Exam 3 review sheet Flashcards
CAD non-modifiable and modifiable risk factors
Non-modifiable
- Age:
- Increased age-disease process begins early and develops gradually.
- Gender:
- Highest for middle-aged white caucasian
- Race:
- Caucasian males highest risk
- Genetic:
- Inherited tendencies for atherosclerosis
Modifiable
- Tobacco
- Hypertension
- Physical Activity
- Obesity
- Dyslipidemia
- Diabetes
- Stress
- ETOH abuse
- HRT
Where do we want out patients with CAD for BP?
less than 120/less than 80
prehypertension
120-139/80-89
high blood pressure stage 1
140-159/90-99
high blood pressure stage 2
160 or higher/100 or higher
hypertensive crisis
higher than 180/higher than 110
what does exercise really help with regards to HDL, LDL, TG?
eally helps HDL and TG
How does diet affect LDL, HDL, TG
LDL: lowers it
HDL: little effect
TG: lowers it
what do omega fatty acids help with?
triglycerides
most used to treat lipid levels
Statins: effects LDL, HDL, and triglycerides
optimal total cholesterol and ldl, HDL,TC/HDL
total: less than 160
LDL: less than 100
HDL: above 45
TC/HDL: less than 3
Type of angina?
Pain w/exertion-relief w/rest
stable Angina
Type of Angina?
Pain onset w/ rest
Caused by vasospams
Prinzmetal’s
type of angina?
Pain onset w/rest
Precursor to AMI
unstable angina
type of angina?
Unrecognized symptoms
Silent agina
causative factors of Angina
- Physical exertion
- Temperature extremes
- Strong emotions
- Heavy meal
- Tobacco use
- Sexual activity
- Stimulants
- Circadian rhythm patterns
Treatment of stable angina?
- etiology: Myocardial ischemia
- Symptoms: episodic, aggravated with exercise, relieved w/NTG
- Treatment: NTG, beta blockers, ca+ channel blockers, ACE inhibitors
Unstable angina treatment
- etiology: ruptured or thickened plaque with platelet and fibrin thrombus
- symptoms: increasing episodes, occurs with rest and exercise, not relieved with NTG
- treatment: NTG, tPA, morphine (dilates vessels), ASA
Prinzmetals angina treatment
- etiology: Coronary vasospasams
- symptoms: Occurs at rest, Triggered with smoking, May have ST elevation,
- AV Block or Ventricular arrhythmias
- Treatment: Ca+ Channel Blockers
progressive inflammatory disorder of arterial wall that is characterized by focal lipid rich deposits of atheroma that remain clinically silent until they become large enough to impair tissue perfusion
atherosclerosis
Stemi vs NonStemi
ST elevation= stemi. Elevation in the t “firemans cap”
ST depression= non-stemi.
APQRST evaluation of chest pain
- A= Associated Symptoms Dyspnea, nausea, diaphoresis, palpitations, feeling of impending doom
- P= Precipitating Factors Exertion, Cold Exposure, meals, movement. Relieved by: rest, NTG, or position?
- Q= Quality Heaviness, tightness, sharp, stabbing, burning
- R= Region, Radiation, Risk Factors Radiates to: arm, jaw, back, below diaphram. Region: substernal, left lateral, right chest. Risk factors: HTN, DM, Obesity, Dyslipidemia, Smoking
- S= Severity Rate pain on scale 0-10
- T= Timing Onset and duration of pain, nocturnal?, constant? Intermittent?
CPK and Troponin
- CPK MB: rises 4-8 hours, peaks 12-24, remains elevated for a day
- Troponin: (breakdown in cardiac muscle) rises in 3 hours, peaks 12-18 hours, stays elevated for 14 days
- Troponin t: 0.1 or less micrograms per liter
- Troponin I: less than 10 micrograms
C-Reactive protein
- Produced by liver w/ inflammation
- Rules out stable angina
- Good o get pt. baseline
- Reference range
- Low- < 1.0 mg/dL
- Average- 1.0-3.0 mg/dL
- High- > 3.0 mg/dL
normal BUN
10-20
normal creatinine
0.5-1.1
normal creatinine clearance
130-170 ml/min
myoglobin
- Peak levels occur 1-4 hours
- Doubling in 2 hours ++ MI
- Reference range: < 90 mcg/L
nursing immediate action for MI
Pt. placed in semi-fowlers position
- ECG and Cardiac Enzyme Assessment
- IV line started (at least 18 guage)
- ASA 325 mg given: Four baby ASA, Clopidogrel (Plavix) 300 mg (becomes an issue if they need to go to surgery)
- Oxygen
- Beta Blockers
- ACE inhibitors (if CHF present): watch out for asthma patients
-NTG titrate to releive chest pain but keep SBP above 90 mm/Hg
- start drip 5 mics per min, can titrate as high as 400
- Works as a vasodilator
- Decreases peripheral resistance
- Increased coronary blood flow
Heparin vs Lovenox
- Neither lyse the clot only prevents new clots
- Heparin increased risk of HTP
- Lovenox longer more predictable action
- Not preferred if Surgery anticipated
cardiac catheterization
- Procedure which involves placement of a catheter into RT or LT side of heart.
- Invasive
- Coronary angiography is often included together with cardiac catheterization
- Diagnostic procedure and/or
- a therapeutic procedure
- Adults & Children
PTCA
- This procedures provides the doctor with a “road map” of the arteries in the heart
- To find any areas of blockage in the arteries that supply the heart with blood.
- May also look at the valves, chambers & heart muscle
- Can help in making decisions about the treatment of heart disease.
Catheter can be introduced through?
- femoral, brachial or carotid artery to the knob of the aorta for coronary arteries
- It may be advanced to the left heart to look at the LT ventricle
Balloon Angioplasty/PTCA
- Balloon Angioplasty is a technique used to dilate an area of arterial blockage with the help of a balloon catheter.
- It is a way of opening a blocked blood vessel
- Not highly effective, can rupture wall of vessel, or the plaque can just move right back
absolute contraindications to cardiac cath
- Internal Bleeding
- Cerebral Aneurysm
- AV malformation
- Previous Cerebral Hemorrhage
- Pregnant
- CVA recent
- Uncontrolled HTN
- Aortic Dissection
- Traumatic CPR
prevention of re-stenosis
Lifestyle Change
Healthy diet
adequate exercise
No Smoking
Medicine coated stents (apirin, plavix, cholesterol medicine)
ablation
INDICATIONS
- Atrial Fibrillation
- Atrial Flutter
- AV Nodal Reentrant Tachycardia
- AV Reentrant Tachycardia
- Atrial Tachycardia
Most often, cardiac ablation is used to treat rapid heartbeats that begin in the upper chambers, or atria, of the heart. As a group, these are know as supraventricular tachycardias, or SVTs. Types of SVTs are:
Minimally invasive treatment for arrhythmias
- Live fluoroscopy and angiography techniques are used along with special electro physiologic equipment and catheters
minimally invasive CABG
Minimally invasive surgery does not use CPB
- Smaller incision
- Emerging as a replacement for conventional CABG
- Starting in 1990’s, MIDCAB has gained popularity
- Usually conducted for LIMA to LDA grafts
Advantages
- no sternotomy or CPB
- operating time is 2-3 hours
- recovery time 1-2 weeks
- effectiveness 90%
- incision only 10cm
- reduced need for blood transfusion
- less time on anesthesia
- less pain
- less expensive
problem with MIDCAB
- New instruments must be developed
- Requires highly skilled surgeon and learning curve for surgeons limits number performed
- Small incision
- Beating heart
- Blood in field
- Can only be used with patients having blockages in one or two coronary arteries on the front of the heart
- Attempts at operating on other arteries have been moderately successful, but requires even greater skill and practice
Port access CABG
Uses CPB
Balloon catheter system for aortic occlusion and cardioplegic arrest
5-8 cm left anterior thoracotomy incision
No sternotomy!!!
uses LIMA
Benefits:
- Bloodless field
- Heart arrested
- allows more accurate anastomoses than MIDCAB
- Smaller incision than CABG
- No sternotomy
Drawbacks
- Uses CPB
- Technically very difficult
conduits used for CABG
- Saphenous vein used for bypassing right coranry artery and circumflex coronary artery
- Internal mammary artery (IMA) used for bypassing left anterior descending coronary artery (patency rate over 90% after 10 years)
- If more veins are needed, alternative sites such as upper extremity veins can be used (patency rate as low as 47% after 4.6 years)
discharge planning and teaching for CABG
- What to expect at home
- Pain in your chest around the incision area
- Swelling in the leg at harvest site
- Itchiness or tingling feeling at incision site
- Weakness
- Cardiac rehabilitation
- Lifestyle & diet modification
- Smoking cessation
- Cardiac diet (Low salt, low cholesterol, low fat)
clinical presentation of pericarditis
- physical exam: 85% have audible friction rub during the course of their disease: lean them forward, hear Left sternal border, loudest during expiration
- The rub is high pitched scratchy or squeaky
- Chest pain
- Pericardial friction rub: pericardial friction rub is audible throughout the respiratory cycle, whereas the pleural rub disappears when respirations are on hold
- diffuse ST segment elevation on EKG
- Pericardial effusion
- *Presence of at least two of the above feature is necessary to make the dx
Indicative of?
- retrosternal in location
- sudden onset
- pleuritic and sharp in nature
- exacerbated by inspiration
- worsens when supine and improves upon sitting upright or leaning forwardca
- n often radiate to the neck, arms, or left shoulder
- radiation to one or both trapezius muscle riges, suggest a probable ? (bc phrenic nerve traversses the ?)
pericarditis
need for hospitalization with pericarditis
- uncomplicated acute pericarditis can undergo iinitial evaluation in a same day hospital facility or clinic, with an outpatient follow up
features of high risk include:
- subacute symptoms (eg. developing over several days or weeks)
- high fever (.38 C, 100.4 F) and leukocytosis
- evidence suggesting cardiac tamponade
- a larg pericardial effusion
- immunosupressed state
- a history of oral anticoagulant therapy
- acute trauma
- failure to respond within seven days to NSAID therapy, a generous allocation of time
- elevated cardiac troponin, suggestive of myopericarditis
ECG stages of pericarditis vs MI
Stages of pericarditis:
1: diffuse ST elevation and PR segment depression (seen in more than 80%)
2: Normalization of the ST and PR
3: Eidespread T-wave inversion
4: normalization of the T waves
* *Pericarditis** _ Angina, Ischemia_
*PR depression Frequent Almost never
***Q waves **not usual, common with Q
unless infarct wave infarct
*T waves inverted after J inverted while
returns to baseline ST still elevated
*Arrhythmia Rare frequent
*Conduction Rare frequent
Disturbances
features that differentiate pericarditis
- worse when breathing in
- retrosternal pain
- sudden
- sharp and stabbing continuous
- worse when sleeping, best up leaning forward
- does not respons to nitro
- friction rub
- pr segment depression with ST elevation
- normally in trapezius and back
pericarditis treatment
- Goals of accute therapy: relieve pain, treat inflammation, prevent cardiac tampenade
- most viral infections are self-limited
- treat the underlying disease process
- drain purulent effusions
- symptomatic therapy
- NSAIDS: Aspirin (2-5g/day), Ibuprofen (300-800 mg q6-8hr), ketorolac
- Colchicine (0.5-1mg/day) may prevent reoccurance
- Glucocorticoids (prednisone 1mg/kg/day): increased rate of complications. Should be restricted to acute pericarditis due to conncetive tissue disease, autoreactive pericarditis, uremic pericarditis
nursing interventions for pericarditis
- assess pain frequently: evaluate pain within 30 minutes, notify MD if analgesics not effective
- Position of comfort: sit up and leand forward
- Administer medications as ordered: give NSAIDs and steroids with food, monitor for GI bleeding, give antibiotics on time, reassure pt. that chest pain is not a MI
cause of rheumatic heart disease
- inflammatory immune response
- only develops in kids and adolescents following group a beta-hemolytic strep pharyngitis
- genetic studies show strong correlation b/w progression to rheumatic heart disease and human leukocyte antigen (HLA)-DR class II alleles and the inflammatory protein-encoding genes MBL2 and TNFA
most common valves affected by RHD and type of murmur
- valve insufficiency
- most common are: apical pansystolic, apicial diastolic, basal diastolic
- permanent heart valve damage (mitral #1, aortic #2)
Jones Criteria
The jones criteria require the presence of 2 major or 1 major and 2 minor criteria for the diagnosis of rheumatic fever
Major Criteria
- Subcutaneous nodules
- pancraditis
- migratory polyArthritisSyndenham
- Chorea
- Erythema Marginatum of Skin
Minor Criteria
- Fever
- Arthralgia
- Leukocytosis and raised ESR (erythrocyte sedimentation rate)
erythema marginatum
- occurs in 5-13% of patients with acute rheumatic fever
- begins as 1-3 cm in diameter or papules located on the trunk and proximal limbs but never on the face
- the lesions spread outward to form a serpiginous ring with erythmatous raised margins and central clearing
- the rash may fade and reappear within hours and is exacerbated by head
prevention of RHD
- PO penicillin is drug of choice, but ampicillin and amoxicillin are equally effective
- can use single dose of IM benzathine penicillin G or benzathine/procain penicillin combination is therapeutic
- do not use tetracyclines or sulfonamides to treat GABHS pharyngitis
Preload
- the amount of blood the heart must pump with each beat
- determined by: venous return to heart and strength of muscle fibers
- increasing preload–>increased stroke volume in normal heart
- increasing preload–>impaired heart–>decreased SV. Blood is trapped–>chamber becomes enlarged
afterload
- the pressure that must be overcome for the heart to pump blood into the arterial system
- dependent on the systemic vascular resistance
- with increased afterload the heart muscles must work harder to overcome the constricted vascular bed–>chamber enlargement
- increasing the afterload will eventually decrease the cardiac output
dilated congestive cardiomyopathy
heart muscle disorders in which the ventricles enlarge but are not able to pump enough blood for the body’s needs, resulting in HG (example: CAD, myocarditis, etoh, HIV)
hypertrophic cardiomyopathy
heart disorders in which the walls of the ventricles thicken and become stiff, even though the worklaod of the heart is not increased. Ex: congenital HCM, or acquired
restrictive (infiltrative) cardiomyopathy
heart disorders in which the walls of the ventricles become stiff but not necessarily thickened and resist normal filling with blood between heartbeats. EX: ratiation, amyloidosis
adaptive mechanisms of the heart to increase load
- frank sterlin mechanism
- ventricular hypertrophy : increased mass of contractile elemts cuases increased strength of contraction
- increased sympathetic adrenergic activity: increased HR, increased contractility
- increased activity of R-A-A system
systolic cardiac heart dysfunction (systolic HF)
when the heart muscle doesn’t contract with enough force so there is not enough oxygen rich blood to be pumped throughout the body
diastolic cardiac dysfunction (or diastolic HF)
when the heart contracts normally, but the ventricle doesn’t relax properly so less blood can enter the heart
body compensatory mechanisms of HF
- epi and norepi releases which increases HR and contractility which increases myocardial work load
- decrease in salt and water excretion from kidneys which helps maintain BP by increased BV, this leads to stretching of heart’s chambers which can impair ability to contract
- hypertophy and thickening of heart muscle which initially increases contractility but over time leads to stiff chambers
- HF pts have higher levels of epi, norepi, aldosterone, angiotensin 2, enothelin, inflammatory cytokines, and vasopressin which contributes to heart remodeling, progression of HF, and higher levels are associated wiht increased mortality
neurohormonal with HF
- Stimulated by decreased perfusion leadin gto secretion of hormones
- Epi: increases contractility, increases rate and pressure, vasoconstriction leads to SVR
- Vasopressin: pituitary gland, mild vasoconstriction, renal water retention
renin angiotensin mechanism in HF
- Decreased renal blood flow secondary to low cardiac output triggers renin secretion by thte kidneys
- aldosterone is released–> increased sodium retention and water retention
- preload increases
- worsening failure
ventricular hypertophy
- long term compensatory mechanism
- increases size due to increase in work load ie skeletal muscle
- potential reasons
- alternation in ventricular distensibility
- valvular regurgitation
- pericardial restrain
- cardiac rhythm
- conduction abnormalities
- rv function
- also several non-cardiac factors including peripheral vascula fxn, reflex autonomic activity, renal sodium handling, etc
sign and symptoms of HF
- dyspnea
- pnd
- orthopnea
- cough
- exercise intolerance
- edema
- fatigue
- nausea
- abdominal fullness
- rales (usally starts at bases)
- s3 (position patient left lateral to hear)
- pulmonary edema
- jvd
- tachycardia
- cardiomegaly
- hepatojugular reflex (apply pressure, see distention, let go it stays pretty long)
- peripheral edema
- hepatomegaly
physical exam of HF: signs that suggest HF include
- tachycardia
- third heart sound (listen LL recumbent)
- increased jugular venous pressure
- positive hepatojugular reflux
- bilateral rales (not always present, only in L sided HF)
- peripheral edema not due to venous insufficiency
- laterally displaced apical impulse (from midclavicular (normal) to mid-axillary)
- weight gain
Elevated BNP levels have been associated with?
- reduced LVEF, LVH, and elevated LV filling pressure, and acute MI
- evidence supports getting baseline BNP
clinical use of BNP
- levels below 100 may indicate no heart failure
- levels 100-300 suggest heart failure is present
- levels above 300 indicate mild heart failure
- levels above 600 indicate moderate hf
- levels above 900 indicate severe HF
clinical presentations of LVHF
- Severe resp distress evidenced by orthopnea, dyspnea, hx of parozsymal nocturnal dyspnea
- severe apprehension, agitation, confusion, resulting from hypoxia, feels like he is smothering
- cyanosis
- diaphoresi results from sympathetic stimulation
- pulmonary congestion: rales, rhonchi, wheezes
- JVD from backed up pressure
- vital signs: BP elevated, pulse elevated, resp rapid and labored
- LOC may vary, depends on level of hypoxia
- chest pain may be present, masked by the RDs
Clinical presentation of right sided HF
- Marked JVD
- clear chest
- hypotension
- marked peripheral edema
- ascites, hepatomegaly
- poor exercise tolerance
- often will be on lasix, digoxin
- have chronic pump failure
CHF presentation
- thin white sputum
- pink frothy hemoptysis
- PND within oone hour
- common pedal edema with chronic
- orthopnea at night
- substernal crushing pain
- progressing cyanosis
- diaphoresis mild to heavy
- jvd mild to severe
- bp high
- crackles fine to coarse, being in gravity dependent areas
non pharm treatment of HF
- Sodium intake: limit, 203 g a day over 3 meals, recheck sodium intake when weigth gain experienced
- Fluid intake: HF patients wiht hyponatremia, high dose diuretics, severe HF. LImit to 6-8 glasses a day. Fruit=1/2 cup liquid
- exercise: hf patients with stable heart and stable voume status. 5-10 minutes a day 2-3 times a day to start
- monitor wieght gain. Report gain of 2.5 kg a week.
vasodilaters for HF
- dilate blood vessels
- ace inhibitors (prils): block production of chemicals that cause bp to narrow, decreasing the heart pumping easier. Side effects: cough, hyperkalemia (blood tests every 6 weeks), angioedema, orthostasis
- nitrates (african american patients respond well)
diuretics for HF
- lasix (can develop tolerance to lasix)
- hydrochlorothiazide: works as a vasodilator primarliy at low doses
- spironolactone: for patients with stage 3 or 4 heart failure Watch for hyperkalemia
- loop diuretics (furosemide, bumentanide, torsemide) to treat volume overload. No effect on mortality
inotropic agents
- digoxin, lanoxin
- decreased heart rate increases stroke volume, increaseing the CO
- 10-20% develop toxicity
- side effects include arrhythmias, cisual changes, gi complaints, altered mental status
- therapeutic range: 0.8-2.0
- steady state : 7-10 days
- toxic: 2.4
- half life: 33-51 hours
- obtaining levels: determine serum digoxin levels at least 4 hours after IV 6 hours after oral
calcium channel blockers
- slow conduction, allows more time for filling pressures, counteracts natural response to increase hr, relaxing of peripheral blood vessels
- used in pts wiht diastolic bp
- ex: nifedipine, diltiazem, verapamil, amlodipine, felodipine
beta blockers
- useful by blocking beta-adrenergic receptors of the sympathetic nercous system,the heart rate and force of conractility are decreasd
- may worsen HF
- ex: metoproplol, atenolol, propanolol, amiodarone
atrial septal defect
- most commonly asymptomatic
- essentials for dx: right ventricular heave, s2 widely split and usually fixed, grade 1-4/4 systolic murmer at the pulmonary area, widely ratiading systolic murmuer cardiac enlargement on cxr
- treated: closure generally recommended when ratio of pulmonary to systemic bf is .2:1. Operation performed 1-3 years of age
- previously surgical, no often closed interventionally
3 types of atrial septal defects
- ostium secundum: most common, in the middle of the septum in the region of the foramen ovale
- ostium primum: low position, form of av septal defect
- sinus venosus: least common, positioned high in the atrial septum, frequently associated with papvr
ventricular septal defect
- single most common congenital malformation
- can occur both the membranous portion of the septum and the muscular portion
- 3 types
- small hemodunamically insignificant: between 80% and 85% of vsds, less than 3mm, all close spontaneously in school years, muscular close sooner than membranous
- Moderate: 3-5 mm, least common group of children, without evidence of CHF or pulmonary htn, may be followed until spontaneous closure occurs
- large VSD with normal PVR: 6-10 mm in diameter, usually requires surger, otherwise chf and fft by afe 3-6 months
clinical findings of ventricular septal defects
grade 2-3/4, medium to high pitched, harsh pansystolic murmer heard best at the left sternal border with radiation over the entire precordium
patent ductus arteriousus
- persistence of normal fetal vessel joining the pulmonary artery to the aorta
- closes spontaneously in normal term infants at 3-5 days of age
- higher incidence at higher altitueds
- more common in females
- clinical findings course depend on size of the shunt and the degree associated pulmonary htn
- pulses bound and pulse pressure widens
- characteristically has a rough machinery murmer which peaks at s2 and becomes a decreascendo murmur and fades before the s1
tetrology of fallot
- cyanosis result of a small number of cardiac malformations well determines, one is much more frequent than the others. Consissts of stenosis of pulm artery, interventricular communication, deviation of the origin of the aorta to the right, hypertrophy almost always concentric type of the right ventricle. Fialure of obliteration of the foramen ovale may occasionally be added in whilly accessory manner
typical features of tetralogy of fallot
- cyanosis after the neonatal period
- hypoxemic spells during infancy
- right sided aortic arch in 25% of all patients
- systolic ejection murmur at the upper LSB
- most patients are cyanotic by 4 months
- hypoxemic spells are one of the hallmarks of severe tetrology
flail chest
multiple ribs by each other that are compromised and the lung doesn’t expand correctly. Pt. has paradoxical chest movement
tension pneumo thorax
lung completely collapses. That lung presses against the good lung and the heart
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