Cardiovascular Assessment and Diagnostics. Flashcards
Three layers of the heart:
endocardium, myocardium, epicardium
Depolarization:
Electrical activation of cell caused by influx of sodium and also Ca into cell while potassium exits cell
Repolarization:
Return of cell to resting state caused by reentry of potassium into cell while sodium exits
Effective refractory period:
Phase in which cells are incapable of depolarizing (meaning squeezing and cotracting)
Relative refractory period:
phase in which cells require stronger-than-normal stimulus to depolarize
P- wave
Depolarization of the atria in response to SA node firing an action potential
PR segment: it should be called the PQ segment (small one ) but we call it the pr segment for some reason. Or simply how long does the electrical impulse stay in the AV node. It should be 0.02 sec only anything besides this is an abnormality.
Delay of the AV node to allow the filling of the ventricles.
QRS complex
Depolarization on the ventricles. It triggers the main pumping contraction of the left ventricle. It contracts the right ventricle too but the big one is the lft ventricle
ST segment
It is the beginning of ventricular repolarization. It should be flat.
Ejection fraction:
Percent of end diastolic volume ejected with each heartbeat (left ventricle). It is the amount of blood ejected with each heartbeat from the total volume. usually, it is between 55% and 65%.
40% remains in the ventricle. Ejection fraction is a measurement of the percentage of blood leaving the heart each time it squeezes
Cardiac output (CO):
Amount of blood pumped by ventricle in liters per minute
CO = SV × HR
Stroke volume(SV):
amount of blood ejected with each heartbeat
Preload:
Degree of stretch of cardiac muscle fibers at end of diastole
Afterload: It has nothing to do with the heart.
It has nothing to do with the heart. It has more to do with blood vessels and valves. It is the force/pressure that the ventricles must work against/ encounter in order to get the semilunar valves open, so that blood can leave the ventricles and go to the rest of the body.
Contractility:
Ability of cardiac muscle to shorten (squeez) in response to electrical impulse
Control of heart rate:
2 things
Autonomic nervous system, baroreceptors
Control of stroke volume
Preload: Frank–Starling Law (The Frank-Starling Law states that the stroke volume of the left ventricle will increase as the left ventricular volume increases due to the myocyte stretch causing a more forceful systolic contraction.)
Afterload: affected by systemic vascular resistance, pulmonary vascular resistance
Contractility increased by :
Catecholamines, SNS (sympathetic nervous system ), certain medications
Side note: The main types of catecholamines are dopamine, norepinephrine, and epinephrine.
(Catecholamines) A type of neurohormone (a chemical that is made by nerve cells and used to send signals to other cells). Catecholamines are important in stress responses. High levels cause high blood pressure which can lead to headaches, sweating, pounding of the heart, pain in the chest, and anxiety.
Increased contractility results :
in increased stroke volume
What reduces contractility:
Decreased by hypoxemia (because if the heart is not getting enough oxygenated blood through the coronary arteries it can’t produce enough ATP and therefore it can’t contract with enough force), acidosis (NO O2), certain medications like beta blockers (because they cover the sites where adrenaline attaches ).
Objective data of cardiovascular system.
Diagnostics
Cardiac interventions & CV surgeries
Physical examination
- Vital signs
- Assessment of perfusion &
cardiac output
- Inspection, palpation (Palpation includes assessing the arterial pulse, measuring blood pressure),
auscultation of the thorax
-Auscultation of murmurs (indicate valve problems)
-Peripheral vascular system
Subjective data
- Health history (because the pt can lie to us about their past medical history)
- Medications (reconciliation, compliance: pt can lie to us about taking their medication on time etc…)
- Patient perception (perception=feeling not a fact) of effects and outcomes of surgeries and other treatments
Hair:
Brittle, dry. Think poor nutrition (Meaning that the blood is not bringing enough O2 and food)is possibly due to cardiac insufficiency (Cardiac insufficiency, also known as heart failure), if the hair cells don’t get oxygen due to poor blood flow they die.
Eyes:
High BP can cause yellow orange plaque under eyelids. May indicate chronic serum cholesterol elevation
lips and tongue:
blue tingled? Think cyanosis (
Cyanosis is the medical term for when your skin, lips or nails turn blue due to a lack of oxygen in your blood.)
-Dry ? think dehydration
Jugular vein
distended when you are at a 45 degree angle? Think hypervolemia. Right sided heart failure (due to lack of blood return in core pulmonale), pericardial temponade (Cardiac tamponade is pressure on the heart that occurs when blood or fluid builds up in the space between the heart muscle and the outer covering sac (pericardium) of the heart.) or constrictive pericarditis (Constrictive pericarditis is the result of scarring and consequent loss of the normal elasticity of the pericardial sac.)
Chest sound auscultate (left what?)
Auscultate, if crackled (rales) consider left sided heart failure. Assess rate, rhythm, and presence of murmurs.
Abdomen.
Fluid accumulation (ascites) or enlarged tender liver may indicate right sided heart failure. Pulsating ((fast-beating))
mass may indicate AAA (An abdominal aortic aneurysm (AAA) is a swelling (aneurysm : an excessive localized enlargement of an artery caused by a weakening of the artery wall. The aorta is the main blood vessel that leads away from the heart, down through the abdomen to the rest of the body.)
Skin
dry (no nutrition /vitamins/food brought by blood), cool- May be from nutrition (Because the blood is not making it and therefore there is no food ). Blue tinged indicates cyanosis. Pallor (palido amarillo) may suggest anemia or low circulation (Because the blood is not making it and therefore there is no food/iron).
Sacrum: Right ventricular failure.
Check for edema and pressure areas in immobilized clients.
Nails:
Clubbing may indicate chronic low O2 saturation as in congenital cardiac and pulmonary disease. Thick nails think can can be due to poor nutrition or impaired O2 delivery.
Lower extremities. hair
Absence of hair en thin skin are signs of poor circulation.
Legs/ ankles/ feet
Check for edema, presence of pulses, decreased sensation (because it indicates tissue death that can’t feel shit coz it’s dead), pressure areas.
Assessment of the Cardiovascular Risk. Non-Modifiable
Increasing age
Male gender
Gender
Heredity (including race)
- Generally due to increased incidence and prevalence of obesity and diabetes (Mexican-Americans, Native Americans, Native Hawaiians and some Asian- Americans
-African-Americans have high blood pressures than Caucasians
-Children of parents with heart disease
Assessment of the Cardiovascular Risk. Modifiable
-Elevated total cholesterol
**HDL, + LDL + 20 % of triglycerides (This is the total amount of cholesterol that’s circulating in your blood.)
**Goal is low LDL, higher HDL and lower triglycerides
- HTN
-Smoking, vaping, chewing tobacco
-Obesity and being overweight
-Physical inactivity
-Diabetes
***68% of diabetic patients over 65 years die of some kind of heart disease. 16% die of stroke
-Stress
-Alcohol
-Diet & nutrition
Functional health patterns?
-Health perception & health management pattern
-Nutritional-metabolic pattern
-Elimination pattern
-Activity-exercise pattern
-Sleep-rest pattern
-Cognitive-perceptual pattern
-Self-perception & self-concept pattern
-Role-relationship pattern
-Sexuality-reproductive pattern
-Coping & stress tolerance pattern
-Values-belief pattern
Effects of Aging on the Cardiovascular System
-Age alters the cardiovascular response to physical and emotional stress
-Heart valves become thick and stiff
-Frequent need for pacemakers
-Less sensitive to β-adrenergic agonist drugs (beta blockers) Basically drugs that stop the effects of epinephrine
-Increase in Systolic BP; decrease or no change in DBP. Because there is more resistance due to arteriosclerosis that comes with aging, stiffening of valves and arteries the heart finds itself forced to increase the systolic pressure to counteract this and be able to send blood to the body.
Normal physiologic CV effects of aging
-Loss of elastin
-Increase collagen (from scarring through the years )
-Increase of fibrous tissue, fatty deposits, cholesterol
-Stiffening and thickening of heart valves and vessels
-Decrease beta-adrenergic receptors (are adrenergic receptors primarily responsible for signaling in the sympathetic nervous system.)
-Muscle atrophy
-Cell
-Slight enlargement (thicker walls, larger cells because they compensate to fight the vascular resistance)
Manifestations of normal physiologic CV effects of aging
-Cardiac hypertrophy causes a decrease in SV and CO (Because if the heart cells become too bing there won’t be room for fluid ) So the heart gets bigger to fight vascular resistance but it bites its own tail because now there is less room for blood.
-Fewer conducting cells cause an inability for the HR to increase during times of stress (because SA node cells etc go down in numbers )
-Loss of arterial elasticity causes increase resistance & increase HR (Because if the arteries become narrow it means that their resistance to blood flow becomes bigger and that the heart has to increase the rate to make up for it)
-Arteriosclerosis
-Decrease baroreceptor sensitivity causes a decrease in ability to regulate BP
Common Age-Related Cardiovascular Problems
Arrhythmias (big cause is CAD)
Atrial fibrillation
Brady-arrhythmias (Slow heart rate)
PSVT (Paroxysmal supraventricular tachycardia (PSVT) is a type of abnormal heart rhythm, or arrhythmia. It occurs when a short circuit rhythm develops in the upper chamber of the heart. This results in a regular but rapid heartbeat that starts and stops abruptly.)
Aortic Stenosis
Valvular disease
Stroke
PE/DVT: Pulmonary embolism and deep vein thrombosis.
Laboratory Tests
Cardiac biomarkers
Blood chemistry, hematology, coagulation
Lipid profile
Brain (B-type) natriuretic peptide
C-reactive protein
Homocysteine
Blood test: Troponin
Troponin <0.03 ng/mL
Troponin is a type of protein found in the muscles of your heart. Troponin isn’t normally found in the blood. When heart muscles become damaged, troponin is sent into the bloodstream. As heart damage increases, greater amounts of troponin are released in the blood.
Blood test: CK-MB (creatine kinase-myocardial band)
can also mean you have damage to other muscles in your body
CK-MB 0-3 ng/mL
The CK-MB test is a blood test that looks for a specific enzyme. That enzyme, creatine kinase-myocardial band, is most common in your heart but can also mean you have damage to other muscles in your body. The use of this test has decreased because of newer tests that have a better ability to detect heart damage only.
Blood test: BNP
Bentricular !!! not ventricular hahah
BNP <100 pg (picograms)/mL (>100pg/mL positive for HF)
*****ventricular heart failure
A B-type natriuretic peptide (a hormone)(BNP) test gives your provider information about how your heart is working. This blood test measures the levels of a protein called BNP in your bloodstream. When your heart has to work harder to pump blood, it makes more BNP. Higher levels of BNP can be a sign of heart failure.
Blood test: ANP (atrial natriuretic peptide)
ANP 22-77 pg/mL (>77 pg/mL positive for HF)
High levels can mean your heart isn’t pumping as much blood as your body needs.
Low plasma levels of MR-ANP predict development of future diabetes and glucose progression over time
**atrial heart failure
ANP test. ANP stands for atrial natriuretic peptide. ANP is similar to BNP but it is made in a different part of the heart. Metabolic panel to check for kidney disease, which has similar symptoms to heart failure.
So depending on what we have more of we will know where the problem in the heart is. If we have more ANP it means that the atria of the heart is working extra hard to compensate for something.
Blood test: C-reactive protein
C-reactive protein (CRP) < mg/dL (> 3mg/L positive for MI.
C-reactive protein (CRP) is a protein made by the liver. The level of CRP increases when the coronary arteries get inflamed.
Your level of C-reactive protein can be an indicator of how at-risk you are for developing cardiovascular problems. This is because the development of atherosclerosis (accumulation of cholesterol inside the blood vessel walls) is associated with inflammation within the vessel walls. So more C protein indicates a greater chance of developing atherosclerosis which in turn increases the chances of getting a coronary obstruction which leads to more chances of developing an MI.
Blood test: Homocysteine. Homocysteine is an amino acid.
Increased serum homocysteine levels positively correlated with severity of CAD.
An increased cholesterol level promotes atherosclerosis and hence it is a risk factor for CAD. Serum levels of homocysteine were found to be significantly higher in CAD than in non CAD subjects.
Blood test: Triglycerides
Triglycerides < 160 mg/dL (> 400 mg/dL CAD + risk)
High triglycerides are often a sign of other conditions that increase the risk of heart disease and stroke.
Triglycerides are a type of fat that circulates in your blood. Your body makes triglycerides or gets them from the foods you eat. Your body needs some triglycerides for good health. However, high triglycerides in your blood can raise your risk of heart disease and stroke.
Blood test: LDL/ HDL
-LDL (low-density lipoprotein) <100 mg/dL (> 160 mg/dL CAD + risk)
-HDL > greater than 60 mg/dL- (< 40 mg/dL CAD + risk)
Blood test: Phospholipids (fat)
Phospholipids 131-276 ng/mL
phospholipid saturated fatty acids (SFA) are associated with an increased risk of coronary heart disease and hypertension,
Hypokalemia
-Muscle weakness, cardiac cells can’t repolarize
-ECG: Flat or inverted T wave because the ventricles can’t repolarize -ST depression because since there is less K+ ventricular repolarization takes longer.
-Ventricular dysrhythmias
-Increase digoxin toxicity (In states of hypokalemia, or low potassium, digoxin toxicity is actually worsened because digoxin normally binds to the ATPase pump on the same site as potassium. So when K+ is low digoxin has no competitor and too much of it ends up binding to those receptors, causing a much stronger effect by digoxin. When potassium levels are low, digoxin can more easily bind to the ATPase pump, exerting the inhibitory effects slows and regulates heart rate)
Hyperkalemia
-Causes decreased depolarization and early repolarization: Because too much of it doesn’t let NA+ do its job. And too much of it also accelerates repolarization.
-ECG: Tall peaked T waves (because repolarization lasts too long), wide QRS (Because too much K+ inside the cell will ake it harder for NA and Ca to depolarize the cell fast. So ends up depolarizing eventually but it takes a long time), prolonged PR intervals, or flat P waves (because depolarization is very short)
-Ventricular fibrillation, asystole (so much K+ that contraction doesn’t even occur)
Hypercalcemia
-Occurs with dehydration, thiazide diuretics,
-ECG: Wide T waves because there is so much Ca+ inside the cell that it takes K+ a long time to depolarize the cell.
-Tachycardia or bradycardia, cardiac arrest
Hypomagnesemia
serum magnesium < 1.5 mEq/L
- Caused by malnutrition, diabetes (Diabetes reduces renal Mg2+ reabsorption resulting in urinary Mg2+ wasting), diuretics, diarrhea
-Irritates cardiac muscle
-ECG Tall T wave with depressed ST segment (because it helps K+ repolarize and its lack slows polarization)
-Ventricular tachycardia/fibrillation. Because its lack makes depolarizations longer and more frequent. Causing fast heart beats and erratic ones.
Hypermagnesemia
Serum magnesium > 2 mEq/L
-Caused by renal failure and -MgSO4 administration (Magnesium sulfate)
-Causes muscle weakness, hypotension (Hypermagnesemia will cause hypotension by blocking the calcium channels on the adrenal cortex cells and decreasing aldosterone production. Since aldosterone increases blood pressure, an increase in serum magnesium will cause hypotension. The kidneys are responsible for excreting excess amounts of magnesium.)
-ECG: Prolonged PR interval and wide QRS
-Bradycardia (because there is less Ca+ we have less contraction)
12- Lead ECG
-Non-invasive diagnostic tool used to clients with chest pain (differentiates between myocardial ischemia and infarction) or other cardiac symptoms and arrhythmias
-12 lead or rhythm strip, serial ECG for AMI (Acute Myocardial Infarction) times with Troponins
-Leads must be placed in specific locations VERY IMPORTANT, client must lie still (reduces artifact) (Electrocardiographic artifacts are defined as electrocardiographic alterations, not related to cardiac electrical activity.) shaving, staying still etc …. helps reduce them
5 Lead ECG - Telemetry/Cardiac Monitoring
-Wireless, transmitted from a distance with radio signals, continuous ECG monitoring.
-Nurses still need to assess mechanical events (cardiac output, VS, skin, etc.)
Electrocardiography
Telephone/Facsimile/Ambulatory Electrocardiography
Electrocardiograph is a machine which is used to assess electrical activity of the cardiac system by using electrodes placed on a patients body.
*Transtelephonic event recorder
**Phone checks for clients with pacemakers, complete ECGs can be read in 10-15 minutes
*Holter monitor
*Ziopatch
