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Cardiovascular System. Nursing 1120 By: Diana Blum RN MSN Metropolitan Community College. Basics. In the mediastinum Right side is under sternum About the Size of a fist Weighs 10-14 oz. Cardiac Function. Primary function : to pump blood through the pulmonary and systemic circulations.

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cardiovascular system

Cardiovascular System

Nursing 1120

By: Diana Blum RN MSN

Metropolitan Community College

  • In the mediastinum
  • Right side is under sternum
  • About the Size of a fist
    • Weighs 10-14 oz.
cardiac function
Cardiac Function
  • Primary function : to pump blood through the pulmonary and systemic circulations
3 layers of cardiac tissue
3 Layers of Cardiac tissue
  • Endocardium:
  • Myocardium:
  • Epicardium:
blood flow
Blood Flow
  • Right Atrium: receives blood from vena cava and from coronary arteries
  • Tricuspid Valve: passes blood from right atrium to right ventricle
  • Right Ventricle: bottom chamber of the heart that contracts (systole) and pushes blood through pulmonic valve and into pulmonary artery
blood flow continued
Blood Flow Continued
  • Pulmonary artery: carries blood to the lungs
  • Pulmonary veins: carry the newly oxygenated blood back to the heart
  • Left Atrium: accepts blood from pulmonary veins
  • Mitral Valve: moves blood from left atrium to left ventricle
  • Left Ventricle: thickest and strongest muscle
    • Cone shaped and contains apex of heart
    • When the LV contracts (Systole) blood is ejected into aorta and out to Body
coronary arteries
Coronary Arteries
  • Two major coronary arteries
    • arise from the aorta beyond the aortic valve.
    • Blood flows to the coronary arteries during diastole
  • Left main, LAD, Circumflex feeds most of Left side of the heart
  • Right feeds SA node, AV node, RA, RL
Collateral circulation is a network of tiny blood vessels, and, under normal conditions, not open. When the coronary arteries narrow to the point that blood flow to the heart muscle is limited (coronary artery disease), collateral vessels may enlarge and become active. This allows blood to flow around the blocked artery to another artery nearby or to the same artery past the blockage, protecting the heart tissue from injury.
conduction system
Conduction System
  • SA node: (pacemaker)
    • initiates the impulse
    • travels thru atria to the AV node, located on the floor of the RA
    • Impulse is delayed at AV node, then transmitted to bundle of His
cardiac cycle
Cardiac Cycle
  • Contraction and relaxation of the heart:
  • Diastole:
  • Systole:
cardiac output
Cardiac Output
  • the volume of blood ejected by the heart each minute and is determined by stroke volume and the heart rate.
  • Normal stroke volume is 60-100 ml
  • Normal cardiac output is 4 to 8 L / min
  • (CO = HR X SV)
factors affecting stroke volume
Factors affecting Stroke Volume
  • Preload: the amount of blood remaining in the ventricles at the end of diastole or the pressure generated at the end of diastole
  • Contractility: is the ability of the cardiac muscle fibers to shorten and produce a muscle contraction. (Inotropic, + or -)
  • Afterload: amount of pressure the Ventricle must overcome to eject blood volume out
heart rate
Heart Rate
  • SA node : pacemaker of heart 60-100 bpm
  • AV node : 40 -60 bpm
  • Heart is innervated by sympathetic and parasympathetic nervous system
    • Sympathetic: speeds HR, and increases force of contraction
    • Parasympathetic: slows HR and force
heart tones
Heart Tones
  • Murmur: Produced by turbulent sounds across valves
    • Rub: inflamed pericardium-best heard along left sternal border
    • S3 murmur: sounds like “Kentucky”
    • S4 murmur: sounds like “Mississippi”

present illness
Present Illness
  • Fatigue
  • Edema
  • Palpitations
  • Pain
  • Aggravating and relieving factors
past medical history
Past Medical History
  • HTN
  • renal disease
  • pulmonary disease
  • DM
  • CVA
  • rheumatic fever
  • streptococcal sore throat
  • scarlet fever
  • previous cardiac disease or conditions
  • currents meds and allergy
review of systems
Review of systems
  • weight gain
  • fatigue
  • dyspnea
  • cough
  • orthopnea
  • palpitations
  • chest pain
  • fainting
  • concentrated urine
  • edema
functional assessment
Functional assessment
  • effects of illness on ADLs and rest patterns
  • smoker
  • diet
  • stress
  • coping
physical assessment
Physical Assessment
  • General:
  • VS: orthostatic bp in both arms, apical rate and rhythm, respiratory rate and effort
  • peripheral pulses:
  • Skin: color hair distribution, cap refill, temp
  • Thorax: heart sounds, lung sounds, sputum
  • Extremities: pulses, color, temp, edema
age related changes
Age Related Changes
  • Heart less able to adapt to changing needs related to activity
  • Valves thicken and stiffen
  • # of pacemaker cells decrease
  • Nerve fibers decrease
  • Frequent dysrhythmias
diagnostic tests
Diagnostic Tests
  • EKG: rate, rhythm, ischemia (T-inverted), injury (ST segment elevation), arrhythmias, strain, infarction (q wave)
  • Echocardiogram: (TEE) sound wave test detects size of chambers, valve integrity, flow, wall motion, Cardiac Output
diagnostic tests continued
Diagnostic Tests Continued


Troponin will show elevation 3-6 hr after symptoms begin/injury peak in 12 hours stay in system 10-14 days

<0.10 is negative

0.10-0.60 is intermediate and may indicate injury

>0.60 is positive evidence of MI

Myoglobin increases 1-4 hours after MI

CPK-MB will show increase 4-6 hrs after MI peaks in 18-24 hours in system 2-3 days

BNP can be elevated 48 hrs after MI which indicates heart failure

diagnostic tests continued1
Diagnostic Tests Continued
  • CBC: anemia
  • CMP: screening K+, etc
  • PT, INR
  • PTT
  • Lipid profile: see next 2 slides
diagnostic tests continued2
Diagnostic Tests Continued
  • ABG: assess acid/base levels
  • Pulse Oximetry: generally >92%
  • Holter monitoring: 24+ hr of EKG + events
  • Stress test: treadmill or pharmacological
  • Cardiac Catheterization: invasive, NPO 6-8h, consent. Visualizes chambers, valves, arteries, pressures, CO
  • Heart-CT scan: assesses CAD, MRI
  • Nuclear scans: assess heart muscle viability
  • EPS: NPO, consent, IV, assess electrical activity

Video-mysterious heart volume 3 chapter 2

etiology of cad
Etiology of CAD
  • CAD occurs when the intimal lining of the coronaries begin to plaque resulting in jagged edges and narrowed passageway for blood flow
  • Atherosclerosis results in impaired blood flow to the heart muscle
risk factors for cad
Risk Factors for CAD
  • Non-controllable-
  • Controllable-
s s of cad
s/s of CAD
  • Angina which results from a lack of 0xygen to the heart muscle
    • 4Es=
  • Weakness, diaphoresis, SOB
  • N/V
mi myocardial infarction
MI: Myocardial Infarction
  • Occlusion of a coronary artery resulting in necrosis of the heart muscle.
  • Risk factors: same as for CAD
  • Pathophysiology: AMI-over 4-6 hrs ischemia injury and infarction develop. Ischemia=lack of 02 to heart muscle, if not relieved=injury. After 20 min of ischemia=infarction
  • Main S/S: chest pain and accompanying S/S
Within 24 hours after infarction, healing begins, collateral circulation begins.
  • 10-14 days after MI=extension of MI may occur due to myocardial tissue vulnerability to stress
  • Complete scar formation and healing takes about 6 weeks

Video- mysterious heart volume 1 chapter 2

data collection
Data Collection
  • Same as for CAD but will assess symptom of chest pain with accompanying s/s
  • May have EKG changes with or with-out ST-T wave changes or Q wave changes
  • Cardiac Bio-markers (Troponin, Myoglobin, CPK, CKMB)
  • May proceed with Echocardiogram to assess if wall motion sluggish
  • May go to cath lab
angina or mi
Angina or MI
  • Angina without MI} often relieved with rest and NTG
  • Angina with MI } may be relieved with rest, NTG, 02, MS, rescue angioplasty, etc.
      • Think MONA
        • Morphine
        • Oxygen
        • Nitroglycerin
        • Aspirin

treatment continued
Treatment continued
  • May need antiarrhythmic meds
    • like what???
  • Stool softeners to reduce valsalva maneuver and prevent constipation r/t narcotic use and bed rest
  • Treat: HTN, DM other co-morbid illnesses
  • Cardiac Rehab to follow
  • Low fat low cholesterol diet
  • Prescribed exercise program 5-7 days a week
  • Knows correct use of NTG for angina
  • Management of DM, HTN
  • Stop smoking
  • Medications to reduce work load or dilate
low fat 30 low cholesterol 200mg
Low fat <30% Low cholesterol <200mg
  • Lean meat: skinless
  • Dairy limited: egg beaters, skim milk
  • Olive oil, canola oil
  • Avoid: fried, fatty or heavily marbled meats, sausage, lunch meat, spareribs, frankfurters, salt pork, canned fish in oil, yolks, duck. Cream sauces, gravy, buttered vegetables, sweet rolls, other processed foods
  • 5-7 X week is goal to include stretches with warm-up, progressive walking program, light weights, stretches with cool down.
  • Strengthens heart muscle, reduces BP, BS, weight, stress, tension, appetite, LDLs.
  • Increases HDLs, energy and self esteem and improves immune system
principles of exercise
Principles of Exercise
  • Practice on regular basis
  • Know how to do own pulse
  • Strive for target heart rate
  • Stop if chest pain occurs
  • Complications: CHF & Dysrhythmias
nursing interventions for mi
Nursing interventions for MI
  • Comfort measures
  • Freq VS, cardiac monitoring, I&O, CMS checks, spacing activities
  • Heart & lung sounds, assess fluid volume status, IV responsibilities, note BP & Pulse prior to heart meds!!
  • Client education r/t diet, meds, pulse taking activity, elimination, reporting chest pain and correct use of nitro products for angina
medications for heart disease
Medications for Heart Disease
  • Anti-Anginal:
  • Anti-Hypertensive:
  • Anti-Arrhythmic: l
  • Cardiac glycoside:
medication continued
Medication continued
  • Thrombolytic:
  • Anti-coagulant:
  • Anti-platelet aggregate:
  • Lipid-Lowering agents:
  • Diuretics:
  • Electrolyte replacement:
medication continued1
Medication continued
  • 02 to maintain 02 sat > 92% to reduce chance of angina/ischemia
  • If Angina the nurse needs to have the client lie down, take VS then report to charge nurse ,met team, call md.
  • Instruct client: If develops chest pain, sit down take 1 nitro every 3- 5 min x 3. If chest pain not relieved call 911
90% will develop complication
  • 80% will demonstrate arrhythmia
    • the most common cause of death in clients in the pre-hospital period. (VT>>>VF)
  • CHF and severe Left ventricular failure
  • Papillary muscle dysfunction
  • Pericarditis
  • Thromboembolism
  • Ventricle rupture
nursing diagnosis
Nursing Diagnosis
  • Decreased cardiac output r/t Dysrhythmias
  • Acute Pain r/t lack of 02 to myocardium
  • Anxiety r/t to feeling of doom, lack of understanding of medical diagnosis
  • New in 1958
    • purpose to restore the regular rhythm
      • improve tissue perfusion and cardiac output.
  • Temporary / permanent
  • Single chamber or double chamber
  • Teach client how to take 1 min pulse, s/s to report to MD-dizzy, angina, dyspnea
  • Carry card and know precautions
  • Implantable defibrillator to correct a life threatening rhythm disturbance.
    • Has pacemaker back-up.
  • check battery q2months
  • Instruct on how to take pulse for 1 min
  • s/s to report to MD: firing, s/s of dizziness, dyspnea, weakness, carry card and wear bracelet, CPR for family. Know precautions
Nursing care for client with newly implanted pacemaker or AICD.
    • Assess cardiac monitor for capture/pacing (pacer)
    • VS post-op then q 4 hours, IV, bed rest till am
    • Dressing dry and intact until AM then often may remove. Increase activity progressively
    • Instruct client not to raise arm above shoulder for 5days. May shower in 5 days
angioplasty with stent
Angioplasty with Stent
  • Procedure done at the time of cardiac cath.
  • Balloon angioplasty is accomplished to widen or open specific coronary vessel-stent is inserted to maintain patency of the vessel.
  • pre-procedure Plavix given with follow up Plavix

ep with ablation
EP with Ablation
  • Mapping of myocardial tissue to determine irritable focus.
  • Low voltage current delivered to ablate tissue causing SVT or VT
  • 90% effective
nursing care
Nursing Care
  • NPO prior
  • Coumadin stopped 4 days prior, Heparin 4 hours prior
  • Post – procedure same as heart cath
    • Cardiac monitoring
    • Muscloskeletal and groin checks
    • VS
    • Ambulate prior to discharge
cardiac surgery
Cardiac Surgery
  • Coronary artery bypass
  • Valve replacement or repair
  • Septal repair and other congenital repairs
    • CCU post op, chest tubes
    • Pre-op teaching with post op expectations
    • See client teaching for CABG, Valve repair/replacement, care of PTCA, MI
congestive heart failure
Congestive Heart Failure
  • Video..the mysterious heart volume1 chapter 3
causes of chf
Causes of CHF
  • CAD, advancing age
  • HTN is a major factor > CHF x 3
  • DM, Smoking, Obesity
  • Valvular incompetency, alcohol or other chemicals, idiopathic,(unknown)
s s of left sided chf
S/S of Left Sided CHF
  • Fatigue
  • Angina
  • Tachycardia
  • Cool extremities
  • Hacking cough
  • Crackles
  • Frothy sputum
  • Gallop
s s of right sided chf
S/S of Right Sided CHF
  • Jugular distention
  • Anorexia/nausea
  • Dependent edema
  • Distended abdomen
  • Weight gain
  • BP problems
assessment findings
Assessment Findings
  • C/O SOB, weakness, dry cough, fatigue, can not lie down must sit up to breath, has gained weight
  • Auscultation of the heart} rapid HR, extra heart sounds
  • Auscultation of the lungs} rales, wheezing
  • Examination of the extremities for peripheral edema
system compensation
System Compensation
  • Mediated thru Sympathetic Nervous System: as CO drops, baroreceptors alert brain

    • stimulation Beta 1=>>Stimulation Beta 2=
      • Activate Alpha receptors peripherally=constriction=>>
  • Causing S/S of CHF because:
  • Contractility decreases
  • Stroke volume and CO continue to decrease
  • Afterload (pressure on the other side of the aorta) increases
  • Preload ( pressure caused by increase volume to heart creating an exaggerated stretch in the muscle) increases
renal compensation
Renal Compensation
  • CO drops initiating renin-angiotensin mechanism
    • Results in powerful vasoconstrictor
ventricular hypertrophy
Ventricular Hypertrophy
  • The heart enlarges which results in strain
  • The increase in volume causes the ventricles to dilate
  • Eventually remodeling will occur
diagnostic tests1
Diagnostic Tests
  • H&P
  • Chest x-ray
  • EKG:
  • Echocardiogram:
  • CBC:
  • CMP:
  • Thyroid function
  • ABGs
  • BNP=B type natriuretic peptide= hormone released in response to Ventricular stretch ( CHF peptide)
  • Nuclear studies to determine heart function, EF, tissue viability
  • Cardiac Cath to determine exact nature of heart function
chf management
CHF Management
  • Directed at: Improving LV function (Contractility) by decreasing intravascular volume and decreasing vascular resistance
  • Decreasing venous return (Preload)
  • Decreasing BP (Afterload)
  • Improving gas exchange and 02
  • Increasing the CO and reducing anxiety
  • ACE inhibitors to < afterload by dilating vessels and < BP (ARBs)
  • Beta blockers to < 02 demand by reducing the contractility of the heart and HR (not given in acute period)
  • Diuretics
  • ASA in low doses or Plavix to help prevent blood clot formation
  • Anticoagulants for those with poor EFs to prevent CVA
  • Antiarrhythmics to control ectopy
  • Biventricular pacing (CRT=cardiac resynchronization therapy) to improve CO
  • Digoxin to increase contractility of myocardial fibers and improving cardiac output. +inotropic agent
treatment of chf
Treatment of CHF
  • Treat underlying cause
  • Rest and hi Fowlers to reduce work load and improve ventilation
  • 02 at 2-6 L/min with 02 sats >92% to increase available 02 and prevent hypoxemia
  • Freq VS and cardiac monitoring
treatment continued1
Treatment continued
  • I & O q shift
  • Daily am weights before breakfast and after voiding. 2-3# weight gain in 1-4 days call MD
  • Sodium restricted diet
  • Medications: to decrease intravascular volume thus reducing venous return, dilate and reduce BP and improve contractility
educating the chf client
Educating the CHF Client
  • Education re: heart failure
    • Explanation of heart failure
    • Expected S/S and when to call MD
    • Self monitoring of daily weights
    • Know medications and need to take them
    • 2000mg sodium restricted diet
    • Importance of low level daily exercise program (energy conservation)
    • Prognosis / advanced directives
A dysrhythmia is a disturbance of the rhythm of the heart caused by a problem in the conduction system.
  • Categorized by site of origin: atrial , AV nodal, ventricular
  • Blocks are interruptions in impulse conduction: 1st, 2nd type 1&2, 3rd or complete heart block
to map to determine if regular or irregular
To map= to determine if regular or irregular

Each small box measures 0.04

1 big box (5 small boxes) is equal to a HR of 300

2 big boxes is hr of 150

3 big boxes is hr of 100

4 big boxes is hr of 75

5 big boxes is hr of 60

6 big boxes is hr of 50

7 big boxes is hr of 43

8 big boxes is hr of 38

P-wave = atrial electrical activity
  • QRS= ventricular electrical activity
  • T wave= resting phase of ventricle
p wave
P wave

Measures: 0.12-0.20


Measures: 0.06-0.10

heart rates
Heart rates
  • NSR: heart rate is ___bpm
  • ST: heart rate ____ bpm
  • SB: heart rate ____bpm
sinus rhythm
Sinus rhythm
  • PR interval- 0.12-0.20sec
  • QRS-0.06-0.10sec
  • QT segment 0.36-0.44 sec
  • Heart rate 60-100
sinus arrythmia
Sinus arrythmia

Hr= 60-100 bpm

On strip it looks regular but does not map out

PR interval= 0.12-0.20

junctional escape rhythm
Junctional escape rhythm

HR 40-60 bpm

<60 bpm is accelerated

Rhythm is regular

Pwaves not always present

sinus bradycardia
Sinus Bradycardia
  • All criteria same except rate < 60bpm
  • S/S: dizziness, syncope, angina, hypotension, sweating, nausea, dyspnea
  • Sometimes no S/S
  • Treat underlying cause
  • IV atropine, pacemaker
sinus tachycardia
Sinus Tachycardia
  • All criteria same as with NSR except rate >100
  • Causes: fever, dehydration, hypovolemia, increased sympathetic nervous system stimulation, stress, exercise, AMI
  • S/S: Palpations #1, angina and < CO from < V filling time
  • Treatment: correct cause, eliminate caffeine, nicotine, alcohol. Beta blockers may be ordered
first degree heart block
First degree heart block

Rate is usually WNL

Rhythm is regular

Pwaves are normal in size and shape

The PR interval is prolonged (>0.20 sec) but constant

second degree heart block type 1
Second degree heart block type 1

Pwaves are normal in size and shape;

Some pwaves are not followed by QRS

PR interval: lengthens with each cycle until it appears without QRS Complex

then the cycle starts over

QRS is usually narrow

second degree heart block type 2
Second degree heart block type 2

Ventricular rate is usually slow

Rhythm is irregular

Pwaves are normal in size and shape (more pwaves than QRS)

PR interval is within normal limits

QRS is usually wide

3 rd degree heart block of complete heart block
3rd degree heart block of complete heart block

Ventricular rate is regular but there is no correlation between pwaves and QRS

Pwaves are normal in size and shape

No true PR interval

atrial fibrillation
Atrial Fibrillation

Erratic wavy base

Pr is not measurable

QRS 0.10 sec or less usually

a fib continued
A fib continued
  • Atrial rate > 400 bpm with a varying Ventricular rate
  • Overall rhythm irregular
  • No P waves, unable to measure PR interval
  • QRS=normal: Twave undeterminable
  • Causes: Rheumatic fever, mitral valve stenosis, cad. HTN, MI, hyperthyroidism, COPD, CHF see pp. 604
a fib continued1
A fib continued
  • Concern is the development ________________________________________________________________________
  • Treatment: Ca channel blockers and anti- arrhythmics to convert, beta blockers to HR, anticoagulants to prevent embolization.
  • Synchronized cardioversion
atrial flutter
Atrial flutter

Atrial rate of 250-450 bpm ventricular rate varies

Atrial rhythm is regular ventricular rate is irregular

No identifiable p waves

P wave is not measurable

Qrs: 0.10 or less usually

paced beat
Paced beat

Pacer spike should fall before the P wave unless a dual

Chamber pacemaker; if it does not there could be a problem

premature ventricular conduction pvc
Premature ventricular conduction (PVC)

Extra beat


uniform=go the same direction

multifocal= go in different direction

R on T=when the pvc fall on the preceding twave

couplet= 2 pvcs together

bigeminy= pvc every other beat

trigeminy=pvc every third beat

ventricular tachycardia
Ventricular tachycardia



torsades de pointe
Torsades de pointe

This is a polymorphic VT

Usually electrical imbalance in nature r/t NA+ or K+

ventricular fibrillation
Ventricular Fibrillation

Rate can not be determined because of no identifiable waves

Rapid chaotic rhythm with no pattern

No p waves

No PR interval


vtach vfib
  • Both can be life threatening
  • VT= V HR 100-250 bpm
  • Causes: AMI, CAD, hypokalemia, dig toxic
  • S/S: palpitations, dizzy, angina,
  • Treatment: assess for pulse, if none, defib
  • VF=Rate undeterminable Cause: same
  • Treatment: CPR
HTN is described as persistent elevation of arterial blood pressure greater than 140/90 on at least 2 or more readings on different dates.
  • The Joint National Committee, Detection, Evaluation, and Treatment of High Blood Pressure defines normal:
    • BP as S < 120 mm Hg and D < 80 mm Hg
    • PreHTN: SBP 120-139 DBP 80-89
    • Stage 1: SBP 140-159 DBP 90-99
    • Stage 2: SBP >160 DBP >100
types of hypertension
Types of Hypertension
  • Essential HTN: (Primary) which is the most common 90-95% of population
  • Secondary HTN: is a result of another disease, kidney, pregnancy.
factors that determine arterial pressure
Factors that determine arterial pressure
  • Cardiac output
  • Peripheral vascular resistance
possible causes of pvr
Possible Causes of PVR
  • Narrowing of blood vessels, PVD, CAD, kidney disease: renin/angiotensin =vasoconstriction
    • Release of catecholamine (epinephrine and adrenalin) = vasoconstriction
  • blood volume= more work to pump
  • Blood viscosity=harder to pump
  • Ability of blood vessel to stretch
causative factors of htn
Causative Factors of HTN
  • Hyperlipidemia Obesity
  • Atherosclerosis Sedentary
  • DM Family Hx
  • Cigarette smoking
  • Age > 60
  • Men
  • Post menapausal women
  • Often none
  • Occipital headache more severe on rising
  • Lightheadedness
  • Epistaxis
  • Known as the ‘Silent Killer’
  • Damage to blood vessels of the eyes, heart, kidney, brain resulting in:
  • Stroke
  • CHF
  • AMI
  • Renal failure
  • Blindness
lifestyle change education
Lifestyle Change Education
  • Exercise, dash diet, stop smoking, weight management and control, stress reduction, medications and recording BP frequently
  • Avoid OTC meds
  • Instruct on how to do postural BPs
  • Narrowing of the opening of the valves. Limits the amount of blood which is ejected from one chamber to the next.
mitral stenosis
Mitral Stenosis
  • Mitral valve leaflets become thickened and fibrotic. Affect women age 20-40
  • CHF may develop
    • TX if failure develops: Digoxin, Lasix, beta blockers, and anti arrhythmics, lo Na diet, etc
    • Will monitor with yearly echocardiogram
    • Surgery if worsens
  • Prophylactic antibiotics prior to invasive procedure or dental work
  • The inability of the valves to close completely.
  • Allows the blood to backflow.
  • Mitral valve is the most commonly affected
Cardiac insufficiency can be caused by many factors – by a swelling of the heart muscle (1), an enlargement of the hollow chambers in the heart (2), a heart attack (3) or a blood clot (4).
mitral insufficiency
Mitral Insufficiency
  • Often accompanies mitral stenosis as a result of _______________.
  • Valve leaflet become rigid and shorten, prevents closure of valve.
  • Hypertrophy of Left Atrium and Ventricle = L sided heart failure occurs
  • Murmur heard.
  • F/U with echocardiogram
  • TX: vasodilators, same as for stenosis
mitral valve prolapse
Mitral Valve Prolapse
  • When the Left ventricle leaflets become enlarged, and protrude into the left atrium during systole.
  • Benign but may progress to Mitral insufficiency
  • More common in women age 20-55
s s of mitral prolapse
S/S of mitral prolapse
  • Often none
  • Others experience chest pain, palpitations, dizziness, syncope, dysrhythmias
  • Monitor with echocardiogram
  • May do heart catherization
  • Manage stress, beta blockers if tachycardia
aortic stenosis
Aortic Stenosis
  • Occurs when valve cusps become fibrotic and calcify.
  • Most commonly caused by aging and atherosclerosis.
  • Occurs most predominantly in men
  • Untreated will lead to Left sided CHF
aortic insufficiency
Aortic Insufficiency
  • Caused primarily by rheumatic fever
  • May also be caused by chronic HTN
  • Predominantly in men
  • Hypertrophy of the Left ventricle and eventually_______________________
  • Blood may eventually back up into the pulmonary system and lead to _______________________________
s s and treatment
S/S and Treatment
  • Aortic murmur, tachycardia, palpitations, CHF with fatigue, SOB, ascites
  • Monitored with echocardiogram assessing L ventricular dilatation
  • Chest X-ray-enlargement of heart
  • May do cardiac cath
  • May need valve repair or replacement
Inflammation of the heart most often results from systemic infections and may include any layer of the heart:

What are they???

  • Inner layer: tends to affect the valves (Mitral=L).
  • Organisms (Bacterial or fungal) present in blood stream and collect (colonize) on the valves:
    • Rheumatic heart disease, congenital defects or mitral valve prolapse
    • IV drug users or invasive procedures
Clients with known valvular disease need to be treated with prophylactic antibiotics prior to any invasive procedure including dental.
    • Immunosuppression and any source of contamination places clients at risk
  • Bacteria may enter blood stream:
  • Bacteria collect on valves and vegetate
  • Complications: Ventricular septal defect, CHF(#1 cause of death) and embolization
  • Fever- (99-105)
  • Chills and night sweats may accompany
  • Malaise, fatigue and weight loss
  • Appearance of petechiae in the mouth, conjunctiva and legs
  • Chest and abdominal pain indicating embolization
treatment and diagnostics
Treatment and Diagnostics
  • H&P and Lab tests

CBC with diff with leukocytosis, sed rate, (+)blood cultures

  • May have heart murmur Echocardiogram to visualize valves and vegetation
  • Chest x-ray: CHF
  • Long term antibiotics, rest, limited activity, prophylactic anticoagulants, valve replacement after inflammation treated
nursing assessment
Nursing Assessment
  • Frequent VS and assess for fever
  • Assess for heart murmur
  • Note cough
  • Assess peripheral edema
  • Rest with limited activity, administer meds in a timely manner
Muscle layer: Local or diffuse inflammation of the myocardium. May be viral or bacterial, an autoimmune process or drug toxicity.
  • May result in cardiomyopathy=
  • Characterized by degeneration and necrosis of myocardial tissue that is different of that caused by MI
  • Tissue next to necrosed area hypertrophies, loses elasticity, results in CHF and arrhythmias
  • Asymptomatic
  • May have fever, fatigue, sore throat, dyspnea, muscle aches
  • Lymph nodes may be enlarged
  • Chest pain 7-10 days after virus
  • CHF S/S
  • Based on Hx, S/S, and testing-enzymes>
  • May hear friction rub, rales
  • Jugular vein distention
  • Chest x-ray, echocardiogram=hypertrophy
  • EKG=arrhythmias
  • Biopsy (RV) shows lymphatic infiltration and cell necrosis
  • Bed rest
  • 02
  • Meds: cardiac glycoside-Lanoxin, anticoagulants, antiarrhythmic, antibiotics, steroids
  • Cardiac monitoring
  • NI same as for endocarditis
  • ND same as for endocarditis
Outer-surrounds heart
  • Inflammation of the pericardium.
  • Primary or secondary
  • Acute or chronic
  • Acute: virus, bacteria, fungi, chemotherapy, MI
  • Chronic: TB, radiation or metastases
  • Inflammation causes an increase in the amount of pericardial fluid and inflammation of surrounding tissues.
  • Adhesions may occur
  • May lead to tamponade
  • Chest pain is hallmark
  • Most severe on inspiration, sharp, stabbing, or dull and burning.
  • Pain is relieved by sitting up or leaning forward
  • Dyspnea, chills and fever
  • WBC elevated
  • Serial EKG show that ST segment increases and resolves in several weeks. A fib may occur
  • Echocardiogram to see pericardial thickening and effusion
  • Enzymes can be increased
  • Blood cultures to ID organism
  • Analgesics
  • Antipyretics
  • Anti-inflammatory agents
  • Antibiotics
  • May need OR to create a pericardial window to allow for drainage of fluid
  • NI and ND same as for endocarditis
  • Heart rate and rhythm, color, temperature, cognition
  • Circulation: peripheral CMS checks
  • Vital signs to include 02 saturations and telemetry interpretation
  • Subjective: c/o chest pain, SOB, fatigue, lightheadedness, dizziness
  • retrieved on 4/8/07.
  • Images found at Retrieved on 4/8/07.
  • Aehlert, B. RN BSPA (2006). EKGs Made Easy. Mosby (3rd ed). St Louis.