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RN Refresher Course > Module 2: Cardiovascular System > Flashcards

Module 2: Cardiovascular System Flashcards

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1
Q

Heart’s Structure (including the three layers)

A

*Endocardium (thin inner lining)
* Myocardium (layer of muscle)
* Epicardium (outer layer)

*Fibroserous sac called pericardium covers the heart; consists of 2 layers
-Inner (visceral), part of epicardium
-Outer (parietal)

A small amount of pericardial fluid lubricates space between pericardial layers (pericardial space) and prevents friction between surfaces as heart contracts

Septum vertically divides heart
-Intertribal septum creates right and left atrium
-Interventricular septum creates right and left ventricle

**Left ventricular wall is 2-3x thicker than right ventricular wall; why? Strength is needed to pump blood into systemic circulation

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2
Q

What are the four heart valves?

A

4 valves keep blood flowing in forward direction
-Cusps of mitral and tricuspid valves are attached to thin strands of fibrous tissue, chord tendinae; anchored in papillary muscles of ventricles
-pulmonic and aortic valves (also known as semilunar valves) prevent blood from regurgitating back into ventricles at end of each ventricular contraction

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3
Q

Right side of heart

A

-unoxygenated
Blood flow path:
SVC –> IVC –> right atrium –> tricuspid valve –> right ventricle –> pulmonic valve –> pulmonary artery –> lungs

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4
Q

Left side of heart

A

-oxygenated
-Pulmonary veins –> left atrium –> mitral valve –> left ventricle –> aortic valve –> systemic circulation

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5
Q

Heart Conduction System

A

-creates and transports electrical impulse (action potential)
-starts depolarization of heart cells, leading to heart muscle contraction
-electrical impulse normally begins in SA node (pacemaker of heart)
-Travel through interartrial pathways to depolarize atria, resulting in contraction
-Travels from atria to AV node through internal pathways
-Signal then moves to bundle of His and left and right bundle branches
-Left bundle branch - anterior and posterior divisions
-moves through ventricle walls via Purkinje fibers
-Ventricular conduction system triggers synchronized right and left ventricular contraction + ejection of blood into pulmonary and systemic circulations

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6
Q

Coronary Circulation

A

Left coronary artery branches: left anterior descending + left circumflex
-Supply blood to L atrium, L ventricle, inter ventricular septum + part of right ventricle

Right coronary artery branches; AV node and Bundle of His
-Supplies blood to right atrium, R ventricle, part of posterior L ventricle

Coronary veins drain into coronary sinus

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7
Q

What is repolorization?

A

Contractile and conduction pathways cells regain resting polarized condition

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8
Q

What is absolute refractory period?

A

Heart muscle does not respond to any new stimuli

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9
Q

Relative Refractory Period

A

Heart muscle recovers excitability via early diastole

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10
Q

How does aging affect the heart?

A

CVD is leading cause of death for adults over 65
Commonly due to atherioschlorosis
Increased age = increased collagen in heart, elastin decreases; affect heart’s ability to stretch and contract
Less sensitive to B adrenergic agonies drugs
Heart valves thicken and stiffen from lipid accumulation, collagen degeneration and fibrosis
Aortic and mitral valves are most often affected
-What happens as a result? Regurgitation of blood when valve should be closed; narrowing of office of valve (stenosis) if it should be open
-Number of pacemaker cells in SA node and conduction cells decreases with age, develops sinus and atrial dysrthmias and heart blocks
-Arteries and veins thicken, become less elastic
-Edema occurs from blood flow returning to heart less efficiently
-Increased risk of falls from orthostatic hypotension and postprandial hypotension

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11
Q

Heart murmur

A

Turbulent blood flow across affected valve, heard as a whooshing sound (or murmur)
between heartbeats

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12
Q

ECG

A

Electrodes record electrical activity of heart as P, QRS, T, and U waveforms

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13
Q

P Wave of ECG

A

Firing of SA node and depolarization of atria

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14
Q

QRS Complex

A

Depolorization of AV node throughout ventricles

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15
Q

T Wave

A

Repolorization of ventricles

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16
Q

U Wave (if seen)

A

Repolorization of Purkinje fibers (large U wave might occur with hypokalemia)

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17
Q

PR, QRS, QT intervals

A

Travel time of signal from one area of heart to another (changes in timing indicate conditions)

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18
Q

Mechanical System: Systole

A

Contraction of heart muscles, ejection of blood from ventricles

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19
Q

Mechanical System: Diastole

A

Relaxation of heart muscle, ventricles fill with blood

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20
Q

SV (stroke volume)

A

Amount of blood ejected with each heart beat

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21
Q

CO (cardiac output)

A

Amount of blood pumped by each ventricle in one minute

CO = SV x HR
Normal is 4-8L/min

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22
Q

Factors affecting CO

A

Heart rate - controlled by autonomic nervous system (ANS)
*High rate = reduced perfusion and filling

SV - affected by
preload (volume of blood stretching ventricles at end of diastole)
*Frank Starling law = increased stretch, increased force of contraction
contractibility (strength of contraction)
*increased with epinephrine and norepinephrine from SNS; increased contractility increased SV by increased ventricular emptying
afterload (peripheral resistance against which left ventricle must pump)
*Depends on size of wall ventricle, tension, and BP
*Increased BP = increased resistance = increased workload = hypertrophy

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23
Q

Cardiac Reserve

A

Ability of CV system to maintain or increase CO in response to many situations in health and illness
-exercise, stress, hypovolemia

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24
Q

Vascular System: Blood Vessels

A

-Blood circulates from L side of heart
*arteries + arterioles - carry oxygenated blood except for pulmonary artery
*capillaries
*venules/veins - carry deoxygenated blood (except for pulmonary veins)
-Right side of heart

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25
Q

Arteries

A

Thick walls of elastic tissue to handle pressure; recoil propers blood forward
-Large arteries (like aorta and pulmonary arteries) also have smooth muscle

26
Q

Arterioles

A

More smooth muscle
-Control arterial BP and blood flow distribution through dilation and constriction

27
Q

Endothelium

A

Inner lining
-Maintains hemostasis, promotes blood flow, inhibits coagulation
-Disruption results in coagulation and fibrin clot

28
Q

Capillaries

A

thin walls of endothelial cells; no elastic or muscle tissue
-connects arterioles and venules
-exchanges nutrients and metabolic end products

29
Q

Veins and Venules

A

Venules - small muscles with minor amount of muscle and connective tissue (collect blood from capillary bed to larger veins)
Veins - thin wall, large diameter; intermittent valves move blood to heart
-Blood volume in venous system affected by:
*arterial flow
*compression of veins by skeletal muscles
*changes in thoracic and abdominal pressures
*right atrial pressure - distended neck veins

30
Q

Regulation of CVS

A

Autonomic Nervous System (ANS)
-Effect on heart
*Sympathetic stimulation increases; HR, speed of impulse through AV node, force of contraction, B-adrenergic receptors
*Parasympathetic simulation slows HR, impulse conduction from SA to AV node, vagus nerve
-Effect on blood vessels
*sympathetic stimulation of alpha adrenergic receptors causes vasoconstriction, decreased stimulation causes vasodilation

31
Q

Regulation of CVS: 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 peripheral vasodilation; decreased
stretch or pressure does opposite

32
Q

Regulation of CVS: Chemoreceptors

A

Aortic and carotid bodies and medulla
*Increased CO2 results in changes in RR and BP

33
Q

Blood Pressure

A

Force exerted by blood against arterial walls
Systolic: Peak pressure against arteries during ventricular contraction; normally 120 or less
Diastolic: Residual pressure in arteries during ventricular relaxation; normally less than 80

Influencing factors: CO, systemic vascular resistance

34
Q

Pulse Pressure

A

-Difference between SBP and DBP
-Normally about 1/3 of SBP
*Increased with exercise, atherosclerosis
*Decreased with with heart failure, hypovolemia

35
Q

Assessing Pt - CVS

A

Subjective Data:

Health info: history of present illness/why are they seeking care
Direct or indirect with CVS, all current meds
Surgery and treatments (ECG, X-ray)
Risk factors
Weight, dietary habits
Elimination pattern (diuretics, swelling, constipation)
Activity/Exercise - chest pain etc
Sleep/rest patterns
Syncope, language/memory problems, pain
Body image/activity level
Support systems, areas of conflict and stress
Fear of death, fatigue, chest pain
Sources of stress/support
Religion/culture

Objective Data:

Physical assessment
Vital signs
Inspection for skin, hair, edema, etc
Look at right side of neck for jugular venous distention, indicative of right sided heart failure
Palpation for moisture, edema, pulses and capillary refill
Inspect and palpate thorax
*Ausculatory areas: aortic, pulmonic, tricuspid, mitral, erb’s point
Apical pulse

36
Q

Genetic Link CVS

A

Coronary artery disease - lipoprotein gene links
Cardiomyopathy - autosomal and X linked genetic mutations
Hypertension - genetic, environmental, lifestyle

37
Q

Auscultating CVS

A

S1—closure of tricuspid and mitral valves; “lubb”;
beginning of systole
S2—closure of aortic and pulmonic valves: “dubb”;
beginning of diastole
Listen in sequence
* Use diaphragm
Pulse deficit—Palpate radial pulse when listening to
apical

38
Q

Auscultating CVS - Extra Sounds

A

Split S2—pulmonic area
* Normal inspiration; abnormal expiration
S3 or S4—use bell – low frequency vibration
* Lean forward; 2nd ICS aortic and pulmonic
* Left side-lying—mitral
* S3—ventricular gallop
Left heart failure or mitral regurgitation
* S4—atrial gallop
CAD, cardiomyopathy, LV hypertrophy, aortic stenosis

39
Q

Auscultating CVS - Abnormal Sounds (Murmurs and Rubs)

A

Murmurs
* Graded on a six-point Roman numeral scale (I to VI) of
loudness and recorded as a ratio

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

40
Q

Hemodynamic Monitoring

A

-Measurement of pressure, flow, and
oxygenation within cardiovascular system
-Assesses heart function, fluid balance, and
effects of drugs on cardiac output (CO)
-Invasive and noninvasive measurements

41
Q

Hemodynamic Monitoring Terminology

A

CO: volume of blood pumped by heart in 1
minute
CI: CO adjusted for body surface area (BSA)
SV: volume ejected with each heartbeat
SVI: SV adjusted for BSA
Systemic vascular resistance (SVR) or pulmonary
vascular resistance (PVR)
 Opposition to blood flow by systemic and pulmonary
vasculature

Preload, afterload, and contractility determine SV
Preload:
Volume of blood within ventricle at end of diastole
 PAWP: reflects left ventricular end-diastolic pressure
 CVP: reflects right ventricular end-diastolic pressure

Afterload
Forces opposing ventricular ejection
 SVR and arterial pressure indices of left ventricular
afterload
 PVR and pulmonary arterial pressure indices of right
ventricular afterload

Vascular resistance
 Systemic (SVR) and pulmonary (PVR)
 Reflect afterload
 Contractility
 Strength of ventricular contraction
 No direct clinical measures

42
Q

Invasive BP Monitoring: Arterial

A

Various indications when continuous BP
measurements useful
 Non-tapered Teflon catheter used to cannulate
peripheral artery
 HCP sutures in place
 Immobilize insertion site

High- and low-pressure alarms

-Risks/complications
 Hemorrhage
 Infection
 Thrombus formation
 Neurovascular impairment
 Loss of limb

Continuous flush irrigation system
 Delivers 1 to 3 mL of saline per hour
* Maintains line patency
* Limits thrombus formation
 Assess neurovascular status distal to arterial insertion
site hourly

43
Q

Arterial Pressure Based CO (APCO) Monitoring

A

Calculates continuous CO and CCI
 Used to assess patient’s ability to respond to
fluids
 Uses arterial waveform characteristics and
patient demographic data to calculate SV and
pulse rate (PR) to calculate CCO/CCI, and
SV/SVI every 20 seconds

44
Q

Pulmonary Artery (PA) Pressure Monitoring

A

Guides management of patients with
complicated cardiopulmonary problems
 PA diastolic (PAD) pressure and PAWP are
sensitive indicators of heart function and fluid
volume status
 Allows for precise manipulation of preload

PA flow-directed catheter (e.g., Swan-Ganz)
 Distal lumen port in PA
 Balloon inflated to measure PAWP
 2 proximal lumens to measure CVP, inject fluid for
CO, draw blood, administer fluids or drugs
 Temperature sensor near distal tip

 Specialized features
-Atrial electrode
-Fiberoptic sensor for mixed venous O2 saturation
-Continuous measurement of right ventricular volume
and EF
-Continuous CO monitoring
-Additional ports for IV access

45
Q

Central Venous Pressure (CVP Monitoring)

A

Measurement of right ventricular preload that
reflects fluid volume
Obtained from:
 Central venous catheter
 PA catheter
 Similar to PAWP waveforms

46
Q

Diagnostic Studies of CVS

A

-Assess oxygen carrying capacity (RBCs, hemoglobin)
-Coagulation properties (clotting time)
-Cardiac biomarkers; injured cells release enzymes and proteins in blood

47
Q

Diagnostic: Troponin

A

Troponin T (cTnT)
* Troponin I (cTnI)
* Rises within 4 to 6 hours, peaks 10 to 24 hours, detected for
up to 10 to 14 days
* High-sensitivity troponin (hs-cTnT, hs-cTnI) assays may
detect a heart event within 1-3 hours

48
Q

Diagnostic: Copeptin

A

Substitute marker for arginine vasopressin (AVP)
* Detected with acute MI, ischemic stroke, HF
* Copeptin + troponin = rapid diagnosis of acute MI
* High copeptin levels = increased mortality with acute MI

49
Q

Diagnostic: Creatine Kinase (CK); 3 isoenzymes

A

CK-MB cardiac specific; increased with MI or cardiac injury
* Rises in 3 to 6 hours, peaks in 12 to 24 hours, returns to
baseline within 12 to 48 hours
* Rarely used for diagnosis of acute MI

50
Q

Diagnostic: C-Reative Protein (CRP)

A

-Marker for inflammation
-Linked to atherosclerosis and first heart event; predict risk of future heart events

51
Q

Diagnostic: Homocysteine

A

-Hereditary or dietary deficiency of vitamins B6, B12, or folate
* High levels—increased risk for CVD, PVD, stroke

52
Q

Diagnostic: Cardiac natriuretic peptide markers

A

Three types
 Atrial natriuretic peptide (ANP)
 B-type natriuretic peptide (BNP)—heart failure
 C-type natriuretic peptide
* Increased levels of BNP distinguishes cardiac vs respiratory cause of dyspnea
* NT-pro-BNP
* Increased DBP leads to release of BNP and NT-pro-BNP
leads to increased urinary excretion of Na+

53
Q

Diagnostic: Serum Lipids/Lipid Panel

A

Triglycerides—storage form of lipids
 Cholesterol—absorbed from food and made in liver
 Phospholipids—glycerol, fatty acids, phosphates, and nitrogenous compound
 Lipoprotein
**four classes of lipoprotein:
-Chylomicrons
-Low-density lipoproteins (LDLs)
-High-density lipoproteins (HDLs)
-Very-low-density lipoproteins (VLDLs)

Increased Triglycerides and LDL—CAD risk factor
Increased HDL decreases risk—decreased risk of CAD
-Cholesterol: HDL ratio—risk assessment

Other serum lipoproteins used as predictors of risk
for CAD
 Apolipoprotein A-I (Apo A-I)—HDL protein
 Apolipoprotein B (Apo B)—LDL Protein
 Lipoprotein (a) [Lp(a)] + increased LDH
 Lipoprotein-associated phospholipase A2—
atherosclerotic placques

54
Q

Diagnostic: Electrocardiogram

A

Resting 12 lead ECG
Holter
Exercise or Stress Test
External or internal monitoring

55
Q

Diagnostic: Functional Stress

A

Exercise or stress testing
* Heart symptoms with activity—Increased O2 demand
* Assess CVD; set limits for exercise
* Patients walk or ride bike while ECG and BP monitored
 6-minute walk test—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

56
Q

Diagnostic: Chest X Ray

A

Chest x-ray
* Heart displaced or
enlarged
* Pericardial effusion
* Pulmonary
congestion

57
Q

Diagnostic: Echocardiogram

A

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 ejection fraction (EF)—% of end-diastolic blood volume ejected during systole

 Motion made (M-mode)
* Motion, wall thickness, and chamber size
 Two-dimensional (2-D)
* Spatial relationship of structures
 Doppler technology
* Sound evaluation of flow or motion of scanned object
 Color-flow imaging (duplex)
* Combination of 2-D and Doppler—show speed and direction of blood flow

Real time 3-D
* How structures change during cardiac cycle
 Stress echocardiography
* Computer compares images or wall motion and
function before and after exercise
* No exercise—use IV dobutamine and dipyridamole for pharmacologic stress
 Bubble study
* Contrast echocardiography checks for defects in wall between the two upper chambers of the heart

Transesophageal echocardiography (TEE)
* Better visualization of heart with endoscope
* Requires NPO, sedation; check gag afterward
* Evaluates: mitral valve disease, endocarditis
vegetation, thrombus before cardioversion, source of heart emboli, intraoperative heart function, and aortic dissection
* Complications: perforation of esophagus, hemorrhage, dysrhythmias, vasovagal reactions, transient hypoxemia

58
Q

Diagnostic: Tomography

A

Cardiac computed tomography
 Heart anatomy, coronary circulation, great vessels
(multidetector CT scanning—MDCT)
* CT angiography (CTA)
 Noninvasive; faster, less risky, less radiation exposure than cardiac catheterization; must have NSR
* Calcium-scoring screening
 Identifies calcium deposits in coronary arteries
 Confirms suspected CAD; predict future cardiac events
 Electron beam CT (EBCT)

59
Q

Diagnostic: CMRI, No Radiation

A

Cardiovascular magnetic resonance imaging
(CMRI)—no radiation
 3-D view of MI; assess EF
 Predicts recovery from MI
 Diagnosis of congenital heart and aortic disorders and CAD
 Patients with stents can undergo CMRI 6 weeks after placement

60
Q

Diagnostic: Nuclear Cardiology

A

Multigated acquisition—MUGA scan
* Wall motion, heart valves, EF
 Stress perfusion imaging
* Blood flow changes with exercise diagnoses CAD
* Viable heart tissue versus scar tissue
* Determine success of interventions (e.g., CABG or PCI)
* IV medications to dilate coronary arteries and simulate
exercise effects
* SPECT—size of infarction
* PET stress testing—myocardial ischemia and viability

Interventional studies
 Cardiac catheterization—contrast and fluoroscopy
 CAD, coronary spasm, congenital and valvular heart disease, ventricular function, intracardiac pressures and O2 levels, CO, and EF
 Right-sided to measure pressures from vena cava to pulmonary artery
 Left-sided—arterial insertion to evaluate coronary arteries; coronary angiography (dye injected) to identify location and severity of blockages

Cardiac catheterization
 Complications: bleeding or hematoma at puncture
site; allergic reaction to contrast; looping or kinking of catheter; infection; thrombus formation; aortic
dissection; dysrhythmias; MI; stroke; puncture of
ventricles, septum, or lung tissue

Intravascular ultrasound (IVUS)
 Intracoronary ultrasound (ICUS); done in cath lab
 Also uses coronary angiography to provide a 2-D or 3-D view of
the coronary artery walls
 Evaluate vessel response to stent placement and atherectomy
 Electrophysiology study (EPS)
 Electrodes placed in heart to record and manipulate electrical
activity of heart; SA node, AV node, and ventricular conduction information regarding source and treatment of tachydysrhythmias
 Nursing care—similar to cardiac catheterization

61
Q

Nursing Management of Cardiac Cath Patient

A

Preprocedure:
 Assess allergies; contrast dye
 Baseline assessment: VS, pulse oximetry, heart and breath
sounds, neurovascular assessment of extremities
 NPO for 6 to 12 hours
 Assess labs
 Patient education:
* Procedure—local anesthesia, flushed feeling when dye injected; fluttering of heart
 Administer sedation and other meds as ordered

Postprocedure
 Baseline Assessment: compare to preprocedure; note hypotension or hypertension; signs of PE
 Assess neurovascular status of extremity
 Compression device over arterial site for hemostasis; observe for hematoma and bleeding every 15 minutes for 1 hour then per agency policy; bed rest as ordered
 Monitor: ECG, chest pain, IV/oral fluid intake and urine output
 Patient Education: discharge instructions, activity limits

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