Cardiovascular alterations

Question 1

Arteriosclerosis

Answer 1

a group of disorders that have in common thickening and loss of elasticity of arterial walls.

Question 2

Atherosclerosis

Answer 2

thickening and hardening of arterial walls which is caused by deposits of fat and fibrin that harden over time. Sclerosis progresses from a fatty streak to a fibrous plaque, and then ultimately a complicated plaque

Question 3

Fatty streak (atherosclerosis)

Answer 3

A precursor to more advanced lesions and the earliest lesion. They are flat, yellow, lipid filled smooth muscle cell that causes no obstruction of the vessel.

Question 4

Fibrous plaque (atherosclerosis)

Answer 4

white, elevated, protruding lesion in an artery that is characteristic of advancing atherosclerosis.

Question 5

Complicated plaque (atherosclerosis)

Answer 5

calcified fibrous plaque containing various degrees of necrosis, thrombosis, and ulceration. The plaque often causes symptoms, but they don’t generally occur until 60% or more of the tissue’s blood supply is occluded.

Question 6

Non-modifiable risk factors for atherosclerosis

Answer 6

Age ( increased death rates from ischemic heart disease, IHD). Gender (male death rate for IHD is greater than female). Familial Predisposition

Question 7

MALL

Answer 7

Mitral- Aortic Left Lung The acronym for remembering that left sided heart/ valve complications will yield symptoms in the lungs.

Question 8

Modifiable risk factors for Atherosclerosis

Answer 8

hyperlipidemia, Diet ( that is high is saturated fats and cholesterol), hypertension, cigarette smoking, diabetes mellitus, obesity, lack of regular exercise, hyperuricemia, and stress.

Question 9

Clinical manifestations of atherosclerosis

Answer 9

narrowing of vessels leads to ischemic atrophy of tissues, the plaques provide a site for thrombi/emboli formation, which can lead to infarction, plaques also weaken the vessel wall which can lead to aneurysms

Question 10

Hypertension

Answer 10

constant elevated BP > or equal to 140mmHg systolic or 90mmHg diastolic. Diagnosed with these values on at least three clinical visits. HTN depends on any factor that increases the blood volume and/or the peripheral resistance of arteries.

Question 11

Essential HTN (cause? risk factors?)

Answer 11

HTN with unknown cause that affects 95% of people. Risk factors include aging, male gender, and family history of HTN. Also includes smoking, black race, high sodium intake, lack of exercise, hyperchloremia and athersclerosis.

Question 12

Theories on the causes of essential HTN

Answer 12

Increased sympathetic nervous system activity (norepi and epi), overproduction/excess secretions of aldosterone and renin, chronic high sodium intake, prostaglandin deficiencies, and unknown genetic factors

Question 13

Secondary HTN

Answer 13

HTN that is caused by an identifiable systemic disease, 5% of cases. This type is easier to treat cause you can treat more than just the symptoms.

Question 14

Isolated systolic HTN

Answer 14

high systolic, normal diastolic pressures as a result of increased CO, rigidity of the Aorta, or both. Usually in older adults

Question 15

Renin-Angiotensin mechanism

Answer 15

Renal sympathetic nerves secrete renin which ultimately gets converted to angiotensinogen then angiotensin I. Angiotensin I gets converted to Angiotensin II in the lungs and A. II converts to aldosterone in the adrenal cortex. Angiotensin II is a powerful vasoconstrictor. Aldosterone is secreted into plasma and causes increased Na reabsorption and H2O retention.

Question 16

Systemic/Organ Complications of hypertension

Answer 16

Most of these problems are due to accelerated atherosclerosis. Myocardial infarction, left ventricular hypertrophy, CHF, Blurred or impaired vision, papilledema (eyes), Transient ischemic attacks (strokes), Cerebral thromosis, brain aneurysm, encephalopathy, renal insufficiency, renal failure, decreased peripheral circulation and arteriosclerotic aneurysm.

Question 17

Thrombus (definition, cause, sign)

Answer 17

A blood clot that can develop anywhere in the vascular system which leads to narrowing of the vessel. The cause of thrombus formation is injury to a vessel wall which leads to clotting cascade activation and, thus, stasis and pooling of blood. Ischemia to tissue supplied by affected artery is the resulting sign.

Question 18

Embolism (definition, cause, manifestations)

Answer 18

substance that travels in the bloodstream from primary to secondary site which then obstructs the blood flow. It is most commonly caused by a blood clot. Also due to fat, amniotic fluid emboli, air and tumor cells. Manifestation is ischemia or infarction to site distal to obstruction

Question 19

Varicose Veins (definition, causes, manifestations, and increased risk for?)

Answer 19

Tortuous, distended veins where blood has pooled, often the legs. Caused by weak valves, hereditary predisposition, trauma, obesity, or pregnancy. Signs include bulging bluish veins and pooling in legs. These veins increase the risk for thrombi formation.

Question 20

Ischemic Heart Disease (IHD)

Answer 20

a myriad of disorders characterized by inadequate oxygenated blood being supplied to the heart. Most commonly caused by atherosclerosis. Leads to angina pectoris, myocardial infarction, chronic ischemia, death.

Question 21

Angina Pectoris

Answer 21

Chest pain caused by transient, reversible myocardial injury secondary to ischemia. Pain is a squeezing tight feeling that may radiate to lower jaw, left arm or shoulder, and is often related to exertion and relieved by rest and/or vasodilators. Other symptoms= pallor, diaphoresis, dyspnea.

Question 22

Myocardial Infarction (definition, what does the area look like?, manifestations)

Answer 22

IRREVERSIBLE hypoxia and myocardial cell death after 20 minutes of ischemia. Infarction is seen as a central area of necrosis, surrounded by area of injury, surrounded by area of ischemia. Causes release of heart cell enzymes and troponin (most sensitive lab indicator). Manifestations include pain that is more severe/persistant than angina, and not relieved by nitrates, N&V, cool clammy skin, diaphoresis, fever, EKG changes, arrhythmias.

Question 23

How does the heart heal after myocardial infarction?

Answer 23

Heals by scar tissue, usually complete after 6 weeks, but heart muscle is not as efficient.

Question 24

Complications of myocardial infarction

Answer 24

arrhythmia, left ventricular congestive failure, cardiogenic shock, rupture of muscle wall, thromboembolism

Question 25

Normal heart valves allow for what 2 functional characteristics?

Answer 25

unimpeded flow, and unidirectional flow.

Question 26

Stenosis

Answer 26

failure of a valve to open completely

Question 27

Regurgitation/incompetence

Answer 27

failure of a valve to close completely

Question 28

aortic stenosis

Answer 28

diminished blood flow from left ventricle into aorta. May lead to symptoms of left sided heart failure (pulmonary congestion…)

Question 29

Aortic regurgitation

Answer 29

reflux of blood back into the left ventricle (from aorta). MALL symptoms

Question 30

Mitral stenosis

Answer 30

diminished flow of blood from left atrium to left ventricle. MALL symptoms

Question 31

Mitral regurgitation

Answer 31

reflux of blood back into the left atrium from the left ventricle. MALL symptoms

Question 32

Tricuspid regurgitation

Answer 32

reflux of blood back into right atrium from right ventricle. Leads to volume overload, increased systemic venous BP and right sided heart failure. Person may have symptoms of peripheral edema, weight gain, enlarged organs, and distended jugular veins.

Question 33

Rheumatic Fever

Answer 33

inflammatory disease caused by a delayed immune response to strep throat ( from hemolytic streptococcus).

Question 34

Rheumatic heart disease

Answer 34

A genetic predisposition and major cause of acquired cardiac valve disease (usually affecting mitral and aortic valves). 10% of those with rheumatic fever develop this condition. Manifestations include: history of strep throat ( + for hemolytic streptococcus), migratory polyarthritis, SC nodules, marginatum erythema, chorea, behavioral changes

Question 35

Chorea

Answer 35

rapid jerky movements

Question 36

Heart failure

Answer 36

state of abnormal heart functioning where the contractility of the muscle is reduced and CO declines. Onset may be acute or insidious and is related to systolic/diastolic overloading and myocardial weakness

Question 37

Frank starling effect

Answer 37

refers to the dilation and increase force of contractions of ventricular muscles in response to increased blood volume

Question 38

Ventricular hypertrophy

Answer 38

long term compensatory response to increased volume of blood in the ventricles. Allows the ventricle to push excess volume out, but causes increased metabolism of O2 and energy by myocardial cells.

Question 39

Dilation

Answer 39

enlargement of cardiac chamber size. Often a response to chronic increased blood volume and often occurs with hypertrophy

Question 40

Cardiac Reserve

Answer 40

ability of the heart to increase its output under stress. This is accomplished by increasing SV and HR, which can increase output 4-5X normal. With heart failure, persons under stress will experience symptoms cause reserve also fails

Question 41

Backward effects of Left Heart Failure

Answer 41

Failure of left ventricle –> increased volume/pressure in L ventricle –> increase volume/pressure in L atrium –> increased volume in pulmonary veins –> increase volume in pulmonary capillary bed–> transudation of fluid from capillaries to alveoli –> rapid filling of alveolar spaces –> respiratory signs and symptoms.

Question 42

S&S of Left Heart Failure

Answer 42

increased respiratory rate, decreased CO2, lower 02 perfusion to tissues, easily fatigued, weakness, dizziness, loss of potassium, secretion of aldosterone, orthopnea, paroxysmal nocturnal dyspnea, and signs of acute pulmonary edema (ADE) including dyspnea, rales, cyanosis, tachycardia, oliguria, pink tinged sputum

Question 43

Signs of Acute Pulmonary Edema

Answer 43

dyspnea, rales, gasping respirations, tachycardia, extreme anxiety, increased venous pressure, oliguria, cool and clammy skin that is ashen grey to cyanotic, frothy pink-tinged sputum

Question 44

Backward effects of right heart failure

Answer 44

decreased emptying of right ventricle–> increased volume/pressure in R ventricle–> increased volume/pressure in R atrium–> increased V/P in great veins–> increase V in systemic venous circulation–> increased volume in distensible organs (liver spleen)–> increased pressure in capillary line–> systemic S&S like edema.

Question 45

S&S of Right Heart Failure

Answer 45

dependent pitting edema, enlarged spleen and liver with organ dysfunction ( liver inactivates aldosterone, thus, dysfunction leads to more retention,), may see jaundice and coagulation problems, ascites, jugular venous distention, weight gain.

Question 46

Forward effects of Left heart failure

Answer 46

decreased CO–> decreased perfusion to tissues–> decreased blood to kidneys and glands–> increased renin-angiotensin-aldosterone–> increased reabsorption of Na and H2O–> increased ECF volume–> increased total blood volume.

Question 47

Forward effects of Right heart failure

Answer 47

decreased volume from right ventricle to lungs–> decreased return to left atrium and then decreased CO—> forward effects of left sided heart failure ( less perfusion, more renin-aldosterone and retention) –> increased total blood volume

Question 48

Shock (definition, compensatory mechanisms involved)

Answer 48

a syndrome that results in inadequate tissue perfusion. Compensatory mechanisms include: 1. SNS stimulation due to low BP causes secretion of epinephrine (increases speed and contractile force of heart) and norepinephrine (arteriolar vasoconstriction). 2. Anaerobic production of ATP (causes accumulation of lactic acid–> cell rupture/death–> metabolic acidosis). 3. Fluid shifts/ Renal conservation (ICF and interstitial fluid move into vasculature, kidney hormones, vasoconstriction causes depressed organ function).

Question 49

Cardiogenic shock

Answer 49

inadequate tissue perfusion due to 1. cardiac pump failure-usually left ventricle failure from MI. or 2. decreased venous flow- where the problem is not the heart muscle but the external compression of the heart from cardiac tamponade, mediastinal shift, acute pericardial effusion… leads to decreased blood to heart and then decreased CO–> venous system engorged with blood

Question 50

A person experiencing cardiogenic shock, due to external compression of the heart, will have visible…?

Answer 50

Jugular veins, even when completely supine, due to increased venous pressure

Question 51

Hypovolemic shock

Answer 51

low tissue perfusion due to:

1. hemorrhage- acute whole (plasma and cells) blood loss >1 liter –> decreased CO, tachycardia, hypotension, vasoconstriction, anxiety.
2. burns- loss of plasma proteins and H2O into interstitial areas
3. dehydration- excess loss through GI leads to decreased circulating plasma and stimulation of compensatory mechanisms

Question 52

Neurogenic shock

Answer 52

Sudden onset of vasodilation and peripheral pooling due to loss of SNS control of arterioles. Precipitated by drug reactions, spinal cord injury, overwhelming stress reactions, brain injury, and anesthesia

Question 53

Septic or Toxic shock

Answer 53

Shock commonly caused by UTI from E. coli entering via foley catheters. This hyperdynamic shock results in increased temp, with chills and cold, clammy skin, mental confusion, tachycardia, increased respirations, severe hypotension, metabolic acidosis, and anuria. Disseminated intravascular coagulation is a common complication (thrombohemorrhaging).

Question 54

Anaphylactic shock

Answer 54

Hypersensitivity reaction to a specific allergen, which causes vasodilation (with increased capillary permeability), hypotension, tachycardia, anxiety, wheezing, coughing, hives, periorbital edema, and laryngospasm

Question 55

General manifestations of shock

Answer 55

anxiety, confusion, deep and rapid respirations, narrowing of pulse pressure, tachycardia (w/ weak and thready pulse), thirst and dry mouth, decreased urine output (less than 30ml/hr), cool and clammy skin, increased capillary refill time, low body temperature, muscle weakness and fatigue

Question 56

Coarctation of the aorta (pediatric disorder)

Answer 56

congenital defect resulting in the narrowing of the aorta as it leaves the left ventricle. The narrowing results in an increased pressure proximal to the defect (head and upper extremities) and decreased pressure distal to the obstruction. Manifestations include CHF, acidosis and hypotension if the condition is severe. Other signs are weak/absent femoral pulses, poor perfusion, dizziness, headaches, fainting, epistaxis (bloody noses), intermittent claudication.

Question 57

Patent ductus arteriosus, PDA (pediatric disorder)

Answer 57

Condition resulting from the ductus arteriosus (connection b/w the pulmonary artery and aorta) remaining open after birth. This results in shunting of blood b/w the two main arteries which will manifest as signs of CHF, or asymptomatic, machinery-like murmur, widened pulse pressure and bounding pulse

Question 58

Kawasaki Disease (pediatric CV disorder)

Answer 58

Acute self-limiting systemic vasculitis that may result in cardiac sequelea. The cause is unknown and the condition begins with inflammation throughout the vasculature that leads to aneurysms and subsequent calcification and stenosis of the coronary arteries.