Cardiac Nursing notes Exam 2

Rheumatic Heart Disease

Most common cause of untreated pharyngeal infection

Strep throat

Group A Betahemolytic

Streptococci

Risk and Prevention of Rheumatic Heart Disease

Take all antibiotics

Rheumatic fever

3rd world countries

Clinical manifestations of Rheumatic Heart Disease

Asymptomatic

Cardiomegaly

Heart murmur S3 AND S4

Joint pain

Chest pain

Friction rub

Diagnostics for Rheumatic Heart Disease

Echocardiogram

Chest XRAY

Labs: BNP/CRP/CBC

Treatment for Rheumatic Heart Disease

Penicillin if allergic then Tetracycline, Qunilones,Macrolides

Doxycycline

Erythromycin

Ciprofloxacin

ASA

NSAIDS

Rheumatic Heart Disease Management

Activity mixed with rest

Assess exercise intolerance

Healing diet

Fluid management

Expect surgery to repair damaged valves if necessary

Complications for Rheumatic Heart Disease

Pericarditis

Cardiac tamponade (emergency)

Myocardial Infarction Risk factors (modifiable)

Smoking

High LDL

Type 2 diabetes

Elevated adrenalin (catecholamines)

Obesity/Inactivity

Hypertension

Myocardial Infarction risk factors (non modifiable)

Male gender

Female gender after menopause(the estrogen)

Family history

Myocardial Infarction

Refers to the destruction of heart muscle from lack of oxygenated blood supply

Typically in the early morning hours

Common cause atherosclerosis(gradual build up of plaque in arteries)

Rupture of the plaque results in thrombosis formation and obstruct coronary blood supply resulting in decreased cardiac output

Stable angina

Not associated with damage to the heart muscle but is a warning sign for potential heart muscle damage

Acute Coronary syndrome

An umbrella term when there is a concern for myocardial ischemia and it encompasses unstable angina, non-ST elevation MI(NSTEMI), ST elevation MI (STEMI)

Unstable Angina

Pain that is not associated with exercise and is not relieved by rest

May present with ECG changes but no elevation in cardiac markers

EMERGENCY

NSTEMI

Non ST elevation MI

A partial occlusion of a major coronary vessel or complete occlusion of a minor coronary vessel causing REVERSIBLE partial thickness heart muscle damage

STEMI

ST elevation MI

A complete occlusion of a major coronary vessel resulting in IRREVERSIBLE full thickness heart muscle damage

Severe occlusion of the right coronary artery

Results in symptoms of right heart failure

Branches of Left coronary arteries

Left Coronary Artery is referred to as- Left Main (LM)

Branches of into the left anterior descending (LAD), and the circumflex (CIRC) coronary arteries

In some individuals the third branch Ramus coronary artery between LAD/CIRC

An occlusion of the LM coronary artery is often referred to as

The wide maker- because the interruption of its extensive coverage is associated with sudden death

Left coronary artery occlusion is most likely to produce extensive cardiac injury with impairment of

Heart function

Pulmonary Congestion

Low Cardiac Output

Clinical Manifestation of Complete occlusion of the vessel resulting in an Myocardial Infarction

Chest pain (stable or unstable)

Shoulder and arm pain, jaw and tooth pain, shoulder blade pain, upper back pain

SOB

N/V

Sweating

Generalized fatigue

Clinical manifestation of Right Sided MI

JVD

Hypotension

Bradycardia; due to damage to the SA node (sinoatrial)

N/V

Clinical manifestations of Left ventricle infarction

The worst prognosis

Dyspnea

Tachycardia Hypertension; result from loss of cardiac output because of damage to the left ventricle and subsequent stimulation of sympathetic compensatory mechanism

Clinical manifestations of MI person to person

Women: neck, shoulder blade, and jaw pain as well as ABDOMINAL pain

Geriatrics: Dyspnea, syncope, weakness, CONFUSION

Diabetics: SOB, fatigue

Types of Myocardial Infarction

Anterior wall: (ECG changes, leads V1-V4/ LAD)

Posterior wall:( Possibly leads V1-V4/ CIRC or RCA)

Lateral Wall: (Leads 1, aVL,V5,V6/ CIRC)

Inferior wall: (Leads 2,3,aVF/RCA)

Diagnosing for Myocardial Infarction

Cardiac markers (Troponin- )

ECG changes (Q wave)

Image testing to reveal loss of viable heart muscle

Labs

ECG/Coronary angiography/Stress test/ECHO

Labs Myocardial Infarction

Troponin, CK, CKMB, BUN,CMP,CBC,BUN/CREAT., COAGS,ARTERIAL BLOOD GAS

CKMB- increased levels can be seen in 3 hours and remain elevated up to 36 hours

Troponin 1&T- specific marker for cardiac muscle damage, levels can elevate within 4 hours and stay elevated up to 10 days

ECG for MI

Th gold standard for diagnosing MI

Typical ECG change of MI: ST- segment elevation and presence of Q waves

ST- segment depression indicates ischemia(NSTEMI)

Evolution from ischemia to infarction include TALL narrow T waves then, ST-segment elevation (STEMI with T- wave)

Presence of a Q wave predicts a large infarction with increased mortality

When are less likely than men to have ECG changes when presenting with an MI

Echocardiogram

Can assist in diagnosing MI by looking for specific areas of heart muscle that are not contracting normally referred to as WALL MOTION ABNORMALITIES

Stress testing for MI

Another way to evaluate heart function

Exercise test

Or with meds- Dobutamine/ Adenosine

Nuclear stress test

The best stress test for diagnosing Myocardial Ischemia

Reveals the amount of viable heart muscle, which helps to determine treatment

Coronary Angiography gold standard for CAD, At the same time a ventriculogram may be obtained

Involves positioning the catheter to allow injected dye to enter the left ventricle.

Demonstrates how efficiently the Left ventricle fills and pumps blood, how well blood flow s through the aortic and mitral valves, and the size of the left ventricle

Treatment for once the diagnosis of MI is made

Maximizing oxygenation and administering medications to control pain, dilate coronaries, prevent clots, and decrease myocardial workload

Medications: Oxygen, Nitroglycerin,asprin, morphine, beta blockers(decrease myocardial workload), heparin infusion(help prevent new clot formation)

Beta blockers will not be used for Right coronary artery MI experiencing Bradycardia

Repercussion Therapy

Revascularization by PCI or Fibrinolytic therapy within 6 HOURS have significantly higher survival rates

PCI or Percutaneous Coronary intervention

Most preferred method for opening a blocked blood vessel causing an MI

Should be done within 90 min. of arrival at hospital (door to balloon 90 min.)

Radial or femoral artery are typically used

Preferred site for Percutaneous Coronary Intervention

Radial preferred site risk of internal bleeding is eliminated(once catheter is removed you place a compression device to remain pressure, and no requirement for patient to remain immobile

If femoral (the patient needs to lie flat without bending for 2-6 hours)

Fibrinolytic’s

Are medications that accomplish revascularization

Should be administered within 30 minutes of arrival to the hospital

Should be considered if not contraindicated and immediate PCI is not available

Fibrinolytics: Success with this med is defined as-

ST-segment reduction greater than 50% at 90 minutes

Contraindications for Fibrinolytic’s

Recent surgery

Bleeding

Presence of a peptic ulcer

Uncontrolled hypertension

Pregnancy

Non compressible vascular punctures

Complication for Fibrinolytic

Intracranial Hemorrage

Bleeding

CABG FOR MI

Is not the first line of interventions because PCI and Fibrinolytic is much faster, and not. a long surgical procedure

CABG

Indication for MI is if PCI is unsuccessful, or critical left main or three vessels disease

A healthy artery or vein typically mamary artery or saphenous vein is grafted to the clocked coronary artery; one end is attached to the aorta, with the other end attached to the blocked coronary distal to the occlusion

Complications associated with CABG

Bleeding

Dysrhythmias

MI

Stroke

Nonunion of of the sternum

Sternal infections

Renal failure because of decreased blood flow

Heart failure

Complications of BYPASS

Induction of a systemic inflammatory response resulting in vasodilatory shock

Heparin induced thrombocytopenia

Activation of platelets

Complications associated with cross clamping the aorta during procedure

Off pumper Beating Heart CABG

Developed to avoid complications related to bypass

Secondary preventions of MI

Cardiac Rehab

Life Simple 7

Cardiac Rehab

Supervised exercise program which also provides education regarding diet, weight, meds purpose/side effects, and psychosocial support.

Goal recovery and to improve quality of life

Life simple 7

1. No smoking cig. or tobacco

2. Maintain normal body weight

3. Exercise at least 75-150 min. a week

4. Eat a healthy diet

5. Maintain total cholesterol level less than 200mg/dL

6. Keep BP les than 120/79 mmHg

7. Keep fasting blood glucose less than 100 mg/dL

Complications of MI

Heart failure (decreased level of ventricular function, from large amount of heart muscle dying, and inability to produce adequate cardiac output to maintain the body metabolic demand)

Sinoatrial node dysfunctions(Systole, symptomatic bradycardia, heart block) Most common after an inferior wall MI because the right coronary artery supplies the SA node. Temporary pacemaker may be used to prevent systole

What is not uncommon after MI

Ventricular Arrhythmias are not

They occur In the first 48 hours

Immediate defibrillation is the treatment of choice for ventricular fibrillation and pulseless ventricular tachycardia

Nurse Assessment for MI

Vitals( tachycardia with a borderline low BP and decreased oxygen are signs of inadequate cardiac output)

Pain(PQRST)

ECG changes (ST-segment depression is indicative of ischemia. Q wave is diagnostic for MI)

Assess restlessness early sign and feeling of anxiety and doom late stage

Assess skin and temp(decreased pulses and pale, cold, clammy, skin are indicative of inadequate tissue perfusion)

Monitor urine output (decreased or absent urine is a sign of decreased perfusion to kidneys)

Monitor Labs

Nurse assessment Post CABG for MI

Monitor heart rate and BP every 15 min initially then every 4 hours when patient is stable

Continuous cardiac monitoring (dysrhythmias are common after CABG)

Assess heart tones(Muffled may indicate tamponade, S3/S4 and crackles may indicate Heart Failure)

Monitor breath sounds( diminished may indicate pleural effusions)

Monitor core temp

Hourly I&O less than 30 ml in 2 hours notify provider

Asses skin color temp edema cap refill (Edema can be an expected response after CABG)

Monitor chest tube output (bright red drainage may indicate hemorrhage)

Nurse actions for MI

Administer oxygen

Insert 2 large bore catheters

Administer meds (aspirin, heparin, nitro, morphine, betablockers, fibrinolytic)

Continous ECG monitoring

Bed rest (to decrease oxygen demands)

Post op actions after CABG

Maintain tight BP control (hypotension may result in graft collapse, hypertension may result in bleeding)

Administer fluids and meds(maintain hemodynamic stability)

Rewarm patient slowly with warm fluids , prevent shivering it increases oxygen needs

Maintain effective sedation and analgesics to decrease anxiety and pain

While intubated reposition frequently, suction as needed, Oral care every 4 hours, pulmonary hygiene like IS/ cough and deep breather every 1-2 hours while awake, chest splinting when coughing

Plan to initiate early ambulation

Initial dressing of wound to be removed or changed by provider!!! then can be changed daily as needed

Teaching for MI

Immediately report signs and symptoms of MI such as chest pain or chest discomfort or increases SOB

Purpose, Dose, and side effects of meds

Life simple 7: No smoking, normal body weight, exercise 75-150 min weekly, cholesterol level less than 200, bp less than 120/79, fasting blood glucose less than 100

Teaching Post CABG

Signs of infection

Sternal precautions; DO NOT lift weight over 10 pounds, DO NOT raise arms over head, DO NOT bend at the waist, DO NOT participate in vigorous activity until cleared by a physician

Participate in cardiac rehabilitation(decreases risk of repeated MI

Evaluating outcomes of MI

A well managed patient is free from pain and has normal vitals with an improved SPO2

Signs of decreased perfusion from inadequate cardiac output such as cool extremities, weak pulses, and decreased urine output are resolving

Goals: Effective care include resumption of a normal active life from pain and feeling of anxiety and doom

Rheumatic Heart disease treatment

Pace maker