-
Was the average size of the heart?
Size of your fist .5" x 3.5"
-
What is the PMI or point of maximal impulse?
- Pulsation arising at the apex of the heart; tip of the left ventricle
- Apical pulse
- 5th ICS midclavicular line
-
What are the four chambers of the heart?
- Right atrium
- Right ventricle
- Left atrium
- Left ventricle
-
What are the layers of the heart?
- Endocardium: inner lining of the heart, chambers and valves
- Myocardium: actual muscle, conductive system
- Pericardium: sac surrounds the heart: composed of visceral and parietal layer
- Epicardium: outer surface of the heart, contains the coronary arteries; visceral layer of the pericardium
- Pericardial space: small amount of fluid in space acts as a lubricant; there is friction caused by movement of the layers with each contraction, contains about 50 mL of serous fluid
-
Valves of the heart
- Prevent backflow of blood; keep blood flowing in one direction
- Atrioventricular valves: tricuspid valve, mitral valve (first heart sound, S1)
- Semilunar valves: aortic, pulmonic (second heart sound, S2)
- Tricuspid and mitral (atrioventricular) prevent backflow of blood into the atria during contraction
- Pulmonic and aortic (semilunar) prevent regurgitation into the ventricles at end of each ventricular contraction
- Chordae tendeneae prevent eversion of the valve leaflets during ventricular contraction
-
Arterial coronary blood flow
- Coronary arteries branch off just as the aorta leaves the heart
- Right coronary artery: supplies blood to the right anterior surface of the heart, part of the inferior wall of left ventricle, and conduction system (SA & AV)
- Left main coronary artery: branches into the left circumflex (supplies the posterior and lateral left atrium and ventricle)
- Left anterior descending: supplies the anterior wall of left ventricle to apex
- Left circumflex: supplies lateral wall of left ventricle
-
What is ischemia?
- Deficiency of blood due to constriction or obstruction of a blood vessel
- Results in tissue hypoxia which reduces the mechanical & electrical activity of the heart
- Indicates there is myocardium that is at risk, but if you intervene may be able to salvage it
-
Is ischemia reversible?
May be reversible, depending on length of time ischemia occurs and the extent of muscle involved
-
What is an infarction?
- Permanent loss of blood flow to myocardium; not reversible
- Results in cell death
- Overall effect depends on the size of area deprived of O2
- Alternate routes are developed in time to nourish the endangered myocardium (collateral blood supply)
- Causes: emboli and atherosclerotic plaque buildup in the arterial blood supply
-
Electrical conduction system
- Conduction system is composed of specialized nerve tissue responsible for creating and transporting the electrical impulse, or action potential
- Cardiac cells have the ability to transmit electrical impulses
-
Depolarization
- Rapid influx of sodium & calcium ions into the cell & outflux of potassium ionsShift in electrolytes
- Causes muscle fibers to shorten and contract
- T wave
- Electrical activity is synchronous with mechanical activity
- Cells become positive insideFiring of SA node depolarizes the atria
-
Repolarization
- Return to resting phase; electrical recovery
- Potassium moves back into cell and sodium and calcium return to extracellular space
- Cell returns to negative state
-
SA node
- Intrinsic pacemaker of the heart; right atria near entrance of superior vena cava
- Creates an electrical impulse
- Intrinsic rate of 60-100.
-
AV node
- Conducts impulse to Bundle Branches
- Internodal pathways to reach the left atrium
- Rate of 40-60
-
Bundle Branches
- Conduct impulse to Purkinje fibers resulting in ventricular contraction
- Impulse terminates in the Purkinje fibers which trigger a uniform ventricular contraction
-
ECG
Electrical activity of the heart detected on one’s body surface
-
ECG waves
- P wave: depolarization of fibers in atria (lasts .06-.12 seconds)
- PR Interval: conduction through A-V node (.12-.20 seconds); time it takes to get thru AV node (if prolonged, indicates conduction problem in AV node)
- QRS: ventricular contraction/depolarization (.04-.12 seconds); if wider than normal, there is a conduction blockage below the AV node
- T wave: ventricular repolarization
- U wave: delayed ventricular repolarization; may be associated with hypokalemia, Digoxin toxicity
- Repolarization of atria is buried under the QRS interval
-
What is the significance of a prolonged PR interval?
- Delayed AV conduction or at atria
- AV block
-
What is the significance of a prolonged QRS interval?
Delay below AV node or at ventricles
-
What is the significance of a prolonged QT interval?
- Rhythm disturbances
- At risk for serious ventricular arrhythmias (ventricular tachycardia)
- There are some drugs that can prolong the interval as well as a genetic component
-
What are the clinical consequences of SA node dysfunction?
- Lower pacemakers should take over and run the heart, however not as efficient
- HR may still be bradycardic (rate at AV node is around 40 to 50 bpm, in ventricles is around 20 to 30 bpm)
-
What is cardiac output?
- Heart Rate x Stroke Volume (SV determined by preload, contractility and afterload)
- Total amount of blood pumped by each ventricle in 1 minute
- Normal adult at rest is 4L to 6L
- Amount of blood ejected from the ventricle with each heartbeat; approximately 70ml
-
What is preload?
- Volume of blood in ventricles at end of diastole before next contraction (end of filling)
- It determines the amount of stretch placed on myocardial fibers
- Heavily influenced by fluid volume status
- Increased in hypervolemia and regurgitation of cardiac valves
- If preload increases, cardiac output increase (due to Starling's Law; the more the ventricle is filled, the more blood that has to go out)
-
What is contractility?
- Ability of the heart to depolarize; the force of contraction
- Affected by the autonomic nervous system
- If contractility increases, cardiac output increases
-
What is afterload?
- Peripheral resistance which left ventricle must pump against to circulate the blood
- Affected by size of ventricle, wall tension, and arterial blood pressure
- Influenced by hypertension, aortic stenosis, peripheral vasoconstriction (the more clamped down the vessels are the more resistence; ex: clamped down water hose)
- If afterload increases, cardiac output decreases (the harder the heart has to work to get blood out against resistance)
-
What is Starling’s Law?
- The more the myocardial fibers are stretched the greater the force of contraction
- The more the heart is filled, the greater the squeeze of the heart and the larger the cardiac output
- As the heart is stretched overtime the likelihood that the muscle will lose contractility increases
-
Autonomic regulation of the cardiovascular system
- Barorecptors in aortic arch and carotids responsive to stretch
- Chemoreceptors in aortic arch and carotids responsive to pH, PO2 and PCO2
- Information conveyed to vasomotor center in brainstem
-
Baroreceptors
- Pressure sensitive
- If pressure decreases, message is sent to brain stem that more cardiac output is needed
- SNS is activated releasing epi and norepi to increase HR and contractility to increase cardiac output
- If pressure gets too high, baroreceptors indicate that there is too much pressure and needs to decrease cardiac output
- PNS is activated via vagus nerve (decreases HR and contractility)
-
Sympathetic stimulation
- Release of Epinephrine and Norepinephrine (stimulates β-1 receptors)
- NE stimulates α-1 receptors in periphery (vasoconstriction causes increase in afterload; increases BP)
- Increases heart rate, conduction, contractility, and peripheral vasoconstriction
-
Parasympathetic stimulation
- Mediated by vagus nerve
- Slows HR, contractility and conduction
- No effect on periphery
-
What are the 3 major types of blood vessels?
- Arteries
- Capillaries
- Veins
-
Arteries
- Carries oxygenated blood away from heart, except for pulmonary artery
- Thick walls and elastic tissue
- High pressure system, major control of arterial BP
-
Veins
- Carries deoxygenated blood toward heart, except for pulmonary veins
- Returns blood to right atrium
- Thin walled and large in diameter
- Low pressure system, high volume
- Reliant on valves, changes in muscle contraction, and changes in thoracic pressure
-
Capillaries
- Endothelial cells
- No elastic or muscle tissue
- Thin walled vessels
- Diffusion of gases; exchange of O2 and CO2 (cellular nutrients and metabolic end products)
-
Diagnostic studies of the heart
- Chest x-ray (size of heart, any fluid volume overload)
- ECG (rhythm disturbances, conduction, heart blocks, ischemia
- Holter Monitor/Event Monitor
- Echo (2D or transesophageal)
- Exercise stress test (patient on treadmill to get HR to increase; looking for EKG changes and areas of ischemia)
- Stress echo (sonogram of heart; stress heart and look for areas that lack perfusion after exercise)
- Nuclear stress test (injection of a nuclear isotope and stress the heart; looking for areas that lack perfusion)
- conduction defects, arrythmias, ischemia
-
Echocardiogram
- Looking at size of heart, chambers and valves
- Any ischemic areas
- Injection fraction (% of volume that is in ventricle that comes out with each squeeze; normally between 50% to 65%; if less than 20% indicates decreased contractility and weak myocardium)
-
Holter Monitor
- Worn by patient when having syncope, palpitations, rhythm disturbances
- Patient keeps monitor on for 24-48 hours and must keep a log of activities at all times (including any symptoms experienced)
- Information is stored in monitor and printed out at a later time
-
Stress test
- Patient walks on treadmill or rides stationary bicycle
- Leads are placed on chest
- BP and O2 level is monitored
- Stop test if reach peak HR, peak exercise tolerance, chest pain, significant ST segment depression (indicates ischemia)
- Helps diagnose left ventricular function.
-
Cardiac enzymes
- Used to diagnose infarction
- Indicate damage to myocardial cells
- CK-MB (5% of total; rise in 3-12 hours; peak in 24 hours; return to baseline in 48-72 hours)
- Troponin T < 0.1 ng/ml is normal.
- Troponin I < 0.4 ng/ml is normal.
- Troponins (elevate within 3 hours; peak in 24-48 hours; return to baseline in 5-14 days)
-
Cardiac catheterization
- Invasive exam of heart
- Looks at valve function, ventricular function and presence of CAD (plaque)
- Catheter is threaded through femoral artery (left cath) or vein (right cath)
- Contrast dye is injected (ask about allergies to iodine, shellfish, renal function, look at BUN and Cr labs; need to hydrate patient after contrast to prevent toxicity)
- Xrays are taken
- Potential complications: aneurysm, hemorrhage, clots, MI, embolus, arrhythmias, death
- Assess patients vitals (decreased BP from bleeding), peripheral pulses (perfusion; clot in artery that breaks off would result in decreased peripheral pulses), puncture site (bleeding or development of hematoma)
-
Cardiac catheterization nursing considerations
- Informed Consent
- NPO 6-12 hours prior
- Assess Allergy History
- Post-procedure must keep leg straight for 6 hours (can dislodge a clot and can start to bleed)
- Monitor V/S, peripheral pulses, puncture site
-
Electrophysiology Study (EPS)
- Invasive study to diagnose, induce and treat arrhythmias
- Catheter inserted to right side of heart via femoral vein
- Electrodes detect site of arrhythmia
- Can ablate aberrant conduction pathways
- Requires informed consent, NPO 6-8 hours prior
- Can put patient into ventricular tachycardia to assess and try to locate site of arrhythmia
-
Cardiovascular effects of aging
- High rates of atherosclerosis (increases with age, even though not normal sign of aging)
- Increased incidence of hypertension
- Increased rates of valvular calcification
- Decreased HR response to exercise
- Decreased baroreceptor function (at risk for orthostatic hypotension)
-
Modifiable cardiovascular risk factors
- Hypertension
- Hyperlipidemia
- Diabetes
- Smoking
- Excessive ETOH
- Obesity
- Sedentary Lifestyle
-
Non-modifiable cardiovascular risk factors
- Family History
- Age
- Race
- Sex
-
Cardiovascular assessment
- Past medical history (heart disease, MI, angina, cardiac testing, arrhythmias, valve disease, rheumatic fever, DM, HTN, Meds)
- Past surgical history (PTCA, CABG, valve replacement)
- Family history
- Social history (smoking, alcohol, drug use, diet, exercise)
- Review of systems (fatigue, chest pain, syncope, dyspnea, palpitations, claudication, edema, orthopnea)
- Paroxysmal nocturnal dyspnea (when laying supine all fluid from extremities goes back up to heart; will back up into lungs if heart is not functioning properly)
-
Cardiovascular physical exam
- Vital Signs (BP, pulse, resp, O2 sat)
- Neck (JVD, carotids palpation and auscultation for bruits)
- Precordium (PMI, heaves, lifts, thrills)
- Auscultation of heart (S1, S2, rate, rhythm, murmurs, rubs, gallops)
- Abdominal vessels (Abdominal aortic aneurysm or bruit)
- Assessment of periphery (peripheral pulses, capillary refill, color, temperature, edema)
|
|
