Week 2- Haemodynamic Dysfunction Flashcards
Define haemodynamics
the factors that govern blood flow
dependent upon the relationship between cardiac output, blood pressure and resistance
What carries blood (oxygenated) to the rest o the body
Aorta
How do we work out cardiac output
HR X SV
Stroke volume = diastole end volume of blood- systole end vol of blood.
What can affect stroke volume
Venous return = pathological conditions (build up in vessels)
Exercise
Contraction= preload, calcium - thyroid disease of noradrenalin all affecting ca2+ (effecting hb) electrolyte imbalances.
Ejection= vascular resistance (clogged)
What can affect hr
Parasympathetic - vagus nerve
Sympathetic
What is an odema
Localised or generalised accumulation of fluid in interstitial space
Outside both the vascular fluid and cellular fluid compartments (in interstitium)
Where can odema occur
Hydrothorax: within thorax, around lungs; also pleural effusion
Hydropericardium: Fluid in the pericardial sac
Hydroperitoneum or ascites: Fluid in the peritoneal cavity
What factors affect intravasvular and interstitial water movement
:
• Increased hydrostatic pressure: Impaired venous return i.e. DVT
• Reduced plasma osmotic pressure (hypo-proteinaemia): Liver cirrhosis,
nephrotic syndrome
• Lymphatic Obstruction: Trauma, fibrosis, neoplastic or post-surgical
• Sodium & Water Retention: Excessive salt intake with renal insufficiency
• Inflammation: Acute or chronic
• Decreased blood volume: Trauma
When would fluid accumulate
When movement of water in tissues (or body cavities) exceeds lymphatic drainage
List types of oedema
Pulmonary
Pitting
Renal
Periorbital
Lymphoedema (red and shiny skin)
Ascites (pregnant looking as in periteneum)
Hyperaemia ( red inflammation.)
Congestion (red or blue)
Describe hyperaemia
Arteriolar dilation causes it
Red tissue due to engorgement of oxygenated blood
Describe hyperaemia
Arteriolar dilation causes it
Red tissue due to engorgement of oxygenated blood
Describe congestion
Passive process from impaired outflow of a tissue
Systemic - cardiac failure
Local congestion- isolated venous obstruction
Blue/ red colour
Deoxygenated hb in affected tissues
Reversible
Compare hyperaemia to congestion
H= active process
C= passive
H= increase blood flow via vasodilation
C-= impaired blood flow
H= during exercise and in inflammation
C= venous obstruction and cardiac failure
H=oxygenated blood is redder
C- deoxygenated blood (cyanosed so blue)
Describe left sided heart failure
Chronic congestion of the lung
Pulmonary congestion and oedema
Caused by aortic valve disease and primary myocardial disease
Feel weak
Not enough blood in body
Blue congestion
Very tired
Describe right sided heart failure
occurs when the right ventricle is unable to pump blood effectively into the pulmonary circulation
Primary symptoms:
-pulmonary embolism (clot blocking pulmonary arteries) can cause this by increase of pressure
-chronic obstructive pulmonary disease (COPD) (vasoconstriction caused by lungs impaired ability to oxygenate blood)
-Congenital heart defects
-Right ventricular infarction : HA involving coronary artery can affect pumping
Secondary symptoms:
-Caused by left sided heart failure causing pulmonary congestion and raised pulmonary arterial pressure
-tricuspid valve disease
Symptoms:
-Congestion and oedema in feet ankles and sacrum
-fatigue and weakness
-Swollen liver and spleen (liver hepotomegaly and spleen spleenomegal)
- jugular vein sitention (elevated pressure in neck)
-Too much blood not being processed by the heart
Shiny red and hot skin (hyperaemia)
What is haemostasis
Process by which blood clots form at sites of injury
Name 2 disorders of haemostasis
Haemorrhagic disorders- excess bleeding)
Thrombotic disorders- blood clots from within intact blood vessel or within heart)
Describe haemostasis and clot formation
- Vascular spasm (vasoconstriction)
Smooth muscles constrict when blood vessel is injured.
Helps limit blood loss
- Platelet plug formation
Placements attracted to site of injury, adhere to exposes collagen (endothelial cells show when injured)
Platelets become activated upon contact with collagen and release chemical signals like ADP to recruit more platyeleyts
These platelets stick to each other causing a temporary plug which seals the wound.
- Coagulation
Enzymatic reactions leads to formation of fibrin mesh which stabilisates this plug forming a clot.
Both intrinsic and extrinsic pathway converge at common pathway. Fibrin weave through placement plug - Clot retraction
Clot undergoes retraction where it contracts nad brings the damage vessel walls closer together
Platelets releases growth factors which stimulate repair of damages vessel - Clot removal
Fibrinolysis occurs to dissolve clot. Plasmin breaks down fibrin mesh allowing normal blood flow.
What is hypoxia
Lack of blood flow to an area
What are the 3 primary causes for thrombus formation
1.endothelial injury
2. Stasis or slowing of the blood
3. Blood-hyper coaguliability
Describe embolism
A mass that is carried by the blood to a site distal to point of origin.
Pulmonary Thrombo-embolism:
• 95% of venous emboli originate from deep leg vein thrombi.
1+ arteries in lungs become blocked by a blood clot
Systemic Thrombo-embolism:
Blood clot travels throug arterial circulation and blocks blood flow in other part of the body
• Emboli travelling within arterial circulation
• 80% arise from intra-cardiac mural thrombi
• 2/3rds associated with left ventricular wall infarcts
• The major sites for arteriolar embolism are lower extremities (75%) and the brain (10%)
List types of embolism
Pulmonary Thrombo-embolism:
• 95% of venous emboli originate from deep leg vein thrombi.
Systemic Thrombo-embolism:
• Emboli travelling within arterial circulation
• 80% arise from intra-cardiac mural thrombi
• 2/3rds associated with left ventricular wall infarcts
• The major sites for arteriolar embolism are lower extremities (75%) and the brain
Fat Embolism
• Microscopic fat globules may be found in the circulation after fractures of the long bones
• Occurring in 90% of individuals with severe skeletal injuries
• Characterised by pulmonary insufficiency, dyspnoea, tachycardia, neurologic symptoms, anaemia
Air Embolism
• Gas bubbles within the circulation can obstruct vascular flow
• Enter circulation during obstetric procedures or as a consequence to chest wall injury
Amniotic Fluid Embolism
• Underlying cause is the infusion of amniotic fluid or foetal tissue into maternal circulation via a tear
in the placental membrane or rupture of the uterine veins.
• Characterised by a sudden sever dysp
Describe infarction and factors affecting it
• An area of ischaemic necrosis caused by lack of blood supply by arterial supply or
venous drainage in a particular tissue.
• Nearly 99% of all infarcts result from thrombotic or embolic event and almost all
result from arterial occlusion.
Factors that affect the development of an infarction include:
1. Anatomy of the vascular supply
2. Rate of occlusion
3. Tissue vulnerability to hypoxia
4. Hypoxe
Describe shock
Body’s tissues and organs do not receive enough blood flow and o2 leading to cell damage and organ failure
Cardiogenic shock= heart failure or function
Cardiomyopathy
Myocardinal infarction (heart attack) or heart valve disease
What is another word for heart attack
Myocardial infarction
how would you assess for right sided heart failure
In an assessment I would ask my patient of any history of COPD, mycardial infarction, congestive heart failure or valvular heart disease.
I would then physicallly assess my patient for symptoms by inspecting if there is any Congestion and oedema in feet ankles and sacrum
i would palpate abdomen for fluid collection due to Swollen liver and spleen (liver hepotomegaly and spleen spleenomegal).
I would assess my patient for elevated blood pressure as a symptom is jugular vein sitention (elevated pressure in neck).
Chest x-ray may show enlargement of right heart, pleural effusions or pulmonary congestion.
prostoglandin function
key mediators of inflammation. They are produced at sites of tissue injury or infection and promote inflammation by increasing blood flow and vascular permeability
brings immune cells and nutrients to area
redness, heat, swelling, pain
Prostaglandins sensitize pain receptors (nociceptors), making them more responsive to other inflammatory mediators like bradykinin.
Identify two chemical mediators of pain.
bradykinin
prostoglanin
bradykinin function
peptide that is produced during inflammation and tissue injury.
It acts on bradykinin receptors, n nociceptive, nerve fibers, leading to pain, vasodilation, and increased vascular permeability.
contributes to the sensation of inflammatory pain and enhances the sensitivity of pain receptors (nociceptors) to other chemical mediators, thus amplifying the pain response.
leading to swelling, redness, and other signs of inflammation.
What are the hallmarks of cancer
Hallmarks of cancer:
1.self-sufficiency in growth signals
2.resistance to growth stop signals
3. Cell immortalisation through action of telomerase
4.angiogenesis : produce new blood vessels
5.Resistance to apoptosis
6.ability to invade and produce metastases
