Cardiovascular

Question 1

Describe how obstructive shock develops in trauma, in particular due to tension pneumothorax and cardiac tamponade

Answer 1

obstructive causes of shock are those not directly associated with loss of fluid, pump failure or vessel dilation, it occurs when blood flow in the heart or great vessels becomes blocked.

2 of most common examples of obstructive shock in trauma are Tension Pneumothorax and Cardiac Tamponade.

Tension Pneumothorax.

• a pneumothorax is a respiratory problem caused by damage to lung tissue allowing the air, normally held within the lungs, to escape into the chest cavity.
• if pneumothorax continues untreated, sufficient air will accumulate within the chest cavity, to begin applying pressure to the structures of the mediastinum.
• when the trapped air begins to shift the chest organs toward the uninjured side, it becomes known as a tension pneumothorax.
• tension pneumothorax is a life-threatening condition because the kinking of the vena cava that occurs as the mediastinum shifts, can precede cardiac arrest.
• pt’s at significant risk are those who have positive pressures in the lung(ie positive pressure ventilation/bag-valve-mask/ventilator)and non-invasive mask ventilation.
• usually the only action that will prevent eventual death is decompression of the injured side of the chest, relieving the pressure in the chest cavity and allowing the heart to expand fully again.
• the decision to decompress the chest should always be based on good evidence that a tension pneumothorax exists with decreased perfusion.

Cardiac Tamponade.

• life threatening condition caused by blunt or penetrating trauma, tumours or pericarditis.
• occurs when blood leaks into the tough fibrous pericardium, quickly causing an accumulation of blood within the pericardial sac, which leads to the heart being compressed.
• as the pericardium has minimal ability to stretch, each contraction of the heart allows more blood accumulation between the heart and the sac, preventing the heart from opening up to allow complete refilling.
• this continued pressure within the pericardial sac obstructs the flow of blood into the heart, resulting in decreased outflow from the heart.
• treatment is removal of the blood/fluid.
• if the tamponade is fluid, pericardiocentesis can be performed-inserting a needle attached to a syringe through the chest, into the pericardium to withdraw the fluid.
• in traumatic cardiac tamponade, the blood may rapidly clot and cannot be removed by pericardiocentesis, thus requiring a thoracotomy.
• vital clues to presence of cardiac tamponade are:
  
  • increasing tachycardia
  • small QRS complexes
  • muffled heart sounds
  • systolic and diastolic BP’s starting to merge

Question 2

Describe how distributive shock develops, in particular due to sepsis and anaphylaxis

Answer 2

distributive shock occurs when there is widespread dilation of the resistance vessels(small arterioles), the capacitance vessels(small venues), or both.
as a result, the circulating blood volume pools in the expanded vascular beds and tissue perfusion decreases.

examples of distributive shock are sepsis and anaphylaxis.

Sepsis/Septic Shock.

• septic shock is defined as the presence of sepsis syndrome plus a systolic BP of less than 90 mm Hg, or a decrease from the baseline BP of more than 40 mm Hg.
• systemic inflammatory response syndrome is defined as the presence of 2 or more of the following in the presence of a trigger such as burns, trauma, pancreatitis, bacterial infection, or hypovolaemia:
  
  • Temp >38.3C or <36C
  • Heart rate >90bpm
  • Tachypnoea >20bpm
  • White cell count <4 or >12 x 10(to the power of 9)/L
• in the presence of suspected infection, it is known as ‘sepsis’, and if this results in organ failure it is known as ‘severe sepsis’.
• this can progress to multiple-organ dysfunction syndrome(when multiple organs are failing) and/or septic shock if the blood pressure is non-responsive to fluid boluses.
• sepsis occurs as a result of widespread infection, usually due to gram-negative bacterial organisms.
• gram-positive bacteria, fungi, viruses, and rickettsia can also be causative agents.
• complex interactions occur between the pathogen and the body’s defence mechanisms, which initially, may keep the infection under control.
• the infection activates the inflammatory-immune response, invoking humoral, cellular, and biochemical pathways, which result in increased microvascular permeability(leaky capillaries), vasodilation, third-space fluid shifts and microthrombi formation.
• in some pt’s an uncontrolled and unregulated inflammatory-immune response occurs, resulting in hypo perfusion to the cells owing to opening of arteriovenous shunts, tissue destruction, and organ death.
• septic shock is complex as initially, there is an insufficient volume of fluid in the ‘container’, because much of the blood has leaked out of the vascular system(hypovolaemia).
• subsequently, the fluid that leaks out, often collects in the respiratory system, interfering with ventilation.
• finally the dilated vascular system is being asked to contain a smaller-than-normal volume of intravascular fluid.
• left untreated the result is multiple organ dysfunction syndrome, and often, death.

Anaphylactic Shock.

• a life threatening, generalised or systemic hypersensitivity reaction, occurring when person reacts violently to a substance, to which they have been sensitised.
• sensitisation means developing a heightened reaction to a substance.
• an allergic reaction typically does not occur, or occurs in a milder form, during sensitisation.
• a pt can report no history of allergic reaction to a substance during a 1st or 2nd exposure, yet each subsequent exposure after sensitisation produces a more severe reaction.
• in anaphylactic shock, there is no loss of blood, minor vascular damage, and only a slight possibility of direct cardiac muscle injury.
• the pt experiences widespread vascular dilation, resulting in relative hypovolaemia. In other words the normal blood volume is less, relative to the size of container it is within. The combination of poor oxygenation and poor perfusion that this causes can easily prove fatal.
• in anaphylaxis, immune system chemicals, such as histamine and other vasodilator proteins, are released when exposed to an allergen. Their release causes the severe bronchoconstriction that accounts for wheezing if the pt is actually moving enough air.
• anaphylaxis is also accompanied by urticarial, widespread vasodilation, which causes distributive shock, and blood vessels that continue to leak. Fluid leaks from the blood vessels into the interstitial space, resulting in hypovolaemia and potentially causing significant swelling.
• in some cases this swelling may occlude the upper airway resulting in a life-threatening condition.
• recurrent large area of subcutaneous oedema of sudden onset, but usually disappearing within 24 hours are called angioedema(mainly seen in young women, as a result of allergy to food or drugs).

Question 3

Describe the pathological processes which lead to acute coronary syndrome, in particular atherosclerosis

Answer 3

Acute Coronary Syndrome(ACS) is a term used to describe any group of clinical symptoms consistent with acute myocardial ischaemia.
It is often caused by atherosclerosis when narrowing/occlusion means that there is insufficient blood supply to the cardiac muscle, causing acute myocardial ischaemia, which presents as chest pain.

Acute myocardial ischaemia could be caused by Myocardial Infarct of the coronary arteries, or Angina Pectoris(because of narrowing, supply of oxygen to the myocardium is insufficient to meet demands, so the cardiac muscle becomes ichaemic and switches to anaerobic metabolism, leading to accumulation of lactic acid and carbon dioxide in the muscle)

The basic lesion of atherosclerosis is a fibrofatty deposit in the intima of blood vessels(fibrous tissue and lipids), known as an atheromatous plaque.

Atheromas occur in large/medium sized arteries, particularly the aorta and its major branches(carotid, coronary, mesenteric,renal, iliac and femoral arteries).

Earliest visible lesions are called fatty streaks as they are almost entirely made up of lipids.

Complications of atherosclerosis:
- decreased blood flow
- thrombosis
- embolism
these can begin to appear in 30'3 but usually don't manifest as signs/symptoms till much later. Female complications usually delayed until after menopause due to protective effect of oestrogen and progesterone. 

Low-pressure pulmonary arteries not usually involved.

Atheromatous plaque formation begins with damage to the endothelium potentially caused by agents like:

• toxins in cigarette smoke
• diabetes
• hypertension
• immune injury
• turbulent blood flow at sites of bifurcation of arteries

Once damaged the endothelial cells become leaky.
Lipid droplets that are normally circulating in the blood diffuse across the endothelium and deposit in the intimate.
In response the endothelial cells recruit monocytes and lymphocytes.
The monocytes scavenge the free lipid, then remain in the tissue as lipid-laden macrophages.
At the same time, smooth muscle cells migrate into the intimate from the media to limit the damage and restore function to the intima.
The activity of the macrophages and smooth muscle cells is regulated by cytokines secreted by the lymphocytes.
Accumulated lipids within the macrophages and smooth muscle cells give the intima the yellow colour seen as the fatty streak.

As atheromatous plaques mature, smooth muscle cells and macrophages become incontinent and release lipids into the extracellular space again, aggravating and accelerating the inflammatory process.
Lipids are deposited extracellularly in the form of cholesterol crystals.
As with any chronic inflammatory lesion, fibrosis also occurs, and over time the plaques become scarred/sclerotic.
Also cells within the lesion die. Their remains undergo dystrophic calcification.
Therefore atheromatous lesions gradually enlarge over years, becoming progressively more fibrous and calcified.
The white/yellow, crusted appearance of advanced atherosclerosis is caused by crystallisation of the cholesterol and calcification.

Atherosclerotic plaques cause harm by:

• significantly narrowing or occluding the lumen of a blood vessel, causing ischaemia of the tissue normally supplied by that artery.
• The plaque surface can ulcerate. Exposed collagen is highly thrombogenic, so a thrombus can rapidly form over an ulcerated plaque, leading to acute occlusion and infarction of the tissue supplied by the artery.
• Bits of a thrombus could also break off, travelling distally before occluding a smaller-calibre vessel.
• Plaques can also damage the structural integrity of a vessel wall, causing it to balloon under pressure, forming an aneurysm. If the wall becomes thin enough an aneurysm can rupture leading to life threatening haemorrhage.

Different vessels suffer different complications from atherosclerosis:

Coronary arteries(smaller calibre).

• narrowing of the lumen
• plaque rupture with thrombosis or haemorrhage into the plaque causes M.I

Carotid arteries.
- plaques cause occlusion

Abdominal Aorta(most common site of atherosclerosis.

• can be asymptomatic even when extensive
• complication occur when plaques overgrow the orifice of an aortic branch artery
• thrombus form and bits of it embolise to different tissues
• aneurysms form

Question 4

Describe the pathophysiology of heart failure in relation to cardiogenic shock

Answer 4

Congestive Heart Failure means the heart is unable to pump the blood that returns to it, resulting in blood ‘backing -up’ into the pulmonary and/or systemic veins, with consequent leakage of fluid into the pulmonary alveoli and other tissues.

Congestive heart failure, like cardiogenic shock is often the result of M.I, but also occurs in late stages of other forms of heart disease:

• hypertensive heart disease
• rheumatic valvular disease
• severe myocarditis
• cardiomyopathies

Congestive heart failure is not a diagnosis but a manifestation of some other underlying disease. Determining the cause is important as it may be treatable or even curable.
Treating heart failure with diuretics and digoxin alleviates symptoms and heart function but doesn’t address the underlying condition.

Congestive heart failure is categorised as left or right sided depending on which ventricle function is compromised.
Commonly left/right sided failure occur together.
Most common cause of right side failure, is left side failure, because increased blood pressure transmitted into the lungs from left heart failure eventually has an adverse affect on the ability of the right side of the heart to pump blood into the lungs.

Left Heart Failure causes:

• increased venous pressure in the lungs as result of a backup of blood, as left ventricle is no longer able to push all of the blood it receives, into the systemic circulation
• manifests as S.O.B(dyspnoea) as a result of transudation of fluid into the pulmonary alveoli
• physical exam detects resonance changes of the thorax during auscultation, as well as the presence of ‘rales’ during inspiration.

Right Heart Failure causes:

• enlargement of the liver and spleen(hepatosplenomegaly) as result of congestion
• oedema particularly noticeable in the ankles
• distention of neck veins caused by increase venous pressure

Severity and duration of congestive heart failure vary.
In mild forms, it is manageable for many years with drugs such as:
- digitalis(digoxin) - improves myocardial contractile force
- diuretics - promote renal excretion of excess fluid
- angiotensin-converting enzyme (ACE) inhibitors
- beta blockers
At its worst, it rapidly leads to cariogenic shock and death

Cardiogenic shock refers to shock caused by failure of the heart - the heart cannot maintain cardiac output(pump sufficient volume of blood) adequate for tissue perfusion - can often be the result of extensive M.I - rapidly leads to death in majority of pt.

Question 5

Briefly describe the pathophysiology of aneurysms

Answer 5

Pulsatile waves of blood place extreme haemodynamic force on artery walls.
Over years this force produces degenerative changes in the media(middle layer) of the artery wall.
The effect is to ‘unglue’ the layers of the wall from one another.
Eventually these degenerative changes to the media, may lead to disruption of the intima(innermost layer of the artery).
Tearing of the intima is likely to occur at areas that are subjected to the greatest stress.
Once the intima tears, the process of dissection, or separation of the artery wall, often begins.
With each ventricular systole, a jet of blood is forced into the torn arterial wall, gradually causing an outward bulging of the artery wall(aneurysm).
As an aneurysm increases in size, the risk of rupture increases.
Rupture of an aneurysm leads to uncontrollable and life threatening haemorrhage.

Question 6

Describe the pathophysiology of sickle cell anaemia and thalassemia

Answer 6

Sickle cell anaemia is a genetic abnormality of haemoglobin structure caused by an altered sequence of amino acids in the globin molecule.

Sickle cell anaemia occurs in people with 2 genes for haemoglobin S (the homozygous state).
People with 1 haemoglobin S gene (the heterozygous state) are said to carry the sickle cell trait.

The abnormal haemoglobin structure results in some red blood cells becoming sickle(crescent) shaped under situations of low oxygen tension.

The defective Red blood cells are much less able to carry oxygen effectively, meaning a person with the disease is more susceptible to hypoxia

The sickle cells are more susceptible to rupture and premature death.
When more cells become sickled, it can lead to vascular obstructions/infarcts(thrombotic crisis) which are more common in the spleen(causing the organ to swell and/or rupture) and bone, and care the cause of high levels of pain for the pt.
The increased breakdown(haemolytic crisis) of red blood cells causes jaundice.
Red blood cell production may temporarily stop(aplastic crisis).

Thalassemia - genetic defect affecting the rate of synthesis of normal haemoglobin - also occurs in homozygous people.
Severe anaemia develops in infancy, leading to death in childhood/adolescence.
There is a decrease in production of red blood cells because of increased destruction of immature red blood cells in the bone marrow.

Question 7

Briefly describe anaemia and its causes

Answer 7

Anaemia is defined as a haemoglobin or erythrocyte level that is lower than normal(<120g/l for women and <130g/l for men).

Usually associated with type of underlying disease process.

May result from:
- acute
or
- chronic blood loss

• decrease in production
  or
• increase in destruction of erythrocytes
• may be outcome of a pre-existing haemolytic disorder(related to the breakdown of red blood cells)

Iron deficiency anaemia:

• most common type
• causes include
  
  • gastrointestinal blood loss
  • menstrual bleeding
  • blood loss through frequent donation/diagnostic tests

Haemolytic disorders:

• such as sickle cell anaemia and thalassaemia
• can result in deficiency of an enzyme known as glucose-6-phosphate dehydrogenase which helps protect cells during infection. Low levels mean cells become damaged.

Autoimmune disorders:
- red blood cells are destroyed by the body’s own antibodies, that think normal blood cells are foreign.

Most common type of acquired anaemia develops when the flow of red blood cells is disrupted due to problems with blood vessel linings(aneurysms, weaknesses) or blood clots.

Red blood cells can also be destroyed by microorganisms in the blood.

Renal failure may also cause anaemia. As the kidneys fail they may not produce enough erythropoietin for red blood cell production.