T2: Ischaemia, Infarction and Shock Flashcards
What is the difference between ischaemia and infarction?
Ischemia denotes diminished volume of perfusion, while infarction is the cellular response to lack of perfusion.
Individual cell death in ischaemic injury is called NECROSIS
Tissue necrosis caused by ischaemia is called INFARCTION
What are the main causes of ischaemia?
Causes of ischaemia:
1. Vascular occlusion
(Severe) atherosclerosis
• Thrombosis
• Embolism
• Hyper viscosity (rare)
2.Vasospasm
3.Vascular damage
• Vasculitis
• Rupture (e.g. AAA)
4.Extrinsic compression
• Tumour
5.Mechanical interruption
• Volvulus
• Intussusception
• Torsion
6. Hypoperfusion
• Cardiac failure
Cardiac malformationDescribe the morphology of infarcts.
Most infarcts are wedged shaped due to the architecture and branching of the blood supply. When a vessel branches deeper, the branches expand into a wedge shape. Therefore when an obstruction occurs upstream, the entire wedge shape supplied by the vessel will be affected and infarcted.
White infarcts - organs with a single blood supply
Red infarction - organs with dual blood supply and venous infarction
What does the outcome of ischaemic tissue depend on?
- An alternative blood supply means less damage. Severe ischaemia would be required to cause infarction. Tissues with a dual vascular supply are generally resistant to infarction of a single vessel.
- The duration of the ischaemia: if sustained or prolonged there is irreversible cell injury. If limited cell injury in ischaemia is reversible. E.g. in myocardium, the first 30 minutes are reversible. This is sometimes referred to as the golden hour in which intervention is critical.
- Collateral blood supply.
- How vulnerable the tissues are to ischaemia: e.g. in the brain if a neuron is deprived of blood it, it only requires 3-4 minutes to undergo irreversible cell damage. This is in contrast to the 2-30 minutes of the myocardium. It depends on how metabolically active the cell is.
- The blood oxygen content - in anaemia for example the patient is more vulnerable top infarction.
What are the effects of reperfusion injury?
In general, it is great if done in the golden hour. This is establishing blood flow back to the infarcted area. The act of reperfusion can augment tissue damage. This may be due to the generation of reactive oxygen species by sudden reperfusion of ischaemic tissues.
Healthy cells have defences mechanisms to prevent the oxygen reactive species doing damage. In necrotic tissue, these defences are gone and so the oxygen species can cause further damage through membrane damage, DNA mutation and protein damage. It is also thought that inflammatory cells recruited by cytokines released during the ischaemic process, that are allowed to flow into the tissue can cause damage. There is also thought to be a role in activation of the complement pathway.
What are the pathological process of shock?
Impaired tissue perfusion leads to ischaemia with derangement of cellular biochemistry which leads to end organ dysfunction and the multi-organ failure which can cause eventually death.
Shock is essentially ischaemia on a systemic level. It is eventually but actually becomes irreversible. Mortality in shock is very high. It is the cause of death in many patients.
Mean arterial pressure = cardiac output * total peripheral resistance
Shock comes from decreased mean arterial pressure or total peripheral resistance. Mean arterial pressure can be decreased due to:
- reduced heart rate - parasympathetic or sympathetic
- reduced stroke volume - decreased venous return
Decreased peripheral resistance:
- decreased arterial radius
What are the causes and features of cardiogenic shock?
Failure of the cardiac pump. To compensate for this the peripheral resistance increases. The patient will be cool and peripherally shut down.
4 categories :
(a) Myopathic - Failure of the myocardium. Myopathic cardiogenic shock includes:
• Heart muscle failure
• Myocardial infarction
• Cardiomyopathies
• “Stunned myocardium”
(b) Arrhythmia-related - electrical abnormalities in the heart causing atrial and ventricular arrythmias. Impaired ventricular contraction or filling decreasing cardiac output.
(c ) Mechanical - Defects relating to blood flow through the heart. Valvular defects e.g. prolapse and ventricular defects.
(d) Extra-cardiac - Anything outside the heart that impairs cardiac filling or ejection of blood from the heart. For example a massive pulmonary embolism, tension pneumothorax, severe constrictive pericarditis or pericardial tamponade.
What are the causes and features of hypovolaemic shock?
- Intra-vascular fluid loss (blood, plasma etc)
- ↓ venous return to heart AKA “pre-load”
- ↓ stroke volume à ↓ cardiac output. Initially the patient will try and compensate by increasing the heart rate and by increasing totally peripheral resistance by constricting peripheral vessels. This determines how they present to you: cool (due to the restriction of peripheral vessels), tachycardic and a normal blood pressure (due to the compensation).
Causes: 1. Haemorrhage • Trauma • Gastrointestinal bleeding • Haemorrhagic pancreatitis • Fractures • Ruptured aortic, abdominal, or left ventricular free wall aneurysm 2. Non-haemorrhagic fluid loss • Diarrhoea +/- vomiting • Heat stroke • Burns • Third spacing! ○ Acute loss of fluid into internal body cavities Third-space losses are common postoperatively and in intestinal obstruction, pancreatitis, or cirrhosis.
What are the causes and features of distributive shock?
Distributive shock Decreased systemic vascular resistance leading to severe vasodilation. You would compensate by boosting cardiac output - high heart rate and large stroke volume. The patient would be flushed and tachycardiac. Types of distributive shock: • Septic shock • Anaphylactic shock • Neurogenic shock • Toxic shock syndrome
What is shock?
A pathophysiological state of reduced systemic tissue perfusion (i.e. systemic hypoperfusion) due to cardiovascular collapse.
