Cardiac Class Lectures

Front 1

Structure of the Heart

Back 1

-4 chambered hollow muscular organ

Front 2

What is the average size of the heart?

Back 2

-Size of your fist. 5 inches by 3.5 inches

Front 3

What is the PMI (Point of Maximal Impulse)?

Back 3

-Point of Maximum impulse—pulsation arising at the apex of the heart.
-Tip of the left ventricle.

Front 4

What are the 4 chambers of the heart?

Back 4

-4 Chambers: separated by septum
-2 chambers on right (right ventricle & right atrium)
-2 chambers on left (left atrium & left ventricle)

Front 5

What are the layers of the heart?

Back 5

-Endocardium
-Myocardium
-Epicardium
-Surrounded by Pericardial Sac

Front 6

Epicardium

Back 6

-outer surface of the heart -contains the coronary arteries
-visceral layer of the pericardium.

Front 7

Myocardium

Back 7

-actual muscle
-conductive system

Front 8

Endocardium

Back 8

-inner lining of heart
-chambers and valves

Front 9

Pericardium

Back 9

-sac surrounds heart
-composed of visceral and parietal layer

Front 10

Pericardial space

Back 10

-small amount of fluid in space acts as a lubricant—there is friction caused by movement of layers with each contraction
-contains 50cc of serous fluid.

Front 11

What is different about the Left Ventricle?

Back 11

-Left ventricle is thicker due to the force/resistance it must overcome to pump blood into the systemic circulation (afterload).

Front 12

What do valves prevent?

Back 12

-Valves prevent the backflow of blood.

Front 13

What are the two Atrioventricular (AV) valves?

Back 13

-Tricuspid valve, Mitral valve – First heart sound S1.
-Tricuspid and mitral (Atrioventricluar) prevent back flow of blood into the atria during contraction

Front 14

What are the two Semilunar valves?

Back 14

-Aortic, pulmonic – Second heart sound S2.
-pulmonic and aortic (semilunar) prevent regurgitation into ventricles at end of each ventricular contraction

Front 15

What is the Chordae Tendeneae?

Back 15

-attach to the cusps of the mitral and tricuspid valves.
-They are anchored in the Papillary muscles of the ventricles.
-Prevent eversion of the valve leaflets during ventricular contraction.

Front 16

What does the Right Coronary Artery do?

Back 16

-Supplies blood to the right anterior surface of the heart and part of the posterior LV. (IWMI, PWMI)
-90% of people AV node.

Front 17

What does the Left Main Coronary Artery do?

Back 17

-branches into the left circumflex (supplies the posterior and lateral LA/LV - LWMI)

Front 18

What does the Left Anterior Descending Coronary Artery do?

Back 18

-supplies the anterior heart to apex – AWMI

Front 19

Where are the Coronary Veins?

Back 19

-dump into the coronary sinus which drains directly into the right atrium.

Front 20

What is ischemia?

Back 20

-Deficiency of blood due to constriction or obstruction of a blood vessel.
-Results in tissue hypoxia which reduces the mechanical & electrical activity of the heart

Front 21

Is ischemia reversible?

Back 21

-May be reversible, depending on length of time ischemia occurs and the extent of muscle involved.

Front 22

What is an infarction?

Back 22

-Permanent loss of blood flow to myocardium-results in cell death, overall effect depends on the size of area deprived of O2.---alternate routes are developed in time to nourish the endangered myocardium, collateral blood supply.

Front 23

What can cause an infarction?

Back 23

-emboli
-atherosclerotic plaque buildup in the arterial blood supply.

Front 24

What are Specialized Nerve Tissues responsible for?

Back 24

-Conduction system is composed of specialized nerve tissue responsible for creating and transporting the electrical impulse, or action potential.
-Cardiac cells have the ability to transmit electrical impulses.

Front 25

What is Depolarization?

Back 25

-Rapid influx of sodium & calcium ions into the cell & outflux of potassium ions—shift in electrolytes.
-Causes muscle fibers to shorten and contract.
-Electrical activity is synchronous with mechanical activity.
-Cells become positive inside.

Front 26

What is Repolarization?

Back 26

-electrical recovery
-resting phase
-potassium moves back in, sodium & calcium return to extracellular space.
-Cell returns to negative state.

Front 27

SA node

Back 27

-Intrinsic pacemaker
-It is the pacemaker of the heart, it creates an electrical impulse, right atria near entrance of superior vena cava.
-Intrinsic rate of 60-100.
-Internodal pathways to reach the left atrium.

Front 28

AV node

Back 28

-Conducts impluse to Bundle Branches
-AV node – rate of 40-60.

Front 29

Bundle Branches

Back 29

-Conduct impulse to Purkinje fibers which trigger a uniform ventricular contraction.

Front 30

ECG

Back 30

-Electrical activity of the heart detected on one’s body surface ---recorded—and yes ECG and EKG are the same terms

Front 31

P wave

Back 31

-depolarization of fibers in atria—lasts .06-.12 seconds

Front 32

PR Interval

Back 32

-.12-.20 sec Conduction through A-V node.

Front 33

The QRS

Back 33

-.04-.10 seconds, ventricular contraction

Front 34

T wave

Back 34

-ventricular repolarization

Front 35

U wave

Back 35

-if seen, not normally seen
-delayed ventricular repolarization
-may be associated with hypokalemia, Digoxin toxicity.

Front 36

Info about ECG Tracing

Back 36

-Measured horizontally – time in seconds.
-Each small square .04 sec.
-Measured vertically – amplitude or voltage, measured in mm.
-Each small square is 1mm amp.
-3 seconds hash marks.

Front 37

What is the significance of a prolonged PR interval?

Back 37

AV node problem

Front 38

What is the significance of a prolonged QRS interval?

Back 38

Ventricular conduction delay or defect

Front 39

What are the clinical consequences of SA node dysfunction?

Back 39

Cardiac arrest

Front 40

To Calculate Heart Rate:

Back 40

Count the number of "R" waves in 6 seconds (6 large blocks X's 10 = 1 min rate)

Front 41

What is cardiac output?

Back 41

HR X SV
Total amount of blood pumped by each ventricle in 1 minute. Normal adult at rest is 4L to 8L.

Front 42

amount of blood ejected from the ventricle with each heartbeat

Back 42

approx. 70cc

Front 43

What is Stroke Volume determine by?

Back 43

preload, contractility and afterload.

Front 44

What is preload?

Back 44

Volume of blood in ventricles at end of diastole before next contraction—it determines the amount of stretch placed on myocardial fibers

Front 45

What is contractility?

Back 45

Contractility of the heart refers to the ability of the heart to depolarize, the force of contraction. It is affected by the autonomic nervous system.

Front 46

What is afterload?

Back 46

Peripheral resistance which Left ventricle must pump against---affected by size of ventricle, wall tension, and arterial blood pressure.

Front 47

What is Starling’s Law?

Back 47

Up to a point the more myocardial fibers are stretched the greater the force of contraction

Front 48

What can cause an increase in Preload?

Back 48

Hypervolemia, Regurgitation of cardiac valve

Front 49

What can cause an increase in Afterload?

Back 49

Hypertension, Vasoconstriction

Front 50

Autonomic Regulation of the Cardiovascular System

Back 50

-Barorecptors in aortic arch and carotids responsive to stretch
-Chemoreceptors in aortic arch and carotids responsive to pH, PO2 and PCo2
-Information conveyed to vasomotor center in brainstem

Front 51

What do Baroreceptors respond to?

Back 51

Stretch

Front 52

What do Chemoreceptors respond to?

Back 52

pH, PO2 and PCo2

Front 53

Sympathetic Stimulation

Back 53

-Release of Epinephrine and Norepinephrine
-Epi and NE stimulate β-1 Receptors
-NE stimulates α-1 receptors
-Increases Heart rate, conduction, contractility, and peripheral vasoconstriction.

Front 54

Parasympathetic Stimulation

Back 54

-Mediated by Vagus Nerve
-Slows Heart Rate, Contractility and Conduction.
-No Effect on periphery

Front 55

What are the 3 major types of blood vessels?

Back 55

Arteries, capillaries, & veins

Front 56

Carries blood away from heart (O2)?

Back 56

Arteries—carries O2 blood except for pulmonary artery—thick walls & elastic tissue, high pressure--major control of arterial BP

Front 57

Carries blood toward heart (no O2)?

Back 57

Veins—carry no O2 blood except for pulmonary veins—return blood to right atrium—thin walled and large in diameter vessels—low pressure, high volume

Front 58

Exchanges cellular nutrients & metabolic end products?

Back 58

Capillaries—endothelial cells-no elastic or muscle tissue—thin walled vessels

Front 59

What is the difference between the arterial system and the venous system?

Back 59

The arterial system differs from the venous system in that it has thick walls composed mainly of elastic tissue. It cushions the impact of the pressure created by ventricular contraction and provides recoil to propel blood forward into the circulation.

Front 60

What is the difference between arteries and veins?

Back 60

Arterioles control blood pressure and respond by dilating or constricting.
Veins are thin-walled. Contain semi-lunar valves to maintain blood flow back to the heart.

Front 61

DIAGNOSTIC STUDIES OF HEART

Back 61

-CXR
-ECG
-Holter Monitor/ Event Monitor
-Echocardiogram (2-D or Transesophageal)
-Exercise Stress Test
-Stress Echo
-Nuclear Stress Test

Front 62

HOLTER MONITOR

Back 62

Patient keeps monitor on for 24-48 hours and must keep a log of activities at all times—information is stored in holter monitor and printed out at a later time

Front 63

STRESS TEST

Back 63

Stress testing: patient walks on treadmill or stationary bicycle—leads are placed on chest and watch BP, and O2 level—stop test if peak HR, peak exercise tolerance, chest pain, significant ST segment depression (indicates ischemia). Helps diagnose left ventricular function.

Front 64

What are the different types of Cardiac Enzymes?

Back 64

CK-MB & Troponin

Front 65

What is the importance of Cardiac Enzymes?

Back 65

-Indicate damage to myocardial cells.
-Markers of MI

Front 66

CK-MB

Back 66

-> 5% of total
-Rise in 3-12 hours
-Peak in 24 hours
-Return to baseline in 48-72 hours

Front 67

Troponin

Back 67

-Troponin T < 0.1 ng/ml is normal.
-Troponin I < 0.4 ng/ml is normal.
-Elevate within 3 hours
-Peak in 24-48 hours
-Return to baseline in 5-14 days

Front 68

Cardiac Catheterization

Back 68

-Invasive Exam of Heart +/- -Coronary Vessels
-Catheter Threaded through -Femoral Artery or Vein
-Contrast Dye injected and -X-rays taken.
-Looks at valve function, ventricular function and presence of CAD
-Vein for right cath. Artery for left cath
-Assess patient for allergy to Iodine, Shellfish or contrast Dyes. Dye injection causes flushing sensation.
-Patient can be sedated but awake.

Front 69

Potential Complications of Cardiac Catheterization?

Back 69

MI, Embolus, Ventricular Puncture, Bleeding, Hematoma, Allergic Reaction, Arrhythmias, Death.

Front 70

Nursing Considerations - Cardiac Catheterization

Back 70

-Informed Consent
-NPO 6-12 hours prior.
-Assess Allergy History
-Post-Procedure must keep leg straight for 6 hours.
-Monitor V/S, peripheral pulses, puncture site.

Front 71

Electrophysiology Study(EPS)

Back 71

-Invasive study to diagnose, induce and treat arrhythmias.
-Catheter inserted to right side of heart via femoral vein.
-Electrodes detect site of arrhythmia.
-Can ablate aberrant conduction pathways.
-Requires informed consent, -NPO 6-8 hours prior.

Front 72

Cardiovascular Effects of Aging

Back 72

-High rates of atherosclerosis
-Increased incidence of Hypertension.
-Increased rates of Valvular Calcification
-Decreased Heart Rate response to Exercise.
-Decreased Baroreceptor Function.
-Difficult to differentiate normal aging from disease.
-Decreased CV reserve.
-Increased risk of orthostatic hypotension

Front 73

Modifiable Cardiovascular Risk Factors

Back 73

Hypertension
Hyperlipidemia
Diabetes
Smoking
Excessive ETOH
Obesity
Sedentary Lifestyle

Front 74

Not modifiable Cardiovascular Risk Factors

Back 74

Family History
Age
Race
Sex

Front 75

Cardiovascular Assessment History
Past Medical History

Back 75

Any heart disease, MI, Angina, Cardiac testing, Arrhythmias, Valve Disease, Rheumatic Fever, Diabetes, HTN, Meds

Front 76

Cardiovascular Assessment History
Past Surgical History

Back 76

Any PTCA, CABG, Valve replacement etc.

Front 77

Cardiovascular Assessment History
Family History

Back 77

Any relatives with CV disease age at onset, death

Front 78

Cardiovascular Assessment History
Social History

Back 78

Smoking, Alcohol, Drug use, Diet, Exercise

Front 79

Cardiovascular Assessment History
Review of Systems

Back 79

Fatigue, Chest Pain, Syncope, Dyspnea, Palpitations, Claudication, Edema, PND, Orthopnea

Front 80

Cardiovascular Assessment Physical Exam
Vital Signs

Back 80

BP, Pulse, Resp, O2 sat

Front 81

Cardiovascular Assessment Physical Exam
Neck

Back 81

JVD, Carotids palpation and auscultation for bruits

Front 82

Cardiovascular Assessment Physical Exam
Precordium

Back 82

PMI, heaves, lifts, thrills

Front 83

Cardiovascular Assessment Physical Exam
Auscultation of Heart

Back 83

S1 S2 rate rhythm, murmurs, rubs, gallops

Front 84

Cardiovascular Assessment Physical Exam
Abdominal Vessels

Back 84

AAA or bruits

Front 85

Cardiovascular Assessment Physical Exam
Assessment of Periphery

Back 85

Peripheral Pulses, Cap refill, Color, temperature, Edema

Front 86

What is BP?

Back 86

-Force exerted by blood against artery wall during ventricular contraction (systolic) and ventricular relaxation (diastolic) must be adequate to maintain tissue perfusion during activity and rest.
-Cardiac Output X Systemic Vascular Resistance

Front 87

What regulates BP?

Back 87

SNS (sympathetic nervous system), cardiovascular system, renal and endocrine systems.

Front 88

How is BP measured?

Back 88

Non-invasive via syphygnomanometer and stethoscope, or electronically dynamap. Invasively by arterial line.

Front 89

How do we ensure accurate measurement?

Back 89

Re-check questionable readings, check dynamapps, correct size cuff, arm supported, release valve at steady even pace, beware of ausculatory gap.

Front 90

How Does the body recognize changes in blood pressure?

Back 90

-Baroreceptors
-Transmitted to Vasomotor Center in the Brainstem

Front 91

BARORECEPTORS & BP

Back 91

-Baroreceptors: carotid arteries and the aortic arch.
-If B/P rises, inhibitory messages are sent to medulla to inhibit SNS activity. As a result, the parasympathetic (vagus nerve) assumes control and decreases HR, vasodilation occurs in arterioles.
-When B/P drops, SNS is activated by the release of epi and nor epi, HR increases, vasoconstriction occurs.
-Play an important role in the maintenance of B/P stability. In the presence of long standing hypertension, the baroreceptors become adjusted to elevated levels of B/P and recognize the level as “normal.”

Front 92

SNS & BP

Back 92

-SNS releases epi and norepi at terminal nerve endings.
-Specialized receptors are stimulated in the SA node, myocardium, and vascular smooth muscle. These receptors are classified as:
-Alpha 1 & 2 and Beta 1 & 2 receptors
-Adrenergic: activated by epi, norepi, or secreting epinephrine. Sympathomimetic (an agent that produces effects similar to the SNS.
-Alpha-adrenergic receptors located in vasculature cause vasoconstriction when stimulated by NE.
-Beta-adrenergic receptors located in vasculature cause vasodilation.
-Alpha receptors in the heart respond by increasing contractility (inotropic effects).
-Beta-adrenergic receptors located in the heart respond to NE with increased heart rate (chronotropic) and increased force of contraction (inotropic).

Front 93

Renal System and BP

Back 93

-Response to sympathetic stimulation, decreased blood flow to kidneys, decreased serum NA concentration. Renin-enzyme excreted by the kidney, converts aniogtensinogen to angiotensin I to angiotensin II which increases BP—potent vasoconstrictor.
-A II stimulates the adrenal gland to secrete aldosterone which causes NA+ and water retention by the kidneys, resulting in increased blood volume & increased CO.
-Prostaglandins (fatty acids): vasodilator effect on systemic circulation—decrease SVR & decrease BP

Front 94

What is hypertension?

Back 94

Sustained elevation of BP—systolic is > or = 140 mmHg and diastolic is > or = to 90 mmHg for extended periods of time—diagnosis based on 3 occasions of elevation within a several week period.

Front 95

What effects does hypertension have on the body?

Back 95

HBP means the heart is working harder than normal—both heart and blood vessels under strain. Endothelial damage.

Front 96

What are hypertensive patients at risk for?

Back 96

MI, CHF, CVA, Renal Failure, PVD, Retinal damage.

Front 97

What are the symptoms?

Back 97

People often do not seek treatment. Symptoms may not occur until there is damage to target organs.

Front 98

How prevalent is hypertension?

Back 98

65 million in US 1/3 of adults

Front 99

Who is at risk?

Back 99

Increased age, African-Americans, more prevalent in men than women—women after the age of 55—equal in men and women from 55-75 years of age and after 75 years of age more prevalent in women.

Front 100

Primary (essential) HTN

Back 100

Elevated BP without an identified cause. Accounts for 90-95% of all cases of Htn.

Front 101

What can be considered a contributing factor of Primary HTN?

Back 101

Increased SNS activity (stres, illness), increased NA+ intake, high renin activity, obesity/overweight, high insulin concentration in bloodstream (stimulates SNS activity).

Front 102

Secondary HTN

Back 102

Elevated BP with specific underlying cause—identify it and correct it. Main cause of Htn in children (80%).

Front 103

What are the causes of Secondary HTN?

Back 103

Causes: Hypokalemia, narrowing of the aorta, tachycardia, renal disease, Meds (NSAID’s), Neurologic disorders (brain tumors), endocrine disorders (Hyperaldosteronism), Obstructive Sleep Apnea.

Front 104

What causes the types of hypertension?

Back 104

Strongly familial, BP increases as we age due to loss of tissue elasticity, decrease in renal function, increase in peripheral vascular resistance.

Front 105

Clinical Manifestations of HTN

Back 105

May be asymptomatic, also known as “silent killer”, until it causes damage to target organs, secondary symptoms: fatigue, decrease in activity, dizziness, palpitations, angina, and dyspnea, HA

Front 106

Complications of HTN: Target organ diseases - CAD

Back 106

Htn is major risk factor, exact mechanism unknown, thought to be caused by a disruption of coronary artery endothelium due to high pressures.

Front 107

Complications of HTN: Target organ diseases - Left Ventricular Hypertrophy

Back 107

sustained high pressures increase cardiac workload. Adaptive mechanism to increase CO by increasing contraction. Heart failure occurs when the heart can no longer compensate for the increased pressures and demand to supply oxygen (enlarged heart on X-ray, SOB on exertion, fatigue, ECG changes-wide QRS, inverted T wave).

Front 108

Complications of HTN: Target organ diseases - CVD

Back 108

Atherosclerosis is the most common cause of CVD. Risk for stroke is 4 times higher in people with Htn. If atherosclerotic plaque forms in the carotid arteries, portions may break off and travel to the brain producing TIA’s or a stroke. Hypertensive encephalopathy may occur after prolonged Htn. When blood pressure remains high, the cerebral blood vessels dilate producing edema and marked loss of consciousness. Death may occur from brain damage.

Front 109

Complications of HTN: Target organ diseases - PVD

Back 109

Htn speeds up the process of atherosclerosis in the peripheral blood vessels. Classic symptom: Intermittent claudication (ischemic muscle pain caused by activity, relieved with rest).

Front 110

Complications of HTN: Target organ diseases - Nephrosclerosis

Back 110

Htn is the leading cause of end-stage renal disease. Direct result of ischemia caused by the narrowed lumen of intrarenal blood vessels. Leads to atrophy of the tubules, destruction of the glomeruli, and eventual death of the nephron itself. Lab tests to confirm are: BUN, creatinine, proteinuria, albuminuria, hematuria. Nocturia is the earliest sign of renal dysfunction.

Front 111

Complications of HTN: Target organ diseases - Retinal damage

Back 111

The retina is the only place in the body where blood vessels can be directly visualized. Include blurring of vision, retinal hemorrhages, loss of vision. Damage to the retina gives an indication of cardiac vessel damage.

Front 112

Diagnostic Studies for HTN

Back 112

Manual BP
BUN
Creatinine
Urinalysis
Electrolytes
Blood Glucose
Cholesterol
ECG
Echo
Sleep Study

Front 113

Evidence Based Care of HypertensionJNC-VII

Back 113

Important to control isolated systolic HTN.
Thiazide Diuretics are first line for most patients.
Adequate control may require drug combinations.

Front 114

Classification of Hypertension

Back 114

Normal: SBP < 120 DBP < 80
-Encourage healthy lifestyle
Prehypertension: SBP 120-139 DBP 80-89
-Strongly pursue lifestyle modification
Stage 1 HTN: SBP 140-159 or DBP 90-99
-Initiate drug therapy Thiazide preferred
Stage 2 HTN: SBP >160 or DBP > 100
-Initiate two drug combination

Front 115

AHA 2007 Recommendations - Target BP < 130/80 For:

Back 115

Diabetics, CAD, CKD, Carotid Disease, PAD

Front 116

AHA 2007 Recommendations - Target BP < 120/80 For:

Back 116

Heart Failure

Front 117

AHA 2007 Recommendations - First Line Agents for HTN:

Back 117

Thiazides, ACE, ARB, CCB

Front 118

AHA 2007 Recommendations - Beta Blockers for:

Back 118

CHF, Angina, Post MI

Front 119

Lifestyle Modifications for HTN

Back 119

Dietary Changes - DASH diet
Limit alcohol consumption
Regular physical activity
Avoid tobacco use
Stress management

Front 120

Teaching Low Sodium Diet

Back 120

Ideal 2 grams or less per day.
Read labels.
Do not cook with salt.
Avoid using salt shaker.
Try using different spices.
Limit processed, pickled or cured foods.
Be cautious with canned soups, vegetables.
Avoid fast food and salty snacks.

Front 121

First-line Therapy for HTN - Diuretics

Back 121

rid excess water and sodium

Front 122

First-line Therapy for HTN - Angiotensin inhibitors

Back 122

Two types of angiotensin inhibitors:
-Angiotensin converting enzyme inhibitor – prevents the conversion of angiotensin I to II thus reducing the resultant vasoconstriction.
-A-II receptor blockers (ARB’s)- prevents angiotensin II from binding to receptors in the walls of blood vessels.

Front 123

First-line Therapy for HTN - Ca channel blockers

Back 123

increase sodium excretion and cause arteriolar vasodilation by preventing the movement of extracellular Calcium into the cells.

Front 124

First-line Therapy for HTN - Beta Blockers for certain indications

Back 124

Beta-adrenergic receptors located in the heart respond to NE with increased heart rate (chronotropic) and increased force of contraction (inotropic).

Front 125

What is drug choice for HTN influenced by?

Back 125

cost, presence of other medical conditions, and side effects

Front 126

What effects do Diuretics have on preload, contractility and afterload?

Back 126

decreases preload

Front 127

What effects do Beta Blockers have on preload, contractility and afterload?

Back 127

decrease afterload and contractility

Front 128

What effects do Calcium Channel Blockers have on preload, contractility and afterload?

Back 128

decrease contractility

Front 129

What effects do ACE inhibitors have on preload, contractility and afterload?

Back 129

decrease preload and afterload

Front 130

Nursing Considerations of HTN Drug Therapy

Back 130

Always monitor BP and pulse prior to administration.
Beware of orthostatic hypotension.

Front 131

Nursing Considerations of Drug Therapy - Diuretics

Back 131

monitor fluid and lytes.

Front 132

Nursing Considerations of Drug Therapy - Beta Blocker

Back 132

monitor for bradycardia, bronchospasm, masks hypoglycemia.

Front 133

Nursing Considerations of Drug Therapy - Calcium Channel Blockers

Back 133

monitor for headache, edema, CHF

Front 134

Nursing Considerations of Drug Therapy - ACEI

Back 134

monitor for cough, angioedema. Monitor renal function and K+

Front 135

Nursing Considerations of Drug Therapy - ARB

Back 135

monitor for renal function and K+

Front 136

Causes of Lack of Responsiveness to HTN Therapy

Back 136

Nonadherence to therapy
Drug related causes
Secondary hypertension
Pseudohypertension

Front 137

Reasons for Non-Adherence to HTN Therapy

Back 137

Cost.
Side Effects: sexual dysfunction, fatigue, frequent urination.
Knowledge Deficit.
Lack of Symptoms.
Ask the Questions.

Front 138

Hypertensive Crisis

Back 138

Severe abrupt elevation in BP
Diastolic > than 140 mm Hg

Front 139

What is the etiology of HTN Crisis?

Back 139

non-compliance, drug side effect, rapid withdrawal of antihypertensives (Beta Blockers or Clonidine), ecclampsia, street drugs such as cocaine, amphetemines, PCP, LSD.

Front 140

Hypertensive Emergency vs. Urgency

Back 140

Emergency: Evidence of evolving organ damage

Front 141

Mean Arterial Presssure (MAP) =

Back 141

SBP + 2(DBP)/ 3

Front 142

Hypertensive Emergency
Target Organ Damage

Back 142

MI
Angina
TIA/CVA
Encephalopathy
Renal Failure
Aortic Dissection

Front 143

Hypertensive Encephalopathy
What are the symptoms?

Back 143

HA, N/V, seizures, confusion, coma

Front 144

Hypertensive Encephalopathy
What is the pathophysiology?

Back 144

Changes in capillary permeability
Cerebral edema

Front 145

Hypertensive Emergency
Nursing Care

Back 145

-Admit to ICU.
-Continuous Monitoring.
-IV Nitroprusside,
-Alternative Cleviprex (IV Ca Channel Blocker)
-Gradually reduce MAP
(25% in one hour; 160/100-110 within 2-6 hours)
-Monitor for signs of target organ damage.
-Patient education when crisis resolved.

Front 146

Hypertensive Emergency
Nursing Care
Continuous Monitoring

Back 146

A-line, Telemetry, CVP monitor etc.

Front 147

Hypertensive Emergency
Nursing Care
Nitropursside

Back 147

potent vasodilator. Decreases preload and afterload. Adminster on pump. Titrate to BP. Light resistant bag. Monitor thiocyanate levels if used > 24-48 hours.

Front 148

Hypertensive Emergency
Nursing Care
Gradually reduce MAP

Back 148

reduce 10-20 % in 1-2 hours. Too rapid can precipitate CVA.

Front 149

Hypertensive Emergency
Nursing Care
Target Organ Damage

Back 149

Frequent neuro exams, EKG, cardiac enzymes, urine output, BUN, creatinine, CHF.

Front 150

Hypertensive Urgency

Back 150

-Treated inpatient, ED or outpatient. - Monitor response to treatment and can go home if stabilizes. Requires follow-up within 24 hours.
-Can be given oral drugs - Clonidine or Captopril drugs of choice.

Front 151

What questions should you ask the patient to determine the etiology of a hypertensive crisis?

Back 151

If they stopped taking their medication, illicit drug use, taken other medications (OTC)

Front 152

HTN Nursing Care

Back 152

Daily weight
I & O
Urine output
Response of BP
Electrolytes
Take Pulses
Ischemic Episodes (TIA)
Complications: 4 C's (CAD, CRF, CFH, CVA)

Front 153

CAD Facts - Definition

Back 153

Narrowing of coronary vessels with atherosclerotic plaques. Synonymous terms are: ASHD, CVHD, IHD, CHD, CAD. Compromises blood flow to myocardium.

Front 154

CAD Facts

Back 154

Major cause of death in US - Heart attacks are the leading cause of all cardiovascular deaths and deaths in general. CV disease is now the #1 cause of death in women, breast cancer is #2. More women now die from CV disease than men.
Asymptomatic - Normally asymptomatic until the disease process is well advanced

Front 155

Pathophysiology of CAD

Back 155

-Endothelial injury
-Lipid deposits.
-Lipids calcify over time
-Platelets release growth factors/ smooth muscle proliferation
-Platelets, thrombin, and fibrin formation
-Thrombus
-Unstable plaque
-Collateral circulation

Front 156

Pathophysiology of CAD
Endothelial injury

Back 156

Endothelial injury predisposes to lipid deposits and platelet activation

Front 157

Pathophysiology of CAD
Lipid deposits.
Lipids calcify over time

Back 157

Fatty streaks: the earliest lesions of atherosclerosis: streaks of fat develop in the smooth muscle cells of the blood vessel—turn yellow. Observed by age 15 and increase with age. Believed to be reversible.

Front 158

Pathophysiology of CAD
Platelets release growth factors/ smooth muscle proliferation

Back 158

Platelets release growth factors cause smooth muscle proliferation which further traps lipids.

Front 159

Pathophysiology of CAD
Platelets, thrombin, and fibrin formation

Back 159

Raised fibrous plaque. Beginning of progressive changes in the arterial wall. Observed by age 30 and increase with age. Initiated by elevated BP, high cholesterol, heredity, carbon monoxide damage due to smoking, immune reactions. In the person with CAD, the endothelium is not rapidly replaced, lipids adhere to damaged blood vessel wall and gradually increases in size. Calcify over time. Platelets accumulate at the site in large numbers which lead to thrombus formation.

Front 160

Pathophysiology of CAD
Thrombus

Back 160

Complicated lesion stage—plaque consists of core of lipid materials (mainly cholesterol)---continues to grow in size as more lipids and platelets adhere. Lesion hardens causing more damage to arterial wall and may eventually produce narrowing or total occlusion of the artery.

Front 161

Pathophysiology of CAD
Unstable plaque

Back 161

Plaque ruptures and can precipitate MI

Front 162

Pathophysiology of CAD
Collateral circulation

Back 162

Attributes to two factors: Arterial branching due to chronic ischemia or inherited predisposition to develop new blood vessels—when occlusion of artery happens slowly over a period of time there is a greater chance of collateral circulation developing and myocardium receiving the adequate amount of O2—if it is rapid there is not a chance for collateral circulation to develop—myocardium does not get ample amount of O2 which results in severe ischemia or infarction.

Front 163

Unmodifiable RISK FACTORS FOR CAD

Back 163

Age
Gender
Ethnicity
Genetic inheritance

Front 164

Modifiable RISK FACTORS FOR CAD

Back 164

-Elevated serum cholesterol (>200mg/dl)
-Hypertension
-Smoking (6 Xs higher & proportional to the number of cigarettes smoked)
-Physical inactivity
-Obesity (heart grows in size, causes increased myocardial oxygen consumption)
-Diabetes
-hs-CRP > 2 mg/L (indicative of inflammation)

Front 165

Serum Lipids
Total Cholesterol

Back 165

Least important. Ideal less than 200

Front 166

Serum Lipids
Low Density Lipoprotein (LDL)

Back 166

“bad” cholesterol. Deposits cholesterol in artery walls Ideal less than 130

Front 167

Serum Lipids
High Density Lipoprotein (HDL)

Back 167

“good” cholesterol cleans up cholesterol from arteries. Average risk greater than 45. negative risk factor > 60.

Front 168

Serum Lipids
Triglycerides

Back 168

Another blood fat that contributes to atherosclerosis. Ideal less than 150

Front 169

What are Serum Lipids determined by?

Back 169

12 hr fasting lipid profile

Front 170

Treatment of Hyperlipidemia

Back 170

-Low fat low cholesterol diet
-Exercise and weight loss.
-If target not met consider drug therapy
-Statins mainstay of drug therapy for lipids

Front 171

Treatment of Hyperlipidemia
Low fat low cholesterol diet

Back 171

Decrease intake of red meat, eggs, butter, high fat dairy products. Make teaching simple. Review diet recall. Encourage sustainable changes

Front 172

Treatment of Hyperlipidemia
Exercise and weight loss.

Back 172

Can raise HDL

Front 173

Treatment of Hyperlipidemia
Statins mainstay of drug therapy for lipids

Back 173

Statins have proven benefits to decrease morbidity/mortality.

Front 174

Treatment of Hyperlipidemia
Nursing implications of statins

Back 174

Monitor LFTs and for myositis. Often given in evening.

Front 175

Angina Pectoris

Back 175

Chest pain resulting from reversible myocardial ischemia.

Front 176

Angina Pectoris
Pathophysiology

Back 176

-Results from anaerobic metabolism and lactic acid build up.
-Usually at least 75% stenosis of involved coronary artery.
-Imbalance between myocardial oxygen supply and demand.
-Ischemia evidenced by ST depression on EKG

Front 177

Factors decreasing myocardial oxygen supply

Back 177

Atherosclerotic Plaques.
Anemia.
Hypoxia.
CHF.
Tachycardia.
Arrhythmias.
Coronary Spasm.

Front 178

Factors increasing myocardial oxygen demand

Back 178

Hypertension.
Cardiomegaly.
Exertion.
Hyperthyroidism.
Aortic Stenosis.

Front 179

Stable Angina

Back 179

-Classic—chest pain occurring intermittently over 3-5 minutes with the same pattern of onset, duration, and intensity of symptoms-predictable
-Usually exercise induced, and subsides with rest or nitroglycerin, ECG has ST depression, discomfort is mild or disabling
-Can be controlled with medications as an outpatient

Front 180

Unstable Angina

Back 180

-Progressive and unpredictable—patient with stable can develop unstable.
-Increasing frequency of pain provoked by minimal or no exercise—can happen during sleep or even total rest
-Has been associated with plaque that has ruptured—increased risk of complete thrombosis of the lumen with progression to MI
-Requires immediate hospitalization.

Front 181

Prinzmetal Angina

Back 181

Often occurs at rest, rare form of angina—thought to be caused by coronary artery spasm. Clean coronaries. Treatment with CCBs or nitro.

Front 182

PRECIPITATING FACTORS FOR ANGINA

Back 182

-Physical exertion
-Strong emotions
-Consumption of a heavy meal
-Temperature extremes
-Cigarette smoking
-Sexual activity
-Stimulants (cocaine & crack)
-Circadian rhythm patterns

Front 183

PRECIPITATING FACTORS FOR ANGINA
Physical exertion

Back 183

increases HR—it decreases the time the heart spends in diastole which is the time of greatest coronary blood flow

Front 184

PRECIPITATING FACTORS FOR ANGINA
Strong emotions

Back 184

Stimulate the SNS and increase work of heart-results increase HR, BP, and myocardial contractility

Front 185

PRECIPITATING FACTORS FOR ANGINA
Consumption of a heavy meal

Back 185

Especially if the person exerts afterward—it increases work of the heart—during the digestive process, blood is diverted to the GI system, causing low flow rate to the coronary arteries

Front 186

PRECIPITATING FACTORS FOR ANGINA
Temperature extremes

Back 186

Either hot or cold—increases workload of heart—response to cold blood vessels constrict—blood vessels dilate and pools in skin in response to hot stimulus

Front 187

PRECIPITATING FACTORS FOR ANGINA
Cigarette smoking

Back 187

Causes vasoconstriction and increased HR because of nicotine’s stimulation of catecholamine release and it also diminishes available O2 by increasing level of carbon monoxide

Front 188

PRECIPITATING FACTORS FOR ANGINA
Sexual activity

Back 188

Increases the cardiac workload and sympathetic stimulation

Front 189

PRECIPITATING FACTORS FOR ANGINA
Stimulants (cocaine & crack)

Back 189

Increase HR and myocardial O2 demand—stimulation of catecholamine release is precipitating factor

Front 190

PRECIPITATING FACTORS FOR ANGINA
Circadian rhythm patterns

Back 190

Symptoms tend to occur in the early morning after awakening

Front 191

Anginal Pain

Back 191

-Usually substernal pressure.
-May radiate to arm or jaw.
-May be associated with diaphoresis or dyspnea.
-Not positional, sharp, pleuritic
-Atypical presentations for females, diabetics, elderly

Front 192

Atypical presentations of Anginal Pain for females, diabetics, elderly

Back 192

less pain may be fatigue, weakness, dizziness, dyspnea.

Front 193

Treatment of Stable Angina

Back 193

-Risk factor modification.
-Antiplatelets: ASA or Plavix
-Statins
-Nitroglycerin
-Β-Blockers
-Calcium Channel Blockers
-Possible PTCA or CABG

Front 194

Treatment of Stable Angina
Risk factor modification.

Back 194

Low fat diet, smoking cessation, control of BP and diabetes.

Front 195

Treatment of Stable Angina
Antiplatelets: ASA or Plavix

Back 195

Decreased risk of MI.

Front 196

Treatment of Stable Angina
Statins

Back 196

Decrease lipids and plaque stabilization, anti-inflammatory effects on endothelium.

Front 197

Treatment of Stable Angina
Nitroglycerin

Back 197

Decreased pre-load and afterload. Decreases myocardial O2 demand. Some degree of coronary vasodilatation. Side effects headache, hypotension, tachycardia.

Front 198

Treatment of Stable Angina
Β-Blockers

Back 198

Decrease HR, contractility, BP. Decrease myocardial O2 demand.

Front 199

Treatment of Stable Angina
Calcium Channel Blockers

Back 199

-Decrease myocardial O2 demand by decreases in afterload and contractility.
-Some coronary vasodilatation.
-Cause headache, edema, hypotension.
-Contraindicated in acute MI or CHF.

Front 200

Ranolazine (Ranexa®)

Back 200

-Anti-ischemic effects independent of heart rate or BP
-Used in combination with β blockers, calcium channel blockers and nitrates
-Prolongs QT interval
-GI effects, dizziness, headache

Front 201

Patient Teaching on Nitroglycerin

Back 201

-One tab under tongue Q 5 minutes X 3.
-Call 911 if pain worsens or fails to improve after 5 minutes.
-Common side effects. (HA, dizziness, tachycardia, ortho hypo)
-No Viagra, Levitra, Cialis (Can cause fatal hypotension and MI).
-Beware of “supplements”
-Store in cool dry place. In tightly sealed dark glass bottle.
-Discard 6 months after opening.
-Use of transdermal nitro - Rotate patches. Nitrate free period. Remember to remove.

Front 202

Treatment of Unstable Angina

Back 202

-Equals unstable plaque/ Acute Coronary Syndrome.
-Hospitalize.
-Bedrest.
-Continuous EKG monitoring.
-Administer ASA (chew 162-325 mg) +/- Heparin.
-Nitro Drip titrate to pain and BP.
-Beta Blockers.
-Consider PTCA.

Front 203

MYOCARDIAL INFARCTION
Pathophysiology

Back 203

-When ischemic intracellular changes become irreversible and necrosis results. Cell death begins in 20 minutes.
-Angina causes reversible cellular injury and infarction is result of sustained ischemia causing irreversible cellular death
-Contractile function of heart stops in the area of necrosis—degree of altered function depends on area of heart involved and size of infarct

Front 204

Types of MIs

Back 204

Non-ST elevation (Subendocardium) ST elevation more extensive damage. Transmural in 4-6 hours.

Front 205

Most infarcts involve which part of the heart?

Back 205

left ventricle
Described by the area of occurrence as anterior, inferior, lateral or posterior wall

Front 206

Infarctions by location and coronary anatomy.
Right Coronary Artery (RCA)

Back 206

Inferior Wall and AV node in 90% of people

Front 207

Infarctions by location and coronary anatomy.
Left Main (LMA)

Back 207

Massive Anteriolateral. “widowmaker”.

Front 208

Infarctions by location and coronary anatomy.
Left Anterior Descending (LAD)

Back 208

Anterior wall.

Front 209

Infarctions by location and coronary anatomy.
Circumflex

Back 209

Lateral and posterior wall.

Front 210

MI initial presentation
Typical

Back 210

Classic substernal crushing chest pain. May radiate. Severe and persistent. Possible associated diaphoresis, dyspnea, nausea/vomiting. More severe and persistent than angina. Elevated BP and pulse. EKG changes.

Front 211

MI initial presentation
Atypical

Back 211

-Women: Less pain more shortness of breath.
-Diabetics: Silent MI.
-Elderly: May be syncope, mental status change or pulmonary edema.

Front 212

Area of Infarction

Back 212

-O2 Deprived
-Damage Irreversible
-Cause "Q" wave on EKG

Front 213

Area of Injury (MI)

Back 213

-Next to infarct.
-Tissue is viable as long as circulation remains adequate.
-Increasing O2 may save this area from necrosis.
-Causes S-T Segment Elevation on EKG.

Front 214

Area of Ischemia (MI)

Back 214

-Viability may not be damaged as long as MI doesn't extend and collateral circulation is able to compensate.
-Causes depressed ST Segment.

Front 215

Relationship of EKG leads to coronary anatomy

Back 215

Inferior: Leads II, III, AvF
Anterio-Septal: Leads V1-V4
Lateral: Leads I, AvL, V5-V6.

Front 216

MI Natural History

Back 216

-Initial Myocardial Necrosis.
-2-3 days inflammatory process
-10-14 days scar formation
-6 weeks scar formed.
-Myocardial remodeling.

Front 217

MI Natural History
Inflammatory process

Back 217

Inflammatory process: Macrophages and neutrophils remove necrotic tissue. Can be associated with low grade fever.

Front 218

MI Natural History
scar formation

Back 218

Initial scar tissue fragile.

Front 219

MI Natural History
Remodeling

Back 219

Remodeling: surrounding myocardium dilates and incease myocardial O2 demand. Can lead to late-onset CHF. Minimized with ACEI and B-Blockers.

Front 220

COMPLICATIONS OF MI

Back 220

-Arrhythmias
-CHF
-Cardiogenic Shock
-Pericarditis
-Dressler’s Syndrome
-Pulmonary embolism
-Papillary Muscle Dysfunction
-Papillary Muscle Rupture
-Ventricular Aneurysm

Front 221

COMPLICATIONS OF MI
Arrhythmias

Back 221

Most common complication following MI is arrhythmias which are present in 80% of MI patients. The most common cause of death in the pre-hospital period (usually V-fib).

Front 222

COMPLICATIONS OF MI
CHF

Back 222

CHF: pumping action of the heart is diminished. Inadequate CO and pulmonary edema.

Front 223

COMPLICATIONS OF MI
Cardiogenic Shock

Back 223

Cardiogenic shock: severe LV failure, renal failure, worsened myocardial ischemia. Requires intubation, vasopressors, IABP, Swanz-Ganz. High mortality.

Front 224

COMPLICATIONS OF MI
Pericarditis

Back 224

Pericarditis may occur 2-3 days post-MI as a complication of infarction. S/S: Chest pain aggravated by inspiration, coughing, and upper body movement. Pain relieved by sitting in a forward position. Heard as a friction rub. Best heard with diaphragm of stethoscope over lower sternal border. ST-T wave elevations on ECG indicating inflammation. Tx: ASA, steroids, or NSAID’s.

Front 225

COMPLICATIONS OF MI
Dressler’s Syndrome

Back 225

Dressler syndrome – pericarditis that develops 1-4 weeks post MI. Caused by immune response to necrotic heart tissue. Treatment short course corticosteroids.

Front 226

COMPLICATIONS OF MI
Pulmonary embolism

Back 226

PE: due to immobility. Source may be leg veins or the damaged endocardium.

Front 227

COMPLICATIONS OF MI
Papillary Muscle Dysfunction

Back 227

Ischemia or injury to papillary muscles causes new mitral regurg. New onset systolic mitral murmer. Impaired CO, CHF.

Front 228

COMPLICATIONS OF MI
Papillary Muscle Rupture

Back 228

Sudden Severe Mitral Regur. Flash Pulmonary Edema. Necessitates rapid afterload reduction with IV nitroprusside, IABP. emergent mitral valve replacement.

Front 229

COMPLICATIONS OF MI
Ventricular Aneurysm

Back 229

Bulging of ventricular wall. Contributes to CHF, angina, arrhythmias, thrombi and ventricular rupture which is fatal.

Front 230

Nursing care of the patient with chest pain

Back 230

-Acute Chest Pain is MI until proven otherwise.
-“Time is Muscle”
-Administer O2 at 4L .
-Establish IV access.
-Continuous EKG monitoring.
-Draw Labs.
-Administer Meds.
-On-going Assessment.
-Emotional Support.

Front 231

Medications for MI

Back 231

-Aspirin (Administer 325 mg stat. Have patient chew.)
-Morphine Sulfate (Controls pain decreases myocardial oxygen demand.)
-IV Nitroglycerin (Titrate to pain and BP)
-Heparin
-β Blocker

Front 232

Nursing Assessments for MI

Back 232

-Vitals signs and pulse oximetry.
-EKG ischemic changes and arrhythmias
-Chest pain.
-Associated symptoms (Dyspnea, dizziness, N/V)
-Cardiopulmonary assessment: Assess onset, location, character, duration, aggravating factors, relieving factors, radiation, severity, response to meds.

Front 233

Diagnostics for MI

Back 233

-Chest X-Ray (CXR)
-Serial 12 Lead EKGs
-Serial Cardiac Enzymes
-Rule out pulmonary pathology or aortic dissection.

Front 234

CK-MB

Back 234

-Rise 3-12 hours after onset of MI
-Peak in 24 hours.
-Return to baseline in 2-3 days.

Front 235

Troponins

Back 235

-Rise in 3 hours.
-Peak in 24-48 hours.
-Return to baseline in 5-14 days.

Front 236

Treatment of NSTEMI

Back 236

-Admit to CCU.
-Bedrest.
-Continuous monitoring.
-Assess for complications.
-Consider PCI (PTCA) or CABG

Front 237

Treatment of STEMI

Back 237

Emergent PCI (PTCA) or Thrombolytics.

Front 238

PCI (PTCA)

Back 238

-Alternative to surgical intervention: catheter is inserted with balloon on end, ambulatory after procedure, decreased length of hospital stay
-Complication is dissection of dilated artery causing death, cardiac tamponade, ischemia, and MI, allergic reaction to dye

Front 239

STENT PLACEMENT

Back 239

Treat abrupt or threatened closure following PTCA—meshlike structure maintain vessel patency
Complications: hemorrhage and vascular injury, acute MI, emergency CABG, stent embolization, coronary spasm

Front 240

Nursing Care of the PCI (PTCA) patient

Back 240

-Risks of Procedure (MI, vessel rupture, arrhythmia, emergent CABG, death)
-Post procedure sheaths in place.
-Continue to monitor vital signs, pulse ox, telemetry, cardiopulmonary assessment.
-Care of femoral artery site as per cardiac cath.
-Continue ASA and Plavix post stent placement.

Front 241

CABG

Back 241

-If patient has left main coronary artery obstruction, triple-vessel disease, two vessel disease unresponsive to medical therapy
-Graft from saphaneous vein, internal mammary artery. Or radial artery.
-Requires Cardiopulmonary Bypass

Front 242

Nursing Care of the CABG patient.

Back 242

-2 surgical sites.
-Sternotomy.
-Chest tube care
-Initially intubated.
-Critical care monitoring of vital signs, CVP, telemetry, urine output.

Front 243

What is the significance of urinary output?

Back 243

Renal Perfusion (30 ml/hr)

Front 244

Thrombolytic Therapy

Back 244

-Produces lysis of clots
-Indication: STEMI within 6-12 hours of onset.
-No contraindications or active bleeding.
-Types: tPa, Streptokinase,

Front 245

Thrombolytic Therapy
Absolute Contraindications

Back 245

-Active Bleeding.
-Coagulation Defects.
-Peptic Ulcer Disease.
-GI Bleed within 6 months.
-Past hemorrhaging stroke.
-Pregnancy.
-Surgery within 3 months.
-Suspected Aortic Dissection.
-SBP > 180
-DBP > 110

Front 246

Thrombolytic Therapy
Relative Contraindications

Back 246

-Patient on Coumadin.
-Recent CPR.
-CVA or TIA in last 12 months.
-Severe renal or liver disease.
-Hemorrhagic retinopathy.

Front 247

Thrombolytic Therapy
Nursing Care

Back 247

-Draw labs prior.
-Establish 2-3 IV lines.
-Initiate infusion with close monitoring. (VS every few minutes)
-Observe for reperfusion.
-Observe for bleeding.

Front 248

Thrombolytic Therapy
Nursing Care
Observe for Reperfusion

Back 248

resolution of ST elevation, rapid rise in CK, reperfusion arrhythmias.

Front 249

Thrombolytic Therapy
Nursing Care
Observe for Bleeding

Back 249

Bleeding: Decreased BP, Increased HR, Change in LOC, Oozing of IV sites, hematuria, blood in stool etc.

Front 250

Post-MI Nursing Care

Back 250

-Gradually advance activity.
-Educate patient on meds, diet, activity.
-Encourage smoking cessation.
-Confirm activity prescription with cardiologist.
-Refer to cardiac rehab.
-Possible follow-up stress test.
-Reinforce need to control diabetes, hypertension, lipids.
-Screen for depression

Front 251

ACS Discharge Meds

Back 251

-ASA and Plavix
-Beta Blocker
-ACE Inhibitor
-Statin

Front 252

Sudden Cardiac Death

Back 252

-Unexpected sudden cardiac arrest.
-Usually underlying CAD
-Usually results from V-fib.
-Death is first symptom of CAD in 25% of cases.
-20% are discharged without brain damage.

Front 253

Sudden Cardiac Death Survivors

Back 253

-Work-up for MI.
-Cardiac Catheterization.
-EPS Study.
-CABG if indicated.
-ICD: Implanted -Cardioversion Defibrillator.

Front 254

What is CHF?

Back 254

-Cardiovascular condition in which the heart is unable to pump an adequate amount of blood to meet the metabolic needs of the body’s tissues. Impaired cardiac pumping. -Leads to fluid overload and congestion in lungs or periphery.

Front 255

How prevalent is CHF?

Back 255

Currently 5 million people in the U.S. with CHF. Leading cause of hospitalization for those older than 65

Front 256

What causes CHF?

Back 256

Long-standing hypertension, CAD, and DM. The risk of CHF increases with the severity of Htn. DM predisposes a person to CHF.

Front 257

What is the prognosis of CHF?

Back 257

High rate of morbidity and mortality. Variable prognosis. Annual health care costs exceed $57 billion.

Front 258

RISK FACTORS FOR CHF

Back 258

-Hypertension (Major risk factor. Due to strain of pumping against high SVR. Dysfunctional hypertrophy.)
-CAD
-Congenital Heart Disease
-Rheumatic Heart Disease
-Cardiomyopathy
-Valvular Heart Disease
-Atrial Fibrillation. (loss of atrial kick)
-Cor Pulmonale (caused by chronic lung disease)

Front 259

Pathology of Ventricular Failure
Impaired Ventricular function

Back 259

Inability of Ventricle to adequately pump or fill. Impaired ability to meet metabolic demands leads to fatigue, decreased organ function.

Front 260

Pathology of Ventricular Failure
Pulmonary Congestion

Back 260

LV dysfunction results in excessive fluid backs up into pulmonary system resulting in congestion. Results in cough, rales, dyspnea.

Front 261

Pathology of Ventricular Failure
Systemic Congestion

Back 261

RV dysfunction causes back up of fluid into periphery cause JVD, edema, hepatomegaly.

Front 262

Cardiac Output & CHF

Back 262

Preload elevated beyond ventricular capacity. Failure of starlings law. Impaired contractility. Excessive Afterload due to increased systemic vascular resistance.

Front 263

TYPES of CHF
Systolic

Back 263

-Most common cause—LV looses its ability to eject blood forward through the high pressure aorta (impaired ventricular emptying). -Hallmark sign is the decrease in EF (the fraction of total vent. filling volume ejected on each contraction. Normal is greater than 50%).
-Results from not able to pump blood to aorta: decreased LVEF, increase in LVEDP, increase in PAWP, pulmonary congestion
-Caused by: impaired contractile function (MI), increased afterload (HTN)), or mechanical abnormalities (VHD)

Front 264

TYPES of CHF
Diastolic

Back 264

-Not a disorder of contractility but of relaxation and ventricular filling. Impaired ability of the ventricles to fill during diastole. Results in decreased stroke volume. Normal systolic function.
-High filling pressures with resultant ventricular engorgement in both the pulmonary and systemic vascular systems
-Diagnosis made based on pulmonary congestion and pulmonary hypertension with normal ejection fraction
-Result from LVH from chronic hypertension or hypertrophic cardiomyopathy (aortic stenosis).

Front 265

TYPES of CHF
Mixed Systolic & Diastolic failure

Back 265

Mixed origin, dilated cardiomyopathy (weakened muscle function, dilated LV wall), poor ejection fractions, poor exercise tolerance, pulmonary congestion and edema. Both ventricles are affected with poor emptying and filling capacity.

Front 266

TYPES of CHF
Left Sided

Back 266

-Ventricular failure of any type: Low CO, poor renal perfusion, exercise intolerance, ventricular arrythmias.
-Left sided will eventually cause right sided failure.

Front 267

TYPES OF CHF
Left Sided (cont)

Back 267

Left sided: most common initial heart failure, results from LV dysfunction, blood to back up through the left atrium and into pulmonary veins results in pulmonary congestion and edema—causes are coronary arteries, hypertension, cardiomyopathy, and rheumatic heart disease, MI

Front 268

TYPES of CHF
Right Sided

Back 268

-Ventricular failure of any type: Low CO, poor renal perfusion, exercise intolerance, ventricular arrythmias.
-Chronic Lung Disease.

Front 269

TYPES OF CHF
Right Sided (cont)

Back 269

Decreased right ventricle causes backflow to right atrium and venous circulation—peripheral edema, hepatomegaly, splenomegaly, vascular congestion of GI tract, and jugular venous distention—primary cause is left sided failure, can be caused by chronic hypertension, Cor pulmonale (right ventricular dilation caused by pulmonary pathology)

Front 270

TYPES OF CHF
Right & Left Sided (cont)

Back 270

Eventually both sides will fail: one side may fail first then the other so the other side continues to function normally for a period of time but due to prolonged strain it will fail—biventricular failure

Front 271

TYPES of CHF
High output Failure

Back 271

Results when normal CO inadequate to meet hypermetabolic state. E.g. Anemia, hyperthyroidism.

Front 272

Left Sided Heart Failure

Back 272

-Paroxysmal Nocturnal Dyspnea
-Elevated Pulmonary Capillary Wedge Pressure
-Pulmonary Congestion (Cough, Crackles, Wheezes, Blood-Tinged Sputum, Tachypnea)
-Restlessness, Confusion, Orthopnea, Tachycardia, Exertional Dyspnea, Fatigue, Cyanosis

Front 273

Right Sided Heart Failure (Cor Pulmonale)

Back 273

Fatigue, Increased Peripheral Venous Pressure, Ascites, Enlarged Live & Spleen, May be secondary to chronic pulmonary problems, Distended Julgular Veins, Anorexia & Complaints of GI Distress, Swelling in Hands & Fingers, Dependent Edema

Front 274

COMPENSATORY MECHANISMS of CHF

Back 274

-Attempts to increase cardiac output.
-Ventricular dilation
-Ventricular hypertrophy
-Increased SNS activity
-Hormonal response
-Myocardial Remodeling

Front 275

COMPENSATORY MECHANISMS of CHF
Attempts to increase cardiac output.

Back 275

Initially help maintain CO but ultimate worsen heart function.

Front 276

COMPENSATORY MECHANISMS of CHF
Ventricular dilation

Back 276

Enlargement of chambers of heart—pressure in heart is elevated over time (LV)—increase CO, adaptive mechanism to cope with increasing blood volume, becomes inadequate because the elastic elements of muscle fibers are overstretched and overstrained

Front 277

COMPENSATORY MECHANISMS of CHF
Ventricular hypertrophy

Back 277

An increase in muscle mass and cardiac wall thickness in response to overwork and strain, slowly occurs, increase in CO and maintenance of tissue perfusion, has poor contractility

Front 278

COMPENSATORY MECHANISMS of CHF
Increased SNS activity

Back 278

First mechanism triggered in low CO states, least effective compensatory mechanism, happens because of inadequate SV and low CO, thus a release of epi and norepi which increases HR, myocardial contractility, and peripheral vasoconstriction. Increases myocardium’s need for O2 and workload of an already failing heart Increases SVR and afterload. Diastolic failure intolerant of increased HR.

Front 279

COMPENSATORY MECHANISMS of CHF
Hormonal response

Back 279

CO decreases blood flow to kidney decreases causing decrease in glomerular blood flow—juxtaglomerular apparatus release renin, increase in peripheral vasoconstriction- release of aldosterone causing sodium retention. Increases Preload and afterload. Hypothalamus senses and causes posterior pituitary to secrete ADH causes water retention

Front 280

COMPENSATORY MECHANISMS of CHF
Myocardial Remodeling

Back 280

Compensatory mechanism cause ventricle to remodel becomes less effective pump.

Front 281

Natriuretic Peptides
Atrial Natriuretic Peptide

Back 281

Atrial Natriuretic Peptide
Natrecor
B-type Natriuretic Peptide

Front 282

Natriuretic Peptides
Atrial Natriuretic Peptide

Back 282

Produced by atrium when stretched. Promotes vasodilation and diuresis. Decreases preload and afterload.

Front 283

Natriuretic Peptides
Natrecor

Back 283

Drug given IV in acute CHF. Chemically similar to ANP.

Front 284

Natriuretic Peptides
B-type Natriuretic Peptide

Back 284

Originally brain but actually produced by ventricles. Serum level diagnostic marker.

Front 285

Interpretation of BNP levels

Back 285

-Less than 100 no heart failure.
-Between 100-500 possible heart failure.
-Greater than 500 confirms heart failure
-Greater than 900 severe heart failure.

Front 286

CLINICAL MANIFESTATIONS OF ACUTE CHF

Back 286

Manifests as Pulmonary edema - Acute and life-threatening. Because of the decreased LV function, pulmonary venous pressures rise causing engorgement of the pulmonary vascular system. Fluid moves into the interstitial space causing interstitial edema. Alveoli are disrupted (alveolar edema) as they are flooded with fluid and lungs fill with serosanguineous fluid.

Front 287

Signs and Symptoms of Acute CHF

Back 287

-Acute Dyspnea
-Tachypnea
-Tachycardia
-Hypoxia
-Change in Mental Status
-Course Rales
-Wheezes
-Frothy Pink Sputum

Front 288

Pulmonary Edema
Medical Management

Back 288

-Acute Care Admission.
-High Flow O2
-Continuous monitoring
-Labs, CXR, 12 lead EKG
-IV Lasix (Assess for hemodynamic/renal status)
-IV Morphine
-IV Nitrogylecrin or Nitroprusside
-IV Dopamine
-IV Natrecor

Front 289

CLINICAL MANIFESTATIONS OF CHRONIC CHF

Back 289

-Factors (age, type, extent, ventricle)
-Fatigue
-Dyspnea
-Tachycardia
-Peripheral Edema
-Nocturia
-Behavioral Changes
-Chest Pain
-Weight Changes
-Arrhythmias

Front 290

CLINICAL MANIFESTATIONS OF CHRONIC CHF
Fatigue

Back 290

Fatigue caused by decreased CO, impaired circulation, and decreased O2 of tissues “sick fatigue”

Front 291

CLINICAL MANIFESTATIONS OF CHRONIC CHF
Dyspnea

Back 291

Dyspnea: increased pulmonary pressure, poor gas exchange, SOB, get rapid shallow breaths—orthopnea: patient is in recumbent position---Paroxysmal nocturnal dyspnea (PND) occurs when patient is asleep dry cough. Bibasalar rales.

Front 292

CLINICAL MANIFESTATIONS OF CHRONIC CHF
Tachycardia

Back 292

Tachycardia due to decreased CO—increase in SNS

Front 293

CLINICAL MANIFESTATIONS OF CHRONIC CHF
Peripheral Edema

Back 293

Edema: legs liver ascites. Pitting.

Front 294

CLINICAL MANIFESTATIONS OF CHRONIC CHF
Nocturia

Back 294

Nocturia: decreased CO, impaired renal perfusion, decreased urinary output during day—at night fluid moves from interstitial spaces back into circulation—increases renal blood flow and UO

Front 295

CLINICAL MANIFESTATIONS OF CHRONIC CHF
Behavioral Changes

Back 295

Behavioral changes: restlessness, confusion, and decreased attention span from impaired cerebral circulation due to low oxygen state

Front 296

CLINICAL MANIFESTATIONS OF CHRONIC CHF
Chest Pain

Back 296

Chest pain: decreased CO and increased myocardial workload

Front 297

CLINICAL MANIFESTATIONS OF CHRONIC CHF
Weight Changes

Back 297

Weight changes: fluid retention, ascites, hepatomegaly. Renal failure contributes to symptoms. Patients are nauseous and anorexic. Best Indicator of fluid status

Front 298

CLINICAL MANIFESTATIONS OF CHRONIC CHF
Arrhythmias

Back 298

Atrial fib due to dilated LA worsens CHF loss of atrial kick. Increased rate decreases ventricular filling and coronary perfusion. Increased risk of ventricular arrhythmias.

Front 299

What is the single best assessment of fluid balance changes?

Back 299

Daily Weights under constant conditions

Front 300

Chronic CHF
Diagnostics

Back 300

-CBC, CMP - Look for anemia, renal function, liver function lytes.
-CXR - Look for pulmonary congestion, cardiomegaly.
-EKG - Ischemia, arrhythmias, LVH.
-Echo - EF, valve function, wall motion, chamber size.
-BNP - Confirmatory and marker of response to therapy.
-Stress Testing - Determine if CAD is a causative factor.
-Cardiac Cath - Plan for possible re-vascularization or valve procedure.

Front 301

New York Heart Associated
Functional Classification

Back 301

-Class I - Ordinary activity does not cause symptoms - 1 yr mortality: 8%
-Class II - Ordinary activity results in symptoms - 1 yr mortality: 14%
-Class III - Limitation of physical activity - 1 yr mortality: 20%
-Class IV - Symptoms are present at rest - 1 yr mortality: 65%

Front 302

Treatment of Chronic CHF

Back 302

-Low sodium diet.
-Daily weight.
-O2 if needed.
-Control hypertension.
-Correct CAD.
-Control or correct arrhythmias
-Correct Valve disorders.
-Medications.
-Bi-ventricular pacing.

Front 303

Treatment of Chronic CHF
Low Sodium Diet

Back 303

Improves diuresis and decreases fluid overload/ edema.

Front 304

Treatment of Chronic CHF
Daily weight

Back 304

Best measure of fluid status. Weight gain of 3 pounds in 2-5 days indicative of a problem.

Front 305

Drug Therapy for CHF

Back 305

-ACEI
-ARB
-Beta Blockers: Carvedilol (Coreg), Metoprolol (Toprol XL)
-Loop Diuretics
-Digoxin
-Spironolactone (Aldactone)
-Nitrates
-Statins
-BiDil® (Isosorbide and Hydralazine)

Front 306

Drug Therapy for CHF
ACEI

Back 306

Proven reduction in morbidity and mortality. Decreases preload, afterload and myocardial remodeling.

Front 307

Drug Therapy for CHF
ARB

Back 307

If ACE not tolerated.

Front 308

Drug Therapy for CHF
Beta Blockers: Carvedilol (Coreg), metoprolol (Toprol XL)

Back 308

Counter-intuitive due to decrease in myocardial contractility.Proven to decrease morbidity and mortality. Interrupt sympathetic over stimulation. Control BP and HR. Prevent myocardial remodeling. Start low and go slow.

Front 309

Drug Therapy for CHF
Loop Diuretics

Back 309

Decrease Preload.

Front 310

Drug Therapy for CHF
Digoxin

Back 310

Especially for rate control in A-fib. Positive Inotropic action. Negative Chronotropic action. Low therapeutic index. Watch for Toxicity e.g. headache, nausea, vision changes, arrhythmias, heart block. Monitor levels and serum lytes. No reduction in mortality. Benefit to reduce hospitalization and symptoms.

Front 311

Drug Therapy for CHF
Spironolactone (Aldactone)

Back 311

K sparing diuretic. Helpful in severe CHF. Must have adequate renal function. Watch K with ACEI.

Front 312

What is the risk of combining spironolactone with an ACEI?

Back 312

HyperK

Front 313

Which drugs have been shown longer survival in heart failure?

Back 313

ACEI, Beta-blockers

Front 314

Nursing Care of CHF

Back 314

-Assess: Vital signs, O2 sat, Heart sounds, lung sounds, cardiac rhythm, weight, urine output, edema, JVD, PND, orthopnea, dyspnea, mental status.
-Labs: BNP levels. Lytes. Renal function.
-Multiple meds. Beware of side effects and interactions.
-Education: How to do daily weights e.g. 1st in AM after void same clothes. Report weight gain of 2 pounds in 1 day or 3 pounds in 2-5 days. Low salt diet. Alternate rest and activity. How to take meds.
-D/C: How to avoid future exacerbations. Follow-up appointments, Home health, Medications Need to report changes early.

Front 315

Teaching Low Sodium Diet

Back 315

-Ideal 2 grams or less per day.
-Read labels.
-Do not cook with salt.
-Avoid using salt shaker.
-Try using different spices.
-Limit processed, pickled or cured foods.
-Be cautious with canned soups, vegetables.
-Avoid fast food and salty snacks.

Front 316

Decompensated or end-stage heart failure
Inotropes

Back 316

Dopamine, Dobutamine, Milrinone

Front 317

Decompensated or end-stage heart failure
Intra-aortic Balloon Pump (IABP)

Back 317

-Inflates during diastole
-Improves coronary perfusion
-Decreased workload for LV

Front 318

Decompensated or end-stage heart failure
Ventricular Assist Device (VAD)

Back 318

-Surgically implanted pump
-Bridge to transplant
-“Destination Therapy”

Front 319

Cardiomyopathy

Back 319

-Group of disease resulting in damage to heart muscle structure and function.
-3 Types (Dilated, Hypertrophic, and Constrictive)

Front 320

Dilated Cardiomyopathy

Back 320

-Most Common 90%
-Cardiomegaly (enlargement of the heart) with ventricular dilatation, impaired systolic function, atrial enlargement, stasis of blood in LV. -Increased risk of thrombi and arrhythmias. Patients often younger than CHF patients.

Front 321

Primary Dilated Cardiomyopathy

Back 321

Idiopathic

Front 322

Secondary Dilated Cardiomyopathy

Back 322

Alcohol, Viral, Doxorubicin (Adriamycin), ischemia, drug abuse.

Front 323

Difference between dilated cardiomyopathy and CHF.

Back 323

This disorder resembles CHF, but the walls of the ventricles do not hypertrophy as they do in CHF.

Front 324

Dilated Cardiomyopathy
Dx

Back 324

Echo and Cardiac Cath

Front 325

Dilated Cardiomyopathy
Tx

Back 325

Same as CHF, +/- anticoagulants, +/- antiarrthymics

Front 326

Dilated Cardiomyopathy
Transplantation

Back 326

Accounts for 50% of heart transplants.

Front 327

Hypertrophic Cardiomyopathy

Back 327

Also known as Idiopathic Hypertrophic Subaortic Stenosis (IHSS)Enlarged ventricular wall and septum impede systolic outflow and diastolic filling. Usually young healthy people. Results in exertional dyspnea, syncope, angina, arrhythmias. Cause of sudden death in athletes.

Front 328

Hypertrophic Cardiomyopathy
Causes

Back 328

Genetic, Aortic Stenosis, HTN

Front 329

Hypertrophic Cardiomyopathy
Physical Exam Findings

Back 329

May be none. May have S3 S4 or systolic murmur.

Front 330

Hypertrophic Cardiomyopathy
Dx

Back 330

Echo

Front 331

Hypertrophic Cardiomyopathy Treatment

Back 331

-Beta Blockers and Calcium Channel Blockers. (Decrease contractility, improve outflow and ventricular filling)
-ICD (Implanted cardiac defib) or antiarrhythmic if indicated.
-Surgery (Shave down ventricular septum)
-Percutaneous transluminal septal myocardial ablation (PTSMA) - Inject ETOH into septal artery
-Patients must avoid strenuous activity and dehydration.

Front 332

Restrictive Cardiomyopathy

Back 332

Ventricles stiffen. Resistant to diastolic filling. Systolic function unaffected.

Front 333

Restrictive Cardiomyopathy
Causes

Back 333

Idiopathic, tumors, radiation, sarcoidosis, amyloidosis.

Front 334

Restrictive Cardiomyopathy
Symptoms

Back 334

Exercise intolerance, angina, syncope, dyspnea on exertion. Cannot tolerate increased HR or increased CO to meet demand.

Front 335

Restrictive Cardiomyopathy
Dx

Back 335

Echo

Front 336

Restrictive Cardiomyopathy
Tx

Back 336

Same as CHF, treat arrhythmias, transplant, avoid exertion, dehydration.

Front 337

Cardiac Transplant

Back 337

-Demand Exceeds Supply
-Criteria - Age restriction > 67, otherwise good health, able to comply with complex medical regimen, no active infection, no active or recent malignancy.
-Procedure - Evaluated for place on wait list. Must be matched. If condition dteriorates may be hospitalized. May require pressors or IABP.
-Life Long Immunosuppressants - risk for infection and malignancy

Front 338

What is Endocarditis?

Back 338

An inflammation of the lining of the heart and valves.

Front 339

Pathophysiology of Endocarditis

Back 339

Previously damaged valve surface seeded with bacteria released during invasive procedures. Infection causes valve damage. Can infect myocardium and or result in sepsis. Valve damage can lead to CHF.

Front 340

What are vegetation?

Back 340

Clumps of bacteria, fibrin platelets and leukocytes that can embolize to brain, kidneys, lungs, limbs.

Front 341

Invasive Procedures

Back 341

-Dental Procedures
-Cystoscopy
-Endoscopy
-GYN procedures
-Surgery
-IV Drug Abuse
-Cardiac Cath
-IV Therapy

Front 342

Endocarditis 
Clinical Manifestations

Back 342

-Fever, Chills, Weakness.
-Myalgias, Arthralgias
-New onset murmur
-Splinter Hemorrhages and Petechiae
-Osler’s Nodes - Painful tender red or purple pea sized lesions on finger tips or toes.
-Janeway’s Lesions - Painful tender red or purple pea sized lesions on finger tips or toes.
-Embolic Complications

Front 343

Endocarditis
Diagnostics

Back 343

-CBC elevated WBC.
-Blood Cultures 2-3 sets. Usually strep, staph or enterococci.
-2-D Echo or TEE - To visualize valves. TEE better to see vegetations.

Front 344

Endocarditis 
Treatment

Back 344

-IV antibiotics for weeks - Usually PCN, Cephalosporin or Vancomycin.
-May be discharged with PICC.
-May require valve replacement.

Front 345

Endocarditis
Nursing Care

Back 345

-Vital signs, heart sounds, examine skin for lesions. Observe for symptoms of embolization, cardiac decompensation or sepsis.
-Telemetry.
-Draw cultures prior to 1st dose of antibiotics. Await results 2-5 days. Track CBC.
-IV antibiotics - Maintain IV access. Review allergy history. Observe for response to therapy and for adverse reactions.
-Acetaminophen - Control fever to decrease workload on the heart.
-Education - Explain need to follow-up until infection eradicated. Explain need for future antibiotic prophylaxis prior to invasive procedures.

Front 346

Endocarditis Prophylaxis

Back 346

-Required for patients with prosthetic heart valves, pacemakers, ICDs, some heart murmurs, rheumatic fever and prior history of endocarditis
-Usually single dose of PCN or Erythromycin 1 hour prior to procedure.
-Educate patient - inform dentist and other hcp

Front 347

What is Pericarditis?

Back 347

An inflammation of the pericardial sac.

Front 348

Pericarditis Pathophysiology

Back 348

Inflammation results from infection, autoimmune responses mechanical or biochemical sources. Inflammation results in chest pain and can cause increase in pericardial fluid which impedes cardiac function. Normal is less than 50 cc

Front 349

Complications of Pericarditis

Back 349

Cardiac tamponade, chronic constrictive pericarditis, myocarditis.

Front 350

Pericarditis
Etiology

Back 350

-Viral.
-MI.
-Dressler’s Syndrome.
-Bacterial.
-Trauma.
-Neoplasm.
-Radiation.
-Tuberculosis
-Uremia

Front 351

Pericarditis
Clinical Manifestations

Back 351

-Chest Pain - Sharp, pleuritic, worse with cough, swallow , movement or lying down. Relieved by sitting up or leaning forward.
-Fever.
-Pericardial Friction Rub.
-EKG changes - Diffuse ST segment elevation in all leads except AvR V1

Front 352

Pericarditis
Diagnostics

Back 352

-EKG and Cardiac Enzymes - to rule out MI
-Echo - To look for inflammation, effusion or tamponade.
-Pericardiocentesis or Pericardial biopsy - To determine etiology.

Front 353

Pericarditis
Treatment

Back 353

-NSAIDS or Corticosteroids
-Treat underlying cause if not viral.
-Rest.

Front 354

Pericarditis
Nursing Care

Back 354

-Assess pain.
-Observe for medication effects.
-Observe for signs or symptoms of tamponade.
-Assist to position of comfort.
-Provide emotional support.

Front 355

Cardiac Tamponade

Back 355

-Rapid accumulation of fluid compresses the heart impeding it’s ability to fill. -Results in severely compromised cardiac output.
-Timing - Severity depends on how rapidly it develops.

Front 356

Cardiac Tamponade
S&S

Back 356

Hypotension, Tachycardia, Tachypnea, Dyspnea, Anxiety, Confusion, JVD, Muffled Heart Sounds Low voltage EKG.

Front 357

Cardiac Tamponade
Pulsus Paradoxus

Back 357

An inspiratory drop in systolic BP of > 10 mm Hg

Front 358

Cardiac Tamponade
Tx

Back 358

Emergent Pericardiocentesis

Front 359

Risks of Pericardiocentesis

Back 359

-Arrhythmias
-Pneumomediastinum
-Pneumothorax
-Myocardial Laceration
-Coronary Artery Laceration.

Front 360

Myocarditis

Back 360

Inflammation of the myocardium causes impaired contractility.

Front 361

Myocarditis
Etiologies

Back 361

-Viral
-SLE
-Idiopathic.

Front 362

Myocarditis
Clinical Manifestations.

Back 362

Similar to pericarditis with CHF, crackles, S3, JVD, edema

Front 363

Myocarditis
Tx

Back 363

No specific treatment. Rest and treat underlying CHF. Most will resolve. Some will progress to dilated cardiomyopathy.

Front 364

Rheumatic Fever

Back 364

An inflammation of the heart resulting from an immune reaction to an infection with group A Beta hemolytic strep. Occurs 2-3 weeks after infection. Inflammation can occur throughout the heart but primarily affects valves.

Front 365

Rheumatic Fever
Complications.

Back 365

Permanent valve damage. Usually mitral or aortic. Can be stenosis or regurgitation.

Front 366

Rheumatic Fever
Clinical Manifestations

Back 366

-Fever.
-Cardiac effects (New onset murmur, CHF, pericardial effusion, pericarditis)
-Migratory Polyarthritis (Inflammatory arthritis. Joints are red, swollen, tender)
-Subcutaneous Nodules (Firm, small, round, painless swellings over bony prominences)
-Sydenham’s Chorea.
-Erythema Marginatum

Front 367

Rheumatic Fever
Clinical Manifestations
Sydenham’s Chorea.

Back 367

-Delayed sign.
-Usually 3 months later.
-Weakness, ataxia, rapid spontaneous movements worsen with voluntary activity.

Front 368

Rheumatic Fever
Clinical Manifestations
Erythema Marginatum

Back 368

-Less common.
-Bright pink macular lesions on trunk upper arms and thighs.

Front 369

Rheumatic Fever
Diagnostics

Back 369

-History and Exam (Mostly made be meeting criteria)
-ASO Titer (Anti-Streptolysis O. Indicates immune response to strep)
-Throat Culture (Identify strep source)
-Echo (Assess heart valves)

Front 370

Rheumatic Fever
Treatment

Back 370

-Antibiotics (Treat with PCN or macrolide to eradicate underlying strep infection. -Will require antibiotic prophylaxis for 5 years to life because attacks will recur if re-infected with strep)
-Antiinflammatories (Salicylates or corticosteroids)
-95 % resolve within 6 months.
-Valve damage (may require on-going evaluation and treatment)
-Prevention (Adequate treatment of strep infections)

Front 371

What are the differences between endocarditis and rheumatic fever?

Back 371

-Endo - direct tissue damange caused by the bacteria
-RF - autoimmune response.

Front 372

Mitral Stenosis

Back 372

Impedes flow from left atrium to left ventricle during diastole. Results in left atrial enlargement and pressure. Results in pulmonary congestion.

Front 373

Mitral Stenosis
Etiology

Back 373

Usually Rheumatic Heart Disease.

Front 374

Mitral Stenosis
Clinical Manifestations

Back 374

-Dyspnea
-Atrial Fibrillation
-Emboli from stagnant blood in LA.
-Opening snap.
-Diastolic Murmur at Apex.

Front 375

Mitral Regurgitation

Back 375

Backward flow of blood into LA during systole.

Front 376

Mitral Regurgitation
Etiology

Back 376

-MI
-papillary muscle dysfunction
-severe MVP
-infective endocarditis
-rheumatic heart disease.

Front 377

Acute Mitral Regurgitation

Back 377

Usually MI. Flash pulmonary edema, New systolic murmur at apex.

Front 378

Chronic Mitral Regurgitation

Back 378

LA, LV dilation. Pulmonary congestion. Holosystolic murmur at apex. Will eventually lead to LV failure with CHF.

Front 379

Mitral Valve Prolapse

Back 379

-Most common valve abnormality.
-Structural abnormality in valve leaflet or papillary muscles results in prolapse of valve leaflets into LA during systole. Usually benign. Can cause MR or endocarditis.

Front 380

Mitral Valve Prolapse
Etiology

Back 380

Usually hereditary. Usually found on echo.

Front 381

Mitral Valve Prolapse
Clinical Manifestations.

Back 381

Can be asymptomatic. Mid-systolic click with late systolic murmur. Chest pain (not anginal), SVT, PVCs, palpitations, V-tach, dizziness.

Front 382

Mitral Valve Prolapse
Treatment

Back 382

Non required if minimally symptomatic. Abx prophylaxis id prolapse. Avoid stimulants, caffeine, Beta blockers for palpitations.

Front 383

Aortic Stenosis

Back 383

-Obstruction of outflow from LV during systole. Results in decreased CO, myocardial hypertrophy, increased myocardial O2 demand. Inability to increase CO with exertion.
-Avoid Nitrates - Decrease in preload will reduce outflow needed to force valve open.

Front 384

Aortic Stenosis
Etiology

Back 384

Most common senile calcified, congenital in younger, rheumatic heart disease.

Front 385

Aortic Stenosis
Clinical Manifestations

Back 385

Angina, CHF, syncope, S4 Harsh systolic murmur at base.

Front 386

Aortic Regurgitation

Back 386

Retrograde blood flow from aorta back into LV during diastole. Causes LV dilation and hypertrophy. Eventually leads to dilated LA and pulmonary congestion.

Front 387

Aortic Regurgitation
Acute etiology.

Back 387

Endocarditis, trauma, aortic dissection. Life threatening emergency can lead to CV collapse.

Front 388

Aortic Regurgitation
Chronic etiology.

Back 388

Rheumatic heart disease, congenital bicuspid aortic valve.

Front 389

Aortic Regurgitation
Clinical Manifestations.

Back 389

Water Hammer pulse: quick collapse in diastole. Diastolic murmur at base. CHF, exertional dyspnea, orthopnea, PND.

Front 390

Valvular Heart Disease
Diagnostics

Back 390

-Echocardiogram - Information on valve structures, functions and chamber size.
-Cardiac Cath - Quantifies size of valve area and chamber pressures. Used prior to planned surgical correction.
-Multiple valve disorders can co-exist.

Front 391

Valvular Heart Disease
Treatment

Back 391

-Conservative - Monitor cardiac function. Prevent endocarditis. Treat CHF.
-PTBV - Percutaneous transluminal balloon valvuloplasty. Cardiac cath balloon separates stenotic valve leaflets.
-Valve Repair - Open with sternotomy with CPB. Surgeon repairs damaged valve without use of prosthetic.
-Mechanical Valves - Open. Lasts longer. Increased risk of thromboembolism. Requires life long anticoagulation.
-Biological Valves - Open. Less thrombogenic but do not last as long.

Front 392

Nursing Care for Valvular Heart Disease

Back 392

-V/S, O2 sat, heart sounds, lung sounds.
-Tx of CHF: Same nursing care as CHF.
-Post-Op valve repair or replacement - Similar to post CABG patient.
-Education: Anticoagulation, Endocarditis prophylaxis.

Front 393

Aortic Aneurysm

Back 393

Bulging of artery wall. Results from atherosclerosis which weakens media. Most AAA. Incidence 5-7 % over 60. Likely have advanced atherosclerosis

Front 394

Aortic Aneurysm
Risk Factors

Back 394

Smoking
Diabetes
HTN
Hyperlipidemia

Front 395

Aortic Aneurysm
Clinical Manifestations

Back 395

Often asymptomatic. Found on sono or CT. May note pulsatile mass on exam. Thrombi and plaque can embolize to lower extremities causing blue toe syndrome. Rupture is usually fatal. Posterior rupture may be tamponaded. Leads to retroperitoneal bleed, grey turner’s sign.

Front 396

Aortic Aneurysm
Dx

Back 396

Sono good for screening. CT more accurate to determine length and diameter.

Front 397

Aortic Aneurysm treatment
Small Aneurysm

Back 397

Less than 4 cm may be watched. Serial monitoring. Control of BP, risk factor modification.

Front 398

Aortic Aneurysm treatment

Back 398

-Repair indicated for > 5-6 cm unless not a surgical candidate. (E.g. terminal illness, unlikely to survive surgery.)
-Endovascular Repair. - Risk of leakage - Synthetic graft threaded into aneurysm via femoral artery. 8-44% experience some degree of leak.
-Open Repair. - High surgical mortality - Aorta cross-clamped for 30-45 minutes. Diseased segment removed and synthetic graft sutured in. Mortality up to 10%. High risk of ARF if above renal arteries.

Front 399

Aortic Aneurysm RepairPost-Op Nursing Care

Back 399

SICU post-op: intubated, CVP monitor, A-line, NG tube, multiple IVs and foley, telemetry.
-Thoracic will have thoracotomy: chest tubes
-Maintain BP - Too high could rupture graft, too low could lead to graft thrombosis.
-Pain control.
-Monitor renal function: QH urine output (at least 30 cc), CVP, monitor BUN, creatinine, lytes.
-Monitor for infection: WBC, temp, wound drainage, foley, IV sites. Graft infection serious complication.
-Monitor GI function: return of bowel function. NG to LIS until bowel sounds return COLA of NG drainage.
-Monitor Neuro status - LOC, mental status, peripheral neuro.

Front 400

Why is monitoring urine output critical?

Back 400

Gives idea of renal perfusion & Fx

Front 401

Aortic Aneurysm Repair
Discharge Teaching

Back 401

-No lifting X 4-6 weeks.
-Monitor for infection.
-Antibiotic Prophylaxis
-Risk Factor Modification

Front 402

Aortic Dissection

Back 402

Tear in the intima. Allows blood to enter between intima and media (false lumen). May impede blood flow to brain, spinal cord, kidney, extremities. Rupture is usually fatal.

Front 403

Aortic Dissection
Risk Factors.

Back 403

Marfan’s syndrome. Chronic HTN, Elderly.

Front 404

Aortic Dissection
Clinical Manifestations.

Back 404

-Sudden Severe Chest pain described as tearing radiating to back and shoulders.
-Significantly different BP and pulses between extremities. Neurological compromise, aortic valve insufficiency, cardiac tamponade.

Front 405

Aortic Dissection
Diagnostics

Back 405

CXR shows widened mediastinum.

Front 406

Aortic Dissection
Treatment

Back 406

Lower BP with nitroprusside or beta blockers. Plan for surgical repair.

Front 407

Aortic Dissection
Nursing Care

Back 407

-Critical Care Monitoring - A-line, tele.
-Titrate meds to BP. (Esmolol β Blocker) - Adjust drips to keep BP within parameters.
-On-going Assessment - Peripheral pulses, Neurological status, Heart and Lung Sounds.
-Pain Management.
-Psychosocial Support.
-Prepare Patient for Surgery.
-Help patient cope with anxiety.

Front 408

Peripheral Arterial Disease

Back 408

Severe atherosclerosis occludes blood flow to extremities. Result in ischemia of muscle and nerve tissues.

Front 409

Peripheral Arterial Disease
Risk Factors

Back 409

Smoking, diabetes, HTN, hyperlipidemia.

Front 410

Peripheral Arterial Disease
Clinical Manifestations

Back 410

-Intermittent Claudication.
-Neuropathy.
-Diminished Pulses. (DP & PT)
-Trophic Changes.
-Arterial Ulcers.
-Gangrene.

Front 411

Intermittent Claudication.

Back 411

Muscle ischemia during exertion results in pain from anaerobic metabolism and lactic acid build-up. Resolves with rest. Femoral or Popliteal results in calf pain. Iliac Artery pain in buttocks and thighs. Will progress to rest pain with severe disease.

Front 412

Peripheral Arterial Disease
Diagnostics

Back 412

-Arterial Duplex - Non-invasive ultrasound to determine degree of arterial flow and location of blockages.
-Ankle-Brachial Index (ABI) - Ratio of Ankle BP to highest brachial BP. Normal 0.9 to 1.3. 0.4-.0.9 mild to moderate disease. Less than 0.4 severe disease.
-Angiography - Invasive study. Dye injected and X-rays taken. Definitive study of degree and location of stenosis. Done if surgery planned.

Front 413

Peripheral Arterial Disease
Treatment

Back 413

-Risk factor modification. (smoking cessation, control of BP, lipids, DM)
-Exercise. (helps improve tissue O2 utilization
-Medications. (statins, antiplatelets)
-Pentoxipfylline (Trental®)
-Cilostizol (Pletal®)
-Angioplasty with Stent Placement - Must be on antiplatelet post stent placement.
-Bypass Surgery - Utilizes autologous or synthetic graft.
-Amputation - For gangrene, osteomyelitis or severe disease.

Front 414

Pentoxipfylline (Trental®)

Back 414

Increases erythrocyte flexibility.

Front 415

Cilostizol (Pletal®)

Back 415

Inhibits platelet aggregation and promotes vasodilation. Side effects diarrhea, headache, worsened CHF.

Front 416

Peripheral Arterial Disease
Patient Education

Back 416

-Smoking Cessation.
-Inspect feet daily.
-Protect feet from injury.
-Podiatry Referral.

Front 417

Arterial Bypass Surgery
Post-Op nursing care

Back 417

-Monitor Surgical Site.
-Monitor peripheral neurovascular status (6 P’s)
-Pain Management.
-Promote mobility.
-Discharge Teaching.

Front 418

Arterial Bypass Surgery
peripheral neurovascular status (6 P’s)

Back 418

-Pallor
-parasthesias
-pulselessness
-pain
-paralysis
-poikilothermia

Front 419

Arterial Bypass Surgery
Discharge Teaching.

Back 419

-Teach about medications
-foot care
-monitor incision
-need for exercise etc.

Front 420

Venous Disease
Vein Function

Back 420

-Low Pressure High Volume System - Most of blood volume in venous system.
-Valves - Prevent back flow of blood against gravity.
-Muscle Activity - Compresses vessel and pushes blood back towards heart.
-Thrombophlebitis - Inflammation and thrombosis of vein.

Front 421

Virchow’s Triad
Factors predisposing to thrombophlebitis.

Back 421

-Venous Stasis - Elderly, Immobility, CHF, Atrial Fib, Bedrest, CVA, Varicose Veins, Pregnancy, Orthopedic Surgery.
-Endothelial Damage - IVs, Trauma, Previous Clot, Leg fractures.
-Hypercoagulability - Smoking, Dehydration, Malignancy, OCPs, HRT, Coagulation defects, Sepsis.

Front 422

Superficial Thrombophlebitis

Back 422

-Etiology - UE usually IV site. LE usually trauma to varicose vein.
-Clinical Manifestations - Palpable cord-like vein. Tenderness, erythema, low grade fever.
-No Embolization Risk.
-Treatment - Remove IV, analgesics, elevate extremity, warm moist heat.

Front 423

Deep Vein Thrombosis (DVT)

Back 423

-High risk of embolization.
-Effects 5 % of surgical patients.
-Clinical Manifestations - Unilateral edema, pain, erythema, low grade fever, +/- Homan’s sign
-Complications - PE, Chronic Venous Insufficiency, Arterial Compromise due to severe edema (rare)

Front 424

DVT Prevention

Back 424

-Mobilization
-Ankle Pumps - Promotes venous return
-TEDS - Compression Hose encourage venous return. Important that they are properly fitted without wrinkles.
-Sequential Compression Devices (SCDs) - More effective than TEDS.
-Anticoagulation - LMWH is becoming treatment of choice for DVT prevention in orthopedic and trauma patients. Fewer bleeding complications. No need to titrate.

Front 425

DVT Diagnosis and Treatment

Back 425

-Venous Doppler.
-Anticoagulation with Heparin and Warfarin.
-3-5 day overlap once therapeutic INR. (INR goal of 2.0-3.0)
-Admission for IV unfractionated heparin or outpatient treatment with LMWH.
-Continue Warfarin 3-6 months after resolution.
-TEDS when ambulating.
-Recurrent DVT requires life long anticoagulation.
-IVC Filter for high risk of embolization or recurrent DVT. - placed by INT Rx
-Catheter-Directed Thrombolysis (CDT)

Front 426

Heparin Facts

Back 426

Heparin drip APTT 1.5-2.5 X control. Monitor for HIT and bleeding. LMWH must teach patient or family SC injection technique.

Front 427

Why is it necessary to overlap coumadin® and heparin?

Back 427

Initiate both because warfarin will take days to become therapeutic.

Front 428

Bleeding Complications

Back 428

-Monitor CBC, coagulation studies - Look for new anemia, platelet counts.
-Assess for bruising, mental status change, hematuria, GI bleed, epistaxsis - Observe for indications of hemorrhage or excessive anticoagulation
-Antidote to heparin - Protamine Sulfate.
-Antidote to coumadin - Vitamin K.
-Fresh Frozen Plasma (FFP) - For acute hemorrhage. Contains multiple clotting factors.

Front 429

Warfarin (Coumadin®)
Teaching

Back 429

-Observe for bleeding.
-PT/INR.
-Missed Dose. - Don't double-up
-Avoid OTC - Especially ASA & NSAIDs
-Multiple Drug Interactions - Inform all HCP
-Vitamin K foods - avoid excess consumption
-Avoid Trauma - soft tooth brush, electric razor, no contact sports
-Medic-Alert Bracelet.
-Direct Pressure to Stop Bleeding.

Front 430

Pulmonary Embolism (PE)

Back 430

-Blockage of pulmonary artery or main branches by thrombi, fat or air.
-Sources. - Usually Thrombus. Thrombi from deep veins in legs or RA. Fat from long bone fracture. Air from open central line.
-Pulmonary Infarction Rare Due to Bronchial circulation.

Front 431

Clinical Manifestations of PE

Back 431

-Dyspnea, tachycardia, tachypnea, hypoxia.
-Anxiety
-Pleuritic chest pain - worse with cough, deep breath
-Cough and Hemoptysis.
-Hypotension, Shock - Impaired CO due to inadequate return to LV
-Pulmonary Hypertension - results from recurrent PEs
-Sudden collapse and death.

Front 432

PE Diagnosis

Back 432

-Spiral CT - Becoming diagnostic test of choice. -Minimally invasive good specificity and sensitivity.
-V/Q Scan - Nuclear Med. Injection and inhalation of tracer. Looks for ventilation perfusion mismatch. Reports probabilities. Neither sensitive or specific.
-D-Dimer - Blood test looks for fibrin degradation products. If normal low probability of PE.
-Venous Doppler - Look for source. Confirms diagnosis if in doubt.
-Pulmonary Angiography - Definitive. Invasive.

Front 433

PE Treatment

Back 433

-Hospitalization.
-Heparin Drip.
-O2 to maintain sats.
-Morphine for pain.
-Monitor ABG’s, coags, V/S, EKG, Cardiopulmonary status.
-Possible IVC filter.
-Emergent embolectomy low survival rate.

Front 434

Varicose Veins

Back 434

-Large dilated subcutaneous veins.
-Familial, usually result from valvular incompetence.

Front 435

Varicose Veins
Risk Factors.

Back 435

Obesity, Pregnancy, DVT

Front 436

Varicose Veins
Symptoms

Back 436

ache after prolonged standing, edema.

Front 437

Varicose Veins
Tx

Back 437

-Conservative Tx: Avoid prolonged sitting or standing. Avoid constrictive clothing. Walking to promote venous return. Support/Compression stockings
-Invasive Tx: Sclerotherapy or vein stripping.

Front 438

Venous Insufficiency

Back 438

Incompetent valves in deep veins. Results in increased hydrostatic pressure, interstitial edema, leak of rbcs. Causes edema, staining of skin, dermatitis

Front 439

Venous Insufficiency
Nursing Care

Back 439

-Compression - Patients often require high grade medical compression stockings to control edema.
-Leg Elevation - Above heart level
-Low Sodium Diet - To decrease edema
-Skin Care - To treat dermatitis, prevent breakdown, cellulitis

Front 440

Venous Stasis Ulcers

Back 440

-Etiology severe venous insufficiency.
-Painful, weeping ulcers with irregular borders.
-Often above medial malleolus.
-Must have compression to heal.
-Ensure adequate arterial circulation prior to applying high levels of compression.
-Slow healing.
-Maintain moist wound bed but absorb excess drainage.
-Observe for cellulitis.
-Consider WOCN referral.
-May require grafting.
-ABI to ensure adequate arterial flow. ABI < 0.8 contraindication to high grade compression.

Front 441

Heart
SA node

Back 441

The normal heartbeat is the result of an electrical impulse that originates in the sinoatrial node. This is about 8 mm long and 2 mm thick and lies in the upper posterior portion of the right atrium. Normally, the cells of the SA node spontaneously reach threshold and depolarize more rapidly than other cells, dominating other areas that may be depolarizing at a slower rate, thus it becomes the pacemaker of the heart. The SA node initiates electrical impulses at a rhythmic rate of 60-100 bpm.

Front 442

Heart
AV node

Back 442

the nonbranching portion of the bundle of His. This consists of specialized conduction tissue that provides the electrical links between the atrium and ventricle. The AV node is a group of cells located in the posterior septal wall of the right atrium immediately behind the tricuspid valve and near the openin of the coronary sinus. This is 22 mm long, 10mm wide and 3 mm thick. In most people, this is supplied by the RCA. Can fire 40-60 bpm

Front 443

Heart
Bundle of His

Back 443

After passing through the AV node, the electrical impulse enters the bunddle of His, or common bundle. This is normally the only electrical connection between the atria and ventricles. This is located in the upper portion of the interventricular septum and connects the AV node with the two bundle branches.

Front 444

Heart
Right and Left Bundle Branches

Back 444

Right bundle branch innervates the right ventricle and the left bundle branch spreads the electrical impulse to the interventricular septum and left ventricle, which is thicker and more muscular than the right.

Front 445

Heart
Purkinje Fibers

Back 445

Special network of fibers in the ventricular myocardium that have intrinsic pacemaker ability at 20-40 bpm.

Front 446

Properties of Cardiac Tissue
Automaticity

Back 446

Ability to initiate a spontaneous impulse.

Front 447

Properties of Cardiac Tissue
Contractility

Back 447

Ability to respond mechanically to an impulse.

Front 448

Properties of Cardiac Tissue
Conductivity

Back 448

Ability to transmit an impulse along a membrane in a orderly manner.

Front 449

Properties of Cardiac Tissue
Excitability

Back 449

Ability to be electrically stimulated.

Front 450

Intrinsic Rate of Conduction System

Back 450

SA node: 60-100
AV node: 40-60
Purkinje fibers: 20-40

Front 451

P wave

Back 451

P Wave- represents atrial depolarization and the spread of the electrical impulse throughout the right and left atria. Atria contact at the height of the P wave. Smooth, round, no more than 2.5 mm, positive in 1, 2, aVF, and V2-V6. Tall and pointed or wide and notched P waves may be seen in COPD and CHF, or valve disease

Front 452

PR Interval

Back 452

PR interval- An interval is a waveforma nd a segment. The P wave plus the PR segment equals the PR interval. This reflects the depolarization of the right and left atria nad the spread of the impulse through the AV node, bundle of His, etc. It does not include the duration of conduction from the SA node to the right atrium. This is measured from the point where P wave leaves baseline to the beginning of QRS. Normally measures 0.12-0.20 sec and shortens with increase heart rate.

Front 453

PR Segment

Back 453

PR segment- A segment is a line between waveforms and is named by the waveform that precedes or follows it. This is part of the PR interval and is the horizontal line between the end of the P wave and beginning of the QRS complex

Front 454

QRS Complex

Back 454

QRS complex- This represents ventricular depolarization. Normally 0.06-0.10 sec.

Front 455

ST Segment

Back 455

ST segment- Portion of the ECG between the QRS complex and the T wave. This represents the early part of ventricular repolarization. ST segment depression- ischemia or hypokalemia, elevation, MI, (Digoxin may cause a dip)

Front 456

T Wave

Back 456

T wave- Ventricular repolarization. Slightly asymmetric. Negative T waves suggest Myocardial ischemia, Tall, pointed T waves common in hyperkalemia

Front 457

QT Interval

Back 457

QT interval- Represents ventricular activity. A prolonged QT puts ventricals at risk for dysrhythmias such as torsades. A QT interval that is more than half of the R-R interval is considered prolonged

Front 458

U Wave

Back 458

U Wave- May not be seen, may be repolarization of purkenje fibers. Rounded symmetric. . If it is taller than 1.5 mm, may indicate electorolyte imbalance, medication, hyperthyroidism. Negative U waves strongly suggestive of organic heart disease.

Front 459

EKG Strips

Back 459

ECG paper is graph paper made up of small and large boxes measured in millimeters. The smallest boxes are 1 mm wide and 1 mm high. The horizontal axis is measured in time. The horizontal unit (1mm/ small box) measures 0.04sec. The lines between every five boxes are heavier and indicate a large box. This represents 0.20 sec. Five large boxes represent 1 sec.
The vertical axis represents voltage or amplitude.

Front 460

Etiology of Arrhythmias

Back 460

-Accessory Pathways
-Conduction Defects
-MI
-CAD
-Myocardial Hypertrophy
-Acid-Base Imbalances
-Alcohol
-Drug Toxicity
-Antiarrhythmics
-Electrolyte Imbalances
-Hypoxia
-Thyroid Disease

Front 461

Evaluating an Arrhythmia

Back 461

-Evaluate the patient, not just the monitor - Hemodynamic response
-Assess level of consciousness (LOC).
-Assess Vital Signs, Pulse Ox.
-Assess Skin/Perfusion.
-Assess for Myocardial Ischemia.
-Assess Respiratory.

Front 462

Rate Measurement
Six Second Method

Back 462

-Simplest, quickest way to determine rate
-Number of QRS complexes in six seconds, multiply by 10. (Note that 30 large boxes equal six seconds)

Front 463

Rate Measurement
R-R Method 1

Back 463

Number of Large Squares- divide by 300

Front 464

Rate Measurement
R-R Method 2

Back 464

Number of Small Squares- divide by 1500

Front 465

Analyzing a Rhythm Strip

Back 465

-What is the Rate - Ventricular and Atrial
-Is the rhythm regular or irregular
-Is there a P wave before each QRS
-Is the PR interval within normal limits
-Is the QRS narrow or wide
-Interpret the rhythm
-How is the rhythm clinically significant

Front 466

Sinus Rhythm

Back 466

-Rate: 60-100 beats per minute
-Rhythm: Atrial and Ventricular Regular
-P Wave: Uniform in appearance, upright, normal shape, one preceding each QRS complex
-PR Interval: 0.12- 0.20 seconds
-QRS: 0.10 second or less. (If larger than 0.10- QRS is wide and there may be a bundle branch block)

Front 467

Sinus Bradycardia

Back 467

-Rate: Less than 60 beats per minute
-Rhythm: Atrial and Ventricular Regular
-P Waves: Uniform in appearance, upright, normal shape, one preceding each QRS complex
-PR Interval: 0.12-0.20 seconds
-QRS: Usually 0.10 seconds or less

Front 468

Sinus Bradycardia
Etiology

Back 468

-Athletic Training
-MI
-Hypothyroidism
-Sick Sinus Syndrome
-Medications
-Hypothyroidism
-Increased ICP

Front 469

Sinus Bradycardia
Tx

Back 469

-None may be indicated.
-Treat underlying cause.
-Atropine.
-Pacemaker.

Front 470

Sinus Tachycardia

Back 470

-Rate: Usually 100- 140 beats per minute
-Rhythm: Atrial and ventricular regular
-P Waves: Uniform in appearance, upright, normal shape, one preceding each QRS
-PR Interval: 0.12-0.20 second
-QRS: Usually 0.10 second or less

Front 471

Sinus Tachycardia
Etiology

Back 471

-Stress
-Anemia
-Fever
-Shock
-Hyperthyroidism
-Drugs
-CHF
-Pain

Front 472

Sinus Tachycardia
Tx

Back 472

-Treat underlying cause.
-β Blocker
-Calcium Channel Blocker (Verapamil or Diltiazem)

Front 473

Sinus Arrest (Pause)

Back 473

-Sinus impulses are not generated. May be because of digitalis, quinidine, CAD, rheumatic heart disease, MI, or myocarditis.
-If hemodynamic compromise is present, IV atropine, or insertion of permanent pacemaker.

Front 474

Premature Atrial Contraction (PAC)

Back 474

-Originates in ectopic focus.
-P Waves: Premature, differ from sinus P waves- may be flattened, notched, pointed, biphasic, or lost in the preceding T wave.
-QRS: Narrow (less than 0.10)

Front 475

Premature Atrial Contraction (PAC)
Etiology & Tx

Back 475

-Etiology: CHF, Myocardial ischemia, fatigue, COPD, atrial enlargement, digitalis toxicity, hypokalemia, hypomagnesemia, and excessive use of caffeine, tobacco or alcohol.
-Occasionally occur in healthy individual.
-Treatment: Usually not necessary. Treat underlying cause.

Front 476

Supraventricular Tachycardia (SVT)

Back 476

-Rapid atrial contractions.
-QRS narrow (less than 0.10).
-Etiology: Accessory pathways, MI, stimulants, CAD, COPD.
-Treatment: Carotid massage, Adenosine IV push, βBlocker, Calcium Channel Blocker, Ablation.

Front 477

PAT

Back 477

-Paroxysmal supraventricular tachycardia is a term used to describe SVT that starts and ends suddenly.
-The onset or cessation of the SVT and identification of the underlying rhythm that precedes it should also be known.

Front 478

Atrial Flutter

Back 478

-Rate: Atrial rate 250-350 bpm. Ventricular rate variable.
-Rhythm: Atrial regular, ventricular may be regular or irregular
-No P waves.
-QRS conducted in 2:1, 3:1, 4:1 ratio.
-Loss of atrial kick.
-Risk of Atrial Fib, embolization.

Front 479

Atrial Flutter
Etiology

Back 479

-Valve Disease
-COPD
-CAD
-Medications
-Hyperthyroidism.

Front 480

Atrial Flutter
Tx

Back 480

-Rate control with digoxin, ablation.
-Chemical cardioversion with amiodarone, sotalol, rhythmol.
-DC Cardioversion.
-Ablation.

Front 481

Atrial Fibrillation

Back 481

-Atrial Rate 350-600.
-Ventricular Rate Variable.
-“Irregularly Irregular”.
-Loss of atrial kick.
-Rate control.
-Embolization risk.

Front 482

Atrial Fibrillation
Etiology

Back 482

-Valve Disease.
-CAD.
-Cardiomyopathy.
-COPD.
-Hyperthyroidism.
-Atrial Enlargement.

Front 483

Atrial Fibrillation
Tx

Back 483

-Rate Control.
-Anticoagulation.
-Chemical Cardioversion.
-DC Cardioversion.
-Ablation.
-Maze Procedure

Front 484

Junctional Escape Rhythm

Back 484

-Rate: 40-60 beats per minute
-P waves: May occur before, during, or after the QRS. If visible, the P wave is inverted.
-Etiology: MI, Sinus Node Dysfunction, Digoxin Toxicity.
-Treatment:Do not suppress, Stop Digoxin, Atropine.

Front 485

1st Degree AV Block

Back 485

-Prolonged PR Interval (> 0.20).
-P waves conducted.
-Generally benign.
-No treatment indicated.

Front 486

2nd Degree Mobitz Type 1 (Wenckebach)

Back 486

-PR interval progressively lengthens until non-conducted.
-Etiology: MI, Ischemia, Medications.
-Observe closely prepare to pace patient if it deteriorates.

Front 487

2nd Degree Mobitz Type 2

Back 487

-Rate: Atrial rate is greater than the ventricular rate. Ventricular rate is often slow.
-Rhythm: Atrial regular (P’s plot through) Ventricular irregular
-Intermittent conduction of P’s.
-Hemodynamic Compromise.
-Etiology: MI, Digoxin Toxicity.
-Pacemaker indicated.

Front 488

3rd Degree AV Block

Back 488

-Rate: Atrial rate greater than Ventricular. The ventricular rate is determined by the origin of the escape rhythm
-Rhythm: Atrial regular. Ventricular regular. No relationship between the atrial and ventricular rhythm.
-Etiology: CAD, MI, Myocarditis, Digoxin Toxicity.
-Emergent Treatment: Atropine, Transvenous or Transcutaneous Pacing.

Front 489

Idioventricular Rhythm

Back 489

-A slow V-Tach.
-Etiology: MI, Reperfusion.
-Escape rhythm.
-DO NOT SUPPRESS.

Front 490

Premature Ventricular Contraction (PVC)

Back 490

-Ectopic Ventricular -Contraction.
-QRS wide and bizarre.
-Unifocal vs. Multifocal.
-Bigeminy, Trigeminy.
-Couplets.

Front 491

PVCs
Etiology and Tx

Back 491

-Occasionally occur in healthy hearts.
-Etiology: CAD, MI, Stimulants, Digoxin, Hypokalemia,
-No treatment or treat cautiously - CAST Trial

Front 492

Ventricular Tachycardia (V-Tach)

Back 492

-Rapid rate, Wide QRS
-May be pulseless.
-Can deteriorate into -Ventricular Fibrillation
-IF IT IS UNCLEAR WHETHER A REGULAR, WIDE-QRS TACHYCARDIA IS VT OR SVT WITH AN INTRAVENTRICULAR CONDUCTION DEFECT, TREAT THE RHYTHM AS VENTRICULAR TACHYCARDIA UNTIL PROVEN OTHERWISE

Front 493

V-Tach
Etiology

Back 493

-Acute MI
-CAD
-Reperfusion
-Hypokalemia
-Prolonged QT
-Antiarrhythmic

Front 494

V-Tach
Tx

Back 494

-Hemodynamically Stable: Amiodarone
-Hemodynamically Unstable: Cardioversion.
-Pulseless: Immediate Defibrillation

Front 495

Torsades De Pointes

Back 495

-“Twisting around a point”.
-Triggered by prolonged QT.
-Treatment: Magnesium Sulfate, Overdrive pacing, Cardioversion.

Front 496

Ventricular Fibrillation

Back 496

-No ventricular contractions.
-No cardiac output.
-Brain cells die in 4-6 minutes.
-Immediate defibrillation, ACLS.
-Initiate CPR until defibrillator available.

Front 497

Asystole

Back 497

-V-fib deteriorates into asystole.
-Rule out fine V-fib.
-Poor prognosis.
-Treatment: CPR, ACLS, epinephrine, atropine, pacing

Front 498

Etiology of Cardiac Arrest
H and T pneumonic

Back 498

-Hypovolemia
-Hypoxia
-Hydrogen Ions (Acidosis)
-Hyper or Hypo kalemia
-Hypoglycemia
-Hypothermia
-Toxins
-Tamponade
-Tension Pneumothorax
-Thrombosis or coronary artery or pulmonary artery
-Trauma

Front 499

Artifact

Back 499

Make sure you don’t mistake artifact for v fib/ v tach and vis versa.

Front 500

Pulseless Electrical Activity (PEA)

Back 500

-Electrical activity does not result in contraction.
-Poor prognosis
-Etiology: Acidosis, potassium imbalances, drug overdose, cardiac tamponade, PE, MI, tension pneumothorax.
-Treatment: Correct cause, CPR, Epinephrine, Atropine, ACLS

Front 501

Pacing

Back 501

-Indications: Heart blocks, Tachyarrhythmias, Sinus node dysfunction
-Temporary: Transcutaneous, Transvenous, Epicardial
-Permanent

Front 502

Nursing Care for Pacemaker Insertion

Back 502

-Monitor for signs/symptoms of infections.
-Know type of pacer and settings
-Monitor telemetry for sensing and capture.
-Assess and treat pain.
-Educate patient.

Front 503

Pacemaker Patient Education

Back 503

-Keep site dry until healed.
-Avoid using operative side arm until healed.
-Monitor Pulse
-Avoid MRIs.
-Must be interrogated.
-Can use microwave.
-Carry pacemaker card.

Front 504

Elective Cardioversion

Back 504

-Informed consent if patient alert and stable.
-IV Sedation.
-Manage Airway.
-Synchronization.

Front 505

Cardioversion

Back 505

-Elective Procedure
-Client awake & frequently sedated
-Synchronized with "QRS"
-50-200 Joules
-Consent Form
-EKG Monitor

Front 506

Defibrillation

Back 506

-Emergency
-V-Fib/V-Tach
-No Cardiac Output
-Begin with 200 Joules - up to 360
-Client Unconscious
-EKG monitor

Front 507

Implantable Cardioverter-Defibrillator

Back 507

-Indicated for cardiac arrest survivors, recurrent arrhythmias, high risk patients.
-Include pacemaker functions.
-Post-op care similar to pacemaker insertion.