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113 Cards in this Set
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Cardiac - Hemodynamics
cardiac ouput (CO) |
amount of blood ejected from L ventricle into aorta each minute, about 8.0L its calculated by multiplying HR x SV.
Stroke Volume (SV) represents amount of blood ejected from L ventricle during each contraction. |
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Cardiac - Hemodynamics
Preload? |
before contraction. all about stretch. represents the VOLUME work of the heart. it is determined by volume of venous return and amount of stretch imposed on the heart.
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Cardiac - Hemodynamics
Afterload? |
after contraction. all about resistance. represents the tension work of the heart. it is determined by the amount of pressure the heart must generate to push blood through aortic valve.
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Cardiac - Vessels
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histamine= ^ blood flow
Serotonin= vasoconstrictor, needed in clotting, Kinins= vasodilator Prostaglandins= E vasodilators, F vasoconstrictors |
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Cardiac - Vessels
all vessels except capillaries have 3 layers in their walls. 1st inner layer is? |
tunica intima- thin layer of endothelial cells that perform a number of functions such as maintain surface for blood flow & vascular reactivity through secretions of constrictors & dilators
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Cardiac - Vessels
other tunica intima (epithelial) functions? |
can remove vaso active agents from blood- produce enzymes that convert precursors to active forms-
produce nitric oxide a dilator & platelet blocker- produce angiotensin II a constrictor- |
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Cardiac - Vessels
2nd middle layer is? |
tunica media- a smooth muscle layer that constricts to regulate diameter of vessel. contraction rely on extra-cellular Ca+, hence Ca+ blocking agents will cause vasodilation-
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Cardiac - Vessels
3rd outer layer is? |
tunica externa (adventitia):
composed of fibrous and connective tissues to support the vessel. |
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Cardiac - ANS stimulation
is by both the parasympathetic & sympathetic systems- |
parasympathetic- through vagus nerve, stimulation produces slowing of HR,
sympathetic- through postganglionic neurons that innervate the heart, stimulation increases HR and contractility |
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Vascular- ANS stimulation
is by sympathetic system- |
sympathetic- controls smooth muscle tone, maintained at state of slight contraction therefore slight constriction, dilation & constriction are a result of altering basal input
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ANS neurotransmitters
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Acetylcholine- postgang NT for parasympathetic. Norepinephrine- NT for postgang. in sympathetic. Sympathetic also react to epinephrine released from adrenal medulla as well as to dopamine-
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Disorder of Arterial Circulation
Hyperlipidemia- What? |
^ risks for atherosclerosis-
major cause of CV disease- contribute to MI, and Stroke |
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Disorder of Arterial Circulation
Hyperlipidemia- |
LDL main carrier of cholesterol
HDL = 50% proteins, carry less cholesterol: Two sites of lipoprotein synthesis: small intestine & liver: HDL thought to clear cholesterol by transport back to liver and excreted To increase HDL moderate alcohol and exercise: Smoking lowers HDL |
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Disorder of Arterial Circulation
Hypercholesterolemia What? |
Primary hypercholesterolemia- genetic basis
Secondary hypercholesterolemia- obesity and high calorie diets, and diabetes mellitus |
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Disorder of Arterial Circulation
Hypercholesterolemia |
all adults > 20 yr need fasting lipoprotein profile done every 5yrs.
Total cholesterol should be: <200mg/dl & HDL > 40 mg/dl |
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Disorder of Arterial Circulation
Hypercholesterolemia Personal recommendations? |
persons with no major risk factors LDL goal of 160mg/dl or less:
. . . with 2 or more major risk factors LDL goal of <130mg/dl . . . with high risk factor (CHD, DM) LDL goal of <100mg/dl . . . with very high risk factors (i.e. acute coronary syndromes) LDL goal of<70 mg/dl |
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Disorder of Arterial Circulation
Atherosclerosis What? |
hardening of the arteries. formation of lesions in the intimal lining of arteries:
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Disorder of Arterial Circulation
Atherosclerosis 3 types. |
fatty streaks: present in children
fibrous atheromatous: clinical atherosclerosis; lesion is gray or pearly white, thickening of vessel COMPLICATED LESION: characterized by hemorrhage, ulceration, and scar tissue deposits. Thrombosis is the most important complication of atherosclerosis. |
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Disorder of Arterial Circulation
Atherosclerosis Cause/Risks |
hypercholesterolemia, > age, family hx. of premature CHD, ^ in males til 7th/8th decade of life, then MI frequency equalizes. MODIFIABLE RISKS? hyperlipidemia, hypertension, smoking, DM type II
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Disorder of Arterial Circulation
Atherosclerosis other causes? |
Homocysteine- ^ levels, ^ risk of atherosclerosis (inhibits elements of anticoagulation & is associated with endothelial damage)
Inflammation- use test CRP (C-reactive protein) which measures systemic inflammation |
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Peripheral Arterial Disease
What? |
disease resulting in occlusion and/or destruction of the arterial circulations in the extremities. most notably the disease affects the lower extremities.
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Peripheral Arterial Disease
Cause/Risks? |
atherosclerosis is most important cause- most common in men in their 7th & 8th decades.
*same risk factors as for atheroscleosis: smoking, DM type II, family hx, ^ cholesterol |
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Peripheral Arterial Disease
How it presents? |
**intermittent claudication** thin skin; atrophy of leg muscle; cool extremity; popliteal and pedal pulses weak/absent; brittle toenails; hair loss; limb color blanches with elevation; becomes deep red when in dependent position
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Peripheral Arterial Disease
Treatment? |
walking (slowly) to the point of claudication is encouraged b/c it will ^ collateral circulation; avoid injury; quit smoking; treat hypertension; decrease lipids; DM management
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Thromboangiitis Obliterans (Buerger disease)
What? |
vasculitis of the med. sized arteries of the hands and feet-
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Arterial Disorders
Thromboangiitis Obliterans (Buerger disease) Why? |
affects men between ages 25-40 who are heavy cigarette smokers-
pain is the predominant symptom of the disorder Tx? stop smoking. |
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Arterial Disorders
Raynaud Disease What? |
disorder of intense spasm of arteries and arterioles in the fingers and, less often, the toes; seen in healthy young women; precipitated by exposure to cold or strong emotions: Hx. of vasospasms
Tx. Protect from trauma, stop smoking, protect from cold, no stress; give Ca+ channel blockers |
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Aneurysm
What? |
abnormal localized dilation of a blood vessel-
most common in aorta a. |
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Aneurysms
Types? |
Berry Aneurysm consists of a small, spherical dilation of the vessel at a bifurcation:
Fusiform Aneurysm involves the entire circumference of the vessel and is characterized by progressive dilatation of the vessel: Saccular Aneurysm extends over part of the circumference of the vessel and appears saclike: |
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Aneurysms
Causes? |
atherosclerosis is most common-
degeneration of the vessel media- |
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Aneurysms
Abdominal Aortic Aneurysms What? |
Aneurysm located most commonly below the level of the renal artery and involve the bifurcation of the aorta and proximal end of the common iliac arteries
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Aneurysms
Abdominal Aortic Aneurysms Why? |
> than 50 more in men than women-
atherosclerosis- hypertension- |
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Aneurysms
Abdominal Aortic Aneurysms How it presents? |
most are asymptomatic; may see a pulsating mass; pain or mild mid-abdominal or lumbar discomfort; sever back pain; stasis of blood may cause thrombus
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Aneurysms
Abdominal Aortic Aneurysms |
ultrasound; echo; CT scans; MRI
Tx: Surgery, replace with Dacron graph Marfans Syndrome may also cause* |
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Aortic Dissection
What? |
a tear in the intimal layer of the vessel that allows blood to enter the vessel wall, dissecting its layers to create a blood-filled cavity.
Acute life threatening condition |
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Aortic Dissection
Why/How? |
men 40-60yr with hx. of hypertension or in younger persons with connective tissue diseases.
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Aortic Dissection
How it presents? |
intense pain described as a 'ripping' or 'tearing' feeling*, BP initially elevated, later drops
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Aortic Dissection
Dx & TX? |
Dx. H&P, TEE, CT scans, MRI
Tx. Medical or surgical, control BP, decrease systolic ejection force- |
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Disorders of Arterial Blood Pressure
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systolic pressure ideally less than 120mmHg; diastolic pressure less than 80mmHg
Mean Arterial Pressure (90-100mmHg)- represents avg pressure in the arterial system during contraction and relaxation, a good indicator of tissue perfusion |
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Disorders of Arterial Blood Pressure
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The components of BP are determined by the CO & the peripheral vascular resistance. It can be expressed as the product of the two (BP = CO x peripheral vascular resistance)
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Mechanisms of BP Regulation
Short Term |
correct temp. imbalance-
CV center in lower pons and medulla- transmits PSN impulses to heart through vagus nerve and SNS impulses through peripheral nerves. |
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Mechanisms of BP Regulation
Short Term. Intrinsic reflexes? |
baroreceptors & chemoreceptor-reflexes essential for rapid short term BP reg.
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Mechanisms of BP Regulation
Short Term. Intrinsic reflexes? |
Baroreceptors- located in walls of vessels (esp. carotid & aorta), and in heart. respond to stretch & send to CV center for adjustment if nec.
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Mechanisms of BP Regulation
Short Term. Intrinsic reflexes? |
Arterial Chemoreceptors- located in carotid & aortic bodies. respond to changes in O2, CO2, & pH in arterial blood.
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Mechanisms of BP Regulation
Short Term. Humoral mechanisms? Renin-angio-aldosterone mech |
kidney responds to decrease in BP, ex-cell fl. volume or Na+ or ^ in SNS activity by releasing Renin, renin= angiotensinogen= angiotensin I= angiotensin II (in lungs) leads to release of aldosterone & ^ sodium reabsorption and constricts arterioles
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Mechanisms of BP Regulation
Short Term. Humoral mechanisms? Antidiuretic hormone (ADH) aka Vasopressin |
released from posterior pituitary d/t decrease in BP or blood volume etc.
Vasopressin has direct constrictor effect on vessels- though not long-term nor does it enhance already induced actions of other constrictors or sodium retainment |
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Mechanisms of BP Regulation
Long term. |
regulation long term rests mostly in the kidneys ability to regulate extra-cell fl. volume.
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Essential or Primary Hypertension
What? |
High blood pressure-
Most common health problem and leading risk factor for CV disorders pre: 120-139 or 80-89 stage 1: 140-159 or 90-99 stage 2: > 160 or > 100 |
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Essential or Primary Hypertension
How it presents? |
usually asymptomatic. until the long-term effects show in affected organs such as kidneys, heart, eyes, and blood vessels
it will ^ LV workload and can cause renal insufficiency |
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Essential or Primary Hypertension
Causes/Why? |
Risk: family hx. race, age, more prevalent in African Americans and more severe; type 2 DM, hyperlipidemia, obesity
Lifestyle: high NA intake, ^ caloric intake, obesity, physical inactivity, excessive alcohol consumption, sleep apnea |
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Essential or Primary Hypertension
Treatment? |
wt reduction, regular physical activity, reduce dietary NA intake, and moderate alcohol.
Pharmacologic tx.: use a stepwise approach |
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Secondary Hypertension
What? |
is hypertension d/t another disease process
only 5 - 10 % of hypertensive cases- many of these can be resolved- < than 30 yr and > than 50 yr **renal disease** |
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Malignant Hypertension
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Secondary w/ accelerated and potentially fatal effects
African-American men, hypertension of preg, renal and collagen diseases: marked ^ in BP Can cause hypertensive encephalopathy Patient may have: HA, restlessness, confusion, stupor, motor/sensory deficits and visual disturbances; coma, convulsions |
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Orthostatic Hypotension
What? |
Abnormal drop in blood pressure on assumption of the standing position
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Varicose Veins
What? |
Dilated or tortuous veins of the lower extremities which can lead to venous insufficiency.
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Varicose Veins
Cause? |
impaired flow in deep venous channels, DVT, pressure on abdominal veins, standing, incompetent valves, wall weakness
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Varicose Veins
How it presents? |
unsightly appearance, aching in the lower extremities, and edema
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Varicose Veins
Common after 50 yr, women. |
treat with elastic support stockings, Sclerotherapy, surgical treatment
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Chronic Venous Insufficiency
What? |
Valve leaflets damaged rendering them incapable of closure, emptying of deep veins cannot occur
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Chronic Venous Insufficiency
How it presents? |
tissue congestion, edema, brown pigmentation of skin, stasis dermatitis, stasis or venous ulcers
Venous ulcers located over the ankle and lower leg (chronic venous hypertension) |
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Venous Thrombosis
What? |
Presence of thrombus in a vein with accompanying inflammatory response in the vessel wall
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Venous Thrombosis
How? |
Vircows Triad: 1) stasis of blood (ex. Immobility) 2) vessel wall injury (ex. Trauma and surgery) 3) increased blood coagulability
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Venous Thrombosis
How it presents? |
50% asymptomatic; fever, general malaise, elevated WBC, and sed rate; + Homans sign
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Chronic Venous Insufficiency
Prevent- Diagnose - Treat |
early ambulation, support stockings, Kendalls, prophylactic anticoagulation, ankle flexion and extension; venography, ultrasonography, D-dimer
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Pericardial Effusion
What? |
an abnormal accumulation of fluid in the pericardial cavity-
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Pericardial Effusion
Cause? |
injury, inflammation, virus, and surgery
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Pericardial Effusion
#1. Complication? |
Cardiac Tamponade
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Cardiac Tamponade
What? |
life-threatening, slows or rapid compression of the heart d/t accumulation of fluid, pus, or blood in the pericardial sac
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Cardiac Tamponade
Diagnostic? |
pulsus paradoxus is key to Dx. of cardiac tamponade.
pulsus paradoxus- a 10 mm Hg or more fall in systolic BP during normal breathing- |
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Pericardial Effusion
Diagnose & Treat |
echocardiogram
Tx.: Pericardiocentesis |
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Acute Pericarditis
What? |
an inflammation of the pericardium due to viral infections, after cardiac surgery, connective tissue disorders
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Acute Pericarditis
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> in men than women
S&S: chest pain, pericardial friction rub, EKG changes Pain relieved by sitting up and leaning forward and slow shallow breathes |
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Acute Pericarditis
Diagnose and Treat |
clinical manifestations, EKG, chest x-ray, echo
Tx.: depends on cause, usually give ASA, NSAIDS |
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Coronary Heart Disease (CHD)
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heart disease d/t impaired coronary blood flow-
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Coronary Heart Disease (CHD)
Normal Circulation |
generally begins with 2 main arteries the RCA & the LCA.
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Coronary Heart Disease (CHD)
RCA- right coronary artery |
the RCA supplies the RV-
it usually branches to form the posterior descending artery (PDA) that supplies posterior heart & papillary muscle, the IVS, and SA & A/V nodes- |
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Coronary Heart Disease (CHD)
LCA- left coronary artery |
the LCA branches anteriorly into the left anterior descending and circumflex arteries. The LAD supplies the LV, anterior IVS and papillary muscle. The circumflex supplies the L lateral wall of LV.
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Coronary Heart Disease (CHD)
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Significant lesions usually occur in first several centimeters of LAD and left circumflex or entire length of RCA
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Coronary Heart Disease (CHD)
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even at normal rest the heart uses 60-80% of the O2 in coronary blood flow- leaves little reserve-
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Coronary Heart Disease (CHD)
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as a general rule: blood flow to the myocardium is greatest during diastole. decreased diastole time decreases O2 delivery*
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Coronary Heart Disease (CHD)
2 types of plaqued lesions? |
fixed/stable-
vulnerable/unstable- |
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Coronary Heart Disease (CHD)
Fixed/Stable Plaque |
obstructs blood flow-
common in stable angina- |
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Coronary Heart Disease (CHD)
Stable Angina? |
CP precipitated by an ^ in the work demands of the heart-
pain is constricting, steady, ^ intensity at onset and end, located substernally may radiate as MI pain- goes away @ rest or with Nitro- |
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Coronary Heart Disease (CHD)
Vulnerable/Unstable Plaque |
^ potential to rupturem cause platelet adhesion, thrombis formation-
common in unstable angina and/or MI |
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Coronary Heart Disease (CHD)
Unstable Angina? |
is more persistent and severe than stable angina, it occurs @ rest, lasts longer than 20 min, pain is severe/frank @ onset, presents a patten that is progressively worse than previously exp.
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Coronary Heart Disease (CHD)
Silent MI |
myocardial ischemia that occurs in the absence of angina-
(DM induced neuropathies) |
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Coronary Heart Disease (CHD)
Variant,Vasospastic Angina |
caused by spasm of coronary arteries. usually during rest, nocturnally.
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Coronary Heart Disease (CHD)
Acute Myocardial Infarction (AMI) |
ischemic death of myocardial tissue-
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Coronary Heart Disease (CHD)
Acute Myocardial Infarction (AMI) How it presents? |
a severe, crushing pain, may radiate to the left arm, neck, and jaw, nausea and vomiting; not relieved by rest or nitroglycerin
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Coronary Heart Disease
(CHD) Acute Myocardial Infarction (AMI) - EKG |
T-wave: represents repolarization of ventricles.
. . . tissue ischemia leads to alterations in repolarization and T-wave inversion. |
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Coronary Heart Disease
(CHD) Acute Myocardial Infarction (AMI) - EKG |
ST segment changes occur during tissue ischemia that produce damage.
transmural injuries usually result in ST segment elevation. injuries to the subendocardium result in ST segment depression. depression |
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Coronary Heart Disease
(CHD) Acute Myocardial Infarction (AMI) - serum markers |
Serum markers include myoglobin, creatine kinase MB (CK-MB), troponin I and troponin T
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Coronary Heart Disease
(CHD) Acute Myocardial Infarction (AMI) - Treatment? |
O2, analgesic agents, ASA, B-adrenergic blockers, nitrates; thrombolytics and revascularization within 60-90 min of symptoms
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Cardiomyopathies
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disorders that affect the myocardium-
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Dilated Cardiomyopathy
What? |
progressive hypertrophy and dilation of the heart muscle. in one or both ventricles.
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Dilated Cardiomyopathy
Cause? |
myocarditis, alcohol & other toxins, metabolic influences, neuromuscular diseases, autoimmune disorders.
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Dilated Cardiomyopathy
How it presents? |
heart failure, EF < 40%, dyspnea on exertion, paroxysmal nocturnal dyspnea, orthopnea, fatigue, ascites, peripheral edema, S3, S4, ventricular arrhythmias, thrombus
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Dilated Cardiomyopathy
Treatment? |
Tx is aimed at cause. decrease workload of heart (decrease preload and afterload
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Infective Endocarditis
What? |
Uncommon, life-threatening infection of the endocardial surface of the heart and valves (may see vegetations to the valves)
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Infective Endocarditis
Why? Primarily 2 factors: |
damaged endocardial surface creates port of entry by which organisms gain access to the CV system. The presence of valvular diseases, prosthetic valves, or congenital defects provide environment ideal for bacterial growth.
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Infective Endocarditis
How it presents? |
fever, S&S of infection, small petechial hemorrhages
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Infective Endocarditis
Dx & Tx |
blood cultures, echo, TEE, antibiotic therapy
Prevent: antibiotics before dental procedures, surgery, urology procedures |
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Rheumatic Heart Disease
What? |
Acute, immune-mediated, inflammatory disease following a group A (B-hemolytic) strep throat infection (1-4 wk after strep)
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Rheumatic Heart Disease
How? |
common school age children 5-15 yrs of age
Most often affects mitral and aortic valves |
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Rheumatic Heart Disease
Dx. and Tx. |
echo, sed rate, C-reactive protein, TEE, antibiotics, anti-inflammatory drugs, After RHD & valvular damage the risks of infective endocarditis ^
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Stenosis: 'narrowing'
Mitral: Cause RHD Aortic: Cause RHD and older persons d/t Ca+ deposits; ^ workload of LV |
SxS will be related to increased L atrial pressure and decreased LV output along with potential thrombi activity-
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Rheumatic Heart Disease
Dx. and Tx. |
echo, sed rate, C-reactive protein, TEE, antibiotics, anti-inflammatory drugs, After RHD & valvular damage the risks of infective endocarditis ^
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Stenosis: 'narrowing'
Mitral: Cause RHD |
Mitral Stenosis SxS will be related to increased L atrial pressure, resistance of flow to LV, and decreased LV output along with potential thrombi activity-
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Stenosis 'narrowing'
Aortic: Causes are RHD, congenital, Ca+ or plaque deposit along the leaflets |
SxS are related to increased resistance of blood flow into aorta, work demands of heart ^, CO declines, LV hypertrophy, declined BP, low pulse amplitudes, syncope
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Regurgitation 'leak'
Aortic: Causes are RHD, failed prosthetic, possible congenital. |
most will be asymptomatic (except for soft systolic murmur) until later. As deformity increases, diastolic pressure falls & LV enlarges as does SV.
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Regurgitation 'leak'
Aortic: |
as disease progresses SxS of LV HF appear such as exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, abnormal drop in diastolic BP, decrease in coronary blood flow, major find is widening in pulse pressure
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Regurgitation 'leak'
Mitral: Causes are RHD, failed prosthetic, ruptured chordae tendineae or papillary muscle, possible congenital. |
characterized by divided LV volume during systole. patho changes usually occur slowly such as ^ in LV end-diastolic volume, augmented preload, reduced or normal afterload
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Regurgitation 'leak'
Mitral: |
also increase in L atrial size, may remain asymptomatic for many yrs, severe progression impedes LV fx, forward SV decreases, L atrial pressure ^, pulmonary congestion ensues, a-fib
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