Cardiac

Question 1

• Discuss the pathophysiology of heart failure

Answer 1

• Defined as: cardiac impairment with inability to fill or eject blood volume
- this may be due to rhythm problems, preload, afterload or contractility problems
• Causes: ischaemic heart disease, hypertension, idiopathic dilated cardiomyopathy

Question 2

What are the layers of the heart wall and examples of pathology?

Answer 2

Pericardium: thin, external layer, double walled membranous sac. Parietal and visceral pericardium.
Functions: prevents displacement of heart and barrier for infection +inflammation
Pathology: pericarditis, pericardial tamponade.

Myocardium:
cardiac muscle, thick middle layer, left thicker than right.
Function: pumps blood around the body
Pathology: myocardial infarction, myocarditis, hypertrophy

Endocardium: epithelial tissue that lines the entire vasculature, thin layer. Prone to infection

Question 3

What is myocarditis?

Answer 3

A rare infection of the myocardium, inflammatory substances infiltrate the heart muscle causing thickening or heart gets dilated.
This alters filling, pumping and causes a big drop in BP.
often occurs in young people who are healthy.
Usually requires heart transplant

Question 4

What is myocardial hypertrophy?

Answer 4

it will develop to some degree through aerobic training. As the disease develops the thickened muscle wall makes it difficult for the heart chambers to fill and muscle contraction becomes less effective. The conductions system runs through the muscle layers and alters rhythm problems.

Question 5

What are alterations to normal valve physiology?

Answer 5

Valve Regurgitation
– Blood flows back and forth across valve
– Blood flow from the heart reduced
– Poor cardiac output

Valve Stenosis
– Blood trying to squeeze through narrow valve opening
– Blood flow from the heart reduced
– Poor cardiac output
– ?poor coronary artery filling

Question 6

What influences normal heart rate?

Answer 6

can increase due to:

• exercise
• physical size- children
• age: young people
• gender: faster in women
• hypotension
• adrenaline and thyroxine
• increased temp

Can decrease due to:

• larger body size
• inactivity
• parasympathetic
• sleep
• hypertension

Question 7

Discuss the different types of cardiac arrhythmias and their effect of cardiac output.

Answer 7

Slow Rhythm causes: some medications, natural degeneration of the SA and AV nodes, surgery of the valves, inadequate blood supply to the nodes.
Bradycardia: slow HR may cause minimal diastolic filling and decreases cardiac output.

Fast rhythm causes: re-entry circuits, myocardial irritability, acute infections, myocardial scarring.
It it seen as a narrow QRS. Tachycardia reduces cardiac output because of decreased preload and high contractility.

Question 8

Describe the measurements used to assess cardiac function

Answer 8

ECG, BP, arterial blood gasses, HR, Echocardiography, Chest X rays

Question 9

Explain the meaning of haemodynamics

Answer 9

Can be defined as the physical forces that determine blood flow.
– Can be influenced by the
heart rate, radius of the
blood vessel and the viscosity and volume of the blood

Question 10

Briefly describe the cardiac conduction system.

Answer 10

SA node to the AV node then pass to the Av bundle ( in the septum), sent to the apex of the ventricles splitting into the purkinje bundle (left and right)

Question 11

Briefly describe cardiac contraction.

Answer 11

atrial depolarization is first- contracting the right atrium. atrioventricular valves open
- QRS wave is ventricle depolarization when it reaches the purkinje fibres, semi-lunar valves open

Question 12

Describe the role of the sympathetic nervous system in the pathogenesis of hypertension.

Answer 12

1. increases HR and peripheral resistance leads to hypertension
2. insulin resistance leads to endothelial dysfunction leading to narrowing of vessels and vasospasm causing hypertension
3. vascular remodel-ling and pro-coagulant effects lead to the narrowing of vessels and vasospasm causing hyper tension

Question 13

Compare and contrast the different types of shock.

Answer 13

Hypovalaemic: inadequate circulating volume
Cardiogenic : impaired forward pumping of the heart, heart failure, MI
Distributive: mal distribution of circulating blood volume. Three types:
- anaphylactic - hypersensitivity reaction > chemical mediators> vasodilation
- neurogenic- loss of sympathetic tone
- septic shock- severe infection

Question 14

Describe the pathogenesis of coronary heart disease.

Answer 14

– Begins with the development of fatty streaks in between the endothelium and internal elastic lamina.
– Over time this leads to progressive luminal narrowing which is associated
with acute coronary syndromes.
– Inflammation is a critical component – patients who are obese or have diabetes are therefore at increased risk.

Question 15

Explain how hyperlipidaemia and atherosclerosis can disrupt arterial circulation.

Answer 15

Hyperlipidaemia:
– causes the build up of lipids,
cholesterol, calcium and
cellular debris in the vessel
wall.
Atherosclerosis causes turbulent
flow and obstruction of oxygen
to target organs.

Question 16

Define turbulent flow.

Answer 16

Blood flow is generally laminar.
– Turbulent flow can occur when the laminar flow is disrupted.
– e.g. large artery branch points, diseased and stenotic arteries and across stenotic heart valves.
– This increases the perfusion pressure required to drive a given flow.
– Turbulence can create sound waves (e.g., ejection murmurs, carotid bruits) that can be heard with a stethoscope.

Question 17

Describe chronic ischaemic heart disease and explain how it can develop.

Answer 17

It is an obstruction of flow of blood to the heart.
– With ageing, fatty plaques develop within our arteries (LDLs and VLDLs)
– The arteries harden and narrow.
– Reduction in blood flow leads to areas of ischaemia developing

Question 18

Define angina.

Answer 18

Chest pain caused by myocardial ischaemia.
– Discomfort is transient (lasting approx. 3-5mins)
– Pain may range from discomfort to a feeling of heaviness or pressure to
moderately severe pain.

Question 19

Define and outline what an acute myocardial infarction is.

Answer 19

Commonly known as a heart
attack.
– Caused by interruption of blood
supply to the heart (myocardial
ischaemia) which then leads to cell
death (myocardial infarct).
– Most commonly there is occlusion
of a coronary artery.

Question 20

Describe the pathophysiology of myocardial infarction

Answer 20

MI occurs when the oxygen demand of the myocardium is not met by a
sufficient blood flow
– May be due to:
– Narrowing of the coronary arteries, leading to insufficient blood supply
to cause myocardial ischaemia.
– Plaques may occlude the coronary arteries.

Question 21

Define what is meant by the term is endocarditis and explain what risk factors are associated with its development.

Answer 21

Inflammation of the endocardium.
– Usually involves the heart valves
– Characterised by a mass of
platelets, fibrin and microbial
growth (vegetations).
– Auto-immune diseases such as
rheumatic heart disease and
systemic lupus erythematosus can
lead to its development

Question 22

Define what an aortic aneurysm is.

Answer 22

An aneurysm is a
dilation/ballooning/swelling of a
vessel.
– While an aneurysm can occur
anywhere in the body, an aortic
aneurysm occurs in the aorta.
– If they rupture, they can cause
sudden death.

Question 23

What is an aortic dissection?

Answer 23

Begins with a tear in the inner
layer of the aortic blood vessel
(there are three layers).
– Blood is channelled into the wall
separating the layers of tissue.
– Weakens the wall and increases
the risk of rupture.
– Life threatening.
– Caused by hypertension,
atherosclerosis, trauma etc.

Question 24

Explain what is meant by the term cardiomyopathy and list the
risk factors that increase the chance of developing cardiomyopathy.

Answer 24

Cardiomyopathy is a disease of the heart muscle cells.
– The contractility of the myocardium (heart muscle) decreases.
– Often a result of long term hypertension
– Genetic history, diabetes etc. can increase the risk.
– May be extrinsic – associated with pathology outside of the myocardium
e.g. ischaemia, diabetic cardiomyopathy.
– May be intrinsic – a weakness of the heart muscle not attributed to extrinsic
causes e.g. mitochondrial myopathy

Question 25

Explain what is aortic valve stenosis. How is it treated

Answer 25

``` Aortic valve does not open fully thus decreasing the blood flow from the heart. – Treatment: – Monitoring – Diuretics, nitrates and beta blockers – Surgery to repair/replace the valve ```

Question 26

Describe heart failure.

Answer 26

Is defined as a condition where the heart cannot pump enough blood to meet its demands. – heart cannot fill with enough blood – heart cannot pump with enough force – Most cases affect both sides of the heart but can affect one side only. – R HF – heart cannot efficiently pump blood to the lungs for gas exchange. – L HF – heart cannot pump oxygenated blood efficiently to the rest of the body.

Question 27

Describe the different alterations that can occur in veins.

Answer 27

Thromboembolism: – Most often associated with restricted mobility such as post-operative patients, bedridden individuals and travel – Varicose veins – a vein where blood has pooled producing distended, palpable vessels. Occurs when a valve is damaged or absent. – Venous ulcer disease, a consequence of poor venous return – Superior vena cava syndrome – progressive occlusion of the superior vena cava leading to venous distension in the upper extremities and head. May be caused by pressure on the superior vena cava most commonly due to cancers.

Question 28

Describe the process of thrombus formation.

Answer 28

1. Endothelial injury 2. Stasis or turbulence (abnormal blood flow) 3. Blood hypercoagulability

Question 29

What is venous thrombosis, how is it diagnosed and treated?

Answer 29

``` A blood clot (thrombus) which has formed in the vein – Pathophysiology is still debated – vessel injury initiates coagulation which triggers clot formation. – Patients may experience a sharp pain in the leg, ultrasound may be used to visualise clot. ```

Question 30

What is a Pulmonary Embolism (PE)?

Answer 30

Is a thrombus that occludes pulmonary arterial circulation. – Usually begins as a thrombus in the deep veins of the pelvis or lower limbs. – A small part of the thrombus (an embolism) breaks away and travels to the lungs.

Question 31

Describe the cellular changes that occur in cardiac muscle in response to increased workload.

Answer 31

Hypertrophy can be seen in response to an increased workload. It is also called physiological enlarged heart. (or pathological if the stimuli is due to heart disease) ‘Physiological’ cardiac hypertrophy can be provoked by exercise training and can lead to increase cardiac size that is characterized by normal cardiac morphology with a normal and/or enhanced cardiac function. ‘Pathological’ cardiac hypertrophy is a condition that is characterized by the thickening of the heart muscle, a decrease in the size of the chambers of the heart, and a reduced capacity of the heart to pump blood to the tissues and organs around the body. Two common causes of pathological cardiac hypertrophy are high blood pressure (hypertension) and heart valve stenosis, and this type of hypertrophy is considered to be a major independent risk factor for morbidity and mortality. (Kavazis A. N. (2015). Pathological vs. physiological cardiac hypertrophy. The Journal of physiology, 593(17), 3767. https://doi.org/10.1113/JP271161)

Question 32

Define the term shock and explain how it may develop.

Answer 32

Shock is when the body is not getting enough blood flow resulting in widespread impairment of cellular metabolism. shock progresses to organ failure and death unless compensatory mechanisms reverse the process or clinical intervention succeeds. Untreated severe shock overwhelms the body's compensatory mechanisms through positive feedback loops that initiate and maintain a downward physiological spiral. The impairment to cellular metabolism includes impairment of oxygen AND glucose. Different types: - hypovalaemic: inadequate circulating volume - Cardiogenic : impaired forward pumping of the heart, heart failure, MI - Distributive: mal distribution of circulating blood volume. Three types anaphylactic *hypersensitivity reaction > chemical mediators> vasodilation *neurogenic- loss of sympathetic tone *septic shock- severe infection

Question 33

Describe the causes of microcytic, normocytic and macrocytic anaemia.

Answer 33

· Anaemia: too few RBC or too little or abnormal haemoglobin - Blood is deficient in either the Quality or Quantity of RBC - An abnormality in Hb leads to hypoxia as RBC cannot transport sufficient O2 - Causes: either a defect in quality or quantity 1. Impaired RBC production 2. Blood loss 3. Altered RBC destruction 4. Combination - Classification of anaemia: ○ Hypochromic Microcytic: small pale RBC, normal or low RBC count. Thalassaemia- anaemia of the sea and chronic disease ○ Normochromic normocytic anaemia: cells normal size and colour but low RBCC. Blood loss, haemolytic anaemia. Sickle cell anaemia- mosquitoes ○ Normochromic/Hyperchromic macrocytic: large RBC, low RBCC, no central pallor. Megablastic anaemia- folate or B12 deficiency, may be genetic. Aplastic anaemia- bone marrow failure

Question 34

Discuss the common causes/risk factors of myocardial infarction

Answer 34

Acute myocardial infarction (AMI) results when there is prolonged ischaemia causing irreversible damage to the myocytes (heart muscle cells). Plaque disruption occurs because of shear forces, inflammation with release of multiple inflammatory mediators, secretion of macrophage-derived degradative enzymes, immune cell activation and apoptosis of cells at the edges of the lesions. The underlying layer of plaque is then exposed and this causes activation of the coagulation cascade. The resulting thrombus can form quickly. The thrombus may break up before permanent myocyte damage has occurred (unstable angina) or it may cause prolonged ischaemia by impeding blood flow past the thrombus and causing lack of oxygen and nutrients to the myocardium, resulting in infarction of the heart muscle (acute myocardial infarction) Risk factors: - advanced age - family history - smoking - diabetes mellitus/insulin resistance - obesity - dyslipidaemia - hypertension

Question 35

Discuss the common causes/risk factors of myocardial infarction

Answer 35

Acute myocardial infarction (AMI) results when there is prolonged ischaemia causing irreversible damage to the myocytes (heart muscle cells). Plaque disruption occurs because of shear forces, inflammation with release of multiple inflammatory mediators, secretion of macrophage-derived degradative enzymes, immune cell activation and apoptosis of cells at the edges of the lesions. The underlying layer of plaque is then exposed and this causes activation of the coagulation cascade. The resulting thrombus can form quickly. The thrombus may break up before permanent myocyte damage has occurred (unstable angina) or it may cause prolonged ischaemia by impeding blood flow past the thrombus and causing lack of oxygen and nutrients to the myocardium, resulting in infarction of the heart muscle (acute myocardial infarction) Risk factors: - advanced age - family history - smoking - diabetes mellitus/insulin resistance - obesity - dyslipidaemia - hypertension - ischaemic heart disease

Question 36

Describe the pathophysiology of right-sided versus left-sided heart failure and outline the effects each would have on the bod

Answer 36

Left side heart failure: (most common) commonly called congestive heart failure , can be further categorised as systolic heart failure or diastolic heart failure. Systolic heart failure is defined as an inability of the heart to generate adequate cardiac output to perfuse vital tissues. Diastolic heart failure is defined as pulmonary congestion despite a normal stroke volume and cardiac output. It results from decreased compliance of the left ventricle and abnormal diastolic relaxation EFFECTS: - pulmonary vascular congestion - inadequate perfusion - coughing, fatigue, dyspnoea, decreased urine output - pulmonary oedema - can be fatal Right side heart failure: (lung disease main cause) can result from left heart failure when an increase in left ventricular filling pressure is reflected back into the pulmonary circulation. As pressure in the pulmonary circulation rises, the resistance to right ventricular emptying increases. The right ventricle is poorly prepared to compensate for the increased afterload and dilates and fails. EFFECTS: - systemic congestion= blood backs up into the veins - impairs kidney function - impaired gastro function - swellings/oedema around the body such as ankles, legs, and sometimes lungs

Question 37

Discuss what factors may promote a blood clot.

Answer 37

When blood vessels are damaged, platelets release chemicals that promote blood clotting to prevent blood loss. (equivalent to thrombocytes). There are other clotting factors such as calcium ions, inactive enzymes synthesised by hepatocytes, roughened endothelial blood vessel surface. Factors that can promote blood clotting or induce the injury to the vessel can include: obesity, smoking, age, diabetes, hypertension, high cholesterol, cancers, trauma, atrial fibrillation, DVT, PAD, metabolic syndrome and immobility These factors promote blood clotting with the damage to vessels such as hypertension, or slowed blood flow which accumulates in the vessels, plaque accumulation (atherosclerosis), inflammation etc.

Question 38

Discuss the pathophysiology of stable angina

Answer 38

Stable angina is caused by gradual luminal narrowing and hardening of the arterial walls, so that affected vessels cannot dilate in response to increased myocardial demand associated with physical exertion or emotional stress. = stable plaque compared to unstable which is prone to rupture or ulcer leading to ischaemia.

Question 39

Describe the modifiable and non-modifiable risk factors for myocardial infarction and explain how they contribute to its development

Answer 39

``` modifiable risk factors: smoking diabetes physical inactivity being overweight high blood cholesterol. hypertension ``` ``` Non-modifiable: age ethnic background family history of heart disease. genetic factors gender/sex ```

Question 40

Describe the pathophysiology of deep vein thrombosis and pulmonary embolism.

Answer 40

Venous thrombi are more common than arterial thrombi because flow and pressure are lower in the veins than in the arteries. The two main presentations of venous thromboembolus are deep vein thrombosis (DVT) and pulmonary embolism. DVT is the presence of a blood clot, normally on the lower extremities, it may lead to pulmonary embolism. Pulmonary embolism starts as venous stasis, hyper coagulability leading to thrombus formation (such as DVT in the leg) causing occlusion of part of the pulmonary circulation due to it travelling in the blood to the lung.

Question 41

Outline the relationship between Virchow’s triad and the development of DVT.

Answer 41

Rudolf Virchow described 3 factors that are critically important in the development of venous thrombosis: (1) venous stasis, (2) activation of blood coagulation, and (3) vein damage. These link to the risks and causes of DVT.

Question 42

Explain the changes the pulmonary circulation that would be experienced as a result of a pulmonary embolism and explain what impact this would have on the heart and systemic circulation.

Answer 42

The impact or effect of the embolus depends on the extent of pulmonary blood flow obstruction, the size of the affected vessels, the nature of the embolus and the secondary effects. Pulmonary emboli can occur as any of the following: • massive occlusion: an embolus that occludes a major portion of the pulmonary circulation (i.e. main pulmonary artery embolus) • embolus with infarction: an embolus that is large enough to cause infarction (death) of a portion of lung tissue • embolus without infarction: an embolus that is not severe enough to cause permanent lung injury • multiple pulmonary emboli: may be chronic or recurrent. EFFECTS: - hypoxic vasoconstriction - decreased surfactant - chest pain - release of inflammatory substances - pulmonary oedema - atelectasis - decreased PaCo2 - decreased CO - pulmonary infarction - shock - hypotension or hypertension - increased dead space