50-70%

Answer 149

replace both ventricles long-term results disappointing

Answer 150

Bleeding disorders Hemorrhage Thromboemboli Hemolysis Infection Renal failure Right-sided heart failure Multisystem failure Mechanical failure

Answer 151

one of the fastest growing heart conditions in the U.S. #1 reason for hospitalization of patients age 65 and older More hospitalizations from heart failure than for all forms of cancer combined About 550,000 new cases per year Prevalence is high

Answer 152

Noncompliance with diet and drugs (low fluid and salt) Inevitable progression of disease Rising incidence of chronic heart failure (population aging, improved survival with acute MI [revascularization]) Poor application of chronic heart failure management guidelines Incomplete treatment during hospitalization

Answer 153

inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients

Answer 154

amount of blood in the ventricle at the end of diastole venous return of blood compliance of ventricular (hypertrophy; fibrotic tissue after MI)

Answer 155

amt of resistance to the ejection of blood

Answer 156

R/t contractility percentage of blood volume in the ventricles at the end of diastole that is ejected during systole; a measure of contractility

Answer 157

Impaired contraction of the heart More common than diastolic heart failure Low EF Example: left-sided systolic heart failure

Answer 158

Impaired filling of the heart Stiffened and noncompliant heart muscle like restricted cardiomyopathy Normal EF

Answer 159

CAD HTN Cardiomyopathy Valvular disorder Renal dysfunction with volume overload Diabetics: high risk Pulmonary hypertension (pressure inside lungs is too high so RV needs to work harder to balance the pressure, eventually leading to RVHF

Answer 160

In reaction to the stretch of heart muscles body releases: natriuretic peptides (NPs) ANP and BNP BNP most accurate in identifying CHF (>100), works to lower BP and afterload Elevated with heart related congestion Vascular remodeling

Answer 161

Heart compensates for the increased workload to increase the thickness of the heart muscle (ventricular hypertrophy) Enlarged myocardial cells become dysfunctional and die early--leaving the other normal myocardial cells struggling to maintain CO A “vicious cycle"

Answer 162

First line of defense in mild HF Relieves s/s and decreases morbidity and mortality

Answer 163

Angioedema (rare allergic reaction, go to hospital for treating) Annoying dry cough Hyperkalemia

Answer 164

For HF have many of the same benefits as ACE inhibitors alternatives for those cannot tolerate ACE inhibitors similar side effects Valsartan (diovan) and losartan (cozaar)

Answer 165

hyperkalemia hypotension renal dysfunction

Answer 166

For HF isosorbide dinitrate may be another alternative for those who cannot take ACE inhibitors venous dilation--lowers preload

Answer 167

For HF lowers systemic vascular resistance and left ventricular afterload smooth muscle arterial vasodilator good for those with poor kidney function

Answer 168

For HF reduced the stimulation of the sympathetic nervous system given in addition to ACE inhibitors, diuretics, and digitalis (increases contractility) may prevent the onset of symptoms of HF

Answer 169

pts may feel worse at the beginning and then feel better, big reason for noncompliance Reduced sympathetic nerve stimulation so they feel tired, impotence

Answer 170

watch for dehydration loop first: furosemide (Lasix slow IV push), bumetanide (Bumex) (increase potassium excretion) thiazide (increase potassium excretion) Spironolactone (Aldactone): potassium-sparing diuretic

Answer 171

electrolyte imbalances symptomatic hypotension hyperuricemia (gout) ototoxicity cardiorenal syndrome: not a SE just something to watch for, resistant to diuretics

Answer 172

does not result in decreased mortality rates digoxin: increase the force of myocardial contraction and slows conduction through the AV node

Answer 173

vision changes first (yellow halos) anorexia, nausea, vomiting, fatigue, depression, and malaise changes in heart rate or rhythm; onset of irregular rhythm ECG changes: (sagging ST)

Answer 174

Monitor serum potassium level because the effect of digoxin is enhanced in the presence of hypokalemia and digoxin toxicity may occur A serum digoxin level is obtained if the patient’s renal function changes or there are symptoms of toxicity

Answer 175

IV diuretics fluid restriction pt may want to dangle his/her legs, helps them breathe better oxygen use of positive inotropes: (such as: Amiodarone) Reduce anxiety

Answer 176

short term balancing the good (improved cardiac output, stroke volume) against the bad (increased myocardial oxygen consumption) long-term use: worsen mortality

Answer 177

atherosclerosis--repetitious inflammatory response to injury of the artery wall over many years Atherosclerotic lesions most often form where the vessels branch

Answer 178

Family history of CAD Age: 45 for male, 55 for female Gender: male Race: African Americans

Answer 179

HL Cigarette smoking, tobacco use HTN Diabetes Metabolic syndrome Obesity Physical inactivity

Answer 180

Most common manifestation of myocardial ischemia is the onset of chest pain. burning, bursting, constricting, grip-like, heaviness, pressing, squeezing, strangling, suffocating, a band across my chest, a weight in the center

Answer 181

physical exertion--O2 exposure to cold--vasoconstriction eating a heavy meal--decreased blood flow to the heart muscle stress or emotion-provoking situation--catecholamines--increase blood pressure, heart rate, and myocardial workload

Answer 182

Predictable and consistent pain that occurs on exertion and is relieved by rest and/or nitroglycerin

Answer 183

relaxes smooth muscle--dilating primarily the veins and to a lesser extent, the arteries reduce preload (venous pooling) and afterload--lower the workload of the heart 0.3-0.6 mg SL q5min up to 3 times; use at first sign of angina not for those with severe bradycardia or tachycardia

Answer 184

attacks that increase in frequency and severity not relieved by rest and administering of nitroglycerin should be treated at the closest ED

Answer 185

Nitrates: Nitroglycerin BB: Metoprolol CCB: Amlodipine, Cardizem Antiplatelet medications: Aspirin, Plavix Anticoagulants: Heparin, Lovenox Reperfusion procedures: PCI procedures and CABG

Answer 186

T-wave inversion ST-elevation Or development of an abnormal Q wave. ST elevation will return to normal, but Q wave alterations are usually permanent.

Answer 187

Obtain ECG within 10 minutes from the time a patient reports pain or arrives in ED. Through ECG and lab tests (serial cardiac biomarkers) to clarify whether the patient has

Answer 188

Unstable angina: no ST elevation, no abnormal biomarkers NSTEMI: no ST elevation, with elevated cardiac biomarkers STEMI: ST elevation and elevated cardiac biomarkers

Answer 189

CK-MB: for heart muscle Troponin I and T: Only in myocardium Myoglobin

Answer 190

Indicates an acute MI Increased within a few hours peaks in 24-48 hr

Answer 191

Indicates a recent MI elevated within a few hours during acute MI remains elevated for as long as 2 weeks

Answer 192

Peaks within 12 hours An increase in myoglobin is not very specific in indicating an acute cardiac event; however, negative results used to rule out an acute MI

Answer 193

Managing myocardial oxygen supply with demand minimize myocardial damage preserve myocardial function prevent complications

Answer 194

MONA Morphine, oxygen (first), nitro, aspirin In ICU/CCU, IV beta-blockers (watch for cardiogenic shock, long-term therapy can decrease future cardiac events)

Answer 195

potent narcotic analgesic and anxiolytic vasodilation and can lower heart rate and systolic blood pressure reducing myocardial oxygen demand

Answer 196

respiratory depression; nausea and vomiting (20% of patients); hypotension

Answer 197

antiplatelet and anticoagulant therapies are important components of ACS patient management because of exposure of a ruptured plaque's contents triggers activation of the coagulation cascade

Answer 198

percutaneous transluminal coronary angioplasty: evaluate coronary artery blood flow and open the occluded coronary artery and promote reperfusion to the area been deprived of oxygen STEMI patients can be taken directly to cath lab for PCI better outcome than thrombolytics with good results in elderly door-to-balloon time: 60 min-90 min

Answer 199

fibrinolytic therapy (IV alteplase [Activase[, reteplase [r-PA], and tenecteplase [TNKase]) Given if not able to do PCI or do PCI on time must be given as early as possible (within 3-6 hours onset of pain) door to needle time--30min given to those with ECG evidence of acute MI (STEMI)

Answer 200

dissolve all clots watch for bleeding must have at least two IV lines minimize the number of times the patient’s skin is punctured

Answer 201

had recent surgery (even minor surgery) or hemorrhagic stroke or prolonged CPR Pregnancy

Answer 202

hypothermia treatment for unconscious adults who experience cardiac arrest (including cardiac arrest due to vfib) and who receive CPR within 10 minutes start within 60 minutes after circulation is restored (ASAP)

Answer 203

electrical complications (very common) embolic complications inflammatory complications ischemic complications

Answer 204

very common bradydysrhythmias (sinus bradycardia most common) tachydysrhythmias AV blocks bundle branch blocks sudden cardiac death

Answer 205

stroke deep vein thrombosis pulmonary embolism

Answer 206

pericarditis

Answer 207

angina reinfarction infarct extension: a myocardial infarction that has spread beyond the original area, usually as a result of the death of cells in the ischemic margin of the infarct zone

Answer 208

BB aspirin Ace inhibitor

Answer 209

Purpose of PTCA: improve blood flow within a coronary artery by compressing the atheroma. Measure of success is an improvement in blood flow and a residual stenosis of less than 30% Used for angina, ACS, and to open blocked CABGs

Answer 210

chest pain and the ECG may display ST-segment changes when the balloon inflated inside of the coronary artery

Answer 211

A metal mesh that provides structural support to a vessel at risk of acute closure. placed to overcome "restenosis" coated with medications to minimize the formation of thrombi or scar tissue within the stent

Answer 212

must be on aspirin and clopidogrel Clopidogrel: up to 1 year following drug-eluting stents

Answer 213

coronary artery dissection, perforation, abrupt closure, or vasospasm acute MI, serious dysrhythmias, cardiac arrest bleeding at the insertion site, retroperitoneal bleeding, hematoma, and arterial occlusion (receive anticoagulant during the procedure) acute kidney injury from the contrast agent

Answer 214

20-30% restenosis after 6 months mortality 0-2%

Answer 215

remain flat in bed and keep the affected leg straight until the sheaths are removed and then for a few hours afterward to maintain hemostasis. Sheath removal and the application of pressure on the vessel insertion site may cause the heart rate to slow and blood pressure to decrease (vasovagal response) The patient is instructed to monitor the site for bleeding or development of a hard mass indicative of hematoma. Bleeding!!! Circulation!!! Immobilization!!!

Answer 216

alleviation of angina that cannot be controlled with medication or PCI treatment for left main coronary artery stenosis or multivessel CAD prevention of and treatment for MI, dysrhythmias, or heart failure treatment for complications from an unsuccessful PCI

Answer 217

women Smaller vessels higher risk of complications

Answer 218

severe triple-vessel CAD ventricular dysfunction diabetes

Answer 219

the bypassed coronary arteries must have more than 70% occlusion (50% if in the left main coronary artery) artery must be patent beyond the area of blockage

Answer 220

Arteries do not develop atherosclerotic changes as quickly and remain patient longer. right and left internal mammary arteries are recommended for CABG radial and gastroepiploic arteries

Answer 221

First: the greater saphenous vein Second: lesser saphenous vein Third: cephalic and basilic veins

Answer 222

edema in the extremity from which the vein was taken edema can diminish over time within 5-10 years, atherosclerotic changes often develop in saphenous vein grafts

Answer 223

many CABG procedures are performed with a combination of venous and arterial grafts internal mammary arteries may not be long enough to use of multiple bypasses

Answer 224

extracorporeal circulation mechanically circulates and oxygenates blood for the body while bypass the heart and lungs allows surgeon to complete the grafting in a motionless, bloodless surgical field

Answer 225

During the procedure, hypothermia is maintained at a temperature of about 28C. Reduce the body’s basal metabolic rate, and decrease the demand for oxygen

Answer 226

standard median sternotomy incision performed with CPB beta-adrenergic blocker used to slow the heart rate myocardial stabilization device to hold the site still less incidence of stroke and complications

Answer 227

graft patency rate is higher and long-term mortality may be lower

Answer 228

Hemorrhage (hypovolemia) dysrhythmias MI

Answer 229

neurologic status cardiac status respiratory status peripheral vascular status renal function fluid and electrolyte pain Maintaining cardiac output

Answer 230

Impaired cerebral perfusion hypoperfusion or microemboli during or following cardiac surgery may produce injury to the brain brain function depends on a continuous supply of oxygenated blood the brain does not have the capacity to store oxygen and must rely on adequate continuous perfusion by the heart

Answer 231

Renal function is related to cardiac output. Urine output of less than 1ml/kg/h may indicate a decrease in cardiac output or inadequate fluid volume

Answer 232

chest tube should have less than 200 mL/h drainage during first 4-6 hours

Answer 233

transient perceptual illusions visual and auditory hallucinations disorientation paranoid delusions

Answer 234

long periods of extracorporeal circulation, arterial hypotension during surgery, emboli, and low postoperative cardiac output. Age, and the type and severity of heart impairment are also factors. Delirium is fostered by sensory overload (or deprivation) in the recovery room and intensive care unit, and by staff tension. delirium resolves after the pt is transferred from the unit

Answer 235

Direct pressure monitoring system

Answer 236

IV solution (may include heparin or only NS) tubing stopcocks flush device: provides continuous and manual flushing

Answer 237

maintained at 300 mmHg of pressure must have fluid in the tubing to transduce pressure Pressure bag should ensure the system to deliver 3-5 ml of solution per hour to prevent clotting and backflow of blood into the pressure monitoring system

Answer 238

to convert the pressure coming from the artery or heart chamber into an electrical signal

Answer 239

increases the size of the electrical signal for display on an oscilloscope.

Answer 240

keep the pressure monitoring system patent and free of air bubbles the stopcock of the transducer must position at the level of the atrium (4th intercostal space): phlebostatic axis. make sure to establish the zero reference point for it to function at atmosphere pressure

Answer 241

Pneumothorax during the insertion The longer the the system in place, the higher chance of infection Air embolic can be introduced into the vascular system if the stopcocks are mishandled

Answer 242

intra-arterial blood pressure monitoring (radial artery) pressure should be compared with cuff pressure 2-3 times per day

Answer 243

real time blood pressure ABG drawing

Answer 244

Patients with diabetes, peripheral vascular disease, hypotension, IV vasopressors, or previous surgery

Answer 245

Assess the perfusion of the hand (Allen test) Circulation can also be assessed by the Doppler ultrasonography, and others.

Answer 246

a measurement of the pressure in the vena cava or right atrium Most valuable when it is monitored over time and correlated with the patient’s clinical status. Preferred site for insertion: subclavian vein

Answer 247

indicates an elevated right ventricular preload (hypervolemia or right rided HF

Answer 248

hypovolemia (dehydration, blood loss, vomiting or diarrhea, and overdiuresis)

Answer 249

Pulmonary artery pressure monitoring Assessing left ventricular function balloon-tipped, flow-directed catheters a syringe connected to the hub and can only inflate or deflate the balloon with a capacity of 1.5ml evaluates left ventricular filling pressures measured by blocking the blood flow through pulmonary artery After measuring the wedge pressure, the balloon must be deflated: may cause pulmonary artery infarction

Answer 250

Pressures: right atrial pulmonary artery systolic pulmonary artery diastolic mean pulmonary artery pulmonary artery wedge

Answer 251

Catheter site care is essentially the same for a CVP catheter Monitor for complications

Answer 252

Pulmonary artery rupture Pulmonary thromboembolism Pulmonary infarction Catheter kinking Dysrhythmias Air embolism

Answer 253

Pulse pressure analysis Esophageal doppler probes Fick principle

Answer 254

uses an arterial pressure waveform to continuously estimate the patient’s stroke volume. Limited to those with good waveform

Answer 255

estimates CO

Answer 256

uses carbon dioxide measures for sedated, intubated, on mechanical ventilation patients

Answer 257

a localized sac or dilation formed at a weak point in the wall of the artery. Most common forms of aneurysms: -saccular aneurysm -fusiform aneurysm Most common type of degenerative aneurysm: Abdominal aortic aneurysm (AAA)

Answer 258

85% of all cases of thoracic aortic aneurysm caused by atherosclerosis men age 50-70 thoracic are: the most common site for a dissecting aneurysm (separation of the wall of the vessel) 1/3 of patients with thoracic aneurysms die of rupture of the aneurysm

Answer 259

Most prominent symptom: pain Dyspnea Couth, frequently paroxysmal and with a brassy quality Hoarseness, stridor, or weakness or complete loss of voice Dysphasia

Answer 260

unequal pupils (cervical sympathetic chain pressed) dx made by chest x-ray, CT-angiogram, TEE

Answer 261

control blood pressure: systolic pressure maintained at 90-120 mmHg. BB, hydralazine, nipride

Answer 262

continuous IV drip to emergently lower the blood pressure advantages: rapid onset and short action of duration, and easy to titrate

Answer 263

vascular graft open surgical repair or percutaneously

Answer 264

maintain the cerebrospinal fluid pressure less than or equal to 10mmHg and to keep the mean arterial pressure greater than 90 mmHg for the first 36-48 hours postoperatively to prevent neurologic deficit

Answer 265

surgery right away!!

Answer 266

Most common type of degenerative aneurysm Most common cause is atherosclerosis Common in caucasians Affects men > women Most prevalent in elderly Mostly below renal arteries (infrarenal)

Answer 267

A damaged media layer of the vessel Caused by congenital weakness, trauma, or disease

Answer 268

Genetic predisposition Tobacco use HTN

Answer 269

Only 40% of pts have symptoms Feeling heartbeat in abdomen when laying down May feel abdominal mass or throbbing Thrombus may occlude a major vessel

Answer 270

Pulsatile mass in the middle and upper abdomen Do NOT perform deep palpitation of the abdomen (80% can be palpitated) Systolic bruit may be heard over the mass Duplex ultrasound or CT angiogram is used to determine the size, length, and location of the aneurysm Rupture is likely with coexisting HTN and with aneurysms more than 6cm wide

Answer 271

Ultrasound q6 months Control BP (esp diastolic, high risk of rupture if >100 mmHg) AntiHTN meds

Answer 272

Aneurysm is not repaired until it is at least 5.5cm wide Open repair of aneurysm by resecting the vessel and sewing a bypass graft into place Alternative for treating an infrarenal AAA is endovascular grafting -Transluminal placement and attachment of a sutureless aortic graft prosthesis across an aneurysm

Answer 273

Severe back or abdominal pain (may be persistent or intermittent) Localized in the middle or lower abdomen, left of the midline Constant, intense back pain, falling BP, and decreasing hematocrit Rupture into peritoneal cavity is FATAL

Answer 274

Severe back or abdominal pain (may be persistent or intermittent) Localized in the middle or lower abdomen, left of the midline Constant, intense back pain, falling BP, and decreasing hematocrit Rupture into peritoneal cavity is FATAL

Exam 2 Flashcards

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