Cardiovascular System Flashcards
Angina(chest pain)
Chest pain leads muscles in the chest. Chest pain resulting from myocardial ischemia(ischemia is lack of oxygen in the blood).
What causing Angina
Ischemia myocardial ischemia or infraction and leads to tissue damage necrosis. three types of angina.
Stable angina: (exertional Angina):- occurs with activities that involves exertion,exercise,emotional stress.
Unstable angina:-occurs with unpredictable degrees of exertion or emotion; increases in occurrence, duration, Severity overtime.
Prinzmetal(Variant)angina:-Arterial spasm (cold, weather, stress, smoking, substance abuse) often walking client from sleep.
Angina assessment
Mild or moderate pain,may radiate to shoulder, arms, Jaw,neck, back, usually last less than 5 minutes, relieved by rest and/or nitroglycerin;dyspnea;Pallor;diaphoresis.
Angina diagnostic test
ECG shows inverted T wave,ST depression, or maybe normal.
Stress test causes chest pain or changes in ECG.
cardiac enzyme levels can be normal. Cardiac catheterization provides definitive diagnosis of patency of coronary arteries.
angina interventions
Assist pain,bedrest, assess ECG strip.
Administer oxygen, nitroglycerin as prescribed-side effect headache.
instruct client about diet, weight management, exercise,lifestyle changes following acute episodes.Surgical procedures same as for coronary artery disease.
chest pain initial care
assess airway breathing circulation ABC’s, position of upright.
Apply oxygen , if hypoxic.
Obtain baseline vital signs, heart and lung sound.
Obtain a 12 leads electrocardiogram ECG.
Insert 2 to3 large bore I/V catheters
assess pain-OLDCART, Medicate for pain: morphine/nitroglycerin (sildenafil) +nitro-severe hypotension).
Initiate continuous electrocardiogram (ECG) monitoring
Obtain bloodwork (example:cardiac markers, serum electrolytes).
Obtain portable chest x-ray
Assess for contraindications to antiplatelet and anticoagulant therapy.
Administer aspirin unless contraindicated.
What is OLDCART
O-onset, when? L-location exactly where? D-Duration-how long? C-characteristics-what kind of pain? A-aggravating factor-what makes activity worsen. R-Relieving – what make better? T-Time /T reatment:exact time.
Angina medications
Nitrates: dilate coronary arteries;decreased preload and after load, such as nitroglycerin.
Calcium channel blockers: dilate coronary arteries and reduce Vasospasm, such as nefidepine(Procardia)
Cholesterol lowering medication‘s:Reduce development atherosclerotic Plagues, such as lovastatin. Statin groups Lower the high cholesterol.
B blocker’s: Reduce blood pressure in individuals who are hypertensive, such as sotalol(Betapace)Atenolol.
antiplatelets: to reduce risk of MI.
myocardial infraction
Occurs when myocardial tissue abruptly, severely deprived of oxygen, leading to necrosis and infraction; develops over several hours.
Location of MI
LAD: left anterior descending artery:anterior or septal MI.
circumflex artery: posterior or lateral wall MI.
Right coronary artery: inferior wall MI.
risk factors of MI
Modifiable versus non-modifiable,
atherosclerosis;coronaryartery disease; elevated cholesterol levels; smoking; hypertension;obesity; impaired glucose tolerance; stress.
diagnostic studies of MI
ECG, ST changes, inverted, T; abnormal Q wave.
cardiac enzymes CKMB/creatinine kinase MB isoenzyme(CK-MB)more sensitive to myocardium.
CK total 30to 170 u/L, Elevated levels first 4 to 6 hours. Expected duration of elevated levels three days. troponin (T)0.2nd/l,elevated levels 3to5hrs(Expected levels first detecting following myocardial injury)14to21days.
Troponin I:-0.03ng/l Expected level 3hrs.
Myoglobin less than 90 MCg/ L2hrs
interventions of MI
acute stage: same as chest pain initial care,
interventions following acute episode,
bedrest, range of motion exercise as prescribed, activity progression as tolerated.
Complications of MI
Dysrhythmias;heart failure; pulmonary edema; cardiogenic shock; thrombophlebitis; pericarditis;
papillary muscle rupture- new murmur (Because of valves or not opening proper muscles)
Heart failure
inability of heart to maintain Adequate circulation to meet metabolic needs of body.
Classification:acute, chronic
Right ventricular: RV reduce capacity to pump into pulmonary circulation-back up in the rest of body.
left ventricular: Left ventricle reduced to capacity to pump into system circulation -back up in lungs
Compensatory mechanism:
compensatory mechanism: restore cardiac output to near-normal levels
include increased heart rate, improved stroke volume, arterial vasoconstriction, sodium and water retention, myocardial hypertrophy.
right sided heart failure
right sided heart failure presents as primarily systemic assessment symptoms, including JVD, dependent edema,ascites,nausea,hepatosplenomegaly.
Left-sided heart failure
Left sided heart failure presents as primarily respiratory symptoms including orthopnea, cough, adventitious breath sounds, tachycardia, dyspnea on exertion,S3.
Pulmonary edema
pulmonary edema present says-acute restlessness, anxiety, crackles , pallor,dyspnea ,orthopnea,pink frothy sputum,diaphoresis.
BNP-basil natriuretic peptides:
made and released by ventricles in response to stretching.
causes natriuresis ( excretion of sodium in the urine)
Stretching of the ventricles- increased blood volume (fluid overload) heart failure.
Elevation of BNP>100pg/ml (picogram)helps to distinguish cardiac from respiratory causes of dyspnea.

BNP:Interventional 
client high in Fowlers position ,Rest period between Activities.
Calm environment, administer oxygen as prescribed (N/C)
better gas exchange, decrease workload, suction PRN as prescribed.
monitor vital signs frequently, (watch for hypotension,orthostatic hypo)
Strict intake and output,daily weight , fluid restriction.
Heart Failure Meds
Meds: administer diuretics as prescribed, electrolytes K levels,
vasodilators, nitro:reduce preload
ACE inhibitors/ARB: Reduce afterload
Beta blockers: reduce workload , improve contractions,
administer morphine sulfate as prescribed: sedation, respiration, depression.
Administer digitals as prescribed: improve contractility (hold HR less than 60).
Heart Failure teaching modifiable risk factors
instruct the client about modifiable risk factor, proper administration of medication regimen.instruct the client to avoid over the counter medication.
Diet: eat low sodium, low cholesterol diet, instruct client to balance activity level. Daily weight , – report a 3lb per day or 5lb a week increase.
coronary artery disease
narrowing or obstruction of the one or more coronary arteries as a result of atherosclerosis.
Coronary artery disease symptoms
Maybe asymptomatic – atypical chest pain – especially in women .chest pain, palpitations, dyspnea, syncope, cough, excessive fatigue.
Diagnostic studies: ECG shows ST depression on inverted T-wave.
cardiac catheterization provides definitive diagnosis, blood lipid levels may be elevated.
Coronary artery disease interventions
Interventions: educate client about diagnostic tests, educate client about modifiable risk factors. Diet: instruct client to eat low calorie, low sodium, low cholesterol, low fat diet, with increase in dietary in fiber.
Instruct client about the importance of regular exercise.
Coronary artery disease special procedures
PTCA:-Percutaneous transluminal coronary angioplasty-ballooning, lesser angioplasty, Atherectomy,vascular stent.
Inflammatory disease of the heart(pericarditis)
Pericarditis: inflammation of the pericardium. Commonly follows a respiratory infection.
Can be due to a myocardial infraction (Dressler‘s syndrome).
grating pain, aggravated my breathing. Pain worsen when in supine position, relieved by leaning forward.
Pericarditis interventions 
Position client in high Fowlers position, upright leaning forward, monitor for signs of cardiac tamponade.
nursing care pericarditis
auscultate heart sounds listen for murmur. Assess breath sounds in all lung fields (friction rub). Review ABG, SaO2, ECG and chest x-ray results.
Administer oxygen as prescribed. Monitor vital signs watch for fever.
Monitor for cardiac tamponade and heart failure.
Obtain throat cultures to identify bacteria -antibiotic therapy. Administer antibiotics and antipyretics as prescribed.
Pain assessment-pain med. Increase bedrest.
Provide emotional support to the client and family, and encourage the verbalization of feelings regarding the illness.
Myocarditis
inflammation of the myocardium.
Can be due to viral, fungal, or bacterial infection. Can be a result of pericarditis.
Myocarditis assessment
Fever, pericardial friction rub, murmur.
Interventions: administer analgesics,salicylates, nonsteroidal anti-inflammatory drugs, antibiotics, digoxin (Lanoxin) as prescribed
myocardial infraction risk factors
Modified and non-modified, Atherosclerosis, CAD, elevated cholesterol levels, smoking ,hypertension, obesity, inactivity, impaired glucose tolerance.
Endocarditis
Inflammation of the inner lining of heart and valves by bacteria . (Staphylococcus aureus–acute or strep virus viridans-chronic).
Endocarditis assessment
Fever, positive blood culture, new heart murmur,petechiae, splinter hemorrhages in nail beds.
Osler’s nodes- painful nodes fingers and toes.
Janeway’s lesions (irregular Erythematous, flat, painless macula’s on the palms soles).
Roth’s spots-Retinal lesions surrounded by bleeding.
endocarditis interventions
prevent venous stasis-periods of rest and activity.
Maintain antiembolic stockings as prescribed.
I/v therapy – antibiotic 6 weeks. Monitor cardiovascular status.
Monitor for signs of emboli throughout the body is the bacterial vegetation over the valves can break off and emboli to various organs-lead to stroke, MI, PE, ischemia to extremity etc.
Endocarditis client education
Encourage the client to take rest periods as needed.Wash hands to prevent infection. Avoid crowded areas to reduce the risk of infection. Participates smoking cessation(If the client is a smoker)
educate the client about the importance of taking medications as prescribed.
Ask the client to demonstrate the administration of intravenous antibiotics and management before discharge.
Educate the client family about the illness, and encourage them to express their feelings.
Home in vision therapy:: can have repeated episodes of endocarditis.
Report – fever , anorexia, malaise , gentle, through oral care (vigorous brushing can lead to bacterial to enter blood to gum).
Need prophylactic antibiotics before invasive procedures.
cardiac dysrhythmias EKG
EKG basics: P wave –-arterial depolarization (squeeze/contact)
QRS complex:-ventricle depolarization.
T-wave- ventricular repolarization (relax),
PQ-time taken to reach from SA node to AV node. 40 to 60b/min.
ventricles (Purkinje fibers)=15 to 40b/min.
PR interval=0.12–0.20 seconds 3–5 small blocks.
QT interval=0.36–0.44seconds(9 to 11 small boxes).
Question most important assess your patient
Sinus bradycardia
Arterial and ventricle rates less than 60 bpm.
attempt to get remain causes; if medication is suspected cause,hold meds.notifythephysician.
Administer atropine sulfate as prescribed.atropine 0.5mg only 6times and every 5min.
Symptomatic bradycardia
Asymptomatic bradycardia exists clinically when 3criterias are presents.
1) The heart rate is low,
2) the patient has a symptom,
3) the symptoms are due to the slow heart rate.
Sinus tachycardia.
Arterial and ventricular more than 100 bpm.
assess the patient – are they symptomatic? Are they stable?
Give oxygen,and monitor oxygen saturation,monitor blood pressure and heart rate, start IV if not already established, notify MD, look for the cause of the tachycardia and treat it.
Fever -give acetaminophen or ibuprofen.
Stimulants stop the use (caffeine,OTC meds, herbs,illicit drugs).
Anxiety-give reassurance or anti-anxiety meds.
Sepsis, anemia, hypotension,MI,heart failure, hypoxia.
Atrial fibrillation
No definitiveP wave can be observed.
Hypoxia, hypertension, CAD, CHF. Administer oxygen, and anticoagulants, for cardioversion as prescribed.
Always irregular rhythm.
Atrial flutter
(rate varies; usually regular;saw toothed)
Seen in valve disorder(Mitral): thickening of the heart muscle, ischemia, cardiomyopathy, COPD.
Cardioversion–treatment of choices.
Antiarrhythmics such as procainamide to convert the flutter 
Slow the ventricle rate by using diltiazem,verapamil, digitals, or beta blockers.
Heparin to reduce incidence of thrombus formation.
Supraventricular tachycardia (more than 150 b/min)
causes: stimulants, hypoxia, stress or over-exertion, hypokalemia, atherosclerotic heart disease.
supra ventricular tachycardia
Some types of SVT may run in families,such as wolf Parkinson white syndrome,-additional electrical Pathway between Atrium and ventricles (in addition to AV node).
Treatment: vagal maneuvers, gagging,coughing.
holding breath and bearing down (Valsalva Maneuver)immersing face in ice cold water divinreflex. Drug – adenosine give rapidly 1to2sec+rapid saline flush(short half life -10 seconds
cardioversion.
Sinus tachycardia
Atrial and the ventricle rates >100b/min.
assess patient-are they symptomatic ?are they stable ?
Give oxygen and monitor oxygen saturation,
monitor blood pressure and heart rate, start IV if not already established, notify MD, look for the cause of the tachycardia and read it and treat it. fever-give acetaminophen or ibuprofen.
Premature ventricular contraction.
PVCs not a rhythm, but ectopic beat that arises from an irritable site in the ventricles.
Pvcs “normal beat”.
PVCS can be associated with stimulants (examples caffeine),medication example (digoxin )heart disease, electrolyte imbalance, hypoxia and emotional stress.
ventricle tachycardia
Repetitive firing of irritable ventricular ectopic focus rate of 140 to 250 bpm.
Client stable or unstable no pulse? Begin CPR, Dfib.
If pulses present and patient stable cardiovert, start meds.
Meds:: meds: Amidarone,and LidoCaine,(xylocaine),antiarrhythmics (procainamide)sotalol.
ventricular fibrillation
chaotic rapid rhythm; ventricular quiver 
Defibrillate immediately as prescribed; initiate CPR.
atrioventricular blocks
Always access decreased cardiac output and treat cause.
four types :first-° block,
second-degree block,Mobitz 1, wenckebatch,
Second-degree block mobitz 11 to,
third-degree block (complete.)
heart block: first- degree
A delay of impulse from SA node to reach AV node.
PR interval more than >.20 seconds (3 to 5 small boxes) but same PR interval for each beat.Can be due to meds such as digoxin.
No specific treatment- watch for worsening to second or 3rddegree.
Second -degree heart block
Can be due to MI/meds (digoxin,beta blocker)/cardiac surgery
Second-degree AV block-type 1(wenckebach), (Mobiz 1)
Progressive prolongation of the PR interval,then one droppedQRS
S/s-bradycardia symptoms-give atropine to increase HR
May need temporary pacemaker if med not working
2-Degree AV Block-Mobitz type-2
The PR interval does not lengthen before a dropped beat due BBB.(Bundle branch block)
Seen in-MI,CAD,RHD,Drug toxicity.might need pacemaker.
3-Degree/Complete
Complete absence of conduction between Atria and ventricles
Nursing priority:assess the pt for possible causes
Monitor blood pressure,pulse,and other vital signs.
Assess of syncope,palpitations,or shortness of breath
Hypotension may occur due to a low ventricular rate
For patient safety,
patient lie down to prevent syncope and potential falls.
implantable cardioverter defibrillator (ICD)
ICD system placed subclavian vein to the endocardium
Battery powered pulse generator is implanted subcutaneously. sensing system monitor HR and rhythm identify VT or VF:delivering 25 Joules or less to heart when detects lethal dysrhythmias.
If the first shock is unsuccessful,the device recycles and can continue to deliver to shocks.
Instruct client on basis functions of ICD,complications to report immediately.

ICD implantable cardioverter-Defibrillator how to educate client?
Instruct client how to take pulse, and to avoid strenuous activity or contact sports and report any sign of infections or feelings of faintness,nausea and vomiting.
cardiogenic shock
Failure of heart to pump adequately, does reducing cardiac output, compromising tissue for perfusion
Cardiogenic shock assessment
Hypertension, oligoria, poor peripheral pulses, tachypnea, tachycardia, disorientation, confusion.
Cardiogenic shock intervention
Administer morphine sulfate, diuretics, nitrates to decrease heart workload- help heart to work more effectively.
Inotrops-stimulate and increase the force of contraction of the heart muscle.
Administer oxygen; prepare for intubation and mechanical ventilation as prescribed.
Monitor vital signs, arterial blood gases, strict intake and output, arterial pressure as prescribed
cardiac tamponade.
pericardial effusion ; Occurs when space between parietal and visceral layers of pericardium fill with fluid. 
Cardiac tamponade assessment
Pulses paradoxus (variance of 10 MM Hg or more in systolic blood pressure between expiration and inspiration.
Becks Triad:(low arterial blood pressure, distended neck veins,and distant muffled heart sounds) Intervention: please client in critical care unit as prescribed.
Administered IV fluids as prescribed,prepare clients for pericardiocentesis,as prescribed.
Supine with the head of the bed raised no in Anguilla 45 to 60°.
This Places the The heart in proximity to the chest wall for easier insertion of the needle into the pericardial sac.
monitor for reoccurrences of tamponade following pericardiocentesis.
Valvular heart disease
Occurs when the heart wall are stenosed (cannot fully open) or insufficient or regurgitant (cannot close completely)
Diagnostic test valvular heart disease
Asymptomatic until late in the progression-echocardiogram
Repair procedure:Balloon valvuloplasty;
mitral angioplasty;
commissurotomy (relieve stenosis on leaflet),
valvotomy.
Valvular heart disease:valve Replacement procedure.
Prosthetic ones can be mechanical or tissue.
Mechanical was last longer but required anticoagulant.
Tissue valves last 10 to 15 years.
The aortic valve must be replaced a mechanical (prosthetic ).
Valve because of the velocity of the blood flow through the valve. A tissue or biologic valve would not withstand the force.
Cardiovascular medication anticoagulants
Prevent extension and formation of clots by inhibiting factors including cascadenand decreasing blood coagulability.
Side effects: bleeding, implement bleeding precautions.
Heparin sodium
Normal activated partial thromboplastin time a PTT 20 to 30 seconds therapeutic1.5 to2.5 times the control valve.
Antidote is protamine sulfate.
Warfarin sodium Coumadin
normal PT is 11 to12.5 seconds
therapeutic level of INR with warfarin equal to 2 to 3
avoid green leafy vegetables? – Don’t change routines.
Antidote is vitamin K (phytonadione[AquaMEPHYTON]
Thrombolytic antiplatelet
thrombolytic:Dissolve the clots
Antidote: Aminocaproic acid (Amicar)is antidote to streptokinase
Antiplatelet-inhibit aggregation of platelets and prolonged bleeding time-aspirin.
side effects: bleeding
interventions: monitor for bleeding, implement bleeding precaution.
Contraindication thrombolytics
Absolute :prior intracranial hemorrhage
structural cerebrovascular lesion(example:Atrioventricular malformation)
Ischemic stroke within three months (except within three hours)
Suspected Aortic dissection
Active bleeding or bleeding diathesis
Significant head trauma with in 3months.
valvular Heart Disease Risk Factor
Hypertension,Rheumatic Fever,(Mitral Stenosis and insufficiency)infective endocarditis,congenital malformations,Marfansyndrome(connective tissue disorder that affects the heart and other areas of the body – genetic). In older adult clients causes are degenerative calcification, papillary muscle dysfunction, ineffective endocarditis.
Mitral stenosis
Associated withAfib( may need anticoagulants) meds: diuretics and Digoxin
Pacemaker
Temporary, or permanent device , provide electrical stimulation. Maintain heart rate when clients intrinsic pacemaker fails to provide for perfusing rhythm.
Synchronou or demand pacemaker
Synchronous or demand:paces only if client’s intrinsic rate falls below set pacemaker rate.no bradycardia
Asynchronized Or fixed rate: paces at present rate,regardless of client,s intrinsic rate.
