Cardiovascular alterations Flashcards
Arteriosclerosis
a group of disorders that have in common thickening and loss of elasticity of arterial walls.
Atherosclerosis
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
Fatty streak (atherosclerosis)
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.
Fibrous plaque (atherosclerosis)
white, elevated, protruding lesion in an artery that is characteristic of advancing atherosclerosis.
Complicated plaque (atherosclerosis)
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.
Non-modifiable risk factors for atherosclerosis
Age ( increased death rates from ischemic heart disease, IHD). Gender (male death rate for IHD is greater than female). Familial Predisposition
MALL
Mitral- Aortic Left Lung The acronym for remembering that left sided heart/ valve complications will yield symptoms in the lungs.
Modifiable risk factors for Atherosclerosis
hyperlipidemia, Diet ( that is high is saturated fats and cholesterol), hypertension, cigarette smoking, diabetes mellitus, obesity, lack of regular exercise, hyperuricemia, and stress.
Clinical manifestations of atherosclerosis
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
Hypertension
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.
Essential HTN (cause? risk factors?)
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.
Theories on the causes of essential HTN
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
Secondary HTN
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.
Isolated systolic HTN
high systolic, normal diastolic pressures as a result of increased CO, rigidity of the Aorta, or both. Usually in older adults
Renin-Angiotensin mechanism
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.
Systemic/Organ Complications of hypertension
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.
Thrombus (definition, cause, sign)
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.
Embolism (definition, cause, manifestations)
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
Varicose Veins (definition, causes, manifestations, and increased risk for?)
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.
Ischemic Heart Disease (IHD)
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.
Angina Pectoris
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.
Myocardial Infarction (definition, what does the area look like?, manifestations)
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.
How does the heart heal after myocardial infarction?
Heals by scar tissue, usually complete after 6 weeks, but heart muscle is not as efficient.
Complications of myocardial infarction
arrhythmia, left ventricular congestive failure, cardiogenic shock, rupture of muscle wall, thromboembolism
Normal heart valves allow for what 2 functional characteristics?
unimpeded flow, and unidirectional flow.
Stenosis
failure of a valve to open completely
Regurgitation/incompetence
failure of a valve to close completely
aortic stenosis
diminished blood flow from left ventricle into aorta. May lead to symptoms of left sided heart failure (pulmonary congestion…)
Aortic regurgitation
reflux of blood back into the left ventricle (from aorta). MALL symptoms
Mitral stenosis
diminished flow of blood from left atrium to left ventricle. MALL symptoms
Mitral regurgitation
reflux of blood back into the left atrium from the left ventricle. MALL symptoms
Tricuspid regurgitation
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.
Rheumatic Fever
inflammatory disease caused by a delayed immune response to strep throat ( from hemolytic streptococcus).
Rheumatic heart disease
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
Chorea
rapid jerky movements
Heart failure
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
Frank starling effect
refers to the dilation and increase force of contractions of ventricular muscles in response to increased blood volume
Ventricular hypertrophy
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.
Dilation
enlargement of cardiac chamber size. Often a response to chronic increased blood volume and often occurs with hypertrophy
Cardiac Reserve
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
Backward effects of Left Heart Failure
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.
S&S of Left Heart Failure
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
Signs of Acute Pulmonary Edema
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
Backward effects of right heart failure
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.
S&S of Right Heart Failure
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.
Forward effects of Left heart failure
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.
Forward effects of Right heart failure
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
Shock (definition, compensatory mechanisms involved)
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).
Cardiogenic shock
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
A person experiencing cardiogenic shock, due to external compression of the heart, will have visible…?
Jugular veins, even when completely supine, due to increased venous pressure
Hypovolemic shock
low tissue perfusion due to:
- hemorrhage- acute whole (plasma and cells) blood loss >1 liter –> decreased CO, tachycardia, hypotension, vasoconstriction, anxiety.
- burns- loss of plasma proteins and H2O into interstitial areas
- dehydration- excess loss through GI leads to decreased circulating plasma and stimulation of compensatory mechanisms
Neurogenic shock
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
Septic or Toxic shock
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).
Anaphylactic shock
Hypersensitivity reaction to a specific allergen, which causes vasodilation (with increased capillary permeability), hypotension, tachycardia, anxiety, wheezing, coughing, hives, periorbital edema, and laryngospasm
General manifestations of shock
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
Coarctation of the aorta (pediatric disorder)
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.
Patent ductus arteriosus, PDA (pediatric disorder)
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
Kawasaki Disease (pediatric CV disorder)
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.
