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Sixkiller4 - Med Surg Test 1
Terms in this set (341)
What is Coronary Artery Disease (CAD)?
build-up of plaque in the arteries - narrows the arteries, decreasing blood flow; - eventually can barely get enough blood flow > barely getting enough oxygen
Non-modifiable risk factors for CAD
race - black
genetics > family history of coronary artery disease
Modifiable Risk Factors of CAD
Smoking - toxins cause vasoconstriction
stress - when stressed body releases cortisol
Why do older patients with CAD have a higher chance of surviving and MI than younger patients?
They have collateral circulation
Smaller blood vessels that are used to shunt the blood around the area that is blocked - builds slowly over time
Management goals for patients with CAD?
Prevent, Stop, Slow
Drug used to control LDL and HDL cholesterol?
CAD can progress to...
Acute coronary syndrome
Acute Coronary Syndrome (ACS)
progressing CAD causes myocardial ischemia which can lead to damage and death of heart tissue - plaque builds up in the coronary artery blocking the blood flow
Manifestations of Acute Coronary Syndrome
No blood supply to heart tissue in one or more areas
2 causes of Myocardial Infarction (MI)
plaque from coronary artery disease become dislodged then blocks artery
lack of blood flow to the heart tissue (is still getting some but not enough)
Chronic Stable Angina Pectoris
- "strangling of the chest"
- temp imbalance between the coronary artery's ability to supply O2 and the cardiac muscles' demand for O2
- ischemia is limited in duration and does not cause permanent damage to myocardial tissue - can cause cells to die but doesn't kill the heart muscle
- occurs with exertion
- patient is familiar with the pattern - what causes it and what makes it stop
- pain stops with use of nitroglycerine
chest pain that is:
- occurs at rest, sleep, with little exertion
- change in pattern from stable angina
- increased frequency from chronic stable angina
Clinical Manifestations of Unstable Angina
-tightness - squeezing
- heavy pressure - jaw pain
- mid-epigastric pain - back pain
-dyspnea - pallor
- increased fear and/or anxiety
Myocardial Infarction (MI)
-no oxygen getting to myocardial cells
What can MI lead to ?
Factors that cause MI
poor perfusion pressure
Why may patients who suffer an MI be confused?
30 % of blood pumped from the heart goes to the brain - brain will not get enough oxygen
Clinical Manifestations of MI
- angina - anxiety
- tachycardia- in beginning as heart tries to compensate
- bradycardia - late when heart wears out, cells dying
-vasoconstriction - feeling of impending doom
- increased temperature - inflammatory response
-nausea/vomiting - lack of blood to medula
- hypertension (early) - hypotension (late)
- decreased level of consciousness - lack of blood flow
-dyspnea - blood backing up in lungs
Complications of MI
cardiogenic shock - heart muscle is dead
Diagnostic studies for MI
-12 lead EKG
-Labs - cardiac enzymes, CBC/BMP, Brain naturetic peptide, C-reactive protein
- echo cardiogram
- stress test
- cardiac catherization
indicator of myocardial death - if have MI, it will be elevated
ultrasound of the heart
on treadmill or use of drugs
- NOT done during active heart attack
How can increased K+ levels effect the heart
can stop it - Na and Ca won't move into the cells to begin action potential
Medical Management of MI
- pain relief - Nitro, sometimes morphine
-decrease myocardial O2 requirements through preload and afterload reduction - nitroglycerine
- drug therapy - nitro
- intra- aortic balloon pump - for heart failure
- immediate reperfusion !! - need to perfuse the heart muscle
Interventions for ineffective tissue perfusion
-drug therapy - aspirin, thrombolytics
- restoration of perfusion to injured area
- complete sustained reprofusion of coronary arteries in the first few hours after MI has decreased morality
Overall goals of nursing management for MI
- pain relief
- preservation of myocardium
- immediate and appropriate treatment
- effective coping with illness
What drug should be given first for MI?
Nursing interventions for accute coronary syndrome
-O2 -IV access
- vital signs - ASA 325 mg chewed
-IV nitroglycerine - Morphine sulfate
- beta blockers - heparin drip
- thrombolyitic therapy
- promote energy conservation
- prepare for vascular procedure
What does heparin do?
Leading cause of death in patients with MI who die before hospitalization?
What is normal blood pressure
What is prehypertension
What is stage 1 hypertension?
What is stage 2 hypertension?
What lifestyle changes can be made with HTN?
- Does not lower BP
- Decrease in CV risk occurs in about 3 years
- Greater effect in black patients, elderly patients, or patients with CRI
- Recommend < 5 g of salt per day
- High in fruits, vegetables & low-fat dairy products; low in saturated fats
Physical exercise and weight loss
blood flow thru arteries diminished, not relieved by nitro or takes more than normal, may occur at rest, may show ST depression, no cardiac enzyme elevation
Typical presentation of pain with MI
pain occurs without cause, early morning, crushing, tight, burning, heavy, squeezing, can radiate, substernal, jaw, neck, back, ears, not necessarily severe, lasts > 20 min, relieved by opioids but not nitro, can mimic GERD
Typical Clinical Manifestations (CMs) of MI in addition to chest pain
N/V, SOB, diaphoresis. also dizziness, weakness, palpitations, denial, feeling of doom, ST w/PVBs, incr temp & BP, S4 gallop, cool extremities w/decr pulses
Atypical CMs of MI
vague ache or poorly localized, absent/silent MI (bc of neuropathy don't feel pain- common w/diabetics, women, elderly), back pain, syncope, N/V, diaphoresis, women more likely to have sleep disturbance, SOB, fatigue.
Discomfort from stable angina:
lasts < 15 min, precipitated by activity, relieved by rest/nitro, few assoc. symptoms, pain retrosternal, epigastric, radiating to jaw, neck, ear, L arm/shoulder
Discomfort from MI:
lasts > 20 min, occurs without cause in a.m., relieved by opioids, freq. assoc. symptoms, substernal, back, radiating to jaw, neck, ear, L arm
MOST specific cardiac enzyme for MI (troponins are released when damage occurs)
quickest elevating enzyme, check @ onset and if doubled in 2 hrs it's a really good indicator of MI
Diagnostic tools for MI
Stress test or exercise tolerance test (cornerstone - usually start with this), MRI, thallium scan, technitium scan, MUGA scan, cardiac cath w/angiogram, PET scan, cardiac CT w/angiography (dye)
Primary goals of MI treatment
limit infarct size, reprofuse ischemic/injured area, prevent/treat complications, provide emotional support & education
Potential complications of MI
DYSRHYTHMIAS most common (normally short lived once heart heals, don't treat unless potentially fatal), HF, thromboembolism, septal/papillary muscle rupture, ventricular aneurysm, pericarditis, extension of MI, cardiogenic shock (most potentially fatal, most severe form of HF)
Medication to relieve angina work primarily by...
Decreasing oxygen demand by heart
-Meds also increase supply to heart, but to a much lesser degree
-Prototypical nitrate--> release NO in body
-Large first-pass effect w/ PO forms
-Use for symptomatic tx of ischemic heart conditions (angina), hypertensive crisis, & uterine tone reduction
-Does NOT reduce mortality
-IV form for BP control in perioperative Htn, tx of CHF, ischemic pain, & pulm edema assoc'd w/ acute MI
-Veins>>Arteries: reduce PRELOAD
-Half-life: 1.5 mins
-Use for prophylaxis of angina & reducing risk of sudden death or re-infarction post MI
-Decrease myocardial oxygen consumption through reductions in HR, BP, & myocardial contractility
-Also in tx of Htn, cardiac arrhythmias, essential tremors, hyperthyroidism sx
is an inflammation of the pericardium. The acute form is defined as inflammation lasting <6 weeks and can be either fibrinous (dry) or effusive with a purulent, serous, or haemorrhagic exudate. It is characterised clinically by a triad of chest pain, pericardial friction rub, and serial electrocardiographic changes. Constrictive pericarditis impedes normal diastolic filling and can be a medium to late complication of acute pericarditis.
What are the 7 conditions included in CVD?
Rheumatic Heart Disease
Congenital Heart disease
Valvular Heart Disease
Coronary Artery Disease
What are the 3 most common symptoms of Congestive Heart Failure?
Shortness of Breath
What are the 5 conditions that lead to heart failure? [CCMDH]
Coronary Artery Disease
Mitral Valve Disease
What are the drugs used for Chronic Heart Failure [VDBDC]
Cardiac Inotropes: dobutamin, milrinone
What agents increase cardiac output?
What drug inhibits sympathetic nervous system activation?
Which 2 classes of diuretics cause hypokalemia?
Loops & Thaizides
What is primary effect of beta blockers?
What are 2 most commonly used beta blockers for CHF?
Carvedilol (nonselective, alpha too)
Digoxin is first-line therapy for patients with CHF and...?
What are adverse effects of digoxin?
What are precautions for digoxin?
Ventricular bigeminy [arrhythmia]
brady cardia [monitor heart rate]
What are 2 ways to treat digoxin toxicity?
1. higher than normal doses of K+
2. Digoxin antibody [Digibind] esp. in life-threatening overdose
Three major categories of drugs to treat CHF?
1. ACE inhibitors
2. Beta blockers
3. Digoxin & diuretics
Chronic high blood pressure left untreated leads to... (3)?
1. Blood Vessel Damage (aterirosclerosis)
2. Heart attack, Heart disease, Heart failure, stroke
3. Kidney failure/disease
Primary Hypertension is caused by genetics and environment leading to..(3)?
1. Insulin resistance
2. Dysfunction of SNS, RAA, adducin & natriuretic hormones
The next step in primary HTN...
Vasoconstriction & Renal Salt/H2O retention
Third step in primary HTN...
Increased peripheral resistance & increased blood volume
Finally leading to...
What are the 7 classes of drugs used to control HTN?
2. Beta blockers
3. Alpha adrenergic blockers
5. ACE inhibitors
7. peripheral vasodilators
What is goal BP after life-style modifications? for a diabetic or patient with chronic kidney disease?
What is initial therapy for Stage 1 HTN?
Thiazide-type diuretic for most; may consider ACE Inhibitor, ARB, Beta blocker, CCB or combo
What are the 3 clinical indications for Beta Blockers?
What conditions are contraindicated for 'olol's?
Name 5 Vasodilators
Sodium Nitroprusside (Nitropress)
Name 9 parenteral Antihypertensives used for Hypertensive Emergency
Chronic Stable CAD factors
Blood Pressure Measurement
Symptom & Activity assessment
Drug therapy for lowering LCL-cholesterol
B-Blocker therapy (Prior MI)
ACE Inhibitor Therapy
Screening for Diabetes
largest artery/blood vessel in the body
inferior vena cava vein
brings blood from the lower body regions and empties into the right atrium
the left side of the heart chamber that pumps oxygen-rich blood from the lungs
receives the oxygen-rich blood from the left atrium, and pumps this blood out through the aorta
or bicuspid valve; a flap like structure that prevents the back flow of blood as it is pumped from the left atrium to the left ventricle
transports blood away from the heart to the lungs
a flap-like structure that prevents the back flow of blood as it is pumped from the right ventricle to the pulmonary artery
transports oxygen-rich blood from the lungs to the left atrium
receives de-oxygenated blood returning from the body
receives the de-oxygenated blood from the right atrium and pumps this blood through the pulmonary artery to the lungs, where the blood absorbs oxygen
separates the right and left side of the heart
superior vena cava vein
brings blood from the head, neck, and upper chest regions and empties into the right atrium
flap-like structure that prevents the back flow of blood as it is pumped from the right atrium to the right ventricle
A hollow, muscular organ about the size of a clenched fist that is located in the chest cavity just behind the sternum, above the diaphragm and between the lungs. It maintains circulation by supplying oxygen-rich blood to all parts of the body.
(peri-:around ; cardia:heart); a serous membrane with two layers that surrounds the heart
outer layer that protects the heart; (epi-:above ; cardia:heart); the innermost of the two layers of the pericardium
(myo-:muscle; cardia:heart); the muscular tissue of the heart responsible for continued rhythmic contraction
(endo-:inside; within: endometrium and cardia:heart); the inner layer of the heart consisting of epithelial tissue and connective tissue, which covers the heart valves
are located in the endocardium. They participate in the contraction of the heart muscle
carry blood to the heart
are elastic blood vessels that carry blood away from the heart
are thin, flap-like structures that are composed of endocardium and connective tissue which are located between the atria and the ventricles and prevent the back flow of blood allowing the blood to flow in one direction; tricuspid valve and mitral valve
flap-like structure that prevents the back flow of blood as it is pumped from the right atrium to the right ventricle
a semilunar shaped flap-like structure that prevents the back flow of blood as it is pumped from the right ventricle to the pulmonary artery
flap-like structure that prevents the back flow of blood as it is pumped from the left atrium to the left ventricle; aka bicuspid valve
a semilunar shaped flap-like structure that prevents the back flow of blood as it is pumped from the left ventricle to the aorta
include the aortic valve, located between the left ventricle and aorta; and the pulmonary valve, located between the right ventricle and pulmonary artery
are strategically located to keep blood flowing in one direction; opening and closing of valves is controlled by pressure changes within the heart chambers
electrical impulses generated by specialized nodal tissue that travel through the heart wall, causing the myocardium to contract the heart chambers in a coordinated fashion
sinoatrial (SA) node
lies in the upper right atrium. It fires an electrical impulse that travels through the walls of the atria, signaling both atria to contract and push blood into the ventricles
atrioventricular (AV) node
after the SA node the impulse then travels to the AV node that lies between the atria and the ventricles. The AV node initially hold the impulse for a fraction of a second, allowing both the atria to relax
Bundle of His (atrioventricular bundle)
after the AV node the impulses are then sent down the atrioventricular bundle
the atrioventricular bundle branches of into Purkinje fibers at the bottom of both ventricles. These fiber signal both ventricles to contract and push the blood out to the lungs and the the rest of the body
refers to the events that occur when the heart beats; 1 SA node, 2. AV node, 3. atrioventricular bundle (Bundle of His), 4. Purkinje fibers
the sequence of relaxation and contraction of the heart chambers as measured by an EKG
refers to the contraction of the heart chambers
refers to the relaxation of the heart chambers
consists of one systole and one diastole of the atria, and one systole and one diastole of the ventricles
network of arteries, veins, and capillaries spread out from the heart. Nutrients and oxygen are distributed to body tissues through the blood; at the same time, waste material is picked up and removed by the blood
vessels that circulate blood through the body - and move blood in and out of body tissues - fall into three categories: capillaries, veins, and arteries
are microscopic tubes that form a network of "beds" throughout the body. They connect with arterioles (the smallest arteries) and venules (the smallest veins); The walls of capillaries are one-cell thick, which allows nutrients and oxygen traveling in arteries to pass through the capillary walls and into body tissues; waste material and carbon dioxide are absorbed from body tissues into the capillaries, and are then carried into the veins for return to the heart
the smallest arteries
the smallest veins
return deoxygenated blood to the heart (except for the pulmonary veins, which carry oxygenated blood from the lungs to the heart; Deoxygenated blood and waste material move into the capillaries first, and then into the venules. Venules feed into larger veins which eventually merge into the vena cavae. The vena cava direct blood back into the heart; The walls of veins are formed of three layers. These layers are thin and collapse when empty. Most veins contain valves (there are exceptions) that keep blood from flowing backward. Valves are most numerous in the veins of the extremities
filter out nitrogenous wastes
removes old red blood cells
receives all the veins from the intestines and stomach; detoxifies the blood before the vena cavae returns it to the heart for reoxygenation
move blood away from the heart (except for the pulmonary arteries, which carry deoxygenated blood from the heart to the lungs).
Arteries carry the oxygenated blood from the heart out through the aorta. The aorta branches and divides into many other arteries, which in turn subdivide into arterioles that terminate in capillaries throughout body tissues.
The walls of arteries have three layers, to include a tough elastic outer coat, a layer of muscular tissue, and a thin inner coat
movement of pulsating blood; can be felt where the large arteries are near the surface of the body
(Class, MOA, Indications, Side Effects, Contraindications, Misc. Notes)
Class: Inotrope (cardiac glycoside) & unspecified antiarrhythmic
MOA: blocks Na+/K+ pump & agonizes muscarinic receptor; ↑ intracellular Ca++, enhances vagal tone, ↑CO, ↑inotropy, ↑natriuresis, ↓LVEF, ↓LVEDP; ↓automaticity of AV node;
Indications: AFib, CHF (Sx despite Tx), AVNRT
Notes: competes w/K+ for Na+/K+ pump, so toxicity increased by ↓K+
Side Effects: arrhythmias (EADs) or SA/AV block; toxicity: CHF exacerbation; GI side effects (nausea, vom), nervous (depression, disorientation, paresthesias); hyperestrogenism
Contraindications: advanced AV block or bradycardia w/o pacemaker; PVCs or VT; hypokalemia; WPW w/AFib (will cause VFib b/c/o AV node delay)
Misc: narrow therapeutic window; no ↑survival, but ↑quality of life for HF; Tx for toxicity = Fab directed against digoxin
(Class, MOA, Indications, Side Effects, Contraindications, Misc. Notes)
Class: nitrate vasodilator
MOA: metabolized to NO; causes arterio-/venodilation; ↓preload, ↓afterload; ↓platelet aggregation
Indications: stable/unstable, acute cardiogenic pulmonary edema (venous pooling of blood), acute MI
Side Effects: reflex tachycardia (give w/BB), excess vasodilation (headache, flushing, weakness, hypotension, GI sphincter weakness); severe myocardial ischemia w/discontinuation; methemoglobinemia
Contraindications: hepatic insufficiency, Viagra (sildenafil, severe hypotension), sympathomimetics (↑ischemia)
Misc: tachyphylaxis, watch out for dependence
Which drugs help prolong survival in HF?
Beta blockers, Ace inhibitors (or ARBs), spironlactone, hydralazine + nitrates, amlodipine in DCM
What drugs help prolong survival post MI?
Beta-blockers, ACE inhibitors, ARBs, (eplerenone if pt also has HF)
How do you treat angina?
Modify risk factors - correct anemia, HTN, drug abuse and noncompliance.
Medications: B-blockers, nitrates are main-stay, CCB help. Nifedipine can help with vasodilatation. ASA decreases mortality
Overall, what do anti-anginal drug help do?
(Nitrates, b-blockers, CCBs) All of these decrease myocardial O2 demand and all decrease afterload.
How do nitrates help with angina?
Decrease preload more than afterload. Can cause devere decompensation in patients with R sided MI. Can cause sympathetic reflex increase in HR. Can develop a tolerance (more likely with dinitrates), so recommend having a 6 hour nitrate free window.
How do b-blockers help angina?
Decrease O2 demand by decreasing HR, BP, and contractility. Complement nitrates well.
What conditions exclude a patient with angina from an exercise stress test?
> 1 mm resting ST depression
Ventricularly paced rhythm
Currently taking digoxin
How do you evaluate chronic stable angina?
1) determine probability of CAD (pre-test probablitity)
2) determine relative risk
3) determine if patient need angiogram
What are the treatment goals of angina?
Keep BP controlled
ACE in all patients
Daily physical exercise (cardio daily and weight at least 2x/week)
Low waist size: M <37-40 F <35
LDL < 100, < 70 if DM, high dose statin (add niacin if non-HDL is too high)
Flu shot yearly
What are some additional CV disease prevention in women?
Hormone therapy is not a primary or secondary prevention
Antioxidants should not be used as primary/secondary prevention
Folic acid should NOT be used
Do NOT use ASA in healthy women < 65 to prevent an MI
What percentage of heart attacks are asymptomatic?
More likely in elderly, diabetic, & women
What are the cardiac markers that are the gold standard for detection of myocardial necrosis?
Troponin I, Troponin T (these are not present in healthy patients)
What is the life-span of the cardiac marker: myoglobin?
Initial elevation: 1-4 hr
Peak elevation: 6-7 hr
Return to normal: 24 hour
What is the life-span of the cardiac marker: troponin I?
Initial elevation: 3-12 hr
Peak elevation: 24 hr
Return to normal: 7-10 days
What is the life-span of the cardiac marker:CKMB?
Initial elevation: 3-12 hr
Peak elevation: 20 hour
Return to normal: 2-3 days
What conditions can cause false elevations of troponin?
Chronic renal failure
Myopericarditis, CHF, PE, cardiac trauma
Which markers are most specific for an MI?
Troponin I and CKMB isoform 1
Which cardiac marker is very sensitive but not very specific for MI?
If a patient had a heart attack 2-3 days ago and has chest pain again, which cardiac marker would be most helpful for help determine if it was his heart again?
Myoglobin - good test to evaluate recurrent chest pain soon after MI
How do you treat a heart attack in the field?
1) Call 911, want ambulance transport only
2) Give ASA 162-325 mg bite and chew x 1
3) Nitroglycerin x1 (if improving, may repeat; if not, stop taking and wait on ambulance)
4) EKG in field by EMS
How do you treat suspected ACS in the Emergency Department?
All following should be done within 10 min
- get EKG
- draw cardiac markers
- give ASA if no contraindication
- directed H&P
How do beta blockers help during ACS?
B-blockers reduce myocardial O2 consumption. Also, by blocking the often excessive sympathetic activity, they reduce the load on the heart and decrease the likelihood of arrhythmias.
What are contraindications to beta-blockers in ACS?
2nd or 3rd degree block
When is atropine needed during ACS?
For temporary management of acute sinus bradycardia with signs of low cardiac output while preparing for temporary pacing
Bradycardia associated with MI (usually inferior) with maybe temporary pacing
When should ACS patient get aspirin?
Immediately and indefinitely
How do glycoprotein IIb/IIIa inhibitors work?
Anti-platelet drugs which are more specific than aspirin. The Gp IIb/IIIa is responsible for platelet aggregation - in which the platelet to plate binding occurs.
Should patient with an NSTEMI or UA get fibrinolytic therapy?
But it is indicated in STEMI or new LBBB and NO PCI is available
What are the primary risk factors for CAD:
Family hx of early CAD
What two factors are INVERSELY related to CAD?
Aerobic exercise and elevated HDL
What factors can modify HDL?
HDL is increased by exercise, estrogen, niacin and small amounts of EtOH
HDL is decreased by smoking and androgens
When should check a lipid panel?
At least every 5 years in healthy persons, starting at age 20
How do you calculate LDL?
LDL = total cholesterol - HDL - 1/5 of triglycerides
When can lipids be falsely low?
Can be upto 2 months post MI or cardiac surgery
What is Buerger's disease?
AKA Thromboangiitis obliterans, it involves medium and small arteries, and often affects the areas of the wrists (positive Allen test) and hands
What is the best way to diagnosis the degree of functional impairment of PVD?
ABI before and after exercise
What is the best test for defining the location of the PVD disease?
Arteriography (CT and MR angiography are very good for noninvasive imaging)
How do you treat PVD?
1) stop smoking
2) regular exercise (30 minutes daily)
3) pentoxifylline tx (Trental)
4) cilostazol (Pletal) (a PDE inhibitor, only use in patient with normal LV)
What are the most two common vasospastic disorders?
Primary raynaud syndrome
How do you treat vasospastic disorders?
Calcium channel blockers, biofeedback and nitroglycerin if needed
What is the treatment of TIAs if no significant lesion is found and h/o of a-fib?
ASA + extended release dipyridamole or plavix
What is the treatment of TIAs if no significant lesion is found, but they do have a-fib?
What is the treatment of TIAs and >70% stenosis?
What should suspect when a patient presents with unilateral headache associated with either TIAs or a dilated pupil?
Suspect spontaneous dissection of the internal carotid artery, look for cholesterol emboli on fundoscopic exam
Relating to the heart and blood vessels
having to do with, composed of, or provided with vessels that convey blood or lymph
pertaining to heart
each small upper chamber of the heart R & L
muscular organ cont contracts at least once evey second to pump blood; has an extns electrical system that initiates contractions to pump blood throughout the system. thicker on the L side of the heart
each large lower chamber R & L
the largest artery that carries fresh oxygenated blood from the L ventricle of the heart to branch arteries
branches off the left ventricle; carries oxygen rich blood to parts of the body above the heart
four: two small upper chambers L & R atrium
two large lower chambers L & R ventricle
pointed lower end of heart
contracts and gathers blood from body; oxygen has been depleted
tricuspid valve allows the blood to go from the R atrium to the R ventricule
R side - opens and contracts and allows blood to go to pulmonary arteries and lung
(or bicuspid valve) btwn L atrium & L ventricule. Contracts and allows blood to flow.
L side - separates the L ventricle & aorta - allows blood to go into the aorta
anchors the tricuspid and mitral (bicuspid) valves.
divides the heart - R side has deficient blood eg, carbon dioxide and L side has the oxygenated blood; the thick muscular wall that separates the L side of the heart to the R side. The septum prevents oxygen rich and oxygen poor blood from mixing in the heart.
composed of cardiac muscle; responds to electrical response
Endothelium (or intima) innermost layer of cells that lines the atria, ventricles, and heart valves.
the middle muscular layer of the heart wall
outermost layer; protective sac enclosing the heart composed of two layers with fluid between
Membrane surrounds the heart and secretes pericardial fluid. U-shaped, the heart is within the U.
(epicardium) part of themembrane that is next to the surface of the heart - is upon the heart.
the outer wall of the pericardial sac.
watery, slippery fluid that allows the two membranes to slide as the heart contracts & relaxes.
contains the heart and parts of the vessels and the thymus, trachea, and the esophagus.
vascular channels thru which blood circulates; have a central opening/lumen thru which blood flows; lined with endothelium, a smooth inner layer that allows flow of blood.
Blood vessels - 3
Arteries, Capillaries, Veins
Largest blood vessels.
Smaller branches of an artery are arterioles;
All arteries have five layers: outer, muscle, elastic, inner and the endothelium (cells) layer.
They carry bright blood that has a high level of oxygen away from the heart. The blood has already gone to the lungs. All have smooth muscle in their walls (exception: pulmonary arteries- pumps oxygen-poor blood out of the body into the lungs from the R ventricules.
smallest blood vessesl; brings nutrients and oxygen to the tissues and absorbs carbon dioxide and waste products
Constriction of smooth muscle in the wall of a blood vessel that causes it to become smaller in diameter.
endothelium cells secretes substance that assists in basil dilation.
of the blood occurs through two pathways:
Systemic Circulation- arteries, arterioles, capillaries, venules and veins everywhere except lungs.
circulation of blood from the pulmonary artery through the vessels in the lungs and back to the heart via the pulmonary vein, providing for the exchange of gases
circulation of blood throughout the body through arteries, arterioles, capillaries, and veins to deliver oxygen and nutrients to body tissues; supplies blood to all of the body except the lungs.
Blood vessel that carries blood from the body back to the heart. This blood has a low level of oxygen & a high level of carbon dioxide and waste products of cellular metabolism from the cells. Exception: the pulmonary veins that carry blood that has a high level of oxygen from the lungs back to the heart.
7-15 ozs (200-425 g/little larger than the size of your fist)
anatomy of the heart
2,000 gallons (7571 liters of blood)
How much does the heart pump blood each day?
right atria, right ventricle, left atria, left ventricle
4 chambers of the heart
left and right ventricles
left and right atria
separates left and right atria
separates left and right ventricles
right atrium (RA)
deoxygenated venous blood from body
right ventricle (RV)
right ventricle (RV)
generates pressure to close tricuspid valve (TV), open pulmonary valve (PV), and propel blood into pulmonary artery and lungs
left atrium (LA)
pumps remaining blood into left ventricles (LV)
left ventricle (LV)
largest and strongest chamber
left ventricle (LV)
chamber walls are only about a half-inch thick but they have enough force to push blood through the aortic valve and into your body
tricuspid (TV), pulmonary valve (PV), mitral valve (MV/bicuspid), aortic valve (AV
regulate blood flow through the heart
takes up to 25% of CO (cardiac output)
tricuspid valve (TV)
regulates blood flow between right atrium (RA) and right ventricle (RV)
pulmonary valve (PV)
controls blood flow from right ventricle (RV) into pulmonary arteries, which carry blood to your lungs to pick up oxygen
mitral valve (MV/bicuspid)
allows oxygen-rich blood from lungs pass from the left atrium (LA) into the left ventricle (LV)
aortic valve (AV)
opens the way for oxygen right blood to pass from the left ventricles (LV) into the aorta, then it's delivered throughout the body
mitral valve (MV)
taking most pressure and if extra pressure in lungs (ex. COPD), this will have more pressure
each has to work efficiently or other parts will be affected
need to close all the way so will have force and not have backflow
cause contraction of heart muscles
sinoatrial node (SA)
Where does the electrical signal in the conduction system begin?
sinoatrial node (SA)
natural pacemaker of the heart
travels through the atria and ventricles causing them to contract
sinoatrial node (SA)
sends electrical impulses at a set rate which may cause a heart rate change depending on physical demands, stress, or hormonal factors
top of RA > SA node > down to atria and ventricles > AV node > Purkinje fibers
path for conduction system if one fails then what backup
SA: 60-100 bpm AV: 40-60 bpm PF: 20-40 (pts cannot tolerate this for long, intervention needed stat)
rates for SA, AV, and Purkinje Fibers
heart and circulatory system
make up the cardiovascular system
to organs, tissues, and cells of your body (to everywhere!)
Where does the heart pump blood to?
delivers oxygen and nutrients to cells and removes carbon dioxide and waste products
main function for blood
through arteries, arterioles, and capillaries
How is blood carried from heart to the rest of the body?
through venules and veins (venous return)
How is blood returned to the heart?
diastole (relaxation and filling of the atria and ventricles) and systole (contraction and emptying of the atria and ventricles)
sequence of events during the cardiac cycle
2/3 of the cardiac cycle
relaxation and filling of the atria and ventricles
contraction and emptying of the atria and ventricles
cardiac output (CO)
amount of blood pumped from the left ventricle (LV) each minute
HR x SV = CO
formula to figure out cardiac output (CO)
heart rate (HR)
number of times the ventricles contract per minute
normal heart rate
stroke volume (SV)
amount of blood ejected by the left ventricle (LV) during contraction
degree of myocardial stretch at the end of diastole and just before a contraction
at the end of diastole and just before a contraction
degree of myocardial stretch (as they fill just before blood is pumped out)
pressure/resistance the ventricles must overcome to eject blood through semilunar valves (PV,AV) and peripheral blood vessels
pulmonary valves (PV) and aortic valves (AV)
force of contraction, independent for preload
pressure to overcome to open aortic valve
autonomic nervous system (ANS), renal system, endocrine system, external factors
regulates and affect blood pressure (BP)
baroreceptors and chemoreceptors (hypercapnia=too much CO2)
What affects the BP in the ANS?
"fight or flight" (ex. if someone from behind jumps and scares you)
an example of an external factor that affect BP
if breathing really fast
the BP will be affected if....
where salt goes
P wave, PR segment, PR interval, QRS complex, QRS duration, ST segment, T wave,QT interval, U wave
phases of an electrocardiogram (ECG/EKG)
representation of the electrical activity of the heart
S1 (first heart sound) and S2 (second heart sound)
normal heart sounds
closure of mitral (MV) and tricuspid (TV) valves; softer, longer, low pitch
lower left sternal border/apex (apical pulse)
Where is S1 best heard?
closure of aortic (AV) and pulmonic (PV) valves; shorter, higher pitched
base of the heart at the end of ventricular systole (apex of heart also?)
Where is S2 best heard?
normal heart sounds (S1="lubb", S2="dubb")
"lubb, dee, dubb" (instead of normal "lubb, dubb"); this can be heard with pts with severe myocardial depression; early closure of pulmonic valve/delay in aortic valve disclosure
turbulent blood flow through normal and abnormal valves
when murmurs occur between S1 and S2
when murmurs occur between S2 and S1
"whoosh" sound (whooshing like a waching machine)
due to backflow since valves did not close all the way
pericardial friction rub
originates from the pericardial sac and occurs with movements of heart during cardiac cycle; transient (lasting only a short time)
may be from MI, cardiac tamponade, post-thoracotomy (lung surgery)
fills with blood and can barely pump and need to release pressure from sac or pt will die (emergency=needs intervention stat)
occurs when the heart is squeezed by fluid that collects inside the sac that surrounds it
have pts breathe in and out slowly so can distinguish that it's not a pleural rub which also sounds the same but from breathing instead of with every heart beat
strep (rheumatic fever)
very important to get this treated and not ignore since can go to heart muscle and ruin mitral valve (if not treated)
Black and Hispanic males
highest risk group for CAD (coronary artery disease)
pt history, nutritional history, family history and genetic risk, current health problems (pain or discomfort, dyspnea, DOE, orthopnea, PND, fatigue, palpitations, edema, syncope, extremity pain esp. legs and arms)
cardiovascular system assessment
labored breathing that occurs when lying flat & improves when standing or sitting up. This is one of the classic symptoms of LVHF, although it ocassionally occurs in other cardiac or respiratory illnesses.
DOE (dyspnea on exertion)
SOB after climbing up the stairs or doing regular activity
retaining too much fluid; apparent especially in feet and legs
lightheadedness,fall on floor,loss of consciousness
general appearance (pale, color, pt status/alertness), skin (if pale, color, ), extremities (if cold or warm, pink, rhttp://quizlet.com/18778553/edit/#auto-defineeddish, blue, mottled?), blood pressure and vital signs
cardiovascular system physical assessment
(in order) Inspection, Palpatation, Percussion (nurses don't do this a lot), Auscultation (I.P.P.A. rhymes with "HIPPA)
assessment of the precordium (area over the heart)
normal heart sounds, paradoxical splitting, gallops and murmurs, pericardial friction rub
What to listen for during auscultation?
position pt is in if they have a barrel chest (harder to hear through stethoscope), COPD (this enables them to breathe better), or pericarditis (more pain if laying down)
more plaque if a lot of fatty/meaty foods are consumed (unless vegetarians)
age-related concern for aorta and large arteries
stenotic (as one gets older, stiffer, then stenotic)
As one gets older, this happens: blood gushing back into chambers because not all blood is forced out due to stiffness
KNOW differences: angina, myocardial infarction, pericarditis, pleuropulmonary, esophageal-gastric, anxiety
chest pain assessment
women: fatigue men: indigestion
symptoms for possible heart problems (women and men)
Troponin (T and I), Creatine kinase (CK), Myoglobin, serum lipids, homocysteine, highly sensitive C-reactive protein
serum markers used for myocardial damage
Troponin (Troponin T and Troponin I)
increased levels indicate cardiac necrosis (death tissue) acute MI
Troponin (T and I)
last longest in system (up to 21 days after an MI)
Creatine kinase (CK)
indicates tissue necrosis/injury
CK specific to skeletal muscle
CK specific to myocardial muscle
CK specific to brain
serum lipids (if fats are increased)
risk factor for CAD (coronary artery disease)
cholesterol, triglycerides, HDL & LDL (know numbers)
amino acid from protein breakdown
if increased, risk for CVD (coronary vascular disease)
highly sensitive C-reactive protein
if increased, this will indicate inflammation
highly sensitive C-reactive protein
if increased, risk for HTN (hypertension, infection, smoking
microalbuminuria (protein in urine), blood coagulation studies (PT, PTT, INR), ABG/H&H, F&E (fluid and electrolytes), erthrocyte and leukocyte count
laboratory tests (if possible, have baseline since these will all go up if pt has had a recent MI)
aka cardiac angiogram
feed wire through femoral (groin area), up to the heart, and where arteries are enclosed due to plaque, balloon is inflatted, and stent is put into place so blood flow is restored
indications for cardiac catheterization
confirm heart disease, determine location and extent of disease, assess: stable, severe angina, unstable angina pectoris, uncontrolled heart failure, ventricular dysrhythmias, cardiogenic shock, papillary muscle dysfunction, ventricular aneurysm, septal perforation, determine best therapeutic option, evaluate effects of medical/invasive treatment
if allergic to iodine (or shellfish) (due to dye being injected) (if chronic kidney disease, dye will also affect pt since it's a diuretic)
important thing to find out before cardiac catheterization/angiogram
femoral vein (bigger and preferable), anticubital vein, basilic vein
common sites for cardiac catherization
(similar to post-op pt) restricted to bedrest 4-6 hrs, extremity kept straight, HOB 30 degree or flat supine, monitor VS q15 min x 1 hr, q30 min x 2 hrs, until stable
nursing interventions for cardiac catherization
insertion site for bleeding/hematoma (a solid swelling of clotted blood within the tissues), peripheral pulses if R femoral artery, check distal pulses on R leg, popliteal, and distal-if white, mottled, or cold, might have a clot and dr will have to go back in), color, temperature of affected extremity, observe for pain, chest pain, nausea, discomfort, lightheadedness, cardiac monitoring, I&Os
assessment for after cardiac catherization
limit activity for several days, observe insertion site for swelling, bruising, redness, warmth, pain (signs of infection), leave dressing in place, avoid heavy lifting and exercise, shower okay but avoid baths (do not soak leg)
discharge instructions for cardiac catherization
aka stress test
stress test (exercise electrocardiography)
assess cardiovascular response to increased workload
helps to determine functional capacity of the heart & screens for asymptomatic CAD or dysrhythmias induced by exercise
monitor ECG and BP during pt recovery, instruct pt to avoid how shower for 1-2 hours after procedure (hypotension)
nursing interventions for stress test/exercise electrocardiography
a non-invasive, risk-free test performed at bedside or in MD office; 30-6o minutes to complete the test
uses ultrasound waves to assess for cardiac structure and mobility as well as valve function
helps assess cardiomyopathy, valvular disorders, pericardial effusion, LV function, ventricular aneurysms, cardiac tumors
cardiac blood pooling
evaluates cardiac motion & calculates ejection fraction
leading cause of death in most patients with MI who die before they can be hospitalized
"sudden death" most common and why AED are in a lot of public places now such as stadiums, schools, airports
identify the dysrhythmia, assess hemodynamic status, evaluate for discomfort
intervention for potential dysrhythmias
the study of pressure, flow, and movement of blood
STERILE! wear mask, wash hands, remind DRs, through skin=sterile technique, central line=major infections, site care and dressing changes per protocol, change transducers/lines per protocol, maintain all access ports with sterile and nonvented caps, monitor flush system, zero/calibrate line per protocol
general nursing care of catheters
Myocardial Infrction (MI)
Signs & Symptoms: 'PASS IT ON'
Shortness of Breath
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