Final Exam: NSG233/ NSG 233 (New 2023/ 2024 Update) Med Surg 3 Exam| Questions and Verified Answers| 100% Correct| Graded A- Herzing
Final Exam: NSG233/ NSG 233 (New 2023/
2024 Update) Med Surg 3 Exam| Questions
and Verified Answers| 100% Correct|
Graded A- Herzing
QUESTION
dissection aneurysm
Answer:
hemorrhage into the vessel wall with longitudinal tearing of the vessel wall to forma a bloodfilled channel
Clinical manifestations: sudden onset of excruciating pain, described as TEARING or RIPPING
QUESTION
PVC (Premature Ventricular Contraction)
Answer:
Irregular rhythm. No Pwave. Wide,bizarre QRS.
Common and harmless
palpations, chest pain, SOB
not frequent- no treatment needed
frequent- medication is needed- amiodarone
QUESTION
Hemorrhage -shock
Answer:
Stop bleeding- pressure
Identify and treat the cause
-BP, +HR, cool clam skin, -H/H(Hgb -7 =Heaven),
Early: restless. Late: metabolic acidosis
QUESTION
Shock- fluid**
Answer:
two large-gauge IV
LR or NS
Blood products for blood loss-give RBC, Platelets, plasma, RBC (+ O2)
QUESTION
Shock symptoms **
Answer:
tachycardia
hypotension
cool/clammy skin
weak peripheral pulses
anxiety
decreased urinary output
low central venous pressure
increase in CO, heart rate
decrease stroke volume
QUESTION
Cardiogenic Shock S&S
Answer:
heart pump fails
-BP
-Cardiac Output
+HR
narrow pulse pressure
S&S: Pain, angina, arrhythmias, fatigue
Correct the cause!
PRIORITY: O2, treat pain, fluids (monitored closely for overload)
Meds: dobutamine, Nitro, dopamine, vasodilator, diuretics, albuterol, quinidine. AE:
photosensitivity, nausea, vomiting, CNS changes
QUESTION
Hypovolemic shock **
Answer:
Reduction of intravascular volume by 15-30 %
Treat underlying cause
Fluid and blood replacement
LR/NS
Blood products: colloids
Vasoactive meds
O2
SS: pale, anxious
tachycardia
hypotension, narrowing pulse pressure
+RR
- Cardiac Out
-urine
Labs: H&H, lactate,
ABGS
Interventions:
Passive leg raise
NO Trendelenburg
Meds: insulin, anti D, antiemetics, vasopressors
first sign: patient bleeding* or loss of fluids
Causes: dehydration, ascites, edema
SPO2: forehead not finger!
QUESTION
Hemoglobin normal range
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heart failure inability of the heart to provide adequate blood to meet the oxygen needs of tissues and organs.
cardiac output measurement of total blood flow through the systemic or pulmonary circulation per minute. affected by HR, myocardial contractility, blood volume and venous return of blood to heart. heart rate x stroke volume = CO
heart contractility the ability of the heart to contract, generating force to pump blood.
heart preload how much the heart stretches out to fill with blood. the ventricles stretch to fill with blood at the end of diastole. preload can be increased by hypertension, aortic valve disease, hypervolemia. preload can be decreased when rapid HR or hypovolemia reduces ventricular filling during diastole.
heart afterload the force the ventricle has to overcome to push blood out. is the peripheral resistance against which the left ventricle must pump. after load depends on the size of the ventricle, wall tension, and arterial BP.
Left sided reduced ejection fraction heart failure (HFrEF) also known as systolic HF. inability to empty during systole, weakened heart muscle and can’t generate enough force to eject blood through aorta
left sided preserved ejection fraction heart failure (HFpEF) also known as diastolic HF. Inability to fill adequately during diastole, primary cause is HTN, results in decreased SV. leads to reduced CO.
right sided heart failure fluid backs up in venous system. caused most often by L sided HF, or RV infarction, pulmonary embolism or Cor pulmonale.
normal ejection fraction 55-65%
Biventricular failure both ventricles have dysfunction which leads to fluid buildup and venous engorgement, decreased perfusion to vital organs.
Acute Decompensated Heart Failure (ADHF) S/S -sudden onset of s/s with decrease in functional status-pulmonary congestion and volume overload-sodium and fluid retention-increase in RR-decrease in PaO2-tachycardic-SOB-pulmonary edema
Chronic heart failure S/S -fatigue-skin changes -dyspnea-neurologic changes-cough -mental and behavioral changes -tachycardia -chest pain-palpitations-edema-weight changes
pleural effusion the build up of excessive fluid between the layers of the pleura outside the lungs.
diuretics 1. loop2. thiazide3. potassium sparing
peripheral artery disease thickening of artery walls which leads to narrowing of the arteries of upper and lower extremities
P wave of ECG beings with the firing of the SA node, it represents depolarization of the atria
QRS complex of ECG represents depolarization from the AV node throughout the ventricles.
T wave of ECG represents repolarization of the ventricles.
Systole depolarization triggers mechanical activity, this is where the heart muscle contracts and ejects blood from the ventricles.
Diastole heart muscle relaxation which allows for filling of the ventricles.
Frank-Starling Law to a point the more the myocardial fibers are stretched, the greater their force of contraction.
SA node “autorythmic group of cells located in the right atrium and is the “”pacemaker”” of the heart. it caused the atrium to squeeze blood into the ventricle and has a pace of about 60-100 beats/min”
AV node autorythmic group of cells located at bottom of right atrium and passes SA nodes signal along. it obey’s SA node but is autorythmic at a slower rate than SA node.
AV bundle (bundle of His) receives electrical signal from AV node and is autorythmic. it can generate its own electrical signal but at a slower rate of 40-60 beats/min. if first two nodes are damaged this is called a heart block and AV bundle sets pace.
bundle branches electrical signal travels from AV bundle travel through these then to cardiac fibers throughout ventricles. there is a branch into each ventricle.
Purkinje fibers fibers in the ventricles that transmit impulses to the right and left ventricles, causing them to contract
Depolarization The process during the action potential when sodium is rushing into the cell causing the interior to become more positive. and potassium is leaving the cells.
Repolarization Return of the cell to resting state, caused by reentry of potassium into the cell while sodium exits the cell.
ECG reading smallest square is 0.04 seconds of time. 5×5 square of these is 0.20 seconds of time
12 lead ECG An ECG that uses 12 leads attached to the patient’s skin; these include the limb leads and chest leads. 6 leads measure electrical forces in the frontal planes. 6 leads measure in the horizontal planes.
calculating HR from ECG Count the number of QRS complexes in 6 seconds and multiply by 10.
Sinus Arrhythmia A sinus rhythm in which the rate varies with respiration, causing an irregular rhythm. it is common in healthy adults and rate remains between 60-100.
Sinus Bradycardia same as sinus rhythm but rate is <60 Sinus Tachycardia has a sinus rhythm but rate is 101-150 Supraventricular tachycardia (SVT) HR of 151-220. rhythm is regular or slightly irregular and p wave may be abnormal or hidden in the preceding t wave. atrial flutter is an atrial tachydysrhythmia identified by recurring, regular, sawtooth-shaped flutter waves that originate from a single ectopic focus in the right atrium, or less often in the left atrium atrial fibrillation is characterized by a total disorganization of atrial electrical activity because of multiple ectopic foci. Premature Atrial Contraction (PAC) irregular heart rhythm characterized by atrial contractions occurring before the expected time. ventricular fibrillation Disorganized, ineffective twitching of the ventricles, resulting in no blood flow and a state of cardiac arrest. Asystole absence of contractions of the heart, ECG shows flat line. Korotkoff sounds series of sounds that correspond to changes in blood flow through an artery as pressure is released. This is the sounds of your heart while taking a BP. Baroreceptors in the arctic arch and carotid sinus that are sensitive to stretch or pressure within the arterial system. stimulation of these receptors caused decrease in HR and peripheral vasodilation. Chemoreceptors chemical sensors in the brain and blood vessels that identify changing levels of oxygen and carbon dioxide and cause changes to respiratory rate and BP. Stroke volume the volume of blood pumped out by a ventricle with each heartbeat Systemic Vascular Resistance (SVR) the force opposing the movement of blood within the blood vessels blood pressure equation BP = CO x SVR determinants of systemic vascular resistance blood viscosityvessel lengthvessel radius blood pressure regulation 1. sympathetic nervous system – first responder to a drop in BP which leads to increased HR, increased cardiac contractility, vasoconstriction, release of renin from kidneys.2. vascular endothelium – regulates and maintains vasodilation and vasoconstriction substances3. renal system – controls sodium excretion, RAAS, Prostaglandins secreted by renal medulla have vasodilator effects lowering BP. 4. endocrine system – SNS causes adrenal medulla to release epinephrine which increases HR and CO which then raises BP. Elevated BP is defined as systolic pressure >120 and and diastolic pressure >80
stage 1 hypertension Systolic: 130-139Diastolic: 80-89
Stage 2 hypertension systolic: >140 diastolic: >90
primary hypertension (essential or idiopathic) is elevated BP without an identifiable cause. accounts for 90-95% of all hypertension cases.
secondary hypertension is elevated BP with a specific cause that often can be identified and corrected.
renin-angiotensin-aldosterone system (RAAS) a hormone cascade pathway that helps regulate blood pressure and blood volume.when BP falls kidneys release Renin, an enzyme that converts angiotensin to angiotensin I. Angiotensin I is then converted to angiotensin II by angiotensin-converting enzymes. A-II is a vasoconstrictor that results in an immediate increase in BP and over a period of hours or days stimulates the adrenal cortex to secrete aldosterone. Aldosterone causes kidneys to retain sodium which raises the BP further.
Prostaglandins effects on BP PGE2 and PGI1 secreted by the renal medulla have vasodilator effect on the systemic circulation which results in decreased SVR and lowers the BP. Prostaglandins oppose the effects of RAAS
HTN risk factors age, smoking, diabetes, weight, alcohol, blacks have higher prevalence. more common in men before middle age, 2-3x more common in women who are on oral contraceptives. after age 64 more common in women.
Thiazide diuretic reduce blood volume and reduce arterial resistance. Middle strength diureticEx: hydrochlorothiazide
loop diuretic greater diuretic effect, reduces blood volume and promote vasodilation. strongest diuretic. Ex: Furosemide
Potassium sparing diuretic weakest diuretic that spares the loss of potassium Ex: spironolactone
Adrenergic inhibitors suppresses the influence of the SNS on the heart, blood vessels and other structures.
B-adrenergic blockers blocks the effects of epinephrine and reduces BP, decreases CO, reduces vasoconstriction. ends with -ololEx: Metoprolol (Lopressor)NOTE: not to be given in someone with asthma
Angiotensin-converting enzyme (ACE) inhibitors Block conversion of angiotensin I to angiotensin II. ends with -prilEx: Lisinopril (Zestril)
Angiotensin II Receptor Blockers (ARBs) Lower blood pressure by blocking the angiotensin II enzyme from causing vasoconstriction. Ends with -sartanEx: Losartan (Cozaar)
Calcium Channel Blockers agents that inhibit the entry of calcium ions into heart muscle cells, causing a slowing of the heart rate, a lessening of the demand for oxygen and nutrients, and a relaxing of the smooth muscle cells of the blood vessels to cause dilation. two types: non-dihydropyridines – Ex: Diltiazem (Cardizem)Dihydropyridines – Ends with -Dipine. Ex: Amlodipine (Norvasc)
Direct Vasodilators Decrease the BP by relaxing vascular smooth muscle and reducing SVR.Ex: Hydralazine
Nitrates relaxes arterial and venous smooth muscle, reducing preload and SVR and lowers BP.Ex: nitroglycerine
first-line drug therapy for HTN thiazide diuretic, calcium channel blocker, ACE inhibitor, and ARB. note: for most patients diuretics are the first drug.
Hypertensive crisis is a term used to indicate either a hypertensive urgency or emergency. occurs when systolic BP is >180 and/or diastolic is >120. Can lead to MI, stroke and seizures.
Hypertensive emergency a situation in which blood pressure is severely elevated and there is evidence of actual or probable target organ damage. often requires hospitalization.
Hypertensive urgency a situation in which blood pressure is severely elevated but there is no evidence of target organ damage and usually does not need hospitalization.
coronary artery disease (CAD) is a type of blood vessel disorder that we consider in the general category of atherosclerosis. it is characterized by fatty lipid deposits that build up on the inside walls of arteries.
CAD stages 1. Fatty streak – lipids accumulate and migrate into the smooth muscle cells. 2. Fibrous plaque – collagen covers fatty streak and vessel lumens become narrowed which reduce blood flow.3. complicated lesion – plaque ruptures, thrombus forms and further narrows or totally occludes vessel.
atherosclerosis condition in which fatty deposits called plaque build up on the inner walls of the arteries
collateral circulation circulation formed by smaller blood vessels branching off from or near larger, occluded blood vessels. small vessels extend and make connections with other surrounding small vessels to bypass occluded artery.
Risk factors of CAD total cholesterol >200Triglycerides >150LDL >130HDL <40 in men or <50 in women and everything else associated with cardiac disease
Lipid lowering agents decrease the levels of lipids that contribute to atherosclerosis and result in blood vessel occlusion by reducing the synthesis of cholesterol. they lower LDL ends with -statinEx: Atorvastatin (Lipitor)
Antiplatelets inhibit platelet aggregationEx: Clopidogrel or baby aspirin
Chronic stable angina chest pain that is primarily caused by atherosclerosis, which results in a long-term but relatively stable level of obstruction in one or more coronary arteries. it is caused by increased demand for oxygen and decreased supply due to blocked arteries.
ST depression inversion of T wave and is associated with myocardial ischemia and indicates a vessel is partially or totally blocked and heart isn’t getting enough oxygen. may be a sign of an impending heart attack
ST elevation hallmark sign of myocardial infarction and indicates the heart has suffered damage, a vessel is blocked.
anticoagulants prevent blood clot formationHeparin – prevents conversion of fibrinogen to fibrin and prothrombin to thrombinWarfarin (Coumadin) – Vitamin K antagonist that interferes with vitamin K dependent clotting factorsEnoxaparin (Lovenox) – low-molecular weight heparin.
Cardiac Glycosides drugs used to increase heart output force and decreases the rate of contractions. used to treat HF Ex: Digoxin
Coronary artery bypass graft a piece of vein from the leg or chest is implanted on the heart to replace a blocked coronary artery and to improve the flow of blood to the heart (AKA bypass surgery)
percutaneous coronary intervention (PCI) balloon-tipped catheter is inserted into a coronary artery to open the artery; stents are put in place
myocardial infarction the occlusion of one or more coronary arteries caused by plaque buildup (heart attack)
aortic aneurysm permanent, localized out pouching or dilation of the vessel wall of aorta. they can occur in more than one location.
Aortic aneurysm classification 1. True a. Fusiform – circumferential and uniform in shapeb. Saccular – pouchlike on one side2. False – disruption of all the arterial walls.
dissection aneurysm hemorrhage into the vessel wall with longitudinal tearing of the vessel wall to forma a blood-filled channel Clinical manifestations: sudden onset of excruciating pain, described as TEARING or RIPPING
DVT (deep vein thrombosis) formation of a blood clot in a deep vein of the body, occuring most commonly in the legs or thighs
chronic venous insufficiency inadequate venous return over a long period due to varicose veins or valvular incompetence
CVI manifestations -lower leg is leathery with brownish appearance -edema-itching eczema -venous ulcers
peripheral arterial disease (PAD) thickening of artery walls which leads to narrowing of the arteries of upper and lower extremities
Varicose veins abnormally swollen veins, usually occurring in the superficial veins of the legs
Peripheral artery disease vs venous insufficiency PAD is when limbs are not getting enough oxygen/nutrients and legs should not be elevated. Pts get relief when you dangle themVenous insufficiency is when blood in the limbs is not able to return to the heart and causes edema. elevating legs facilitates blood return.
PAD surgical interventions bypass surgery which takes a native vein or a synthetic graft and bypasses the blocked artery to restore blood flow to lower limbsEndarterectomy which surgical removes the plaque build up in the arteries to restore blood flow.Stents to widen artery lumen
HF dilation an enlargement of the heart chambers that occurs when pressure in the heart is elevated over time the muscle fibers stretch out in response to the volume of blood in the heart at the end of diastole
HF hypertrophy is an adaptive increase in the muscle mass and heart wall thickness as a slow response to overwork and strain.
HF remodeling change in the structure of the heart over time where it becomes less elliptical and more spherical due to increase in muscle mass. ventricles become larger but are less effective at pumping.
Types of MIs usually damage the left ventricle and are described by the location of damage.The right coronary artery supplies blood to the inferior and posterior walls of the left ventricleThe left anterior descending artery (LAD) supplies blood to the anterior walls. left circumflex artery supplies blood to the lateral walls.
Digoxin toxicity Blurred or yellow visionN/V, anorexia, fatigueBradycardia