Cardio Exam 2 Flashcards
The heart has 3 layers what are these layers
epicardium
myocardium
endocardium
Epicardium
outside protective layer
Myocardium
middle layer of specialized cardiac muscle
Endocardium
endothelial lining of of chambers
What is the pericardium
protective sac encasing the heart;
2 fibrous layers with small amout of serous fluid separating layers for lubrication
Upper chambers of the heart
artium
lower chambers of the heart
ventricle
atria are smaller than
ventricles
Blood flows
body into right atrium and from lungs into left atrium
Atrial contraction
blood is pumped from atria into ventricles
Ventricular contraction
blood is pumped from righ ventricle into pulmonary artery and lungs, and left ventricle into aorta and arterial circulation
AV (atrioventricular) valves
- separate atria from ventricles
- they control blood flow between atria and ventricles
Tricuspid valve
between right atrium and right ventricle
has 3 leaflets
Mitral valve
between left atrium and left ventricle
has 2 leaflets
Leaflets of AV valves are connected to
papillary mucles by chordae tendons to prevent backflow
s1
first heart sound, is heard when AV valves close
Semilunar valves separate .
cardiac chambers from great vessels and control blood flow out of cardiac chambers
pulmonic valve
between right ventricle and pulmonic artery and deoxygenated blood flows through the valve to lungs
Aortic valve is between
left ventricle and aorta and oxygenated blood is pumped from heart through this valve into systemic circulation
Each semilunlar valve has
3 cusps that prevent backflow
s2
second heart sound is heard when semilunar valve close
Circulation
each side of the heart acts as a pump to circulation blood through lungs or through body to perfuse tissues
Double pump
right side responsible for pulmonary circulation, left side responsable for systemic circulation
Right heart circulation
deoxygenated blood Venous system (1 and 2) -> right atrium ( 3) -> right ventricle (4) -> lungs for oxygenation via pulmonary artery (5)
Left Heart circulation
oxygenated blood Lungs via pulmonary veins (6) -> left ventricle (8) -> aorta (9) -> systemic circulation for tissue perfusion
Coronary arteries
brance off aorta to supply oxygenated blood to heart electricle impulses through heart, stimulate depolarization and resulting muscle contraction of chambers in a specific sequence, and initiate pumping action of heart
Sinoatrial (SA) node
natural pacemaker
- concentration of cells responsible for initiating conduction impulse in a healthy heart; located in right atrium at junction with superior vena cava
- 60-100 bpm in healthy adult
Internodal pathways
carry impulse from SA node to AV node through both right and left atria
- impulse initates process of depolarization in both atria
- depoilzarization results in myocardial contraction of both atria
AV node
located in the base of the atrial septum
- slows impulse
- allows atria to fully empy before initiating depolarization of ventricles
- when sac node is functioning, can initiate an impulse at 40-60bpm
Bundle of HIs
short branch of conductive cells connecting AV node to bundle branches at intraventricular septum
Bundle branches
Right (RBB) and Left (LBB) split off on either side of intraventricular septum; carry impulse to Purkinije Fibers
Purkinje Fibers
diffuse network of conduction pathways
- are terminal branches of conduction system
- conduct impulses rapidly throughout ventricles
- initiate rapid depolarizatio wave throughout myocardium and resulting ventricular contractin
- when SA and AV nodes fail, can initiate impulses at rate of 20-40bpm
Cardiac Cycle
each cardiac cycles one complete heartbeat
- includes 2 parts
1. ventricular contraction
2. diastole (relaxation and ventricular refilling)
Systole
portion of cardiac cycle when ventricles depolarize and contract to pump blood into pulmonary adn systemic circulation; begins with closure of AV valves ends with closure of semilunary valves
Diastole
portion of cardiac cycle when ventricles repolarize and refill with blood; begins with closure of semilunar valves; ends with closure of AV valves
Atrial systole
depolarization and contraction
- is part of late ventricular diastole and atrial diastole occurs during ventricular systole
Cardiac Output (CO)
- volume of blood in liters ejected by heart each minute
- indicator of pump function of heart
- Normal adult CO 4-8L/min
- Co is measured directly by PA catheter
- clinical indicators of decreased CO include signs of decreased tissure perfusion such as a change in level of consciousness (early) and decreased blood pressure (late)
- CO=HRxSV
Heart Rate
number of complete cardiac cycles per min
Stroke Volume (SV)
volume of blood ejected from left ventricle with each cardiac cycle; stroke volume and ultimately CO are influenced by preload; afterload and contractility
Preload
degree of myocardial fiber stretch at end of ventricular diastole
- infulenced by ventricular filling volume and myocardial compliance
Afterload
resistance that ventricles must overcome to eject blood into systemic circulation; directly related to atrial BP
Contractility
strength of contraction regardless of preload; decreased by hypoxia and some drugs (for example, beta blockers, and calcium channel blockers)
- increased by drugs (example digoxin, dopamine)
Autonomic nervous system
regulates cardiac function and BP; balance exits between sympathetic and parasympathetic brances
sympathetic nerve stimulation
- produces epinephrine and norepinephrine and norepinephrine
- results in increased HR
- increased myocardial contractility
- increased peripheral vasoconstriction
- results in increased atrerial BP
Parasympathetic nerve stimulation
- produces acetylocholine
- results in lowered HP and decreased contractility
- is the opposite effect of sympathetic stimulation
Changes in sympathetic and parasympathetic activity
occur in response to sensory receptors in body, chemoreceptors, baroreceptors, and stretch receptors
Chemoreceptors
located in aortic arch and carotid bodies
- sense chemical changes in blood
- primarily hypoxia and to a lesser degree hypercapina
- respond by inducing vasoconstriction
Baroreceptors
provide a rapid response to changes in pressure
- sensation of low pressure initiates sympathetic stimulation, resulting in increased HR, vasoconstriction and consequently increased pressurel sensation of increased pressure sends impulses to medulla decreasing HR and BP
(vagal response)
infarction
damage to myocardium from decreased oxygenation
creatine kinase (CK)
formerly known as creatine phosphokinase (CPK)
elevation indicates muscle injury
- CK-MB is isoenzyme specific to myocardial muscle
- Rises within 6 hrs of injury
- peaks at 18 hrs postinjury and returns to normal in 2-3 days
- useful in myocardial infarction (MI)
Troponin
onset is before CK-MB in MI
- peaks at 24 hrs and returns to normal around 2 weeks
- provides early sensitivity
- extended blood levels
- is more specific to cardiac injury for diagnosis of MI
- test 8 hrs for 24 hrs
Lactic dehydrogenase (LDH)
found in may body tissues
- cardiac origin is confirmed with analysis of isoenzymes
- elevation is detected within 24-72 hours after MI
- peaks in 3-4 days
- returns to normal in around 2 weeks
Brain natriuretic peptide (BNP)
is a hormone found in left ventricle
- elevated in heart failure (normal 0-99)
- but my be higher with aging and in women
CHF
Drug levels
blood tests to detect toxic levels of cardiac medications
Digoxin
therapeutic rage is 0.5-2 early signs of toxicity include nausea, vomiting, anorexia, abdominal Bradycardia (HR less than 60bpm) dysrhythmia and visual dysrhytmias
Quinidine
therapeutic range is 2-6mcg
signs of toxicity include tinnitus hearing loss visual distruabnces nausea dizziness widened QRS
ventricular dysrhymias
Electrolytes
normal levels are essential for proper cardiac function; some medications, renal or cardiac conditions may contribute to electrolye imbalance
Potassium (K+) Normals
3.5-5.1
Hypokalemia
can occur with diretic therapy (especially loop diuretics such as furosemide)
- cardiac effects include increased risk of digoxin toxicity ventricular dysrhythmias, flattening and inversion of T wave or presence of U wave
- is usually related to renal dysfunction or intake of excess potassium dietary supplements
- cardiac effects include ventricular dysrhymthmias tall peaked T waves on ECG and asystole
Sodium (Na+) normal
135-145
Hyponatremia
with long term diuretic therapy
Hypernatremia
may result in dehydration
hypo-or hypernatremia
may result in tachycardia (HR greater than 100 beats per min)
Calcium (CA) norms
- 5-5.5
- blood levels are affected by hormonal imbalances, renal failure and several meds
Cardiac effects of hypocalcemia
ventricular dysrhythmias
prolonged QT interval
cardiac arrest
Magnesium Mg
- 5 - 2.5
- cardiac effects of decreased Mg include ventricular tachycardia and fibrillation
- Cardiac effects of increased Mg include bradycardia, hypotension, prolonged PR and QRS intervals
Serum lipid profile
aid to determine risk of developing atherosclerosis
total serum lipds nomrals
400-800
triglycerides
lipids stored in fat tissue, readily available for energy production
normal serum vale is 10-190 (without elevated cholesterol up to 250 my be acceptable)
cholesterol
main lipid associated with atherosclerosis disease, norm is less than 200
lipoproteins
proteins in blood to transport cholesterol; triglycerides and other fats;
high density lipoproteins (HDL)
- happy cholesterol
- transport cholesterol to liver for excretion
- HDL/ total cholesterol ratio should be at least 1:5, 1:3 more ideal
low density lipoproteins (LDL)
ransport cholesterol to peripheral tissues associated with increased risk of coronary heart disease
preprocedure for lipoprotein tests
fast for 12-14 hrs before testing
Electrocardiography
-recording of the electrical activity of the heart electrodes on body surface
12 lead or resting ECG
recording of electrical activity of heart from 12 different views
- used to determine cardiac rhythm, as well as ischemia , injury, infarction, hypertrophy, electrolyte imbalance and drug effects
Holter monitoring
continuous ambulatory ECG monitoring over time ( usually 24)
Stress test
continuous multilead ECG monitoring during ocntrolled and supervised exercise, usually on treadmill
- clients who can not tolerate exercise cardic stress can be drug induced Dobutamine (Dobutrex)
stress test prep
obtain written consent explain procedure instruct to eat a light meal 1-2 hrs before exam (no caffeine, alcohol, or smoking ) wear comfortable clothing rubber soled walking shoes
Nursing care during stress test
secure electrodes
obtain baseline vidal signs
monitor ECG continuously
record at frequent ST segments or cardiac rhythm
Echocardiography
- is an ultrasound of heart to evaluate structure and function of chambers and valves
- client preparation: instruct to remain still during test, secure electrodes for simulationeous ECG tracing
- explain that is typically painless
- tell patient the gel will be cool
Photocardiography
- is a graphic recording of heart sounds with simultaneous ECG
- Client preparation; instruct to remain quiet and still during the test
no pain or electrical shocks - no postproceudre nursing care
Coronary angiography/arteriography
- is an invasive procedure during which cardiologist injects dye into coronary arteries and immediately records a series of x-ray films
- client prep: obtain written consent; explain procedure assess for history of allergies to contrast dye or iodine; initiate IV access; begin fluids as prescribed
- Postprocedure nursing care; same as for cardiac catherterization
Radionuclide tests
are safe methods of evaluating left ventricular muscle function and coronary artery blood distribution; can provide some of the same information as radiographic angiography with less risk to client
ejection fraction (EF)
portion of blood ejected during systole, compared with total ventricular filling volume
- normal 55-65%
PET positron emission tomography scan
evaluates cardic metabolism and assess tissue perfusion
Hemodynamic monitoring
is measurement of pressures in heart and calculation of hemodynamic parameters
Central venous pressure (CVP) monitoring
appropriate for clients who require accurate monitoring of fluid volume status do not require more invasive PA pressure monitoring
- normal CVP 2-6
PA pressure monitoring
appropriate for critically ill clients requiring more accurate assessments of left heart pressures including those undergoing cardiac surgery shock or with serious MI
Normal Sinus Rhythm
rate 60-100 Regular rhythm P:QRS 1:1 PR INTERVAL: 0.12-0.20 SEC QRS: 0.06 -0.10 sec
Sinus tachycardia
rate 101-150 bpm regular rthythm P:QRS 1:1 ( P wave may be hidden in preceding T wave with fast rate) PR Interval 0.12-20 sec QRS 0.06-0.10 sec
sinus tach treatment
treat only if client is symptomatic or is at risk for myocardial damage
- beta blockers or verapamil
sinus bradycardia
Rate 60-100 bpm regular P:QRS 1:1 PR Interval 0.12-0.20 sec QRS 0.06-0.10
Sinus bradycardia treatment
treat only if client is symptomatic
intravenous atropine and/or pacemaker therapy may be used
Sinus arrhythmia
60-100bpm
Rhythm: irregular, varies with respiration
P:QRS 1;1
PR interval 0.12-0.20 sec but may be prolonged
QRS 0.06.0.10
Sinus arrhythmia treatment
generally none; considered a normal rhythm in very young and very old
Premature atrial contractions (PAC)
rate: variable
rhythm: irregular, underlying normal rhythm interrupted by early atrial ectopic ebats
P:QRS 1:1
PR interval 0.12-0.20 but may be prolonged
QRS 0.06-0.10
PAC treatment
usually require no treatment
advise client to reduce alcohol and caffeine and reduce stress and stop smoking
Paroxysmal supraventricular tach. (PSVT)
100-280 (usually 200 bpm) regular p waves often not identifiable PR is not measured QRS 0.06-0.10
PSVT treatment
treat if client is symtomatic many include vagal maneuvers
oxygen therapy. adenosine, varapamil, procainamide, propranolol and esmolol and synchronized cardioversion
Atrial flutter
atrial 240-360 ventricular rate depends on degree of AV block and usually is less than 150 bpm
rhythm: atrial regular ventriular usually regular
P:QRS 2:1, 4:1 may vary
pr interval not measured
QRS 0.06 -0.10 sec
atrial flutter treatment
Atrial fibrillation
atrial 300-600 (too rapid to count) ventricular 100-180 in untreated clients irrgegular PQRS variable PR not measured qrs 0.06-0.10
treatment for A fib
syncronized cardioversion
drugs to convert rhythm ( amidoarone) or reduce ventricular response rate, verapamil propranolol digoxin anticoagulants to reduce risk of clot formation and stroke
First degree av block
usually 60-100 bpm regular pqrs 1:1 pr interval greater than 0.20 seconds QRS 0.06 -0.10 sec requires no treatment
Premature ventricular contractions (PVC)
variable rate irregular PVC interrupts underlying rhythm and is followed by compensatory pause No P wave PR absent with PVC QRS complex wide greater than 0.12 ec
treatment for PVC
treat client if experiencing symptoms
advise against stimulant use
drugs include lidocaine, procainamide, quinidine propranolol phenytoin, bretylium
VENTRICULAR TACHYCARDIA (VT AND V Tach)
100-250 regular p waves usually identifiable PR not measured QRS 0.12 sec or longer bizarre shape
treatment for VT and V tach
treat if VT is sistained or if client is symptomatic
treatment includes procainamide amiodarone or lidocaine and immediate defib if client is unconscious or unstable
Ventricular fib
too rapid to count
grossly irregular
no identifable P waves
IMMEDIATE DEFIBRILLATION
Percutaneous transluminal coronary angioplasty (PTCA)
procedure to increase coronary artery blood flow by inserting a balloon tipped catheter into a narrowed segment of affected artery inflating ballon to expand arterial lumen and removing the catheter , may also include insertion of expandable intracoronary stent
Coronary artery bypass grafting (CABG)
surgical treatment of CHD for clients with more than 50% occlusion in left main coronary artery or several blockage in several vessels
Myocardial infarction
myocardial injury from sudden restriction of blood supply to a portion of heart is a potentially life threating condition
- main cause CAD
Coronary artery disease
the buildup of atherosclerotic plauqe in coronary arteries that restricts blood flow to heart
CAD nonmodifiable risk factors
age, gender, family history, ethnic background
CAD modifiable risk factors
smoking obesity stress elevated holesterol diabetes and hypertension
Stable angina
predictable response to increased activity
unstable angina
unpredictable occurance and increasing severity
prinzmetal angina
caused by arterial spasm and often awakening client from sleep; treated with calcium channel blockers
Medication therapy
MONA morphine oxygen nitroglycerine aspirin
Heart failure (HF)
the inability of heart to pump adequate blood to meet metabolic needs of body
Causes of HF
damage from MI, incompetent valves, inflammatory conditions of heart, cariomyopathy, pulmonary, hypertension
Right side HF
has reduced capacity to pump blood into pulmonary circulation, causing back op of blood into venous circulation ( jvd, full body edema)
Left side HF
left ventricle has reduced capacity to pump blood into systemic circulation causing decreased CO and black up of blood in pulmonary ciruclation
signs of pulmonary edema
restlessness, anxiety, crackles, tachypenia, tachycardia, pink frothy sputum decreased SO2 and PO2
ACE inhibitors
to reduce after load and consequently increase CO
ARBs
interrupt vasoconstrictor andaldosterone secreting effects of angeiotension II prescribed for similar reasons as ACE inhibitors
Diuretics
decrease preload pulmonary congston which degrease cardic work and increase CO monitor potassium
vasodilators
nitroglycerine to reduce preload mointor for hypotension
morphine
sedate and vasodilate decreasing cardiac workload monitor or hypotension or resp. depression
digoxin
improve contractility and correspondingly increase stroke volume, and CO . take apical pulse for 1 full min and withhold dose if HR is below 60-120
inotropic agents
dopamine (intropin) and dobutamine (dobutrex) are used in critical care when decompresation of CO leads to hypotension
Endocarditis
inflammation of inner layer and heart usually involves cardiac values
Endocarditis
caused by microorganisms in blood
risk factors are IV drug use, structure dects of heart or valves
acute endocarditis
sudden onset with staph aureus as most common organism
subacute endocaritis
gradual onset with strep viridans or other less virulent bacteria
microorganisms in bloodstream
colonize on fibrin and platelet strands in endothelium multiply and develop new strands seen as vegetation attached to endothelum particularly valves causing valve damage segments of vegetation may break off and travel to extremities manifeted as petechine
endocarditis assessment
- high fever with chills signs of HF and WBC elevation
- subacute - fever of unknown origin, cough, dyspena , anorexia, malaise normal WBC anemia and elevated erthyrocyte sedimentation
- both positive blood cultures , or new murmur or change in previous murmur
stenosis
heart valve leaflets are fused together opening is narrow stiff and unable to open or close properly
regurgitation
there is improper or incomplete closure of heart valves resulting in backflow of blood
Causes of Valvular disorders
rheumatic heart diseases (most common) congential MI and Endocarditits
- calcium depositis or car tissue from MI or endocarditits cause stiffening
Mitral stenosis
low pitched rumbling diastolic
common in young women
Atrial dystrthmias
mitral regurgitation
murmur high pitched blowing systolic
usually asymptomatic
A-fib common with low incidence of embolization
(diuretics, nitrates, ACE inhibitors maintain sodium restricted diet)
mitral prolapse
murmur systolic click most clients asymptomatic may have PVCs and palpitations syncope, weakness and anxiety * give beta blockers for syncopy * prophylactic antibiotics
Aortic stenosis
murmur harsh systolic
late course symptoms angina S3 and S4
-restrict activity
-symptomatic aortic stenosis has a poor prognosis without surgery
aortic regurgitation
murmor blowing diastolic widened pulse pressure palpitations tachycarda and PVC
- medical management
valvular disorders meds
treat with anticoagulatns
Cardiomyopathy
an abnormality of the heart muscle that leads to functional changes in heart
causes of cardiomyopathy
unknown
may be linked to vital infections alcohol abuse pregnancy
types of cardiomyopathy
- dilated- most common enlargement of all four chambers of the heart
- hypertrophic- unexplained progressive thickening of ventricular muscle mass
- restrictive cardiomyopathy excessively rigid ventricular walls not stretch during diastolic filling external dyspnea syncope angina
SUDDEN DEATH - restrictive dyspnea-right side heart failure , rigid ventricular walls not strech duringdiastolic filling
assessment of cardiomyopathy
Fatigue with all types
dilated weaknes s S3 and S4 heart sound
Pericarditis
inflammation of the pericardium
acute pericaditis
may have many causes including infections , viral are most common, post MI, trauma,
chronic pericarditis
causes fibrous thickening of pericardium constricting cardiac walls movement and strestircting diastolic filling
pericarditis assessment
substernal pain, radiatig to neck aggravated by breathing or cough
