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NURS 231 SG F21 Disorders of Blood Flow
and Blood Pressure Study Guide Portage
Learning 2024
Disorders of Blood Flow and Blood Pressure Study Guide
Before you get started… The main function of the cardiovascular (circulatory) system is to transport oxygen and nutrients to the tissues for metabolic process, carry waste products to the kidneys and other excretory organs for elimination, and circulate fluids, electrolytes, and hormones needed for body function. Knowing normal A&P will help you understand the pathophysiology of disorders affecting this system. If you need a refresher, review the normal A&P chapter of your pathophysiology text, and/or view Khan Academy Circulatory System and the Heart (14:56)
Many of the disorders we’ll look at are due to issues with arteries. It’s a good idea to understand the artery structure and function: 3 layers.
- Inside layer: tunica intima; composed of endothelial cells; roles: serves as transfer acrossvascular wall, platelet adhesion, blood clotting, modulation of blood flow and vascular resistance, hormone metabolism, immune and inflammatory reactions.
- Middle layer: tunica media; composed of vascular smooth muscle cells that constrict and dilate blood vessels in response to hormonal and neural stimulation.
- Outside layer: tunica external; composed of collagen and elastic fibers.
Skim section on Regulation of Systemic Arterial Blood Pressure as needed; figure 26-6 on p. 635 is especially helpful.
Disorders of Systemic Arterial Blood Flow Define ischemia: Decreased blood supply to a body organ or part, usually due to functional constriction or actual obstruction of a blood vessel.
Define infarction: Necrosis or death of tissues due to local ischemia resulting from obstruction of bloodflow.
Dyslipidemia: imbalance of lipid components (triglycerides, phospholipids, cholesterol) Re: lipoproteins … in summary, LDL is considered the BAD cholesterol and HDL is considered the GOOD cholesterol.
Atherosclerosis Hardening of the arteries characterized by what? The formation of fibrofatty lesions in the initial lining of large and medium sized arteries.
1. Describe the risk factors, pathogenesis and mechanisms involved in the development of atherosclerosis (p. 641-645).
List the risk factors here. Circle the major risk factor and put a line under the risk factors that are modifiable by dietary and lifestyle changes and medications.
- hypercholesterolemia and elevations in LDL cholesterol levels. Hypercholesterolemia is one of several risk factors for atherosclerosis that can be modified by dietary and lifestyle changes and medications.
- increasing age, family history of heart disease, and male sex. Women after menopause.
- Cigarette smoking, obesity and visceral fat, hypertension, and diabetes mellitus are also risk factors for atherosclerosis. -hypertension OR diabetes mellitus increases the risk by twofold.
(injury to cells)
- Migration of inflammatory cells. Monocytes adhere to endothelium > become macrophages that engulf lipoproteins > turns into foam cells (oxidized engulfed LDL).
- Lipid accumulation and smooth muscle cell and proliferation due to growth factors. Foam cell macrophages die, depositing what where? necrotic cellular debris and lipids within the vascular wall.
- Plaque structure consists of a lot (see picture 4 on p. 644). This “vulnerable plaque” can rupture, ulcerate, or erode > leading to what? hemorrhage into the plaque or thrombotic occlusion of the vessel lumen.
Clinical Manifestations: A BIG problem with this disorder is manifestations won’t show until the artery isseverely narrowed or totally obstructed. Manifestations depend on what? depend on the vessels/arteries involved and the extent of vessel obstruction can see: hemorrhage, thrombus formation, emboli, ischemia, infarction
What organs/tissues are most frequently involved? the arteries supplying the heart, brain, kidneys, lower extremities, and small intestine
GREAT summary: Atherosclerosis (6:05) Think for a minute. Do you know someone who has had a heart attack or stroke? Do you know if it was due to atherosclerosis? Did they have any risk factors for atherosclerosis? Which ones?
Arterial Diseases of the Extremities
2. Compare the etiology, pathogenesis, and clinical manifestations of acute arterial occlusion, atherosclerotic occlusive disease (peripheral artery disease), thromboangiitis obliterans (Buerger disease), and Raynaud disease and phenomenon (p. 646-648). Disorder Etiology/Pathogenesis Clinical Manifestations Acute Arterial Occlusion
Real patient with acute arterial occlusion (7:26)
Sudden interruption to blood flow toan affected tissue or organ or limb; commonly caused by what? Most acute arterial occlusions are the common result of an embolus or a thrombus. Less commonly, trauma or arterial spasm caused by arterial cannulation can also cause acute arterial occlusion.
Most emboli start where? in the heart and are caused by conditions that cause blood clots to develop on a heart chamber wall or valve surface
Depends on what? on the artery involved and the adequacy of collateral circulation
List the 7 Presentation Ps: pistol shot (acute onset), pallor, polar (cold), pulselessness, pain, paresthesia, andparalysis
Thrombi arise from where? from erosion or rupture of the fibrous cap of an arteriosclerotic plaque.
Disorder Etiology/Pathogenesis Clinical Manifestations femoral and popliteal arteries). When lesions develop in the lower legand foot, the tibial, common peroneal,or pedal vessels are most commonly affected. The disease is seen commonly with advanced age
Other signs of ischemia? atrophic changes and thinning of skin and subcutaneous tissues of the lower leg and reduced size of leg muscles, weak or absent pedal pulses, foot might be cool to the touch
Describe the color changes with position changes. Limb color blanches with leg elevation because of the effects of gravity on perfusion pressure and becomes deep red when the leg is in the dependent position because of an autoregulatory increase in blood flow and a gravitational increase in perfusion pressure. When it is severe enough and blood flow is restricted enough, can see ulceration and necrosis of the tissues Thromboangiitis Obliterans (Buerger disease)
VERY helpful mnemonic for Buerger disease (9:11, can stop at 1:45)
Inflammatory arterial disorder that causes thrombus formation to occur: notice ‘itis’ in the name?
Affects medium sized arteries in what? usually the plantar and digital vessels in the foot and lower leg. Arteries in the arm and hand may also be affected. Cause unclear but cigarette smoking is involved. Heavy smokers
Describe Pain is the predominant symptom and is usually related to distal arterial ischemia.Sensitivity to cold Early stages: pain in arch of foot and digits. Mod Advanced case: extremity becomes cyanotic when in a dependent position, anddigits may turn reddish blue even when in a nondependent position. thin shiny skin, thick nails Severe Case: Pain at rest, ulceration and necrosis Raynaud Disease, Phenomenon
Johns Hopkins video for Raynaud’s (5:05, can stop at 1:44))
Intense Vasospasm of arteries and arterioles, usually fingers, higher inwomen
Disease – no known cause Phenomenon – due to other disorders/diseases, vasospasm
Triggered by cold temperatures or intense emotion stress
Skin color changes first noted in fingertips, then distally.
Ischemic phase: due to vasospasm = pallor
cyanosis + cold sensation > numbness +tingling. Hyperemic phase: intense redness + throbbing, paresthesias > return to normal.
On to another disorder affecting the arteries … actually a big artery … the aorta!
3. Differentiate the etiology/pathogenesis and clinical manifestations of thoracic aortic aneurysms, abdominal aortic aneurysms, and aortic dissection (p. 648-650). Define aneurysm: an abnormal localized dilation of a blood vessel.
Most common in the aorta. What’s the difference between a true aneurysm and a false aneurysm?A true aneurysm is bounded by a complete vessel wall, and the blood remains within the vascular compartment.
Aortic Dissection (^) Acute, life threatening condition.
Hemorrhage into vessel wall with tearing to form a blood filled pocket. Causes: conditions that weaken the elastic and smooth muscle layers of aorta 2 risk factors:
Major symptom: abrupt presence of excruciating pain, described as tearing or ripping.
Early stages: increased BP
Etiology/Pathogenesis Clinical Manifestations hypertension and degeneration of the medial layer of the vessel wall.
Potential complication of what? proximal lesions involving the ascending aorta only or both the ascending and the descending aorta, are designated type A.
Later: the blood pressure and the pulse rate become unobtainable in one or both arms as the dissection disrupts arterial flow to the arms.
What else? Syncope, hemiplegia, or paralysis of the lower extremities may occur because of occlusion of blood vessels that supply the brain or spinal cord. Heart failure may develop when the aortic valve is involved
Grey’s Anatomy Aortic Dissection (4:54). Pretty cool video.
We’re done with arteries … now on to veins. But first, review summary concepts on p. 651.
Disorders of Venous Circulation Just a reminder … veins move ( oxygenated or deoxygenated? ) blood from the body to left or right? side of the heart. There are 2 mechanisms that prevent retrograde flow: valves and action of leg muscles. Look at figure 26-16. Can you see how healthy valves and activity/exercise helps with venous return? If not, read the content above the figure.
4. Describe the etiology and clinical manifestations of varicose veins (p. 652), chronic venous insufficiency (p. 653), and venous thrombosis (p. 653-654). Disorders Etiology/Pathogenesis Clinical Manifestations
Varicose veins: dilated, tortuousveins of lower extremities.
Most common cause? deep vein thrombosis (DVT)
List here: aching in the lower extremities and edema but can subside with elevation, especially after long periods of standing, may occur. The edema usually subsides at night when legs are elevated. When the communicating veins are incompetent, symptoms are more common
More common in male or female? Higher incidence in obese, and those who stand for long periods of time, e.g. nurses!
Prolonged standing > increases venous pressure and causes dilation/stretching ofvessel wall.
Disorders Etiology/Pathogenesis Clinical Manifestations
not close properly. Reflux of blood causes what?
further venous enlargement, pulling the valve leaflet apart and causing more venous failure Chronic venous insufficiency: persistent venous hypertension in lower extremities
List causes:
increased venous hydrostatic pressure (as with prolonged standing), incompetent valves in the veins, deep vein obstructions (as with DVT), skeletal muscle malfunctions, inflammatory processes, and endothelial dysfunction
Tissue congestion, swelling/edema, thinning atrophy, impaired tissue nutrition.
Necrosis of subQ fat deposits, skin atrophy. Brown pigmentation of skin due to what? hemosiderin deposits resulting from the breakdown of red blood cells
- Ineffective blood flow, retrograde blood flow (backflow of blood). Advanced^ stages: Stasis dermatitis: thin, shiny, bluish brown skin, without subQ tissues, poor healing
Can cause Venous (stasis ulcers) Google venous stasis ulcers … these are really tough wounds to treat.
Venous thrombosis (thrombophlebiti s):thrombus + inflammation
Most common in lower extremities, and can cause pulmonary embolism. YIKES! Critical thinking … how can a DVT cause aPE?
Many
asymptomatic.
Symptoms r/t
what?
List signs and symptoms here:
Presence of thrombus in the accompanying inflammatory response in the vein.
Can be superficial or deep. Which one is more common? DVT
Associated with stasis of blood, increased blood coagulability, and vessel wall injury (“Virchow Triad”).
inflammatory process, including pain, swelling/edema, and deep muscle tenderness. Fever, general malaise, and an elevated white blood cell count and erythrocyte sedimentation rate are accompanying indications of inflammation.There may be tenderness and pain along the vein. Swelling may vary from minimal to maximal Identify examples of each: Stasis: Bed rest and immobilization (longcar/airplane rides)
Hypercoagulability:
Acquired: Oral contraceptives and hormone
DVT survivor story (4:35); pretty
chromaffin tissue, which contains sympathetic nerve cells that release catecholamine.
- Coarctation of the Aorta - a congenital condition in which there is a narrowing inthe area of the arch of the aorta. Narrowing increases resistance to blood flow, causing the left ventricle to increasepressure to overcome resistance.
- Oral Contraceptive Drugs - cause is largely unknown, although it has been suggested that the probable cause is volume expansion because both estrogens and synthetic progesterones cause sodium retention.
Clinical Manifestations: in primary, typically asymptomatic until long term effects on target- organ systems, such as: kidneys, heart, eyes, and blood vessels
Can see Angina (chest pain), MI, Heart failure, atherosclerosis, coronary artery disease, peripheral artery disease, stroke, TIA, Chronic kidney disease/failure, retinopathy but not until later on
Increased perfusion pressure > damage target organs; increased intravascular pressure > damage endothelial cells in vessels > atherosclerosis.
Hypertension > atherosclerosis because it promotes what? Plaque formation & rupture
Predisposed to what conditions? Coronary heart disease, heart failure, stroke, PAD
Hypertension > increases workload of the left ventricle (heart pumps against high pressure in
arteries)Hypertension > nephrosclerosis (glomerular perfusion is decreased)
Hypertension > dementia and cognitive impairment, stroke
Hypertension > microvascular changes in retina (retinopathy)
Take a look at table 26-3. What BP is considered ‘normal’? <120/ < This classification is used for diagnosis and management of hypertension.
Now we’re shifting gears to LOW BP.
6. Define orthostatic hypotension and describe the symptoms, etiology, and pathogenesis (p.659- 660).
Orthostatic hypotension is when BP drops after a person stands after sitting or lying down. Systolic BP drop of 20 mmHg and/or diastolic BP drop of 10 mmHg. May be asymptomatic or have what orthostatic symptoms? Dizziness and syncope, light headed when standing (stand up
Etiology: when moving to standing position, 500-700 ml shifts to lower part of body (that’s 2- cups!). Several normal body responses act to maintain blood pressure with this shift. Without those responses,blood pools in lower extremities > inadequate blood flow to brain > symptoms.
The mechanisms of contributing factors:
✔ Effects of aging: increased arterial pressure instability and deficiencies in circulatory system
✔ Reduced blood volume: just not enough blood circulating around
✔ Bed rest and impaired mobility: reduced plasma volume, decreased venous tone, failed
peripheral vasoconstriction, weakness of skeletal muscles that support veins
✔ Drug-induced hypotension: antihypertensives, antipsychotics
✔ Disorders of autonomic nervous system: sympathetic stimulation increases _heart rate and cardiac contractility, causes constriction of peripheral arterioles and veins; diabetes mellitus and spinal cord injury puts people at risk.
Orthostatic hypotension animation (4:02, can stop at 2:55) GREAT SUMMARY!
Reference: Norris, T. L. (2020). Porth’s Essentials of Pathophysiology, 5th edition. Wolters Kluwer.
