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Cardiac/Vascular nursing exam
Ascending Aorta -
- begins from the aortic valve and extends from the left ventricle of the heart to the aortic arch.
- Supplies the Coronary Arteries Aortic Arch - Supplies the Brachiocephalic Artery, Left Common Carotid Artery, and the Left Subclavian Artery Descending Aorta - major portion of the aorta that extends from the aortic arch to the trunk of the body. It forms the thoracic aorta and abdominal aorta. Coronary Arteries and the myocardium are perfused during - diastole P- wave represents - atrial depolarization Q wave represents - beginning of ventricular depolarization Inferior chest leads - II, III, aVF RCA occlusion Anterior chest leads - V3, V LAD occlusion Septal chest leads - V1, V LAD occlusion Lateral chest leads - I, aVL, V5,V Circumflex occlusion T wave represents - ventricular repolarization Sympathetic nervous system releases - norepinephrine ( causes pupil dilation, increased sweating, increased heart rate, and increased blood pressure)
Parasympathetic nervous system releases - acetylcholine (decreases heart rate, decreases blood pressure, pupils constrict, increases digestion and urinary output) RCA supplies - Right atrium, right ventricle, SA/AV nodes, posterior portion of right bundle branch Occlusion causes AV blocks and bradycardias Circumflex artery supplies - side wall of the left ventricle and posterior portion of Left bundle branch LAD supplies - Anterior portion of heart, portion of the septum, left ventricle, left bundle branch Occlusion causes BBB's, Vtach, Vfib Peripheral vascular resistance - a resistance to the flow of blood determined by the tone of the vascular musculature and the diameter of the blood vessels. It is responsible for blood pressure when coupled with stroke volume. Cardiac output - Stroke volume x heart rate Preload - volume returned to the heart. The force exerted on the walls of ventricle at the end of diastole Contractility - force of myocardial contraction After load - pump or resistance against which the ventricles must pump to open the semilunar valves normal stroke volume - 60 - 130 mL's each beat 4 - 6 L per minute Frank-Starling's Law of the Heart - to a point, the greater the volume of blood in the ventricle at the end of diastole, the more forceful the cardiac contraction Estrogen - decreases LDL oxidation, promotes endothelial vasodilation and enhances glucose metabolism
1 risk factor of stroke -
HTN Sleep Apnea - causes decreased cerebral perfusion, increases coagulability and diurnal HTN
Infarct - Irreversible myocardial necrosis EKG shows Q-wave abnormality Acute Coronary Syndrome - Unstable angina, Stemi, Non-stemi pulsus paroxodus - An alteration of the blood pressure on inspiration Aortic regurgitation - floppy valve causing back flow of blood into the left ventricle (increases preload). Causes- rheumatic heart disease (#1 cause) marfan syndrome, infective endocarditis, trauma signs- Widened pulse pressure, cough, SOB, pulmonary congestion, DeMusset's sign (head shaking with pulse) Aortic regurgitation murmur - Early diastolic murmur heard upon left sternal border pulse alternans - alternating strong and weak pulse in a regular rhythm. associated with heart failure water hammer (Corrigan pulse) - rapidly rising and falling pulse seen with aortic insufficiency S1 heart sounds are caused by - mitral and tricuspid valve closure S2 heart sounds are caused by - pulmonic and aortic valve closure Murmur grades - Grade I: Very faint, barely audible Grade II: Soft, quiet but easily heard Grade III: Moderately loud; no thrill Murmur is as loud as S1 and S Grade IV: Loud, thrill is present Grade V: Very loud, thrill is present GradeVI: Able to be heard with stethoscope off chest; thrill is present Systolic Murmurs - Mitral Regurgitation Physiologic murmurs Aortic Stenosis Mitral valve prolapse Diastolic Murmurs -
Mitral Stenosis Aortic Regurgitation Diastolic murmurs are always pathologic Mitral regurgitation - Floppy valve that causes blood to back up into left atrium and lungs. Causes- Anything that causes the left ventricle to dilate or enlarge PAD risk factors - age >70, smokers(#1 risk factor), diabetic patients, abnormal pulse examination, or other established cardiovascular disease ischemia - St depression 1st non-invasive test to assess PAD - ABI at rest. If results are borderline or normal (>0.9) and symptoms of claudication are suggestive an exercise ABI is recommended ABI Results - PAD is indicated if the ABI is less than 1.0; the lower the ABI, the more severe the disease imaging studies to diagnose PAD - arterial duplex ultrasound, CTA, MRA, and contrast arteriography. In the absence of risk factors, history, signs, or symptoms of PAD. - Do not perform routine screening Treatment for intermittent claudication - Smoking cessation, statin therapy, anti-platelet therapy, Cilostazol (Pletal) for patient's without CHF, diabetic control, exercise therapy(walking 3 times a week for 30-60 mins), surgery AHA lifestyle recommendations to reduce risks of CVD - Reduce saturated fat(less than 5-6% of daily intake), trans fat and sodium intake(less than 2,400 mg a day), moderate-vigorous exercise 3-4 times a week for an average of 40 mins., manage cholesterol and blood pressure Abdominal Aortic Aneurysm S/S - A throbbing feeling in the abdomen Deep pain in the back or the side of your abdomen Steady, gnawing pain in the abdomen that lasts for hours or days CK, and CK-MB - levels rise within 4-6 hours of injury, peak at 12-24 hours and return to normal within 3-4 days Myoglobin - Not cardiac specific Early to rise and early to fall elevate 1-3 hours after injury and peak in 8-12 hours return to normal 12-30 hours
- Most common type
- can be ischemic or non-ischemic (if it is ischemic, coronary arteries should be evaluated) ventricles become stretched and thin NYHA classes of HF - Symptoms occur with Class I unusually high levels of activity Class II moderate levels of activity Class III low levels of activity Class IV at rest of with ADL's or any activity Domains of learning - Cognitive, affective, psychomotor 5 moral virtues for health professionals - compassion, discernment, trustworthiness, integrity, conscientiousness treating hypertension in renal patients - A limited rise in serum creatinine of as much as 35 percent above baseline with ACEIs or ARBs is acceptable and is not a reason to withhold treatment unless hyperkalemia develops JNC8 Na restriction recommendations - 2.4 g per day JNC 8 Exercise recommendations - Engage in regular aerobic physical activity such as brisk walking (at least 30 min per day, most days of the week). Drugs of choice to tx hypertension in african americas - diuretics or CCBs. metabolic syndrome - the presence of three or more of the following conditions: abdominal obesity (waist circum- ference >40 inches in men or >35 inches in women), glucose intolerance (fasting glucose >110 mg/dL), BP >130/85 mmHg, high triglycerides (>150 mg/dL), or low HDL (<40 mg/dL in men or <50 mg/dL in women) aspirin guidelines in uncontrolled hypertension - do not use aspirin in uncontrolled hypertension due to risk of hemorrhagic stroke acute target-organ damage examples - Eyes, kidney, brain, heart encephalopathy, myocardial infarction, unstable angina, pulmonary edema, eclampsia, stroke, head trauma, life-threatening arterial bleeding, or aortic dissection undesirable effects of thiazide diuretics - may cause gout or severe hyponatremia
undesirable effects of ACE/ARB's - teratogenic, angioedema, hyperkalemia undesirable effects of CCB's - severe constipation, gingival hyperplasia undesirable effects of BB's - asthma exacerbation, bronchospasms in patient's with reactive airways disease, may mask symptoms of hypoglycemia in diabetics, second or third degree heart block. systolic murmurs - Aortic and pulmonic stenosis mitral and tricuspid regurgitation diastolic murmurs - mitral and tricuspid stenosis aortic and pulmonic regurgitation Who sets hypertension guidelines? - Joint National Committee (JNC) - NOT COMMISSION! Which agent is NOT a first line HTN therapy according to JNC 8? - Beta-blockers undesirable effects of amiodarone - interstitial lung disease, thyroid issues, sensitivity to sunlight, corneal deposits Bundle branch blocks cause - ventricles to beat in an unsynchronized pattern statins should be initiated - prior to discharge from hospital. (not on admission) irreversible injury to the heart muscle occurs after cells have been deprived of oxygen for - 3 - 4 minutes CHADS score - determines risk of stroke 1st letter of pacemaker settings represent - the chamber that is paced O= none A= atrium V= ventricle D=Dual 2nd letter of pacemaker settings represent - chamber that is sensed
blocked by angiotensin II. causes vasodilation, inhibits platelet aggregation, and leukocyte adhesion, inhibits sheer force and releases small amounts of tPA primary prevention - promoting health and delaying or preventing disease BEFORE it happens. i.e- education, public law and policy, reducing environmental hazards, and chemoprophylaxis secondary prevention - early detection of disease. i.e- treating risk factors such as HTN, high cholesterol before having a cardiac/vascular event tertiary prevention - treatment of disease or health problem to avoid progression and consequences. i.e- stroke and cardiac rehab after a cardiac/vascular event. The 5 A's of cessation guidelines - Ask Advise Assess Readiness Assit Arrange Cue Extinction - simulates a temporary craving for drugs by having clients recall and describe situations that have made them want to use drugs in the past. By repeatedly exposing clients to their own personal triggers, and teaching them tools for dealing with the cravings that arise from these triggers without letting them resort to using drugs, the program causes cravings gradually to weaken and possibly even disappear. Contingency management - In this type of treatment, individuals are rewarded for improved behavior. Some contingency management programs also punish participants for undesirable behaviors. Drugs that increase BP may cause HTN - cyclosporines, NSAID's, oral contraceptives, anti-rejection meds, cold remedies, cough suppressants Angiotensin II - potent vasoconstrictor. ACE inhibiters block the process of Angiotensin I converting into angiotensin II thus decreasing BP Aldosterone - promotes sodium and water retention and increases blood volume ADH - released from the posterior pituitary and enhances water reabsorption a - angiotensinogen -
is produced in the liver and is excreted by the enzyme renin in response to lowered blood pressure. angiotensin I - This form of the hormone is not known to have any particular biological function in itself but, is an important precursor for angiotensin II. As it passes in the bloodstream through the lungs and kidneys, it is further metabolised to produce angiotensin II by the action of angiotensin-converting enzyme decreased blood pressure against baroreceptors in the aortic arch and carotid sinus - causes sympathetic nervous system release. Increases vasoconstriction, increases heart rate increased blood pressure against baroreceptors in the aortic arch and carotid sinus - (volume overload) causes parasympathetic nervous system release, increases vasodilation, decreases heart rate unequal right and left carotid and radial pulses seen with - aortic dissection or local occlusive arterial disease of the peripheral artery BNP measures - stretch of the myocytes U wave represents - repolarization of the purkinje fibers Aortic and pulmonic stenosis murmur - crescendo-decrescendo systolic murmur, ejection click is present, s4 heart sounds mitral regurgitation murmur - holo-systolic or pan-systolic (means it does not change throughout) murmur mitral valve prolapse murmur - mid-systolic click mitral stenosis - opening snap s3 heart sounds - in diastole(early) indicates volume overload s4 heart sounds - also in diastole (late) stiff ventricles. Always bad Aortic and pulmonic stenosis -
