Cardiovascular system Flashcards
Anatomy of heart
-4 chambers
3 layers: endocardium, myocardium, epicardium
visceral and parietal pericardium
Left ventrical is 2-3x thicker than right
bloodflow through heart
SVC/IVC –> RA –> tricusp –> RV –> pulmonic valve –> pulmonary artery –> lungs –> pulmonary veins –> LA –> bicsup –> LV –> aortic valve –> systemic
chordae tendinae
anchored to papillary muscles –> keep mitral and tricuspid valve from going into atria during ventricular contraction
Coronary circulation
Left coronary artery
-Left anterior descending artery
-Left circumflex artery
-supply blood to LA, LV, interventricular septum, and part of RV
Right coronary artery
-supplies blood to RA, RV, part of posterior LV
-AV node and bundle of His –>imp for conduction
Coronary veins –> drain into coronary sinus
Conduction system
-specialized tissue creates and transports electrical impulses resulting in depolarization causing hear muscle contraction
SA node –> interatrial pathways –> atrial contraction –> AV node –> internodal pathways –> bundle of His –> left and right bundle branches –> Purkinje fibers –> ventricular contraction
Repolarization
Absolute refractory period
Relative refractory period
-contractile and conduction pathway cells regain resting polarized condition
-heart muscle doesn’t respond to any stimuli
-heart muscle gradually returns to normal
ECG waves and intervals
P wave = firing of SA node and depolarization of atria
QRS complex = depolarization from AV node throughout ventricles
T wave = repolarization of ventricles
U wave = repolarization of Purkinje fibers (big one= hypokalemia)
PR, QRS, QT intervals = travel time of signal from one area of heart to another
Mechanical system
Systole = contractin of heart muscles and ejection of blood from ventricles
Diastole = relaxation of heart muscles and ventricles fill with blood
Stroke volume = amt of blood ejected with each beat
Cardiac output and Cardiac index
CO = amt of blood pumped in a minute
-CO = SV x HR
-Normal = 4-8 L/min
Index = CO/BSA (body surface area)
-normal 2.8-4.2 L/min/m^2
Factors affecting CO
Stroke volume
-preload
-contractility
-afterload
Heart rate
-contolled by ANS
-sustained rapid HR = reduced diastolic filling and coronary artery perfusion
Preload
volume of blood stretching ventricles at end of diastole
-Frank starling law: increased stretch = increased force of contraction
**increased by HTN, aortic valve disease, and hypervolemia
Contractility
Increased with epinephrine and NE from SNS
Increased contractility raises SV by increasing ventricular emptying
Afterload
-peripheral resistance against which left ventricle must pump
*depends on size of ventricle, wall tension, and BP
*increased BP increases resistance = higher workload = hypertrophy (w/o change in chamber area or CO)
Cardiac Reserve
Ability of CV system to alter CO in response to situations like exercise, stress, and hypovolemia
Arteries
Arterioles
Endothelium
Arteries
-thick walls of elastic tissue to handle pressure; recoil propels blood forward
*large arteries (aorta/pulm art) also have smooth muscle
Arterioles = more smooth muscle
-major control of arterial BP and blood flow distribution through dilation and constriction
Endothelium = inner lining
-maintain homeostasis, promote blood flow, inhibits coagulation
-disruption results in coagulation and fibrin clot
Capillaries
Thin wall of endothelial cells –> no elastic or muscle
-connect arterioles and venules
-exchange nutrients and metabolic end products
Veins and Venules
Veins
-thin wall; large diameter
-low pressure; high volume
-intermittent valves move blood towards heart
-blood volume in venous sytem affected by: arterial flow, compression of veins by skeletal muscles, changes in thoracic and abdominal pressure, RA pressure (SVC=neck veins; IVC = liver engorgement)
Venules
-small muscle and CT
-collect blood from capillary beds to larger veins
ANS effect on CV syst
Effect on heart
-Sympathetic stimulation increases HR and speed of impulse thru AV node and force of contractions –> mediated by beta adrenergic receptors
-parasymp stimulation slows HR and impluse f/ SA to AV –> mediated by vagus nerve
Effects on blood vessels
-sympathetic stimulation of alpha adrenergic receptors causes vasoconstriction; decreased stimulation causes vasodilation
ANS: Baroreceptors
-Aortic arch and carotid sinus
-sensitive to stretch or pressure in arterial system
-stimulation sends message to vasomotor center in brainstem to inhibit SNS and enhance PNS to decrease HR and cause peripheral vasodilation
-decreased stretch/pressure does opposite
ANS: chemoreceptors
-aortic and carotid bodies and medulla
-increased CO2 = higher RR and changes in BP
Blood Pressure
Pressure exerted by blood on arterial walls
SBP = peak pressure during vent contraction –> under 120
DBP = residual pressure in arteries during vent relaxation –> under 80
Influencing factors: CO and SVR
-SVR = force opposing movement of blood
-BP = CO*SVR
Measurement of Bp
Invasive technique = catheter into artery –> attached to transducer
Noninvasive technique = sypygmomanometer and stethosope
-automated device
-doppler ultrasonic flowmeter
Pulse pressure and mean arterial pressure
Pulse pressure
-dif bt SBP and DBP
-Normally ab 1/3 of SBP
Mean arterial pressure
-average pressure w/in arterial system that’s felt by organs in body
-(SBP + 2DBP) / 3
-needs to be over 60 to perfuse vital organs
Gerontologic considerations
Risk for CVD increases with age
-CAD due to atherosclerosis is most common
CVD is leading cause of death in adults over 65
CV changes result of aging, disease, enviro, lifetime behaviors
Age related changes to CV system
composition
exercise
valves
pacemakers
beta adrenergic receptors
Increased collagen- decreased elastin
-myocardial hypertrophy
Decreased response to stress/exercise
-slower recovery HR, SV, CO
Heart valves become thick and stiff –> murmurs
Number of pacemaker cells decrease –> dysrhythmias; heart block
Decrease in number and func of beta adrenergic receptors –> decreased stress response and sensitivity to beta adrenergic agonists
Age related changes
blood vessels
venous valves
bp
spine
Blood vessels thicken and less elastic –> increase in SBP and decrease or no change in DBP
Incompetent venous valves –> dependent edema
Orthostatic hypotension and postprandial hypotension (fall risk)
kyphosis
Assessment of CV system: history
Direct or indirect CV issues, all symptoms and allergies
-diabetes, alc/tobacco, angina, strep, rheumatic fever…
past and current meds –> prescription, OTC, herbal, noncardiac
surgeries or other treatments
Assessment of CV functional health patterns
health management
nutrition
elimination
activity/exercise
Health management
-risk factors, allergies, genes
Nutrition
-weight and salt/fat
Elimination pattern
-diuretics, swelling, constipation (don’t do valsalva maneuver if heart probs)
Activity/exercise
-SOB, chest pain, claudication
Assessment of CV syst: Functional health patterns
sleep/rest
cognitive
self-perception
Sleep/rest
-SOB, orthopnea, sleep apnea, nocturia
-HF = paroxysmal nocturnal dyspnea and Cheyne-stokes
Cognitive
-syncope, language/memory probs, pain
Self perception
-body image, activity level
Assessment of CV syst: Functional health patterns
role/relationship
sexuality
coping
values/belief
role/relationship
-support systems; areas of stress/conflict
sexuality
-fear of death, fatiguem chest pain SOB
-ED = symptom of PVD or side effect of meds for CVD
-HT for women poses risks
coping
-sources of stress and support
Values
-culture and religion
Genetic risk alert!
Coronary artery disease
-lipoprotein gene links
Cardiomyopathy
-autosomal and X-linked dominant mutations
HTN
-genetic, environmental, and ifestyle factors
Assessment of peripheral vascular system
Inspect
-skin color, hair distribution, venous pattern, edema, clubbing, lesions
-jugular vein distension
Palpate
-Temp, moisture, edema (1+-4+)
-pulse (0 to 3); thrill
-capillary refill <2 secs
Auscultation
-bruit
Physical examination of thorax
Auscultatory areas: aortic, pulmonic, tricuspid, mitral, and Erb’s point
Epigastric area: abdominal aorta
Precordium: look for heaves
Point of maximal impulse (apical pulse) = mitral fifth ICS, MCL
Auscultation
S1 = closure of tricuspid and mitral valves, “lubb”, beginning of systole
S2 = closure of aortic/pulmonic valves; “dupp”; beginning of diastole
use diaphragm
Pulse defecit = dif bt apical and radial pulses –> dysrhythmia
where in ECG to lubb and dupp occur?
lubb = QRS
dupp = post T
Extra sounds
Spit S2 = pulmonic area
-normal during inspiration; abnormal if during expiration
S3 or S4 = low frequency vibrations
-lean forwards and listen to 2nd ICS aortic and pulmonic
-left side-lying - listen to mitral
S3 = ventricular gallop
-from left HF or mitral regurgitation
S4 = atrial gallop
-from CAD, cardiomyopathy, LV hypertrophy, or aortic stenosis
Murmurs and friction rubs
Murmurs
-graded on 6 pt Roman numeral scale of loudness
Pericardial friction rubs: pericarditis
-inflamed surfaces of the pericardium move against each other; high-pitched, scratchy sounds
-may be intermittent and last days to hours
-listen at apex with patient upright, leaning forward, and holding breath
abnormal sounds
record timing, location, and position of patient when sounds occur
Cardiac biomarkers
injured cells release enzymes and proteins into blood
-consider time from onset of symptoms of ACS
-Troponin, Copeptin, and creatine kinase
Cardiac biomarker: troponin
Troponin T
Troponin I
Myocardial infarction or injury
Rises w/in 4-6 hrs; peaks 10-24 hrs; detected for 10-14 days
Cardiac biomarker: copeptin
substitute biomarker for arginine vasopressin AVP
-detected immediately with MI
-copeptin and troponin = rapid diagnosis of acute MI
-high levels with HF patients = increased mortality
Cardiac biomarker: creatine kinase
-3 isoenzymes
-CK-MB cardiac specific –> increases with MI or injury
-rises in 3-6 hrs, peaks in 12-24 hrs, returns to baseline w/in 12-48 hrs
C-reactive protein (CRP)
marker from liver for inflammation
-inked to atherosclerosis and first heart event –> predicts risk of future heart events
Homocysteine (Hcy)
protein catabolism
-hereditary or dietary deficiency of vits B6, B12, or folate
-high levels = increased risk for CVD, PVD, and stroke
Cardiac natriuretic peptide markers
3 kinds: ANP, BNP (heart failure), CNP
Increased levels f BNP distinguishes cardiac vs respiratory cause of dyspnea
NT-pro-BNP (HF)
Increased DBP leads to release of BNP and NT-pro-BNP –> leads to increased urinary excretion of Na+
Serum lipids and lipoprotein
Serum lipids
-triglycerides = storage form of lipids
-cholesterol = absorbed from food and made in liver
-phospholipids = glycerol, fatty acids, phosphates, and nitrogenous compound
Lipoprotein
-serum lipids bind to protein to circulate in blood
4 classes of ipoprotein
- chylomicrons
- low density lipoproteins
- high density lipoproteins
- very low density lipoproteins
Increased triglycerides and LDL = CAD risk
Increased HDL = decreased risk of CAD
Cholesterol:HDL measures risk
Other serum lipoproteins used as predictors of risk for CAD
apolipoprotein A-I = HDL protein
Apolipoprotein B = LDL protein
Lipoprotein (a) + lactate dehydrogenase = atherosclerosis
Lipoprotein-assos phospholipase A2 = atherosclerotic placques
ECG
-12 lead ECG
-ambulatory ECG monitoring (Holter)
-Exercise or stress testing
Event monitor or loop recorder
External = electrodes worn for a month –> activated by patient when symptoms occur
Internal = for serious, infrequent dysrhythmias; continuous monitor when symptoms occur or when HR increases or decreases from set rate
Functional studies
Exercise or stress testing
-hehart symptoms with activity –> increased O2 demand
-assess CVD; set limits for exercise
-patients walk or ride bike while ECG and BP monitored
6 min walk test
-for general fitness
-flat surface; baseline response to treatment and PT
Noninvasive hemodynamic monitoring
-monitors SV, CO, and BP by finger cuff or thoracic bioreactance; used during complex surgery
iMAGING
Chest xray
-hear is displaced or enlarged
-pericardial effusion
-pulmonary congestion
Echocardiogram
-ultrasound waves record movement of heart structures with or without contrast
Determines abnormalities of:
-valve structures and motion
-heart chamber size and contents
-ventricular and septal motion and thickness
-pericardial sac
-ascending aorta
Measures eection fraction = % of end diastolic blood volume ejected during systole
Echocardiogram
Mmode
2D
Doppelr
Color flow/ duplex
Motion made
-single beam
-motion, wall thickness, and chamber size
2D
-sweeping beam
-shows spatial relationships of structures
Doppler
-uses sound evaluation of flow or motion of scanned object
color/duplex
-combo of 2D and doppler –> shows speed and direction of blood flow
Echocardiogram
real time 3D
Stress echocardiography
Real time 3D
-multiple 2Ds
-shows how structures change throughout cardiac cycle
Stress echocardiography
-computer compares images or wall motion and function before and after exercise
-if uable to exercise, use IV dobutamine and dipyridamole to stress heart
Echocardiogram TEE
better visualization of heart with endoscope
-requires NPO, sedation; check gag reflex after
Evaluates: mitral valve disease, endocarditis vegetation, thrombus before cardioeversion, source of heart emboli, intraoperative heart function, and aortic dissection
Complications: perforation of esophagus, hemorrhage, dysrhythmias, vasovagal reactions, transient hypoxemia
Tomography
Cardiac CT
-looks at heart anatom, coronary circulation, and great vessels
CT angiography
-noninvasive; less risky than cardiac catheterization, but not as good; must have NSR
Calcium scoring screening
-identifies calcium deposits in coronary arteries
-confirms CAD and predicts future issues
-Electron beam CT
Cardiovascular magnetic resonance imaging (CMRI)
no radiation
-3D view of MI
-Assess EF
-predicts recovery from MI
-diagnosis of congenital heart and aordic disorders and CAD
Nuclear cardiology
-Multigated acquisition: MUGA scan
-looks at wall motion, heart valves, and EF
Stress perfusion imaging
-looks at blood flow changes with exercise and diagnoses CAD
-differentiates bt viable heart tissue versus scar tissue
-determines success of interventions
-IV meds to dilate coronary arteries and stimulate exercise effects
-SPECT = size of infarction
-PET stress testing = myocardial ischemia and viability
Interventional studies
Cardica catheterization: contrast and fluiroscopy
-CAD, coronary spasm, congenital and calcular heart disease, ventricular func, intracardiac pressure and O2, CO, and EF
-Right sided to measure pressure from vena cava to pulmonary artery
-Left sides = arterial insertion to evaluate coronary arteries; coronary angiography to identify location and severity of blockage (involves dye)
Complications of cardiac catheterization
bleeding or hematoma at puncture site
allergic rxn to contrast
looping/kinging of catheter
infection
thrombus formation
aortic dissection
dysrhythmias
MI
stroke
puncture of ventricles/septum/lung tissue
Pre catheterization
-assess allergies (esp to dye)
-VS, pulse ox, heart and breath sounds, NV assessment of extremeties
-NPO 6-12 hrs
-assess labs
-educate ab anesthesia, flushed feeling with dye, fluttering of heart
-give sedation and other meds
post catheterization
-baseline assessments compare to pre procedure
-note hypo or hyper tension or signs of PE
-NV status again
-compression on arterial site for hemostasis; observe for hematoma and bleeding every 15 mins for 1 hr then per agency policy
-bed rest as ordered
-monitor ECG, pain, IV/oral fluid I and O
-educate ab activity limits
Intravascular ultrasound
-Intracoronary ultrasound done in cath lab
-also uses coronary angiography to provide 2D or 3D view of coronary artery walls
-evaluate vessel response to stent placement and atherectomy
Electrophysiology study
Electrodes placed in heart to record and manipulate electrical activity of heart, SA node, AV node, and ventricular conduction –> info regarding source and treatment of tachydysrhythmias
