Cardiac/Vascular nursing exam 2022 with complete solutions.

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, V4 LAD occlusion Septal chest leads V1, V2 LAD occlusion Lateral chest leads I, aVL, V5,V6 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 Prehypertension 120-139 mmHg/ 80-89 mmHg Hypertension stage 1 BP greater than 140-159mmHg/ 90-99 mmHg Abdominal obesity waist circumference greater than >40inches in men smh > 35 inches in women AHA exercise recommendations 30-60 minutes of vigorous activity 3-4 days/week at 50-75% of maximum heart rate for healthy people Hypertension stage 2 SBP> 160 mmHg or DBP >100 mmHg Stage 1 treatment for uncomplicated HTN Thiazide diuretics DASH diet 27% Fat (less than 8% from saturated fats) 18% Protein 55% Carb 1,500-3,000 mg NA Aortic Stenosis Narrowing or stiffening of the aortic valve. Normally a tricuspid valve Causes- Bicuspid valve (2 cusps doing the work of 3) -Calcification -Rheumatic Heart disease of fever (more common with mitral stenosis Remember SAD for side effects (Syncope, Angina, Dyspnea), Pulsus parvus et tardus, LVH (blood backs up into the left ventricle), anemia Aortic stenosis murmur systolic ejection murmur heard at 2nd intercostal space left sternal border s4 heart sounds Pulsus parvus et tardus smaller weak pulse that is slow to rise ischemia Decreased blood flow that is reversible EKG shows St depression, T-wave inversion Injury Lack of blood flow to the heart that persists beyond the ischemic phase. Full muscle thickness damage. EKG shows ST elevation 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 S2 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 Troponin Troponin I and T are located in the myocardium Elevates in 4-6 hours, peaks in 8-12 hours remain elevated for 5-7 days Cardiovascular examination technique Inspection, palpation, percussion and auscultation Stages of shock 1. Compensatory 2. Progressive 3. Refractory Compensatory stage of shock - BP remains within normal limit "Non Progressive stage", MAP decreases 10 -15 mmHg from client's baseline S/S : cold , clammy, hypoactive bowel sounds, decreased urine output Management-Directed toward identifying the cause of shock,Fluid replacement and medication therapy Nursing Interventions-Monitor tissue perfusion by observing changes in LOC, v/s, pulse pressure, urineoutput, lab values Narrowed Pulse Pressure - early indication of decreased stroke volume Reduce anxiety Promote safety Progressive stage of shock " Intermediate stage " Occurs when there is sustained decrease in MAP of more than 20mmHg from baseline Failure of cardiac pump, autoregulatory function of the microcirculation fails Life-threatening emergency Management-.IV fluids, Medications to restore tissue perfusion,Enteral nutritional support Refractory period of shock " Irreversible stage" severe tissue hypoxia with ischemia and necrosis The body is unable to respond effectively to interventions & shock continues Multiple organ dysfunction Restrictive Cardiomyopathy - most rare form of cardiomyopathy think brick wall Heart size is normal but the muscles can't stretch deposits into the cells the make the ventricles stiff resulting in most commonly diastolic dysfunction (systolic dysfunction occurs as it progresses)