Module 2: Cardiovascular System Flashcards
Heart’s Structure (including the three layers)
*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
What are the four heart valves?
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
Right side of heart
-unoxygenated
Blood flow path:
SVC –> IVC –> right atrium –> tricuspid valve –> right ventricle –> pulmonic valve –> pulmonary artery –> lungs
Left side of heart
-oxygenated
-Pulmonary veins –> left atrium –> mitral valve –> left ventricle –> aortic valve –> systemic circulation
Heart Conduction System
-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
Coronary Circulation
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
What is repolorization?
Contractile and conduction pathways cells regain resting polarized condition
What is absolute refractory period?
Heart muscle does not respond to any new stimuli
Relative Refractory Period
Heart muscle recovers excitability via early diastole
How does aging affect the heart?
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
Heart murmur
Turbulent blood flow across affected valve, heard as a whooshing sound (or murmur)
between heartbeats
ECG
Electrodes record electrical activity of heart as P, QRS, T, and U waveforms
P Wave of ECG
Firing of SA node and depolarization of atria
QRS Complex
Depolorization of AV node throughout ventricles
T Wave
Repolorization of ventricles
U Wave (if seen)
Repolorization of Purkinje fibers (large U wave might occur with hypokalemia)
PR, QRS, QT intervals
Travel time of signal from one area of heart to another (changes in timing indicate conditions)
Mechanical System: Systole
Contraction of heart muscles, ejection of blood from ventricles
Mechanical System: Diastole
Relaxation of heart muscle, ventricles fill with blood
SV (stroke volume)
Amount of blood ejected with each heart beat
CO (cardiac output)
Amount of blood pumped by each ventricle in one minute
CO = SV x HR
Normal is 4-8L/min
Factors affecting CO
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
Cardiac Reserve
Ability of CV system to maintain or increase CO in response to many situations in health and illness
-exercise, stress, hypovolemia
Vascular System: Blood Vessels
-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
Arteries
Thick walls of elastic tissue to handle pressure; recoil propers blood forward
-Large arteries (like aorta and pulmonary arteries) also have smooth muscle
Arterioles
More smooth muscle
-Control arterial BP and blood flow distribution through dilation and constriction
Endothelium
Inner lining
-Maintains hemostasis, promotes blood flow, inhibits coagulation
-Disruption results in coagulation and fibrin clot
Capillaries
thin walls of endothelial cells; no elastic or muscle tissue
-connects arterioles and venules
-exchanges nutrients and metabolic end products
Veins and Venules
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
Regulation of CVS
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
Regulation of CVS: 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 peripheral vasodilation; decreased
stretch or pressure does opposite
Regulation of CVS: Chemoreceptors
Aortic and carotid bodies and medulla
*Increased CO2 results in changes in RR and BP
Blood Pressure
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
Pulse Pressure
-Difference between SBP and DBP
-Normally about 1/3 of SBP
*Increased with exercise, atherosclerosis
*Decreased with with heart failure, hypovolemia
Assessing Pt - CVS
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
Genetic Link CVS
Coronary artery disease - lipoprotein gene links
Cardiomyopathy - autosomal and X linked genetic mutations
Hypertension - genetic, environmental, lifestyle
Auscultating CVS
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
Auscultating CVS - Extra Sounds
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
Auscultating CVS - Abnormal Sounds (Murmurs and Rubs)
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
Hemodynamic Monitoring
-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
Hemodynamic Monitoring Terminology
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
Invasive BP Monitoring: Arterial
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
Arterial Pressure Based CO (APCO) Monitoring
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
Pulmonary Artery (PA) Pressure Monitoring
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
Central Venous Pressure (CVP Monitoring)
Measurement of right ventricular preload that
reflects fluid volume
Obtained from:
Central venous catheter
PA catheter
Similar to PAWP waveforms
Diagnostic Studies of CVS
-Assess oxygen carrying capacity (RBCs, hemoglobin)
-Coagulation properties (clotting time)
-Cardiac biomarkers; injured cells release enzymes and proteins in blood
Diagnostic: Troponin
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
Diagnostic: Copeptin
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
Diagnostic: Creatine Kinase (CK); 3 isoenzymes
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
Diagnostic: C-Reative Protein (CRP)
-Marker for inflammation
-Linked to atherosclerosis and first heart event; predict risk of future heart events
Diagnostic: Homocysteine
-Hereditary or dietary deficiency of vitamins B6, B12, or folate
* High levels—increased risk for CVD, PVD, stroke
Diagnostic: Cardiac natriuretic peptide markers
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+
Diagnostic: Serum Lipids/Lipid Panel
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
Diagnostic: Electrocardiogram
Resting 12 lead ECG
Holter
Exercise or Stress Test
External or internal monitoring
Diagnostic: Functional Stress
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
Diagnostic: Chest X Ray
Chest x-ray
* Heart displaced or
enlarged
* Pericardial effusion
* Pulmonary
congestion
Diagnostic: 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 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
Diagnostic: Tomography
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)
Diagnostic: CMRI, No Radiation
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
Diagnostic: Nuclear Cardiology
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
Nursing Management of Cardiac Cath Patient
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
