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Cardiovascular system Flashcards

1
Q

Anatomy of heart

A

-4 chambers

3 layers: endocardium, myocardium, epicardium

visceral and parietal pericardium

Left ventrical is 2-3x thicker than right

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2
Q

bloodflow through heart

A

SVC/IVC –> RA –> tricusp –> RV –> pulmonic valve –> pulmonary artery –> lungs –> pulmonary veins –> LA –> bicsup –> LV –> aortic valve –> systemic

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3
Q

chordae tendinae

A

anchored to papillary muscles –> keep mitral and tricuspid valve from going into atria during ventricular contraction

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4
Q

Coronary circulation

A

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

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5
Q

Conduction system

A

-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

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6
Q

Repolarization
Absolute refractory period
Relative refractory period

A

-contractile and conduction pathway cells regain resting polarized condition

-heart muscle doesn’t respond to any stimuli

-heart muscle gradually returns to normal

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7
Q

ECG waves and intervals

A

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

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8
Q

Mechanical system

A

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

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9
Q

Cardiac output and Cardiac index

A

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

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10
Q

Factors affecting CO

A

Stroke volume
-preload
-contractility
-afterload

Heart rate
-contolled by ANS
-sustained rapid HR = reduced diastolic filling and coronary artery perfusion

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11
Q

Preload

A

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

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12
Q

Contractility

A

Increased with epinephrine and NE from SNS

Increased contractility raises SV by increasing ventricular emptying

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13
Q

Afterload

A

-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)

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14
Q

Cardiac Reserve

A

Ability of CV system to alter CO in response to situations like exercise, stress, and hypovolemia

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15
Q

Arteries
Arterioles
Endothelium

A

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

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16
Q

Capillaries

A

Thin wall of endothelial cells –> no elastic or muscle
-connect arterioles and venules
-exchange nutrients and metabolic end products

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17
Q

Veins and Venules

A

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

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18
Q

ANS effect on CV syst

A

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

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19
Q

ANS: Baroreceptors

A

-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

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20
Q

ANS: chemoreceptors

A

-aortic and carotid bodies and medulla
-increased CO2 = higher RR and changes in BP

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21
Q

Blood Pressure

A

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

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22
Q

Measurement of Bp

A

Invasive technique = catheter into artery –> attached to transducer

Noninvasive technique = sypygmomanometer and stethosope
-automated device
-doppler ultrasonic flowmeter

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23
Q

Pulse pressure and mean arterial pressure

A

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

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24
Q

Gerontologic considerations

A

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

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25
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
26
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
27
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
28
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
29
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
30
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
31
Genetic risk alert!
Coronary artery disease -lipoprotein gene links Cardiomyopathy -autosomal and X-linked dominant mutations HTN -genetic, environmental, and ifestyle factors
32
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
33
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
34
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
35
where in ECG to lubb and dupp occur?
lubb = QRS dupp = post T
36
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
37
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
38
abnormal sounds
record timing, location, and position of patient when sounds occur
39
Cardiac biomarkers
injured cells release enzymes and proteins into blood -consider time from onset of symptoms of ACS -Troponin, Copeptin, and creatine kinase
40
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
41
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
42
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
43
C-reactive protein (CRP)
marker from liver for inflammation -inked to atherosclerosis and first heart event --> predicts risk of future heart events
44
Homocysteine (Hcy)
protein catabolism -hereditary or dietary deficiency of vits B6, B12, or folate -high levels = increased risk for CVD, PVD, and stroke
45
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+
46
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
47
4 classes of ipoprotein
1. chylomicrons 2. low density lipoproteins 3. high density lipoproteins 4. very low density lipoproteins Increased triglycerides and LDL = CAD risk Increased HDL = decreased risk of CAD Cholesterol:HDL measures risk
48
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
49
ECG
-12 lead ECG -ambulatory ECG monitoring (Holter) -Exercise or stress testing
50
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
51
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
52
iMAGING
Chest xray -hear is displaced or enlarged -pericardial effusion -pulmonary congestion
53
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
54
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
55
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
56
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
57
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
58
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
59
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
60
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)
61
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
62
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
63
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
64
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
65
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

Patho (44 decks)

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