How the CVS can fail

Question 1

Vessel wall tension

Answer 1

The amount of pressure applied on the walls of a blood vessel.

The greater the radius of the vessel, the more tension is being applied.

Tension= pressure x radius of vessel

Question 2

Compliance

Answer 2

The change in volume in a vessel/ chamber, caused by change in pressure (stretchiness)

The higher the compliance, the stretchier the vessel.
Veins have a higher compliance than arteries.

Vascular compliance decreases with age due to calcification, disease.

Question 3

Turbulent blood flow

Answer 3

Flow of blood occurs in ‘eddies’.

This is occurs when blood:
Is at high speed
Is branching
Has low viscosity 
Is mixed

Question 4

Laminar blood flow

Answer 4

Straight, uninterrupted blood flow. Flow of blood is slower closer to the vascular walls.

Due to sheer force, laminar flow is atheroprotective.

Question 5

Reasons for blood vessel damage

Answer 5

Trauma- especially iatrogenic interventions, like percutaneous coronary intervention (PCI)

Atherosclerosis

Diabetes

Question 6

Plaque rupture

Answer 6

In an atheroma- occurs when the fibrous cap bursts open.
This causes the content of the atheroma to leak out to the lumen of the vessel.

This triggers an immune response and can form a thrombus which is deadly. Can cause ischemia and hypoxia.

Question 7

Stroke

Answer 7

Rapid loss of brain function due to loss of perfusion to the brain
Haemorrhagic- cerebral blood vessel rupture (internal bleeding).
Cause- Stress, trauma, atherosclerosis, diabetes.

Ischaemic- Blockage of the cerebral vessel.
 Symptoms: FAST
Face
Arms
Speech
Time

Question 8

Blood vessel stresses

Answer 8

High blood pressure

Large diameter= more tension

Low compliance, less response to change in volume.

Turbulent flow

Question 9

Atherosclerosis

Answer 9

Hardening of a blood vessel wall due to fat deposits made from hyperlipidaemia

Question 10

Coronary heart disease

Answer 10

Obstruction of the coronary arteries.

Possible causes:
Atherosclerosis (mainly)
Coronary vasospasm (rapid contraction of vessels)

Symptoms:
Can be asymptomatic
Angina
Dyspnea

Treatment:
Placing stents to widen arteries
Medication
Replacing vessels with synthetic/ grafts

Question 11

Acute myocardial infarction

Answer 11

Dying/dead myocardial tissue due to ischaemia.
Reduces contractility of the heart and its overall function.

Symptoms:
Most of the time, severe chest pain will be felt (spreading down the arm)
Some pains symptoms are atypical (no in normal places)

Question 12

Functions of the endothelium in blood vessels.

Answer 12

1. Blood vessel tone.
   Releases NO which causes vasodilation. Controls perfusion at local factors.
2. Filtration.
   Filters blood/ fluid. Such as; glomerulus, blood brain barrier.
3. Haemostasis: formation of blood clot.
   Secrete cytokines to facilitate this process.
4. Angiogenesis
5. Transcytosis of hormones- movement of hormones across cells
6. Recruitment of WBCs in inflammation

Question 13

Compensation heart failure

Answer 13

Occurs when stress is placed on the heart but the body tries to combat this through homeostatic means - increasing cardiac output

• Increased function of kidneys: increasing blood volume
• Increased sympathetic activity; Higher HR, release of adrenaline and noradrenaline, increased peripheral resistance.

Question 14

Decompensation heart failure

Answer 14

Failure to maintain sufficient circulation despite compensatory means.

Usually a consequence of other conditions/ diseases:
Vascular diseases
Valvular dysfunction
Myocardial infarction
Pneumonia 
Arthythmias

Consequences:

• Poor perfusion in tissues
• Respiratory distress
• Jugular venous tension

Question 15

Treatment of decompensation cardiac failure

Answer 15

Medication:
Nitroglycerin- blood vessel dilation= increased blood flow

Furosemide- diuretic= decreased blood volume, decreases BP

Intervention:
Non-invasive positive pressure ventilation (NIPPV)- supplying gases and pressure support through a mask.

Question 16

Peripheral oedema

Answer 16

Occurs when arterial pressure is too high, hydrostatic pressure in capillaries too high. Forces fluid to stay out of vessels.

Causes swelling in tissue.

Question 17

Sympathetic activity during myocardial infarction

Answer 17

In response to pain and changes in blood volume- noradrenaline and adrenaline are released.

Allows compensatory mechanism:
Increased heart rate

Increase contractility of the heart

Increased peripheral resistance

HOWEVER- increases tendency to have arrhythmias

Question 18

Pulmonary oedema

Answer 18

Build up of fluid in the lungs due to left heart failure.

Left heart is unable to pump enough blood and is too full. This increase hydrostatic pressure in the veins due to blood damming.

Increased hydrostatic pressure in pulmonary circulation causes excess fluid to leave vessels in the lungs.

Consequences:
Impairs gaseous exchange by making diffusion of O2 longer (travel across liquid)—-> dyspnea, orthopnea, hypoxia.

Question 19

Cardiac remodelling

Answer 19

Change to the ventricular muscle in response to injury, due to changes in preload/afterload.
Includes change in:
Size
Shape
Function

Question 20

Ventricular hypertrophy

Answer 20

Type of cardiac remodelling that causes the cardiomyocytes to enlarge in response to injury.

Eccentric HT: dilation of ventricle- increases volume in ventricle
Concentric HT: thicken of muscular wall- increases pressure

Question 21

Chronic low output heart failure

Answer 21

Low cardiac output due to accumulated heart damaged.

Symptoms include:
Swelling of ankles
Ascites (swelling of the abdominal cavity)

Question 22

Angiotensin II

Answer 22

A peptide hormone that causes vasoconstriction, thus increasing blood pressure.

Mainly produced in the lung through angiotensin converting enzyme (ACE), converting it from angiotensin I.

Angiotensin II also helps to increase blood volume by stimulating the secretion of aldosterone and ADH.
Also involved in ventricular hypertrophy and remodelling.

Question 23

Aldosterone

Answer 23

Corticosteroid hormone, secreted by the adrenal cortex.
Acts on the kidneys to reabsorb more NaCl, which causes further absorption of water.

This increases blood pressure and decreases diuresis.

Question 24

ADH

Answer 24

Antidiuretic (peptide) hormone: released from the pituitary gland.

Stimulates the reabsorption of water at the collecting duct in the kidneys.

This increases blood pressure and decreases diuresis.

Question 25

Thiazide drugs

Answer 25

Diuretics that blocks the reabsorption of water at the distal convoluted tube. This increases diuresis and blood pressure

Example: Indapamide

Question 26

Loop diuretics

Answer 26

Blocks reabsorption of water at the loop of Henle.

This increases diuresis and decreases blood pressure.

Example; furosemide

Question 27

Potassium sparing diuretics

Answer 27

Inhibits the binding of aldosterone to its receptors in the cortical collecting duct.

This increases diuresis and decreases blood pressure.

Example: spironolactone

Question 28

Indapamide

Answer 28

THIAZIDE diuretic used to treat high blood pressure.

Question 29

Furosemide

Answer 29

LOOP diuretic drug used to treat high BP.

Question 30

Spironolactone

Answer 30

K+ sparing diuretic used to treat high BP.

Question 31

Angiotensin II synthesis

Answer 31

1. Angiotensinogen is made in the liver.
2. Enzyme renin is made in the kidneys.
3. Stimulates the production of angiotensin I
4. Angiotensin I is converted to II in the lungs using ACE.

Question 32

Symptoms and treatment of heart failure

Answer 32

Fatigue

Peripheral oedema

Paroxysmal nocturnal dyspnea ( breathlessness at night)

Orthopnea

Treatment:
ACE inhibitors- decreased blood pressure
Diuretics- also increase BP
Beta blockers- increase CO, blood flow.

Question 33

Cardiogenic shock

Answer 33

Low perfusion in tissue due to low cardiac output.

Occurs when systolic pressure is <90 mm Hg in most cases