Blood Vessels 1a
What causes more morbidity and mortality than any other category of disease?
Diseases of the arteries
What are the two ways that vascular abnormalities cause clinical disease?
Narrowing (Progressively by atherosclerosis or precipitously by thrombosis or embolism), or Weakening of vascular walls to cause dilation or rupture.
What storage organelle is contained in endothelial cells (EC's)?
the storage for Von Willebrand factor which is released when vessel is damaged to activate factor VIII in the clotting cascade.
Which two cells make up the walls of blood vessels?
Endothelial cells and Smooth muscle cells.
What is the vasa vasorum?
The vessels that supply the larger vessels with blood/nutrients.
What are the three types of arteries based on size?
Large/elastic—aorta, pulmonary and other large branches, Medium/Muscular—smaller branches of aorta, coronary, and renal arteries, Small arteries--<2mm.
What controls systemic blood pressure?
Vasoconstriction or vasodilation of arterioles.
What happens to pressure if you half the diameter of a vessel?
It increases by 16 or 2^4.
Which types of arteries are affected by ATH?
Elastic and muscular
Which types of arteries are affected by HTN?
Small muscular and arterioles
What layer is missing in the capillaries?
The media....they are usually the diameter of a RBC (7-8 um)
Where with in the CV system does vascular leakage and leukocytic exudation occur in many types of inflammation?
In postcapillary venules.
Due to poor support what are veins predisposed to?
Irregular dilation, Compression, Easy penetration by tumors and inflammatory processes.
Where is most of the systemic blood found?
66% of systemic blood is in the veins where reverse flow is prevented by valves.
What 5 functions do endothelial cells maintain?
Nonthrombogenic blood-tissue interface, Modulation of blood flow and pressure, Metabolism of hormones, Regulation of immune and inflammatory reactions, and Growth regulation of other cell types (SMC's)
What are the anticoagulant/antithrombotic molecules elaborated by EC's?
Prostacyclin, Thrombomodulin, Plasminogen activator, and Heparin-like molecules.
What are the prothrombic molecules elaborated by EC's?
Von Willebrand, Tissue Factor, Plasminogen activator inhibitor
What are 7 functions of EC's?
Make antithrombotic molecules, Make prothrombotic molecules, Produce ECM, Modulate blood flow, Regulate inflammation and immunity, Regulate cell growth, and oxidation of LDL's
What two things can induce endothelial dysfunction?
Cytokines and Bacterial products.
What do SMC's do?
They are the predominant cell of the tunica media and are important in vascular repair (they proliferate after vascular injury) and pathologic processes like ATH.
What promotes the smooth muscles cells in response to injury?
PDGF, FGF, and IL-1
What inhibits the smooth muscle cells in response to injury?
Heparan sulfates, NO, IFN gamma, and TGF-B.
When does Intimal thickening occur?
In response to vascular injury with acute EC loss or chronic endothelial dysfunction...SMC's migrate from media to intima and multiply as intimal SMC's
What makes SMC's of the vessels unique?
As a healing response, SMC's undergo changes that resemble dedifferentiation and gain ability to divide
What can occur if the vacular healing response is exaggerated?
Intimal thickening that can cause stenosis or occlusion.
What are two important congenital vascular anomalies?
Developmental or berry aneurisms of cerebral vessels or arteriovenous fistulas.
What are intentionally created arteriovenous fistulas used for?
To provide vascular access for hemodialysis.
What are the three forms of arteriosclerosis?
ATH/atherosclerosis is the most frequent and important pattern, Arteriosclerosis—small arteries and arterioles disease with two variants....Hyaline and Hyperplastic.
What 2 diseases is arteriosclerosis most often associated with?
HTN, and diabetes.
What characterizes atherosclerosis?
Intimal lesions/atheromas or fibrofatty plaques.
What causes more mortality and serious morbidity than any other disorder in the western world?
Atherosclerosis....up to 50% of all deaths.
How many deaths occur in the US due to MI?
What is the progression of ATH like?
Normal to fatty streaks to fibrofatty plaques to advanced plaques that can be involved in plaque rupture, plaque erosion, plaque hemorrhage, thrombus, or embolism.
Which vessels are primarily affected by ATH?
Elastic arteries (aorta, corotic, iliac) and large and medium sized arteries (coronary)....usually those that supply the heart, brain, kidneys, and legs.
What are 4 major consequences of ATH?
MI, Stroke, aortic aneurism, or peripheral vascular disease (gangrene of the legs).
What is the clinical significance of ATH in small arteries?
May occlude the lumen entirely or precipitate thrombi that can obstruct or embolize.
What three factors have helped reduce the mortality due to ATH?
Prevention through lifestyle changes (diet/no smoking), Improved treatments, and Prevention of recurrences.
What is a fatty streak?
The presumed precursor for atheromas
What is an atheroma?
Aka: fibrous, fibrofatty plaque--A raised focal lesion that begins in the intima and has a soft, yellow, grumous core of lipid and covered by a firm, fibrous cap.
Where are plaques commonly located in humans?
Around the origins of major branches and more in the abdominal aorta than in the thoracic aorta.
What is the descending order of most commonly involved vessels for ATH?
Lower Abdominal aorta, coronary arteries, Popliteal arteries, internal carotid arteries, and the vessels of the circle of Willis.
Which vessels are not common for ATH?
Upper extremities, mesenteric and renal arteries except at their origins (ostia)
What are the three main components of ATH plaques?
Cells (SMCs, macrophages, leukocytes), ECM, and intra and extrcellular lipids.
What are the typical components of an ATH plaque?
It has a superficial fibrous cap, a shoulder, and a necrotic core.
What are foam cells?
Aka xanthomas---located in the necrotic core of ATH plaqes. They are macrophages full of lipids.
What might occur as ATH plaques continue to mature?
They can become calcified.
What can advanced lesions of ATH lead to?
Rupture, ulceration, or erosion, hemorrhage into a plaque, thrombosis, or aneurismal dilation.
What is the most feared complication due to ATH plaques?
Superimposed thrombosis......can occlude the lumen.
How early to fatty streaks appear in humans?
Some children under 1 and all children over 10.
How might vascular injury and ATH be related?
injury/dysfunction causes SMC's to migrate to intima, these activate macrophages which come and engulf lipids from of the fatty streak to form atheromas that are covered by proliferating SMC's (cap)
What does ATH be most attributed to?
Diet and lifestyle. US has 6X the ATH as in Japan, but Japanese that migrate here and adopt our lifestyle get ATH at same rate.
How does age affect the incidence of ATH and MI?
a dominant influence, between 40 and 60 the incidence of MI increases 5 fold.
How does sex affect MI and other ATH complications?
Pre menopausal women seem to be protected pry by estrogen, but after menopause the rates are comparable. (equalized by 7th or 8th decade)
What are 4 major risk factors for ATH that can be changed?
Hyperlipidemia, HTN, Cigarette smoking, and diabetes.
What are the nonmodifiable risk factors for ATH?
Age, male gender, family hx, genetic abnormalities.
How do LDL's affect ATH?
More LDL's = greater risk
How do HDL's affect ATH?
More HDL's = lower risk.
How can you raise your HDL's?
exercise and moderate ethanol consumption. Smoking and obesity lower HDL's.
How does smoking affect the rate of IHD?
It increases death rate by 200%
How does diabetes affect the risk of ATH induced gangrene of lower extremities?
100X increase in risk. Diabetes also induces hypercholesterolemia which predisposes ATH.
How does elevated homocystine levels (homocystinuria) relate to ATH?
Increased levels lead to all sorts of vascular diseases/ATH, increased levels of homocystine can be due to low dietary intake of folate and vitamin B.
How is C-reactive protein related to ATH?
This is elevated in periodontal disease and other types of inflammation and may induce ATH.
What are some other factors that can affect one's susceptibility to ATH?
Stress, Competition, lack of exercise.
What occurs to the risk for ATH when there are multiple risk factors present?
They become multiplicatitve.....two risk factors = 4 times the risk, three = 7 times the risk, etc.
Can ATH occur w/out any risk factors?
What are the main ideas to the theory for the pathogenesis of ATH?
Endothelial injury increases permeability and leukocyte adhesion, lipoproteins are incorportated into vessel wall, mostly LDL and then these are oxidized and engulfed by migrating macrophages to become foam cells, SMC's proliferate to cap the plaque and more lipids accumulate.
What are three agents that can cause endothelial dysfunction in early ATH?
Dirivatives of cigarette smoke, homocysteine, and possibly viruses and other infectious agents.
What are the two most important determinants in endothelial alterations?
Hemodynamic disturbances that accompany normal circulatory function (at the branches and ostia) and the adverse effects of hypercholesterolemia.
What are 4 disorders that can cause dyslipoproteinemias?
Nephrotic syndrome, Alcoholism, Hypothyroidism, and diabetes.
What can lowering the serum cholesterol do?
Slow the rate of progression of ATH, cause regression of some plaques and reduce the risk of CVA's.
How does hyperlipidemia contribute to ATH genesis?
It can impair the EC function via free oxygen radicals, They deactivate NO, and lipoproteins accumulate w/in the intima at thesites of increased endothelial permeability.
How do antioxidants affect the ATH?
Coronary aterial ATH can be decreased by antioxidant vitamins.
Which cells play important roles in ATH genesis?
Monocytes and macrophages adhere to endothelium, migrate between EC's and release lipids into the intima and engulf lipoproteins to form foam cells.
What is the witches brew made by macrophages?
IL-1, TNF, chemokines, toxic oxygen species, and they elaborate growth factors that may contribute to SMC proliferation.
What role do SMC's play in ATH?
They proliferated and then deposit ECM in the intima to form mature atheromas instead of fatty streaks.
Which bacteria can play a role in ATH genesis?
Clamydia Pneumoniae is most likely....also herpes virus and cmv.
When might a disruption of the fibrous cap with a superimposed thrombus might occur?
Usually associated with catastrophic events.
What are the 6 steps of an atheroma formation leading to thrombosis?
Endothelial dysfunction, Monocyte adhesion and infiltration, Lipid accumulation, SMC proliferation, ECM deposition, and Thrombosis.
What are the 5 ways to prevent ATH?
Stop smoking, control HTN, lose weight, Increase exercise, and most importantly....lower total and LDL blood levels.
At what stage in life does ATH begin?
ATH CAD begins in childhood
What are some secondary preventative measure vs. ATH?
Lipid-lowering drugs (statins), Antiplatelet drugs (ASA, Plavix, )
What is the main issue down stream of atherosclerotic CAD?
Blood Vessels 1c
What is considered hypertension?
Who gets HTN?
Older people and Blacks
What percentage of HTN is idiopathic or essential and compatible with life barring an MI or CVA?
What causes the other 5-10% of HTN cases?
Secondary to renal disease, or Endocrine issues like diseases of the adrenal glands like pheochromocytoma or hypo and hyperthyroidism, also cardiovascular issues or neurologic issues (stress/sleep apnea)
What characterizes malignant HTN?
Severe hypertension with systolic >120, renal failure, retinal hemorrhage with or w/o papilledema.
What determines one's BP?
Multiple genetic, environmental, and demographics.
What two hemodynamic variables determine BP?
CO and Total peripheral resistance.
How do NO, kinins and prostaglandins affect vascular tone?
NO is a vasodilator.
What do Alpha and Beta receptors of the vessels do?
Alpha do vasoconstriction while Beta do vasodilation.
How do kidneys play a role in BP?
Via the rennin-angiotensin system, Angiotensin II raises BP by increasing peripheral resistance and increasing Blood volume via ADH and aldosterone.
What happens in renovascular HTN?
Renal artery stenosis decreases glomerular flow and the pressure in the afferent arterioles which induces the rennin-angiotensin system to raise the BP.
What is a pheochromocytoma?
Tumor of the adrenal that releases catecholamines that cause episodic vasoconstriction and induce HTN seen with neurofibromatosis.
What occurs if you decrease sodium excretion?
You increase fluid volume, CO, and peripheral vasoconstriction which all three work to increase BP.
What are 5 exogenous environmental factors that can contribute to HTN?
Stress, Obesity, Smoking, Physical inactivity, and high salt intake.
What 5 things can HTN cause?
Accelerates atherogenisis, potentiates aortic dissection, and cerbrovascular hemorrhage (large/medium vessels) and in small vessels you might get hyaline arteriolosclerosis or hyperplastic arteriolosclerosis.
Where do you typically see hyaline arteriosclerosis?
Elderly patiens with normal or high BP and common in diabetics....you see pink hyaline thickening of the walls of arterioles.
What issues does hyaline arteriolosclerosis pose in the kidneys?
Diffuse impairment of renal blood supply, loss of nephrons, and symmetric contraction of the kidneys.
What is hyperplastic arteriolosclerosis?
Related to acute or severe elevations in BP, usually over 120 on the diastolic, has onion skin, laminated thickening of arteriole walls with progressive narrowing. Layers are composed of SMC's and BM.
When might you see necrotizing arteriolitis?
In maglignant hypertension and particularly in the kidney.
What is an aneurysm?
Localized abnormal dilation of a blood vessel or of the heart.
What is an arterial dissection?
Arises when blood enters the wall of the artery and dissects between its layers.
What are the most important causes of aortic aneurysms?
ATH and Cystic medial degeneration of arterial media.
What are berry aneurysms?
Congenital defects that are small round dilations, usually in the brain.
What are AAA's?
abdominal aortic aneurisms with the most common cause being ATH and normally located below the renal arteries and above the bifurcation of the aorta and commonly accompanied by smaller fusiform or saccular dilations of the iliac arteries.
What are the two variants of AAA's?
Mycotic and Inflammatory.
What might occur secondarily to AAA's?
Rupture, Obstruction, Embolism, Impingement, and presentation.
What type of aneurysm is related to syphilis?
Syphilis causes endarteritis and can lead to aortic aneurysm of the arch and thoracic aorta but never the root of the aorta.
What can occur secondary to a thoracic aorta aneurysm?
Encroachment on mediastinal structures, encroachment on lungs and airways, difficulty swallowing, persistent cough, pain due to bone erosion, Cardiac diseases or rupture.
Do aortic dissection occur secondarily to aortic dilation?
Not necessarily...can occur without dilation.
When might you see an aortic dissection in a younger patient?
If the patient has Marfan's syndrome.
In what portion of the aorta are dissections most serious?
From the aortic valve to the arch. Proximal lesions are the most dangerous.
What can the pain from an aortic dissection mimic?
That of an acute MI.
What most commonly causes death in a patient with an aortic dissection?
The rupture of the dissection into the pericardial, pleural, or peritoneal cavities.
What are the 3 most common clinical manifestations of an aortic dissection?
Cardiac tamponade, aortic insufficiency, and MI.
What is placation?
The folding and shortening of the aortic wall like an accordion, a surgical approach to repairing an aortic dissection.
What are the two most common mechanisms for vasculitis?
Immune mediated inflammation or direct invasion of vascular wall by infectious pathogens.
Why is it important to distinguish between vasculitis due to direct infections and those that are due to immunologic mechanisms?
Because you treat immune mediated vasculitis with immunosuppressive therapy, but this would be bad in the case of infectious vasculitis.
What evidence is there to show immune complexes are involved in vaculitides?
The lesions resemble those found in Local Arthus reaction, serum sickness, or polyarteritis nodosa which are all type III hypersensitivity reactions.
What causes 10% of vasculitic skin lesions through vascular deposits of immune complexes?
Hypersensitivities to drugs.
With what condition are immune complexes w/complement found in the vascular lesions of patients with vasculitis?
Most frequently with PAN or polyateritis nodosa.
What are pauci-immune vasculitides?
Many small vessel vaculitides show a paucity or scarcity of immune deposits.
What are ANCA's?
antineutrophil Cytoplasmic antibodies---they make up a heterogenous group of autoantibodies directed against enzymes.
What are the two main immunofluorescent patterns of staining of ethanol-fixed neutrophils?
Cytoplasmic localization whit targets proteinase 3 and Perinuclear which is specific for myeloperoxidase.
Which type of ANCA specificity occurs in patienst with ANCA asoociated small vessel vasulitis?
Either may occur, c-ANCA is typically seen in Wegener Granulomatosis and p-ANCA is found in most cases of microscopic polyangiitis but 10% of these patients are ANCA negative.
What role do ANCA's play in vasculitides?
There role is unclea, whether just markers or whether they play a role in tissue injury we don't know.
What are Systemic Lupus Erythematosus and Kawasaki disease associated with?
Antibodies to EC's---to give vasculitides.
What are the 3 ways to classify systemic vasculitides?
By size or site of involved vessels, by histological characteristics of the lesions, or by clinical manifestations.
What is the most common vasculitis?
An acute or chronic inflammation of large to small size arteries principally in the head (temporal, Verterbral, and ophthalmic)
What does eveidence show might cause temporal/giant cell ateritis?
A T-cell mediated immune response to an unknown, possible a vessel wall antigen.
What are symptoms like for temporal arteritis?
Some have only vague constitutional symptoms and for others they have facial pain or headache especially along the couse of the superficial temporal artery.
What size vessels does PAN effect?
Small and medium sized...has to have a muscularis layer, typical in vessels of the belly, but never in the lungs.
What specific vessels are most often affected by PAN?
Kidneys > Heart > Liver > GI tract...never lungs.
Who does PAN most often affect?
It is a disease of young adult but may occur in children or elderly.
What are the common manifestation of PAN?
Malaise, fever, HTN, abdominal pain, Renal involvement is the major cause of death. There is no small vessel involvement so no glomerulonephritis
What has PAN been associated with and what not?
30% patient have Hep B antigen in serum and there is no association with ANCA.
What does Kawasaki disease affect?
Mucous membranes, skin, lymph nodes and blood vessels.
What might play an important role in the pathogenesis of Kawasaki disease?
A pre-existing viral infection which are common in kids (0-10 with 80% younger than 4.)
Which size vessels does Kawasaki's affect?
Large, medium, and small vessels.
What is the leading cause of acquired heart disease in children?
Where might you see erosion and erythema associated with Kawasaki's?
in the Conjunctiva and oral mucosa.
What organ seems to be affected commonly with kawasaki's?
The heart specifically coronary aneurisms (up to 20% if untreated).
Who gets Kawasaki's?
A variety of infectious agents can trigger the disease in a genetically susceptible person.
What is the vasculitis in kawasakis like?
It is much like PAN associated with fibrinoid necrosis, but usually less than in PAN.
What occurs in Wegerner Granulomatosis?
Acute necrotizing granulomas of the URT: ear, nose, sinuses, throat, and oral cavity or LRT. This is in our area.
What size vessels does Wegener's affect?
Small to medium sized...most prominent in lungs and upper airways.
What is unique in how Wegener's affects the kidneys?
You see focal necrotizing in crescentic glomerulonephritis.
What is limited wegener's?
it is limited to the respiratory tract.
What do the lesions of Wegeners look like in the oral cavity?
Ulcerative lesions of the palate...looks like many other dangerous conditions.....
Is there a major pathologic difference between Wegeners vs. mycobacterial or fungal infections?
Yes you will see cavitating masses in the lungs.
Are ANCAs associated with Wegener's granulomatosis?
Yes c-ANCA's are associated with 95% of these patients.
What are the typical clinical features for Wegeners?
Chronic Sinusitis in 90%, and mucosal ulcerations in 75%, Renal disease in 80%, and Pneumonitis in 95%.
What can you use following the disease to monitor possible relapse of Wegeners?
Rising c-ANCA titers.
What is Wegeners often called?
ANCA-associated small vessel vasculitis.
How does Wegener's granulomatosis differ from microscopic polyangiitis?
Wegeners has c-ANCA's in serum with necrotizing granulomas where MP has p-ANCA's in serum with out granulomas
In what size vessels is Buerger Disease common?
Medium and small sized arteries. Specifically common in the tibial and radial arteries.
Who gets Buerger Disease?
Heavy smokers and usually younger than 35, and more common in Israel, Japan, and India than in US. (genetic?;)
What are some unique characteristics of Buergers disease?
It cause phlebitis (veins), you see cold sensitivity (Renauds type) in hands, and may get pain in instep of foot after excersize (instep claudication).
Which type agents can directly invade and cause ateritis?
Bacteria and fungi...most common.
Which size arteries does rheumatoid vasculitis affect?
Small and medium to cause visceral infarction.
What causes Raynauds phenomenon?
Usually secondary to arterial narrowing caused by SLE, scleroderma, ATH, or Buerger disease...might be the first sign of these diseases.
What accounts for 90% of clinical venous diseases?
Who gets varicose veins?
15-20% of the general population eventually and more frequently in those who are standing or sitting for long periods of time at their jobs and most common over 50, obese people, and women.
What often causes varicose veins?
Elastic tissue degeneration or phlebosclerosis (calcification in the media)
Are embolism and other serious complications common with varicose veins?
No, not like with deep vein thrombosis.
What accounts for more than 90% of thrombophlebitis and phlebothrombosis?
Deep leg veins.
What predisposes someone to deep vein thrombosis?
Cardiac failure, neoplasia, pregnancy, obesity, post op, prolonged bed rest.
What is pulmonary embolism?
Common sequel to deep leg thrombosis that can be fatal.
What is the most common type of etiologic agent to spread through the lymphatics to cause acute inflammation of these channels?
Group A—Beta-hemolytic strept.
What commonly occurs when the lymphatics are obstructed?
Lymphedema which will give rise to Peau d'orange appearance of the skin.
What are the 3 types of hemangiomas?
Capillary, Cavernous, and pyogenic granulomas.
What are two intermediate grade neoplasms?
KS, and Hemangioendothelioma
What are two malignant vascular tumors?
Angiosarcoma and Hemangiopericytoma.
What are hemangiomas?
Benign vascular tumor characterized by abnormal vessels filled with blood. Make up 7% of all benign tumors.
Where are the majority of hemangiomas found?
Most are superficial lesions of the head or neck but may occur internally.
What is the single largest type of vascular tumor?
What is a cavernous hemangioma?
It is less common than the capillary type and has large dilated vascular channels. Usually just a cosmetic disturbance.
What is a pyogenic granuloma?
Usually on the gingival or oral mucosa and are the most common intraoral lesion to ulcerate.
What can pyogenic granuloma resemble?
Exuberant granulation tissue.
What is a simple lymphangioma made up of?
Small lymphatic channels. Tends to occur subcutaneously in the head and neck region. AKA capillary lymphangioma
How can you distinguish lymph vessels in simple lymphangioma from capillary channels?
Capillary channels have blood cells in them
What is a cystic hygroma?
A cavernous lymphangioma, made up of massively dilated, cystic lymphatic spaces
In what syndrome are cystic hygromas frequently seen?
What is a vascular ectasias?
Acquired exaggeration of preformed vessels composed of prominent capillaries, venules, and arterioles that creates a small focal red lesion
What is Sturge-Weber syndrome?
Encephalotrigeminal angiomatosis, port wine stains distributed alon trigeminal nerve. Characterized by venous angiomatous masses in leptomeninges over the cortex, and ipsilateral port wine nevi of the face
What is Sturge-Weber syndrome often associated with?
Radiopacities in skull (calcification of Falx Cerebri, mental retardation, seizures, and hemiplegia
Where are spider telangiectasias usually found?
Face, Neck, and upper chest. Most frequent in pregnant women and pts w/ cirrhosis
Where is hereditary Hemorrhagic Telangiectasia found?
AKA Rendu-Osler-Weber Disease. Found distributed widely over skin, and mucous membranes of oral cavity and lips
What can happen in Hereditary Hemorrhagic Telangiectasia?
Rarely rupture leading to serious nose bleeds, bleeding into the gut and hematuria
What causes Bacillary Angiomatosis?
Usually opportunistic infection of immunocompromised persons caused by infection w/ gram-negative bacilli of the Bartonella family
What bacteria causes bacillary angiomatosis and causes cat-scratch disease in immunocompetnet persons?
What are the 4 types of Kaposi sarcoma?
Chronic: classic or European KS, Lymphadenopathic: African or endemic KS, Transplant-associated KS, Aids-associated (epidemic) KS
How does transplant associated KS present?
Several months to a few years postoperatively in solid organ transplant recipients who receive high doses of immunosuppressive therapy. Organ or internal involvement is usually fatal
What group is most likely to get AIDS associated KS?
Male homosexuals with AIDS only 5% of others w/ AIDS
Does KS kill the AIDS pt?
most succumb to opportunistic infectious complications rather than directly to the consequences of KS
What is thought to be the pathogenesis of KS?
Virus-associated (if not virus-caused) neoplasm of primitive mesenchymal or ECs. In AIDS HHV8 plays a major role in etiology of tumors
What are workers in the PVC industry at greater risk for?
Increased frequency of angiosarcomas usually of the liver
3A the Heart
What is a common end point for many types of heart disease?
Congestive heart failure (CHF)
What is CHF?
A pathophysiologic state resulting from impaired cardiac function. The heart is unable to maintain an output sufficient for metabolic requirements of the tissues and organs of the body
What are common causes of CHF?
Coronary artery disease, hypertension, alcohol abuse, heart valve disorders
What can NSAIDs do to a person with underlying heart disease?
Worsen the CHF by sodium retention or affect the power of the heart muscle
Where is the pressure elevated in CHF?
The venous pressure is elevated
What causes the heart to get bigger in CHF?
Hypertrophy of the muscles in the chamber walls
Why is hypertrophic myocardium vulnerable to ischemic injury?
Bigger cells, increased oxygen requirements and the capillary be does not always increase sufficiently to meet increased demands
How does dilation chamber enlargement affect the heart?
Increases wall tension leading to increased O2 demand, the failing myocardium cannot propel sufficient blood to meet need of the body even at rest and the pt enters acute decompensated heart failure (ADHF)
What are the traditional signs of ADHF?
Pitting edema greater than 2mm, and presence of pulmonary rales, increased body
What happens to a pt w/ left sided CHF?
Passive congestion of the pulmonary circulation
What does congestion of pulmonary circulation lead to?
Increased pulmonary vascular resistance and workload on right side of heart leading to right side of heart failing
What are the most common causes of left sided cardiac failure?
Systemic hypertension, mitral or aortic valve disease, ischemic heart disease, and primary diseases of the myocardium
What happens when to maintain cardiac output as left ventricular output decreased?
Leads to decreased perfusion of the kidneys and secondary hyperaldosteronism which increases total plasma volume of extracellular fluid
What does systemic and pulmonary venous congestion lead to?
Pulmonary edema and soft tissue edema
What is Dyspnea?
Sense of breathlessness and the most common manifestation of left side CHF when noticeable lying down as in a dental chair its called orthopnea
What does chronic dilation of left atrium lead to?
Development of atrial fibrillation, manifested by an "irregularly irregular" heartbeat
What is Rales?
Inspiratory crackle or crepitation caused by popping open of small airways and alveoli collapsed by fluid, exudates, or lack of aeration during expiration
What is Ronchi?
Abnormal low pitched continous lung sounds similar to wheezes or snoring. Heard during inhalation or exhalation
What is the most common cause of right sided heart failure?
Left ventricular failure w/ associated pulmonary congestion and elevation in pulmonary arterial pressure
What is Cor pulmonale?
Pulmonary heart disease caused by diseases of lung parenchyma and pulmonary vasculature, pulmonary hypertension. NOT LHF or CHD.
What is long-standing right sided heart failure associated w/ congestion of abdominal viscera, soft tissue edema and in some cases fluid in the pleural, pericardial and abdominal cavities
What happens to the liver in CHF?
Chronic passive congestion leading to atrophy and a nutmeg like appearance. Liver may become fibrotic and in extreme cases cirrhotic
What are the major consequences of right sided CHF?
Systemic venous congestion, and soft tissue edema
How does systemic venous congestion look clinically?
Distended neck veins
What type of fluid is common in pleural and pericardia effusions and ascites due to right sided CHF?
Transudate (low protein)
What is the most common cause of IHD?
Narrowing of the lumina of the coronary arteries by atherosclerosis. Often termed coronary heart disease (CHD) or Coronary artery disease (CAD)
What are 4 myocardial responses to IHD?
Angina pectoris, Acute myocardial infarction, Sudden cardiac death, and chronic ischemic heart disease w/ congestive heart failure
What are acute coronary syndromes?
Acute catastrophic manifestations of IHD including, unstable angina, acute MI, and sudden cardiac death
What is the fundamental disorder underlying IHD?
Severe and chronic atherosclerosis causing narrowing of the lumen of one or more coronary arteries
What are the 3 major variants of angina pectoris?
Typical (stable) angina pectoris, Prinzmental (variant) angina, Unstable angina pectoris. Pain may radiate down the left arm or into the jaw
How does Nitroglycerin work?
Causes venous dilation decreasing the work load of the heart. In larger doses coronary vasodilatation occurs
What is prinzmetal angina?
Variant angina that occurs at rest or awakens pt form sleep. Associated w/ coronary artery spasm
How do unstable angina attacks tend to behave?
Precipitated by progreeively less exertion, more intense, and often last longer than stable angina attacks
How many fatalities are caused by MI each year?
500,000 in the united states. In fatal cases half die before reaching the hospital
What are the two types of MI?
transmural infarct - infarction of the full thickness of the ventrical wall and sub-endothelial infarct
Where do significant plaques occur in a transmural infarct?
Proximal 2 cm of left anterior descending and left circumflex coronary arteries, and proximal and distal thirds of right coronary artery
Where are the 3 most frequent occlusion of coronary arteries?
Left anterior descending coronary artery 40-50%, right coronary artery 30-40%, left circumflex coronary artery 15-20%
What are initial event acute plaque changes?
Erosion, ulceration, fissuring, rupture, and hemorrhagic expansion
How long after onset of complete myocardial ischemia does injury become irreversible?