Cardiovascular & Lympathic System Flashcards
Define the term preload and list the factors that determine preload.
The volume of blood returning to the heart and filling the chamber prior to contraction (the end-diastolic volume). Preload is determined by blood volume and venous return.
Explain what afterload is and how it is influenced.
The resistance to the ejection of blood from the ventricle. It is influenced by the elasticity of the aorta and the diameter of the arteries. The higher the aortic systolic pressure the greater the afterload and workload of the heart.
Describe the baroreceptor reflex.
Baroreceptors located in the aortic arch and carotids respond to the degree of stretch in those blood vessels. Increased pressure stimulates a parasympathetic response to slow down heart rate and reduce contractility, which in turn decreases the blood pressure. Conversely, decreased pressure causes sympathetic activation, speeding up heart rate and increasing contractility and blood pressure.
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.
Blood flow is controlled by pressure, resistance, blood viscosity, the type of flow and compliance.
In order for blood to move through the circulation there is a pressure gradient from the arteries to the vena cava and blood flows down the pressure gradient.
• Resistance to blood flow is a product of the length and diameter of the blood vessels. The greater the length and the smaller the diameter, the greater the pressure in the system and the lower the flow of blood. Changes in the diameter of blood vessels are used to alter blood flow in the short term.
• Blood viscosity influences both blood flow and blood pressure. The thicker (more viscous) blood is, the higher the pressure required to pump it through the system and the lower the flow.
• Vessels that have a greater diameter and are straighter have faster flow at lower pressure than those that are smaller and more torturous. The former vessels have laminar flow where the molecules in the blood move in a straight line, whereas the latter have turbulent flow, which slows down the speed of flow. The degree of elasticity or compliance in the vessel also influences blood pressure. The greater the stretch of the vessel the higher the flow that can be accommodated. Blood pressure overall is a product of cardiac output and peripheral resistance. Cardiac output is controlled by a combination of heart rate and stroke volume
Discuss what is meant by peripheral resistance and how the autonomic nervous system controls peripheral resistance.
Peripheral resistance refers to the degree of resistance to blood flow through the blood vessels. It is controlled by the radius of the arterioles, which is in turn controlled by activation of the autonomic nervous system. Notably, sympathetic stimulation generally causes vasoconstriction but the effect is differentially expressed.
Explain the arterial blood pressure.
The mean blood pressure in the arteries depends on blood volume, peripheral resistance and the degree of elasticity in the arterioles. Up to a certain point, the higher the blood volume is the higher the blood pressure will be. Arterial BP is also increased when peripheral resistance is increased, and when arterioles are stiff.
Describe how the rennin-angiotensin-aldosterone system influences blood pressure.
Increased secretion of renin triggered by a fall in blood pressure increases the rate of conversion of angiotensinogen to angiotensin I, which is in turn converted to angiotensin II by the angiotensin converting enzyme (ACE). Angiotensin II is a vasoconstrictor so it increases the blood pressure through increasing TPR. It also causes aldosterone to be secreted, which causes the kidneys to reabsorb sodium and water, thus increasing blood volume and blood pressure.
Explain how the lymphatic system is involved in fluid movements.
During the interaction between capillary hydrostatic pressure and capillary oncotic pressure, there is a net movement of up to 3 L of fluid per day out of the capillaries into the interstitial space. The lymphatic system absorbs this excess interstitial fluid and returns it to the bloodstream via a series of vein-like channels with one-way valves.
Outline the pathway of lymph flow, from entering the lymphatic system to entering the cardiovascular system.
The fluid enters the lymphatic system and moves towards the thoracic cavity via lymphatic venules and then into lymphatic veins. The fluid in the lymphatic vessels returns to the bloodstream via either the right or left lymphatic ducts, which drain lymph into the right and left subclavian veins, respectively.
Describe the clinical manifestations of a patient with Lymphedema.
- Swollen extremities / extremity oedema
- Thick, rough skin, woody texture of limb
- Heavy limbs
Describe the nursing care of a patient with Lymphedema.
- Thorough skin care (clean, dry and moisturise – in between fingers and toes)
- Promoting lymphatic drainage (compression bandaging/stockngs/pneumatic devices) and limb elevation
- Elasticated graduated compression stockings (legs), compression bandage (arms)
- Monitor size of 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.
Arterial aneurysms form due to weakness of the arterial wall. Destruction of elastin can lead to abnormal dilation of the vessel and collagen destruction can allow the vessel to rupture. This is caused by long-term eroding effects from atherosclerosis and hypertension.
Describe the difference between a true aneurysm and a false aneurysm.
True aneurysm are caused by slow weakening of the arterial wall due to long-term, eroding effects of atherosclerosis and hypertension.
False aneurysm (a traumatic aneurysm) are caused by traumatic break In the vessel wall rather than weakening of the vessel.
List two types of aortic aneurysm and identify the clinical manifestations associated with each one.
Thoracic Aortic Aneurysm: Clinical manifestations:
- Back, neck or substernal pain
- Dyspnoea, stridor, or brassy cough if pressing on trachea
- Hoarseness and dysphagia if pressing on oesophagus or laryngeal nerve
- Oedema of face and neck
- Distended neck veins
Abdominal Aortic Aneurysm (AAA): Clinical manifestations:
- Pulsating abdominal mass
- Aortic calcification noted on X-ray
- Mild to severe midabdominal or lumbar back pain
- Cool, cyanotic extremities if iliac arteries involved
- Claudication (ischaemic pain with exercise, relieved by pain)
Discuss the pathophysiology of atherosclerosis.
The first step in the development of atherosclerosis is damage to the endothelial lining of the vessel wall. This encourages the infiltration of monocytes, which differentiate into macrophages that ingest LDL cholesterol, forming foam cells. The macrophages also release growth factors that stimulate hyperplasia of smooth muscle cells in the vessel wall. These changes cause the vessel lumen to bulge inwards. Over time a fibrous coat (collagen cap) forms over the plaque, and calcium is deposited into the plaque, causing it to harden. The plaque may eventually rupture (develop fissures), causing thrombus formation and obstruction in the affected vessel.
