Med surg cardiology Flashcards
Fibrous Pericardium
Loose sac that outlines the heart
Parietal Pericardium
Serous membrane of fluid to decrease
friction
Visceral Pericardium (Epicardium)
Inner most protective layer that covers the
heart muscle directly
Additional protective layer to prevent
friction as the heart beats
Coronary Circulation
– Coronary arteries (which stem from the aorta) provide the heart tissue and muscle with oxygenated blood – Without appropriate coronary artery function, the heart muscle will not receive appropriate oxygen
The heart has:
Four Chambers
Superior Chambers
– Right Atrium
– Left Atrium
Inferior Chambers
– Right Ventricle
– Left Ventricle
Ventricles have thicker
walls than atria
True.
Left side of the heart pumps blood where?
Out to the body.
Cardiac valves:
Prevent backflow.
Atrioventricular (AV) Valves
– Right AV Valve:
■ Tricuspid
– Left AV Valve:
■ Mitral
Semilunar Valves
– Pulmonic/Pulmonary
– Aortic
Veins:
Blood flows towards the heart.
Arteries:
Blood flows away from the heart.
Blood flows through the heart by:
Inferior/Superior Vena Cava »
Right Atrium »
Tricuspid Valve »
Right Ventricle »
Pulmonic/Pulmonary Valve »
Pulmonary Artery »
Lungs (oxygenation occurs)
»
Pulmonary Veins »
Left Atrium »
Mitral Valve »
Left Ventricle »
Aortic Valve »
Aorta »
Body Tissue/OrgansThe heart is:
an electrically driven pump.
The pump is comprised of muscle
If the muscle grows & hypertrophies – the pump
doesn’t function as well
The pump requires both electricity and oxygen to function
– Again, the pump is a muscle, muscle tissue needs
oxygen to survive
– Electricity is derived from electrolytes (potassium,
sodium, calcium, magnesium)
■ Electricity “fires” and sends conduction through
the chambers of the heart
■ If electrolytes are out of normal range, the pump
will not work appropriately
■ Electrical conduction system coordinates both contraction
and relaxation of the heart chambers
Pathway of electrical impulses that generates a heartbeat
Electrical impulses cause the heart to contract and pump blood to the rest
of the body
Sinoatrial (SA)
Node:
Located in wall of Right Atrium •Known as “pacemaker” of the heart •Paces heart rate to body’s current demands; where we develop HR ranges of 60-100 bpm
Interatrial
Node/Pathway/Bundle:
•Also called Bachmann’s Bundle •Connecting fibers rapidly send an impulse from the right atrium to the left atrium •Both atria begin to contract
Atrioventricular
(AV) Node:
•Delays conduction briefly •Gives atria time to contract and pump all blood into the ventricles •If the SA Node fails to depolarize or becomes nonfunctional, the AV node can initiate each heartbeat at a slower rate of 40-60 bpm.
Bundle of His:
Conduction passes from AV node and travels through Bundle of His
Right and Left
Bundle Branches
Conduction bifurcates into the Right and Left Bundle Branches and travels through walls of ventricles
Purkinje Fibers
•Fibers spread widely across the ventricles to cause all cells of the ventricles to contract quickly •This is when blood is expelled from ventricles
A cardiac cycle is the sequence of mechanical events that occur during each heartbeat
Mechanical events occur because of the conduction of electricity
A single cycle of cardiac activity can be divided into two phases:
Systole, Diastole
Systole
– Systole = Squeeze
– Contraction of chambers
■ Blood empties out of the chambers
– Systole of the atria happens simultaneously
– Systole of the ventricles happens simultaneously
Diastole
– Diastole = Fill
– Relaxation of chambers
■ Blood fills into the chambers
– Diastole of the atria happens simultaneously
– Diastole of the ventricles happens simultaneously
Systole of a set of chambers is followed by
diastole of that same set of chambers
Atrial systole occurs at the same time as:
Ventricle diastole.
While systole is occurring with one set of chambers,
the other set of chambers is in diastole
Atrial Systole
– Atria contract, blood flows from atria into ventricles – Ventricles are in diastole, filling with blood sent from atria – Atrioventricular valves are open ■ Blood flows freely from atria to ventricles – Semilunar valves are closed ■ Blood is unable to pass into the pulmonary artery and aorta
Ventricular Diastole
– Ventricles relax, filling with blood sent from atria – Atria are in systole, contracting, squeezing blood into ventricles – Atrioventricular valves are open ■ Blood flows freely from atria to ventricles – Semilunar valves are closed ■ Blood is unable to pass into the pulmonary artery and aorta
Atrial Diastole
– Atria relax, filling with blood from the superior and inferior vena cava – Ventricles are in systole, contracting, squeezing blood into the pulmonary artery and aorta – Semilunar valves are open ■ Blood flows freely from right ventricle to pulmonary artery ■ Blood flows freely from left ventricle to aorta – Atrioventricular valves are closed ■ Blood is unable to pass from atria to ventricles
Ventricular Systole
– Ventricles contract, squeezing blood into the pulmonary artery and aorta – Atria are in diastole, relaxing, filling with blood from the superior and inferior vena cava – Semilunar valves are open ■ Blood flows freely from right ventricle to pulmonary artery ■ Blood flows freely from left ventricle to aorta – Atrioventricular valves are closed ■ Blood is unable to pass from atria to ventricles
Heart Sounds:
■ Heart Sounds caused by valve closure ■ First sound – Closure of AV Valves (tricuspid, mitral) – Makes “lubb” sound ■ Second sound – Closure of Semilunar Valves (aortic, pulmonary) – Makes “dubb” sound
Cardiac Output
Stroke Volume x Heart Rate = Cardiac Output.
•SV = amount of blood pumped per beat (mL/beat)
•HR = # of heart beats in one minute (beat/min)
•Measured in L/min or mL/min must use units when calculating!
•Average cardiac output for a healthy adult is about 5L/min
•Cardiac output increases with metabolic demand
•If HR increases, then cardiac output increased
•Stroke volume increases during exercise
•Increase in venous blood return, thus causing stretching of ventricular
myocardium
Factors Affecting Cardiac Output:
Preload
Amount of pressure stretching the ventricle the end of ventricular diastole Analogy: Blown up balloon •More water in the balloon, the more it stretches What can cause an increased preload? •Increased central venous pressure •Fluid volume overload •Heart Failure
Factors Affecting Cardiac Output:
Afterload
Systemic vascular resistance
Amount of resistance the heart/left ventricle must overcome
to open the aortic valve and push blood out into systemic
circulation
•Balloon must push, squeeze, and work against the knot to get the fluid out of
the balloon
Analogy: Knot at the end of the balloon
•Hypertension
•Increased pressure in the vessels, harder to push fluid into vessels with
increased pressure
•Vasoconstriction
•Narrow vessels, harder to push fluid into them
What can cause an increased afterload?
•Heart needs to work harder to push blood out against the resistance
The cardiac workload must increase if afterload is increased
Ejection Fraction
Amount/Percentage of blood the left ventricle pumps out with each contraction
(each ventricular systole cycle)
■ Measured in percentage;
– Example: Ejection Fraction is 60%, meaning 60% of the total amount of blood
in the left ventricle is pumped out with each squeeze of the ventricle
■ The ejection fraction value shows how well the heart is functioning
■ Normal range 55% to 70%
■ An ejection fraction under 40% may be evidence of heart failure or
cardiomyopathy
■ The most common test performed to determine the Ejection Fraction is an
echocardiogram (ultrasound of the heart, discussed later!)
Epinephrine & Norepinephrine – defined as catecholamines (act as both hormones & neurotransmitters)
•Secreted by Adrenal Medulla: act as hormones •Secreted by the medulla (CNS): act as neurotransmitter •Secreted in stressful situations or whenever the sympathetic nervous system needs to activate •When these catecholamines act on beta one, they cause: •Increased Force of Contraction •Increased Cardiac Output •Increased Impulse Conduction (think cardiac conduction pathway we just discussed!) •Increased Heart Rate •Increase in Systolic BP (due to increased cardiac output.)
Aldosterone
•A mineralocorticoid that comes from the Adrenal Cortex •Regulates serum sodium & potassium levels •Electrolytes required from electrical conductivity of heart •When aldosterone is released, kidneys hold onto sodium and releases potassium via urine •Fluid follows sodium, thus increasing intravascular volume in the body
Blood Pressure
Defined as force of blood against blood vessel walls Blood pressure is measures in millimeters of mercury (mmHg) Average blood pressure is around <120/80 mmHg
As heart pumps, left
ventricle pushes blood
out into aorta
Pressure exerted by blood on
walls of blood vessels is
defined as blood pressure
Blood pressure is greatest
in the arteries
As blood enters the veins, it
decreases and eventually
approaches zero as blood
enters into the right ventricle
Arteries and arterioles
are usually slightly
constricted to maintain
normal blood pressure
This contributes to peripheral
resistance
BP is affected by many
factors
•Will increase if heart rate and force of contraction increases •If heart rate is increased but ventricles are not filling prior to contraction, cardiac output will be decreased, thus resulting in a decreased blood pressure
What is Blood Pressure?
Determined/Influenced by: – Cardiac output – Peripheral vascular resistance ■ Ability of vessels to stretch – Blood viscosity – Blood volume – Sympathetic nervous system – Kidney Fuction: Renin-Angiotensin-Aldosterone System
Mean Arterial Pressure
MAP
■ MAP is defined as:
– The average pressure within the arteries throughout one
cardiac cycle (systole and diastole)
■ The MAP is considered a better indicator of perfusion to vital
organs than the blood pressure
■ MAP should be ≥ 65 mmHg and ≤ 100 mmHg
– If the MAP is below 65 mmHg for prolonged periods of time,
vital organs are not receiving adequate blood flow and
oxygen
– If the MAP is above 100 mmHg for prolonged periods of time,
the heart workload is increased which leads to various
complications
Mean Arterial Pressure (MAP)
■ MAP = SBP + 2(DBP)
3
■ If the MAP results as a number with decimals, round to the nearest
whole number
– Example: 86.7 Round to 87
■ Example: Blood Pressure is 146/86 mmHg, calculate the MAP
■ MAP = 146 + 2(86)= 146 + 172 = 318 = 106 mmHg
3 3 3
■ Example: Blood Pressure is 90/56 mmHg, calculate the MAP
■ MAP = 90 + 2(56)= 90 + 112 = 202 = 67.333 mmHg = 67 mmHg
3 3 3
Hypotension
Defined if blood pressure is <90/60 Always attempt to determine patients baseline A systolic reading of 90 mm Hg is an acceptable value for some patients.
Causes of hypotension:
Dehydration
Hypovolemia
Bleeding
Medications
Signs and Symptoms of hypotension:
Lightheaded, Fatigue Dizziness, Weakness Syncope Possible confusion Decreased O2 to brain! Tachycardia Heart compensating to increase blood flow to target organs Weak, thready pulse upon palpation Poor circulation/perfuson Orthostatic hypotension may be present Cool, pale, dusky, cyanosis (extreme hypotension)
Therapeutic Interventions for hypotension:
- Lay patient supine (if tolerated)
- Will improve blood flow to brain & improve overall circulation
- Encourage rest/restrict activity
- Encourage & provide fluids
- Monitor signs and symptoms
- Reassess frequently
- Vitals and focused assessment
- Keep patient safe!
Treatment for hypotension:
•Determine cause
•If on medications that decrease blood pressure – decrease dose, change
medications
•Give medications to increase blood pressure
•Alpha one agonist: promote alpha one and vasoconstriction of large peripheral
arteries increase blood pressure
If hypotension is acute, body should activate:
Renin Angiotensin
Aldosterone System to increase blood pressure
Renin-Angiotensin-Aldosterone
System/Mechanism/Pathway (RAAS)
Regulated by the kidneys •Kidneys play a vital role in blood pressure regulation •Kidneys release renin to activate the RAAS
Renin-Angiotensin-Aldosterone
System/Mechanism/Pathway (RAAS): What activates this
system?
•Decreased blood flow to kidneys/renal perfusion (renal ischemia) •Decreased arterial blood pressure (hypotension) •Decreased blood volume (extracellular fluid/intravascular volume) •Decreased serum sodium (hyponatremia) •Increased urine sodium
Purpose of the RAAS?
•Increase blood pressure, blood volume, blood flow to kidneys, serum sodium levels
(RAAS) What is involved in this system?
•Renin: Produces and released by the kidneys
•Angiotensinogen: Secreted into the blood from the liver
•When renin and angiotensinogen meet, a chemical reaction occurs and Angiotensin I
is created
•Angiotensin I: No biological activity, exists solely as a precursor to Angiotensin II
•Angiotensin-Converting Enzyme (ACE) converts Angiotensin I to Angiotensin II
•Angiotensin II: Causes increased peripheral vasoconstriction increases blood pressure
•Also stimulates the release of aldosterone from the adrenal cortex
•Aldosterone: Acts on the kidneys to increase sodium and fluid retention
•Thus increasing serum sodium levels and extracellular fluid (blood volume) which increases blood pressure.
Kidneys will stop release of renin when:
BP is elevated, fluid volume is
appropriate, kidney’s are perfused appropriately, or sodium levels are
within normal limits
Excessive renin production:
cause by impaired renal perfusion may be a
contributing factor to HTN
Blood vessels begin to
age
Starts during childhood, but effects are not seen until later in life
Atherosclerosis
Atherosclerosis increases risk for developing cardiovascular disease; increases with age
Build of of fats, cholesterol, & other substances on artery walls
Reduced/restricted blood flow
Resting blood
pressure increases
Increased afterload
Left ventricle workload increases, increased risk for left sided heart failure
Vein valves more
incompetent
Backflow of blood, varicosities
Dependent edema
Decreased HR
Conduction cells less effective
Dysrhythmias Common
Kyphosis
Changes shape of chest wall
Heart sounds distant
Cardiovascular Assessment: Subjective Data: Health History
•Follow up with appropriate questions and assessments based on
patient’s complaints
•If there are cardiac related issues (dizziness, fatigue, chest
tightness/pain, SOB, dyspnea)
•Vital Signs
•Thorough pain assessment
•Ausculate heart sounds and determine heart rhythm
•Ask more details about SOB and dyspnea
Weight
Compare to baseline weight Acute weight gain? Possible fluid overload secondary to heart failure •2-3 lbs. in 24-48 hours
Blood pressure:
Read box 21-1 on accurate blood pressure measurements “Normal” <120/80 mmHg Always ask patient their baseline Assess both extremities for comparison •Use extremity with higher reading Can assess in leg if necessary
Respirations
Observe rate and quality If patient is having respiratory complications or struggling to breathe, perform focused respiratory assessment (see appropriate lecture)
Assessing Pulse: Apical
■ Determine heart rate and rhythm through auscultation
■ If rate and rhythm are regular, listen to the heart for 15 seconds and multiply times four
■ Rate:
– Documented as regular if between 60-100 bpm
– Documented as irregular if <60 bpm or >100 bpm
■ Rhythm:
– Documented as regular or irregular
■ If the rate or rhythm is irregular when assessing vital signs what is your priority?!
– Assess apical pulse for one minute
■ Is it accurate to assess a pulse using a pulse ox?
■ Athletic individuals may have HR between 40bpm -50bpm
■ Heart pumps more efficiently, does not need to pump as fast.
■ Perform thorough assessment to determine patient is stable.
Assessing
Pulse:
Peripheral
Pulses
Palpate for rate: •If rate is regular (60-100), palpate for 15
seconds and multiply by four
•If rate is irregular (<60, >100), must listen
to an apical pulse for one minute
Arterial pulses palpated for
volume and strength equality
•Most common: Radial, Pedal – if issues,
assess other locations
•Absent: 0
•Weak: 1+
•Strong: 2+
•Bounding: 3+
•Palpate bilaterally, compare for equality
•Bilateral radial pulses strong and equal
•Left radial pulse strong, 2+, right radial
pulse weak, 1+
Blood Pressure and Postural
Position Changes
Before you assess your patient’s blood pressure, be sure they are in an
appropriate position•Do not assess a patient’s blood pressure while they are leaning to one side, curled up, asleep,
etc.
•Try to reposition the patient or get them up and out of bed for the day, ensure your reading is
accurate!Blood pressure changes slightly as a patient changes positions
•If the blood pressure changes and decreases too much, it may cause syncope and collapse
•Brain is not receiving enough blood and oxygen!
•Always anticipate possible vital sign changes with position changes, safety first!
Normal blood pressure and heart rate variations with postural position
changes:•Decrease in systolic up to 15mmHg is normal
•Decrease in diastolic up to 10mmHg is normal
•Increase in HR up to 15 to 20 bpm is normal
•This occurs to maintain cardiac output
Example: BP 125/80 while supine changes to 115/76 sitting
•Systolic changed 10 mmHg
•Diastolic changed 4 mmHg
•Appropriate compensation
Assessing for Orthostatic
Hypotension
■ Orthostatic hypotension is also known as postural hypotension
– Hypotension with position changes
■ Causes of orthostatic hypotension
– Deficient fluid volume
– Diuretics
– Analgesics
– Pain
■ If the patient complains of feeling dizzy/lightheaded with position changes,
the nurse should critically think and perform an assessment for orthostatic
hypotension
Assessing for Orthostatic Hypotension
Before performing orthostatic vitals: •Utilize gait belt, stand close to patient.
Blood pressure and heart rate
taken with patient lying, sitting,
and then standing– •Detects abnormal changes with postural
positioning
•Along with assessing BP & HR with position
changes, must ask patient about feeling
lightheaded and/or dizzy with each position
change.
Orthostatic hypotension is present
when: •The systolic BP drops greater than 15 mmHg
•The diastolic BP drops greater than 10 mmHg
•The HR increases more than 20 bpm
Inspection:
■ Remember – inspection begins the moment you lay eyes on the patient! Be
observant, collect data while collecting
■ Inspect the color of the skin, mucous membranes, lips to help determine
oxygenation status
– Pink
■ Appropriate oxygenation and blood flow to area
– Pallor
■ Decreased arterial blood flow or decreased oxygen to tissues, possible anemia
– Cyanosis
■ Gas exchange and/or perfusion issue
■ Tissues are oxygen deficient
More Inspection:
■ Lower extremity skin color changes
– Decreased arterial blood flow to lower
extremities:
■ Causes dependent rubor: legs turn deep
red color in dependent position
■ Shiny, taut, dry skin and decreased hair
distribution may indicate reduced arterial
blood flow
– Venous blood flow problems; venous blood
cannot return to the heart as efficiently
■ Brown discoloration & purple/blue skin of
lower extremities in dependent position
■ Jugular Venous Distention (JVD)
– Veins in neck are distended/visible when
sitting 45-90 degrees
– Caused by increase in venous volume;
fluid overload
Auscultation:
■ Heart rate and rhythm (if not previously performed)
■ Heart Sounds
– S1
■ Heard at the beginning of ventricular systole
■ Closure of AV Valves
■ “Lubb” Sound
– S2
■ Heard at the start of ventricular diastole
■ Closure of Semilunar Valves
■ “Dubb”
– Murmurs
■ Caused by narrowed value opening or a valve that doesn’t close tightly
■ Prolonged swishing sound
■ Heart sounds can be increased if patient leans forward or lies on left side
– Brings heart closer to chest wall
■ Cluster your care and auscultate lung sounds at same time respiratory and cardiac
assessments are performed back to back usually!
Palpation:
■ Capillary Refill
– <3 seconds: indicates appropriate arterial blood flow to extremities
– >3 seconds indicates a decrease in arterial blood flow to the extremities
■ Edema
– Review edema slides from lecture 2 (fluid imbalances lecture)
– Swelling in dependent extremities due to fluid build up/fluid overload
– Swelling is caused by fluid accumulation in a particular area or fluid leaking from vascular system to
tissues (think of a sponge full of water)
■ Fluid then gets stuck, cannot get back into vascular system without help
– If present, fluid volume overload
■ Patient may have heart failure
– Non-Pitting or Pitting Edema?
■ Pulses (discussed previously)
– Assess arterial blood flow to area; determine rate, volume, strength
– How do we document a peripheral pulse strength that is within defined limits?
■ Temperature
– Assess arterial blood flow to extremity: warm, cool, cold, hot?
Neurovascular Assessment (6 P’s)
Assess for peripheral vascular disease & blood flow
issues within the extremities
These symptoms occur due to lack of oxygen and blood
flow to an extremity
•Pain
•Paresthesia (Numbness)
•Pallor (Pale)
•Pulselessness (No pulse)
•Paralysis (Can’t move limb)
•Poikilothermia (Lack of temperature/cool temperature)
If these findings are present, what does it tell us?
•If any of the 6 P’s are present; hypoxemia may be present
emergency
Noninvasive Diagnostic
Studies:
Review of diagnostic Imaging (review lecture one on these specific imaging tests)
■ Chest X-Ray
– Shows size, position, structures of heart
■ CT Scan
– View calcified plaque in the coronary arteries
■ If there is plaque build up in the coronary arteries, what is this called?
■ CTA Scan
– View blood flow within coronary arteries
■ Magnetic Resonance Imaging
■ Can identify ischemia and heart damage
– Ultrasound of extremities:
■ Arterial ultrasound will look at blood flow and any related problems within the arteries
■ Venous ultrasound will look at blood flow and any related problems within the veins
■ Discussed on following slides:
– Echocardiogram
– Cardiac Monitor
– Electrocardiogram
Echocardiogram
■ Ultrasound test specific for the heart
■ A specialized tech performs this test using an
ultrasound probe
■ The machine records:
– The motion of heart structures (valves &
chambers)
– Heart size, shape & position
– Visualize blood flow through heart
– Determine ejection fraction of left ventricle
■ This test does not show blood flow through the
coronary vessels
– What test would show that?
■ CT Angio of Chest
Cardiac Monitoring
■ Also known as telemetry
■ Continuous monitoring of heart activity
■ Consists of 5 leads with electrodes that connect to
a central cardiac monitor
■ Detects changes in heart rate and rhythm
immediately
■ May be worn if patient has:
– Cardiac complaints
– Receiving medications that can change cardiac
activity
– During acute illness
– Electrolyte imbalances
– IV electrolyte replacement
Electrocardiogram (EKG)
■ Also known as: ECG or EKG ■ Quick, fast, painless test that shows cardiac electrical activity in a moment of time – Once image is captured, leads are removed ■ The EKG will reflect abnormalities related to: – Conduction (Cardiac Conduction Pathway) – Heart Rate & Rhythm – Heart chamber enlargement – Myocardial ischemia and/or infarction – Electrolyte imbalances
Lab Values specific to Cardiovascular
System
Troponin, CK-MB, Brain Naturetic Peptide,
Troponin
•Gold star test, ordered for acute cardiac issues
•The more cardiac damage present, the higher the troponin value
•Remember, small changes in troponin can be very concerning!
•Troponins are drawn in serial increments every few hours to see if cardiac
damage is persistent/continuing
CK-MB
•Supports the diagnosis of myocardial injury, will be ordered in
conjunction with Troponin
Brain Naturetic Peptide
•Ordered to diagnose and monitor progression of chronic heart failure
Electrolytes
•Potassium, Calcium, Magnesium, Sodium •Assess specific electrolytes and determine if an imbalance is present •Are s/s of an imbalance shown?
Lipid Panel
Total Cholesterol, HDL, LDL,
Triglycerides
Therapeutic Measures
■ Improve Diet
– Increase fruits and vegetables
– Decrease saturated fats
■ Promote Exercise
– Walking program to promote and improve blood
flow
■ May improve peripheral vascular disease
– Exercise will assist in optimum cardiac function
■ Weight loss if needed
■ Smoking Cessation
– Smoking causes vasoconstriction which reduces
blood flow
More Therapeutic Measures
■ TED Hose/Stocking (commonly called Compression Socks)
– Improve arterial blood flow and venous blood return
– Preventing blood clots and edema
– Put these on in the morning before you patient gets out of bed!
– Used in patients with peripheral vascular disease, on bedrest, or after
surgery/trauma
■ Sequential Compression Devices (SCDs)
– Used to prevent blood clots in the lower extremities
– Devices wrap around the lower extremities and tubing connects to a
machine
– Devices then intermittently squeeze the lower extremities to maintain
blood flow and venous return
– Used commonly after surgery and when a patient is on bedrest
– Be sure these are on your patient and the machine is turned
Therapeutic Measures 3:
■ Leg Elevation
– Venous Insufficiency
■ Elevate legs above the level of the heart
– Arterial blood flow problems
■ Do not elevate lower extremities above the level
of the heart when the patient has with arterial flow
issues
■ Keep in dependent position
■ Supplemental Oxygen
– Administered to ensure heart receives adequate
amount of oxygen to function appropriately
■ Medications
– Various medications may be administered based
on patient’s history and symptoms; these will
discussed in the next lecture
Atherosclerosis & Coronary Artery Disease (CAD)
Atherosclerosis is the formation of plaque buildup in the walls of the arteries throughout
the body
•Narrowed arteries lead to decreased blood flow & oxygen delivery to organs and tissues
•Decreased blood flow can eventually lead to ischemia of the organ/tissue
Coronary artery disease is caused by plaque buildup in the wall of the coronary arteries,
which narrows the coronary arteries
•Narrowed coronary arteries lead to decreased blood flow & oxygen delivery to cardiac tissue
•Obstruction of coronary artery blood flow typically from atherosclerosis
•Decreased blood flow can eventually lead to ischemia of cardiac muscle and tissue
Risk Factors:
•Older adult
•Poor Diet
•Elevated total cholesterol, LDL, and triglycerides
•Decreased HDL levels
•Obesity
•Sedentary Lifestyle
•Excessive Alcohol use &/or Tobacco use
More Coronary Artery Disease (CAD)
■ Prevention – Limit modifiable risk factors ■ Therapeutic Measures – Promote Healthy Lifestyle ■ Smoking & Alcohol Cessation ■ Low fat & low cholesterol diet ■ Exercise – Increased activity can raise HDL levels and improve blood flow/circulation ■ Medications – Lipid lowering medication (statin) ■ Statins are first line drugs to reduce LDL levels in the body by reducing cholesterol synthesis ■ Where does cholesterol synthesis occur? – Antiplatelet Aggregator ■ Inhibit platelet activation and adhesion which assists in preventing the formation of a thrombus – Vasodilators ■ Prevent angina (chest pain) caused by CAD and decreased blood flow to myocardial tissue
Study pages 67-70 of the power point
important!
