Vascular and Lymphatic system Flashcards Preview

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Flashcards in Vascular and Lymphatic system Deck (24):

Define the term preload and list the factors that determine preload.

The pressure on the walls of the ventricles of the volume of blood filling. Preload is influenced by venous return and the compliance of the ventricles. Factors include: Volume, heart rhythm and left ventricular relaxation.


Explain what afterload is and how it is influenced.

It is the resistance to ventricular contraction. Stroke volume. The most common influence on afterload is the vascular tone or resistance to blood flow.


Describe the baroreceptor reflex.

It is one of the body's homeostatic mechanisms that help to maintain blood pressure at nearly constant levels.


Briefly explain each of the factors that contribute to blood pressure and blood flow.

Indicate the main factor that is used to alter blood flow in the short term.

Short-term (within seconds) adjustments are made by alterations in Cardiac Output (CO) and total peripheral resistance, controlled by the autonomic nervous system influences on the heart, veins and arterioles.

Cardiac output: is the measurement of blood flow from the heart through the ventricles, and is usually measured in litres per minute.

Compliance is the ability of any compartment to expand to accommodate increased content.

The volume of the blood: As blood volume increases, pressure and flow increase

The viscosity: of the blood is the thickness of fluids that affect their ability to flow.

Blood vessel length and diameter: the longer the vessel, the greater the resistance and the lower the flow.


Discuss what is meant by peripheral resistance and how the autonomic nervous system controls peripheral resistance.

Peripheral resistance is the resistance of the arteries to blood flow. As the arteries constrict, the resistance increases and as they dilate, resistance decreases.Peripheral resistance is determined by three factors: Autonomic activity, Pharmacologic agents, Blood viscosity

The autonomic nervous system (ANS) controls functions of the internal viscera, blood vessels throughout the body, effectors in the skin and glands, in fact, all organs except voluntarily controlled striated muscle. Its purpose is to adjust these organs so that their activities are most favourable to their own functions and to the balance of activity of the whole body


Explain the arterial blood pressure.

Arterial blood pressure is created by ejection of blood from the heart during systole (cardiac output) and the resistance of flow from the arterial walls (systemic vascular resistance).


Describe how the rennin-angiotensin-aldosterone system influences blood pressure.

When blood volume or sodium levels in the body are low, or blood potassium is high, cells in the kidney release the enzyme, renin. Renin converts angiotensinogen, which is produced in the liver, to the hormone angiotensin I. An enzyme known as angiotensin-converting enzyme found in the lungs metabolizes angiotensin I into angiotensin II. Angiotensin II causes blood vessels to constrict and blood pressure to increase.


Explain how the lymphatic system is involved in fluid movements.

Fluid collects in the interstitial tissue due to reduced capillary pressure.

It is the role of the Lymphatic system to move this fluid back into the cardiovascular system.

In the circulatory system, blood flows from the heart, through the arteries, and into capillaries that surround all cells. When blood reaches the capillaries, a portion of blood plasma (the liquid portion of the blood) seeps out of the capillaries and into the space surrounding cells. That plasma is then known as tissue fluid. Tissue fluid consists of water plus dissolved molecules that are small enough to fit through the small openings in capillaries.

The lymphatic vessels, or lymphatics, form a network around the arterial and venous channels and interweave at the capillary beds. They collect and drain excess tissue fluid, called lymph, that leaks from the cardiovascular system and accumulates at the venous end of the capillary bed. The lymphatics return this fluid to the heart through a one-way system of lymphatic venules and veins that eventually drain into the right lymphatic duct and left thoracic duct, both of which empty into their respective subclavian veins. Lymphatics are a low-pressure system without a pump; their fluid transport depends on the rhythmic contraction of their smooth muscle and the muscular and respiratory pumps that assist venous circulation.


Outline the pathway of lymph flow, from entering the lymphatic system to entering the cardiovascular system.

Tissue fluid is transported from lymphatic capillaries to lymphatic collecting vessels, where along the length of these vessels, lymph nodes occur to filter the lymph and valves occur to prevent backflow of lymph.

Lymph flows from lymphatic vessels into
lymphatic trunks , and finally into collecting ducts where the lymph is disposed into the subclavian veins.


Describe the clinical manifestations and nursing care of a patient with Lymphedema

Enlarged lymph nodes
Increased proliferation of lymphocytes and monocytes

Thorough skin care
Clean, dry and moisturise (in between the fingers and toes).
Promoting lymphatic drainage
Compression bandaging/stockings/pneumatic devices
Limb elevation
Elasticated graduated compression stockings (legs) compression bandage (arms)
Monitor size of the affected limb (use a measuring tape)
Monitor fluid balance and weight
Patient education
Psychological support (Disturbed body image)


Discuss the pathophysiology of an arterial aneurysm.

Occurs when the wall of an artery is weakened. Arterial aneurysms form due to weakness of arterial wall. The main structural proteins of the aorta are collagen and elastin. Collagen provides tensile strength of vessel preventing excessive dilatation. Elastin allows vessel recoil, returns to its original size.
Destruction of elastin can lead to abnormal dilatation of vessel and collagen destruction can allow the vessel to rupture.


Describe the difference between a true aneurysm and a false aneurysm.

• An aneurysm is a dilatation of the artery while pseudo-aneurysm is a walled off collection of blood outside a damaged artery.

• Aneurysm and pseudo-aneurysms can both expand, but pseudo-aneurysms do not rupture with dilatation.

• Mortality of aneurysms is much higher than that of pseudo-aneurysms.


List two types of an Aortic aneurysm and identify the clinical manifestations associated with each one.


Maybe asymptomatic
back, neck or substernal pain
oedema of the face or neck
distended neck veins


pulsations abdominal masses
mild to severe midabdominal or lumbar back pain
Aortic calcification noted on x-ray
Cool clammy, cyanotic extremities if iliac arteries are involved.


Discuss the pathophysiology of atherosclerosis.

Soft deposits of intra-arterial fat and fibrin in the vessel walls that harden over time.

Step 1: Inflammation
begins with injury to endothelial cells that line artery (common risk factors, smoking, hypertension, diabetes, high LDL cholesterol, low HDL cholesterol, stress, infection and periodontal disease.) The injured cells become inflamed and cannot make normal amounts of antithrombic and vasodilating substances, lose the ability to prevent clotting and vasodilate. This causes vasoconstriction, decreased blood flow, ischemia.

Step 2: Formation
Occurs when inflamed endothelial cells express adhesion molecules that bind macrophages, inflammatory and immune cells. Macrophages adhere to injured endothelium and release inflammatory cytokines, the inflammatory process causes toxic oxygen radicals which cause oxidation of LDL cholesterol. The oxidised LDL is engulfed by macrophages which then penetrate into the vessel (called fatty streak, lines the inside on artery) the fatty streaks release growth factors that stimulate smooth muscle cell proliferation, produce collagen and migrate over the fatty streak forming fibrous plaque.


What are the clinical manifestations associated with atherosclerosis?

- Chest pain, angina
- Pains in leg, arm and anywhere that has a blocked artery.
- Shortness of breath
- Fatigue
- Confusion (if blockage affects circulation to brain)
- Muscle weakness in legs from lack of circulation


What are the main focuses in the management for peripheral vascular disease?

- Modifiable risk factors (reduction in)
- Neurological obs
- Doppler ultrasound
- 5 P’s (pain, pulse, pallor, paraesthesia, paralysis)
- Pain Management
- Medication (aspirin, clopidogrel)
- Surgery


What medications are used in the treatment of peripheral vascular disease?

NSAID – Pain and inflammation.  Blood thinner.
300mg-600mg QID enteric coated or dispersible
Gastric irritant – take with food.

Platelet inhibitor – Prevents blood clots from developing
Can be taken in conjunction with Aspirin.


What modifiable risk factors need to be addressed with patients diagnosed with peripheral vascular disease, in order to slow its progression?

 Sedentary lifestyle


Discuss the pathophysiology of acute myocardial infarction.

ST segment elevation myocardial infarction reflects acute myocardial infarction resulting from the rupture or erosion of an atherosclerotic plaque with thrombotic occlusion of an epicardial coronary artery and transmural ischaemia.


Discuss the clinical manifestations associated with acute myocardial infarction.


Chest pain (intense, heavy)
Radiating chest pain that goes to left arm, jaw, back
Unrelieved by nitroglycerin or rest (chest pain)
Sweating (cold)
Hard to breathe (shortness of breath)
Increased heart rate, blood pressure or irregular heart rate
Nausea with vomiting
Going to be anxious and scared


Discuss the characteristics of five complications, which may arise as a result of an acute myocardial infarction.

Arrythmias, disturbances or irregularities of heart rhythm:
Infarcted tissue is arrhythmogenic it affects the generation and conduction of electrical impulses in the heart.

Pump failure:
MI reduces myocardial contractility, ventricular wall motion and compliance, ^risk of heart failure.
Cardiogenic shock:
Impaired tissue perfusion due to pump failure, results when functioning myocardial muscles mass decreases by more than 40%.
Infarct extension:
Extension or reinfarction in the area of original infarction during the first 10 – 14 days after MI. (continued blood flow impairment and ongoing injury, increases necrosis.)

Structural defects:
Necrotic muscle is replaced by scar tissue that is thinner than the ventricular muscle mass, can lead to other complications (aneurysm)


Glyceryl Trinitrate (GTN) is the key drug in the organic nitrate class of medications. Discus GTN’s mechanism of action, indication for use, usual adult dosage and common adverse reactions associated with this medication.

Mechanism of action:

Calcium channel blocker
Direct acting vasodilator, combined reduction of preload and afterload, little effect on vascular resistance and increased CO.
Relaxation of vascular smooth muscles, arterial and venous dilation.
Results in ^ coronary perfusion and O2 delivery ensures more efficient distribution of blood to ischaemic areas of myocardium.

Indication for use:
Used to treat or prevent stable angina and to treat unstable angina and heart failure associated with MI.

Adult dosage:
Tablet: 300-600 microgram every 3-4 min, max dose of 1200-1800 microgram.
Sublingual aerosol: 400-800 microgram (1-2 sprays)
IV infusion: 5-10 microgram/min ^by 5 microgram/min every 3-5 minutes until desired response.
Transdermal patch: related to amount of drug released/ 24h

Adverse reactions:
Facial flushing
Blurred vision
Dry mouth


Describe the clinical manifestations and nursing care of a patient with Lymphedema

- Swelling of part or all of arms or legs, including fingers or toes.
- Swollen lymph nodes
- Felling of heaviness or tightness
- Aching or discomfort, pain
- Recurring infections
- Hardening and thickening of skin (fibrosis)


Identify three drug interactions associated with ACE Inhibitors and two examples where the use of this medication would be contraindicated.

Drug Interactions:
- Loop diuretics – may result in first dose hypotension.
- Lithium – Increased risk of toxicity
- NSAID’s - Increased risk of hyperkalaemia and Decreased hypotensive effect of ACE inhibitors

- Ace inhibitor hypersensitivity
- Angio-oedema or hyperkalaemia