cardiovascular system
TRANSCRIPT
Physical Assessment Vital signs wnl No abnormal heart
sounds Strong & equal
peripheral pulses Even & unlabored
breathing Regular heart beat
No pallor, cyanosis, or clubbing No syncope, fatigue, or chest pain
No edema Can perform ADLs
without dyspnea
Key Points
Discomfort Indigestion Squeezing Heaviness Viselike
Transient loss of consciousness
Common in older adults
Cardiac Pain Syncope
Key Points
Assess the filling volume & pressure on the right side of heart
Swishing sounds that develop in narrowed arteries
Jugular Vein Pressure Bruits
Diagnostic Assessment No serum markers of
myocardial damage Serum lipids within
normal ranges Normal C-reactive
protein Normal ECG
Key Points: Safety Assess for allergy
to iodine After invasive test
monitor insertion site for bleeding and hematoma formation
Assess vital signs carefully
Report new dysrhythmias after testing
Key Points: Health Promotion
Identify pts at risk for
cardiovascular disease
Psychological Stress
Family history Diabetes
Hyperlipidemia HTN Overweight Physical inactivity Smoking
Key Points: Teaching
How to reduce risks of
Disease Exercise Diet modification Smoking
cessation Medications
Inform pt aboutnonmodifiable riskfactors Family history Gender genetics
Coronary Heart Disease Atherosclerotic plaque in coronary
arteries May be asmptomatic May lead to Angina, heart attack,
dysrhythmias, heart failure, or death Cause of atherosclerotic plaque is
unknown May be linked to certain risk factors
CAD Most common cause of ↓
coronary blood flow is plaque formation
Lipoproteins & fibrous tissue in arterial wall
Theory: begins with an injury to or inflammation of endothelial cells lining the artery
Endothelial damage promotes platelet adhesion & aggregation & attracts leukocytes to area
CHD: Diagnostic Tests Diagnosis based on history & risk factors ↑ triglyceride/LDL & ↓ HDL levels Total serum cholesterol Lipid profile (triglyceride, HDL, LDL levels, & ratio
of HDL to total cholesterol (ratio 1:5; ideal 1:3) NPO 10-12 hrs Etoh & many meds affect results
Risk Factor Management Stop smoking improves HDL levels ↓ saturated fat & cholesterol intake ↑ soluble and insoluable fibers Exercise Control HTN (maintaining 140/90 mmHg) Blood sugar control
Risk Factor Management Mevacor, Zocar, Lipitor- Monitor liver
function & muscle pain/tenderness (may cause myopathy)
If taking Digoxin, monitor for digoxin toxicity
If at risk for MI, low dose ASA
CAD Nursing Diagnosis
Imbalanced Nutrition: More than body requirements
Ineffective Health Maintanance
CAD: Assessment Focus on identifying
risk factorsHealth history: CP, SOB, weakness, current
diet exercise patterns,
Meds smoking hx etoh intake h/o heart disease,
HTN, or diabetes family h/o CHD
CAD: Physical Assessment Weight Height BMI Blood Pressure Strenght and equality of peripheral
pulses
Atherosclerosis Injury→ lipoproteins collect in lining of
artery Macrophages go to site as part of
inflammatory process Platelets, cholesterol, & blood
stimulates smooth muscle cells & connective tissue proliferate abnormally
Yellow fatty streak on inner lining of artery →fibrous plaque develops →collagen fibers proliferate → blood lipids accumulate →occludes vessel lumen
Myocardial IschemiaPathophysiology
Oxygen supply inadequate to meet metabolic demands of cardiac cells
Coronary perfusion & myocardial workload critical to meeting metabolic demands
Oxygen content in blood is a factor
Cardiac ischemia Occurs when
blood flow to the heart muscle (myocardium) is obstructed by a partial or complete blockage of a coronary artery.
Angina
Angina: Common Causes Atherosclerotic heart disease Hypertension Coronary artery spasm Hypertrophic cardiomyopathy
Angina: Pain Assessment Heavy, squeezing,
pressing, burning, choking, aching & apprehension
Substernal, radiating to left arm and/or shoulder, jaw, right shoulder
Percipitated by exercise, exposure to cold, a heavy meal, mental tension, sexual intercourse
Relieved by rest and/or nitroglycerine
Angina: Diagnostic Information ECG: ST depression & T wave inversion Exercise stress test: ST depression and
hypotension Stress echocardiogram: changes in wall
motion Coronary angiogram: coronary spasms Cardiac catheterization: detects arterial
blockage
Angina: Nursing Assessment Dyspnea
Nausea, vomiting
Fatigue
Diaphoresis, pallor, weakness
Syncope
Dysthythmias
CHD: Nonmodifiable Risk Factors Age (50% 65 or
older) Gender (Men
affected at early age)
Race (AA ↑ incidence of HTN)
Genetic factors
CHD: Modifiable Risk Factors
Hypertension Diabetes
CHD: Modifiable Risk Factors Hyperlipidemia
LDLs = less desirable lipoproteins
HDLs = highly desirable lipoproteins
CAD: Modifiable Risk Factors Undesirable Desirable
CHD: Modifiable Risk Factors
Modifiable Risk Factors
CHD: Modifiable Risk Factors Physical Activity
CHD: Modifiable Risk Factors
Angina: Nursing Plans & Interventions
Monitor meds & instruct on proper administration
Assess factors causing pain (decrease these factors)
Teach risk factors/identify risk factors
Angina: During an attack Provide immediate rest Take vital signs Record an ECG 3 NTG tablets, 5 minutes apart Emergency if no relief after NTG x 3
Angina: Physical Activity Avoid isometric activity Exercise program Resume sexual activity after exercise
tolerated Climb 2 flights of stairs without exertion Take NTG before intercourse
Angina: Diet Modify saturated fats and sodium Antilipemic meds to lower cholesterol
levels
Angina: Medical InterventionsPercutaneous transluminal coronary angioplasty (PTCA)
Angina: Medical InterventionsCoronary Artery Stent
Angina: Medical InterventionsArthrectomy
Arthrectomy: a cath with a collection chamber is used to remove plaque that is trapped in the chamber
Coronary laser therapy
Inadequate Oxygenation & Tissue Perfusion: Assessment
Report pain: Chest Shoulder Arm Jaw Back abdomen
Indigestion Diaphoresis Nausea Vomiting Anxious behavior Palpitations Fatigue Disorientation/confusion
Peripheral Vascular Disease Can be due to arterial or venous
pathology
PVD: Predisposing factors
Arterioclerosis Advanced age
H/O DVT Valvular
incompetence
Arterial Venous
PVD: Associated Diseases
Raynaud disease Buerger disease Diabetes Acute occlusion
Varicose veins Thrombophlebitis Venous stasis
ulcers
Arterial Venous
PVD: Skin Assessment
Smooth Shiny Loss of hair Thickened nails
Brown pigment around ankles
Arterial Venous
PVD: Color
Pallor on elevation
Rubor when dependent
Cyanotic when dependent
Arterial Venous
PVD: Temperature/Pulses
Cool Pulse decreased
or absent
Warm Pulse normal
Arterial Venous
PVD: Pain Assessment
Sharp Increases with walking
and elevation Intermittent claudication Rest pain when
hortizonal; relieved by dependent position
Persistant aching, full feeling, dull sensation
Relieved when horizonal (elevate and use TEDs)
Arterial Venous
PVD: Ulcers
Very painful Occur on lateral lower
legs, toes, heels Demarcated edges Necrotic Not edematous
Slightly painful Occur on medial
legs, ankles Uneven edges Superficial Marked edema
Arterial Venous
PVD: Nursing Diagnosis Ineffective tissue perfusion Activity intolerance Impaired skin integrity Risk for infection Pain
PVD: Noninvasive Treatment
Stop smoking Topical antibiotic Saline dressing Bedrest,
immobilization Fibrinolytic agents if
clots a problem
Systemic antibiotics
Compression dressing
Limb elevation Fibrinolytic agents
and anticoagulants
Arterial Venous
PVD: Surgery
Embolectomy Endarterectomy Arterial bypass Percutaneous
transluminal angioplasty
Amputation
Vein ligation Thrombectomy Debribement
Arterial Venous
PVD: Nursing Plans & Interventions Monitor extremities
color, temp sensation, pulse quality
Schedule activities Rest Keep extremities
elevated (if venous)
Avoid crossing legs
Wear nonrestrictive clothing
Keep extremities warm
Do not use electric heating pads
PVD: Teach Change position
frequently Wear nonrestricitve
clothing Avoid crossing legs Keep legs in
dependent position
Wear shoes when ambulating
Obtain proper foot and nail care
Discourage smoking (vasoconstriction & spasms of arteries)
PVD: PreOp & PostOp Care
Maintain affected extremity in a level position (if venous)
Slightly dependent position (if arterial)
Assess surgical site for hemorrhage
Anticoagulants continued to prevent thrombosis
Preoperative Postoperative
Key Points: Vascular Problems Take vital signs Assess peripheral
pulses Assess capillary
refill Check sensation
and temperature
Pain assessment Assess ulcer Elevate legs if
swollen unless arterial flow is poor
Electrocardiogram (ECG) Reflection of the heart's electrical circuit
and its activity.
Coronary Circulation
The heart derives its arterial supply from the coronary sinuses which lie either side of the root of the aorta.
The left and right sinus give rise to the left and right coronary artery and their branches,
Right Coronary Artery
Supplies the right side of the heart via the Right Main), Supplies the inferior border (via Right Marginal branch) Supplies the posterior surface (via Right Posterior
Descending branch). It also supplies the Sinoatrial node and Atrioventricular
node in 90% and 65% of people respectively. Impairment of the right coronary circulation causes
inferior and posterior infarction as well as bradycardia and varying degrees of heart block.
Left Coronary Artery
Divides into the Left Anterior Descending Branch Supplies the anterior surface of the left ventricle & the
anterior 2/3 of the interventricular septum. The other branch of the left Main Stem, the Left
Circumflex, winds around the posterior surface of the left ventricle, anastamoses with the Right Posterior Descending artery.
Impairment of the left coronary circulation causes anterior and lateral infarction
Where the left circumflex comes across to supply the territory of the right coronary artery it may also lead to inferior infarction.
Depolarization
In a cardiac cell, two primary chemicals provide the electrical charges: sodium (Na+) and potassium (K+).
In the resting cell, the potassium is mostly on the inside, while the sodium is mostly on the outside.
This results in a negatively charged cell at rest (the interior of the cardiac cell is mostly negative or polarized at rest).
When depolarized, the interior cell becomes positively charged and the cardiac cell will contract.
In Summary
The polarized or resting cell will carry a negative charge on the inside. When depolarized, the opposite will occur.
This is due to the movement of sodium and potassium across the cell membrane.
Depolarization moves a wave through the myocardium.
As the wave of depolarization stimulates the heart’s cells, they become positive and begin to contract.
This cell-to-cell conduction of depolarization through the myocardium is carried by the fast moving sodium ions.
Repolarization The return of electrical charges to their
original state. This process must happen before the cells
can be ready conduct again. Look at the next slide diagram and note the
depolarization and repolarization phases as they are represented on the ECG.
Electric Circuit of the Heart: SA Node
The intrinsic electrical circuit of the heart
‘natural pacemaker' Receives both a
parasympathetic and sympathetic nerve supply.
Lies at the junction of the Superior Vena Cava with the Right Atrium
Connected by a rapid conduction system to the atrio-ventricular node
AV node which lies at the base of the interatrial septum.
Electric Circuit of the Heart: AV Node
Regarded as the ‘gatekeeper' or resistor in the circuit
Tries to maintain normal communications between the atria and ventricles.
Connects to the Bundle of His Bundle of His divides into a
right bundle, supplying the right ventricle and a
Left bundle, which through its anterior-superior and posterior-inferior divisions supplies the two surfaces of the left ventricle.
Electrical conduction The electrical conduction
through circuits causes a rapid wave of depolarization to spread across the atria and then down through the ventricles.
This depolarization and subsequent repolarization is represented by the different waves of the ECG.
Electrical conduction The electrical baseline of the
ECG from is known as the iso-electric line.
Deflections above this line are POSITIVE
Deflections below are NEGATIVE.
R wave is positive, S wave is negative A QRS is iso-electric when
the addition of the positive and negative deflections give a net deflection of zero.
EKG Paper Grid where time is measured along the
horizontal axis. Each small square is 1 mm in length and
represents 0.04 seconds. Each larger square is 5 mm in length and
represents 0.2 seconds.
Calculating Heart Rate When the rhythm is regular, the heart
rate is 300 divided by the number of large squares between the QRS complexes.
For example, if there are 4 large squares between regular QRS complexes, the heart rate is 75 (300/4=75).
Calculating Heart Rate The second method can be used with an
irregular rhythm to estimate the rate. Count the number of R waves in a 6
second strip and multiply by 10.
For example, if there are 7 R waves in a 6 second strip, the heart rate is 70 (7x10=70).
P Wave First small positive
deflection before the QRS complex
Atrial depolarization
width <0.12 sec
PR Interval Distance from
start of P wave to start of QRS complex
Conduction time from SAN through the AV node
< 0.20 sec
Q Wave First negative
deflection after the P wave and before the R wave
Represents conduction from the opposite side of the heart
R Wave First positive
deflection after the P wave
Ventricular depolarization
S Wave First negative
deflection after the R wave
Ventricular depolarization
QRS Complex Complex including
the Q, R and S waves
Complete ventricular depolarization
<0.12 seconds
ST Segment Segment between
the end of the S wave and the start of the T wave
First part of ventricular repolarization
T Wave Positive wave after
the QRS complex
Ventricular repolarization
QT Interval Start of the QRS
complex to the end of the T wave
Ventricular
depolarization and repolarization
0.42 seconds
Normal Sinus Rhythm Regular rhythm Heart rate 60 – 100 P wave for every ORS, identical PR interval 0.12 – 0.20 second ORS complex 0.06 – 0.10 seconds
Sinus Bradycardia Heart rate < 60 Regular rhythm P wave before each ORS, identical PR interval .12 - .20 seconds ORS < .12
Sinus BradycardiaPossible Causes Hyperkalemia Increased vagal
tone-constipation, vomiting
Inferior wall MI Beta blockers,
digoxin, morphine
Signs & Symptoms Possibly asymptomatic Fatigue,
lightheadedness, syncope, palpitations, chest pain
Treatment Treat underlying cause Atropine Pacemaker
Sinus Tachycardia Regular rhythm Heart rate 100 – 160 P wave before each ORS PR interval 0.12 – 0.20 second ORS complex 0.06 – 0.10 seconds
Sinus TachycardiaPossible Causes Caffeine, tobacco,
ETOH Digoxin toxicity Exercise, fever, stress,
pain, dehydration Inflammatory response Hypovolemia
Signs & Symptoms Usually asymptomatic Palpitations or angina
Treatment Treat underlying cause Beta blockers