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121 Cards in this Set
- Front
- Back
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What determines the preload?
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Preload is determined by how much the myocardium is stretched at the end of diastole. It depends on the end-diastolic volume (EDV), which depends on the venous return.
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What determines the afterload?
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Afterload is determined by the force that the ventricles must eject blood against during systole. It depends mostly on the pressure in the aorta, measured by the mean arterial pressure (MAP) which again depends on the total peripheral resistance (TPR).
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How does the Frank-Starling mechanism work?
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The Frank-Starling mechanism is an intrinsic property of the myocardium. The more the ventricular wall is stretched during diastole, the higher the contractility during systole. It causes stroke volume to increase when the end-diastolic volume increases. |
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In what ways can the heart increase the cardiac output?
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The heart can increase the cardiac output by either: - Increasing contractility - Increasing the heart rate - Increasing the stroke volume |
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Which organs will receive less cardiac output in exercise?
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The GI-tract, liver and kidneys will receive less cardiac output in exercise.
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What is the average cardiac output in rest?
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The average cardiac output in rest is 5 L/min
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What is the average cardiac output during exercise?
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The average cardiac output in exercise is 12,5 L/min.
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What is the reserve capacity of the heart?
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The reserve capacity of the heart is the hearts "headroom" to increase the cardiac output to meet the needs of the body.
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How does the reserve capacity change with age?
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Reserve capacity decreases with age.
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How is the reserve capacity in failing hearts?
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The reserve capacity in failing hearts is very low. They may even have no reserve capacity.
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What is the definition of heart failure?
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The definition of heart failure is that the heart is unable to maintain the cardiac output needed to meet the body's needs.
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What are the three compensatory mechanisms a failing heart will use to compensate for insufficient cardiac output?
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The three mechanisms are: - Activated baroreceptor response -> increased sympathetic activity -> tachycardia, increased contractility - Low CO -> GFR decreases -> RAAS is activated -> salt and water retention increases -> preload increases - Increased EDp -> hypertrophy of ventricles -> increased contractility |
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What is cardiac decompensation?
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Decompensation is the state where the compensatory mechanisms of the failing heart become insufficient to keep up with the body's need for cardiac output. The patient will start experiencing symptoms.
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What are the symptoms of cardiac decompensation?
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The symptoms of cardiac decompensation are: - Dyspnoea - Peripheral oedema - Fatigue |
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What does it mean when a heart is subcompensated?
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The state of subcompensation mean that the failing heart is barely sufficiently compensated in rest, but whenever the demand for cardiac output increases, like in exercise or simply walking up stairs, will the heart become decompensated.
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What are the biggest causes for heart failure?
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The biggest causes for heart failure are: - Coronary artery disease (like AMI) - Arterial hypertension - Diabetes mellitus - Heart valve defect |
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What are the biggest risk factors for heart failure?
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The biggest risk factors for heart failure are: - Obesity - Smoking - COPD - Haemochromatosis - Recreational and prescription drug abuse - Alcohol abuse |
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What are the most important causes for decreased ventricular filling in the right ventricle?
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The most important causes for decreased ventricular filling in the right ventricle are: - Decreased blood volume - Hepatic cirrhosis - Tricuspid stenosis - Pneumothorax |
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What are the most important causes for decreased ventricular filling in the left ventricle?
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The most important causes for decreased ventricular filling in the left ventricle are: - Right ventricle insufficiency - Pulmonary embolism - Mitral stenosis or insufficiency - Left ventricle hypertrophy - Constrictive pericarditis - Restrictive cardiomyopathies |
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What are the most important causes for decreased ventricular filling in both ventricles?
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The most important causes for decreased ventricular filling in both ventricles are: - Pericardial tamponade - Ischaemia - Fibrosis - Congestive cardiomyopathies |
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What are the most important causes for decreased ventricular emptying in the right ventricle?
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The most important causes for decreased ventricular emptying in the right ventricle are: - Pulmonary stenosis - Pulmonary hypertension - Tricuspid insufficiency |
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What are the most important causes for decreased ventricular emptying in the left ventricle?
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The most important causes for decreased ventricular emptying in the left ventricle are: - Systemic hypertension - Aortic stenosis - Polycythaemia |
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What are the characteristics of systolic dysfunction heart failure? What is it caused by?
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In systolic dysfunction heart failure is there a problem with the systole. Both stroke volume (SV) and ejection fraction (EF) are reduced, because of a normal end-diastolic volume (EDV) but high end-systolic volume (ESV). Systolic heart failure is caused by decreased ventricular emptying or decreased ventricular contractility. |
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What are the characteristics of diastolic dysfunction heart failure? What is it caused by?
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In diastolic dysfunction heart failure is there a problem with ventricular filling during diastole. Both end-diastolic volume (EDV) and end-systolic volume (ESV) are reduced, so stroke volume (SV) is reduced but ejection fraction (EF) is normal.
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What is cor pulmonale?
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Cor pulmonale is a right-sided heart failure caused by pulmonary pathologies like COPD, pulmonary hypertension, obstructive sleep apnoea or pulmonary embolism.
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What are the most common causes for chronic heart failure?
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The most common causes for chronic heart failure are: - Coronary artery disease - Ventricular hypertrophy - Pulmonary hypertension - Valvular heart disease - Toxic / inflammatory / metabolic degeneration of myocardium - Primary cardiomyopathies |
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What are the forward-failure symptoms of left-sided heart failure?
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The forward-failure symptoms of left-sided heart failure are: - Daytime oliguria with nightly polyuria - Decreased absorption due to intestinal hypoxia - Increased risk for pressure sores due to hypoperfusion of the skin - Exhaustion during mild physical activity - Hypertension - Tachycardia - Cerebral dysfunction |
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What are the forward-failure symptoms of right-sided heart failure?
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The forward-failure symptoms of right-sided heart failure are: - Left-sided heart failure (due to decreased left ventricular filling) |
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What are the backward-failure symptoms of left-sided heart failure?
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The backward-failure symptoms of left-sided heart failure are: - Pulmonary congestion - Dyspnoea, especially on exertion - Paroxysmal noctural dyspnoea - Orthopnoea - Cough - Cyanosis - Pulmonary oedema (only in acute heart failure) |
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What are the backward-failure symptoms of right-sided heart failure?
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The backward-failure symptoms of right-sided heart failure are: * Splenomegaly -> hypersplenism -> haemolytic anaemia * Distended jugular vein * Lower extremity oedema * Jaundice * Impaired nutritional absorption |
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What is high-output heart failure?
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High-output heart failure occurs when the body for any reason has an extraordinarily high demand for cardiac output. The heart will be damaged for trying to supply the body. |
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What are common causes for high-output heart failure?
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Common causes for high-output heart failure are: - Severe anaemia - Arteriovenous fistula - Beri-beri - Hyperthyroidism - Pregnancy - Heat stress - Septic shock - Hypoxia - Hepatic disease and cirrhosis - Obesity |
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What is a cardiomyopathy and what does it mean that we have primary and secondary types?
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A cardiomyopathy is a disease that causes damage to the myocardium. Primary cardiomyopathies have genetic or other predisposing factors, while secondary cardiomyopathies are caused by other diseases. |
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What are the characteristics of dilatative cardiomyopathies?
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In dilatative cardiomyopathies is the ventricular wall thinning, which dilates the lumen of the ventricle. The thin ventricle has low contractility and the ejection fraction (EF) will therefore decrease.
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What are the primary causes of dilatative cardiomypathies?
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The primary causes of dilatative cardiomypathies are: - HLA type DR4 - Coxsackie infection |
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What are the secondary causes of dilatative cardiomypathies?
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The secondary causes of dilatative cardiomypathies are: - Old age - Beri beri - Ethanol, cocaine, amphetamine poisoning - Metabolic diseases (like diabetes mellitus, gout) - Endocrine diseases (like hyperthyroidism, pheochromocytoma) - Ischemic heart disease (caused by atherosclerosis) - Infections (like rheumatic fever, tuberculosis, syphilis) - Pregnancy - Neuromuscular autoimmune diseases (SLE, Duchenne dystrophy) |
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What are the characteristics of hypertrophic cardiomyopathies? What are the two types? |
In hypertrophic cardiomyopathies are the ventricles hypertrophied. Hypertrophied ventricles have reduced compliance, so a high end-diastolic pressure (EDp) is required to fill it. The ejection fraction (EF) is increased, almost to 100%. Two types exist; the obstructive and non-obstructive types. In the obstructive type is septum so hypertrophied that it can obstruct the outflow. In non-obstructive type is the ventricle as a whole hypertrophied. |
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What are the primary causes of hypertrophic cardiomypathies?
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The primary causes of hypertrophic cardiomypathies are: - Mutations to the myosin heavy chain gene |
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What are the secondary causes of hypertrophic cardiomypathies?
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The secondary causes of hypertrophic cardiomypathies are increased afterload, caused by: - Hypertension - Aortic stenosis - Mitral insufficiency - Aortic insufficiency |
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What are the characteristics of restrictive cardiomyopathies?
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In restrictive cardiomyopathies are the walls of the ventricles stiff, however there is no hypertrophy involved. A high EDp is required to fill it, causing decreased ventricular filling.
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What are the secondary causes of restrictive cardiomypathies?
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The secondary causes of restrictive cardiomypathies are: - Amyloidosis - Sarcoidosis - Haemochromatosis |
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What are the characteristics of arrhythmogenic right ventricular cardiomyopathy?
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Arrhythmogenic right ventricular cardiomyopathy is characterized by fatty or fibrotic degeneration of the right ventricle, causing thinning of the wall and dilation of the lumen.
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What are the causes of arrhythmogenic right ventricular cardiomyopathy?
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Arrhythmogenic right ventricular cardiomyopathy is caused by inherited genetic factors.
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What are the causes of acute heart failure?
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The causes of acute heart failure are: * Left side: Pulmonary embolism * Asystole * 3rd degree AV-block * Ventricular fibrillation * Acute valvular rupture * Toxic or metabolic myocardial injury * Myocardial infarction * Aneurysm * Aortic occlusion * Rupture of aortic aneurysm |
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What are the consequences of acute heart failure?
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The consequences of acute heart failure are: - Severe cerebral hypoperfusion - Syncope - Pulmonary oedema - Rapid development of extreme fatigue and dyspnoea - Cardiogenic shock |
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Any type of oedema has the risk of low plasma levels of one ion. Which ion and what is the mechanism?
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Oedema can always cause hypokalaemia. When plasma fluid leaves the vessels and enters the interstitium will the plasma volume decrease. This activates the RAAS, which causes an increase in aldosterone (secondary hyperaldosteronism). Aldosterone retains water and sodium but excretes potassium. |
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What causes the pitting in pitting oedema?
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When the oedema is pressed will fluid move from the pressed area and take some time to move back, which leaves a pit.
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What are the causes of pitting oedema? |
The causes of pitting oedema are: - Cardiac failure - Local inflammation, burn, allergic reaction, trauma |
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What prevents pitting in non-pitting oedema?
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In non-pitting oedema does the oedema fluid contain proteins or mucopolysaccharides. These molecules bind water and therefore don't let the water move freely. Therefore isn't the fluid moved when the oedema is pressed.
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What are the two types of non-pitting oedema?
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The two types of non-pitting oedema are: - Lymphoedema - Myxoedema |
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What are the causes of lymphoedema?
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Lymphoedema is caused when there is a blockage of the lymphatic system, so the lymphatic vessels can't drain fluid. It's often seen after removal of lymph nodes in surgery. |
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What are the causes of myxoedema?
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Myxoedema occurs in: - Hypothyroidism - Hyperthyroidism It's caused by deposition of mucopolysaccharides in the interstitium. |
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What are the causes of generalized oedema?
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All causes for generalized oedema cause low protein content in the blood. Common causes include: - Nephrotic syndrome - Liver cirrhosis - Protein malnutrition |
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Which dysfunctions can cause life-threatening loss of consciousness?
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* Stokes-Adams syndrome
* Asystole * Ventricular fibrillation * Ventricular tachycardia * Papillary muscle rupture due to myocardial infarction * Pulmonary embolism |
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What are the characteristics of the reversible phase of shock?
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The characteristics of the reversible phase of shock are: - Vasoconstriction of arterioles leads to little blood flow in the capillaries and the venules - Interstitial fluid is drained from the interstitium into the venules - Cool and pallor skin |
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What are the characteristics of the compensated (late reversible) phase of shock?
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The characteristics of the compensated (late reversible) phase of shock are: - Hypoxic metabolic products like lactate, CO2, adenosine and K+ accumulate in the tissues, causing opening og pre-capillary sphincters - Some blood starts to enter the capillaries, but it flows very slowly and stagnates |
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What are the characteristics of the progressive (refractory) phase of shock?
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The characteristics of the progressive (refractory) phase of shock are: - Hypoxia causes damage to endothelium in capillaries - Stagnating blood in capillaries causes disseminated intravascular coagulation (DIC) |
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What are the characteristics of the irreversible phase of shock?
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The characteristics of the irreversible phase of shock are: - Fluid leaves the plasma and enters the interstitium - Myocardial contractility worsens - Ischaemic bowel allows bacteria to enter circulation - Multi organ dysfunction develops - Death is imminent |
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What are the causes of hypovolaemic shock?
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The causes of hypovolaemic shock are: Haemorrhagic: - Operation - Trauma Non-haemorrhagic: - Burns - Dehydration (exsiccosis) - Loss of fluid to third space - Anaphylaxis |
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How do the following parameters change in hypovolaemic shock? - Blood volume - Venous return - Central venous pressure - Blood pressure - Heart rate |
In hypovolaemic shock: - Blood volume decreases - Venous return decreases - Central venous pressure decreases - Blood pressure decreases - Heart rate increases |
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What are the causes of cardiogenic shock? |
The causes of cardiogenic shock are: - Acute myocardial infarction (more than 40% of myocardium) - Obstructed or ruptured valves - Cardiomyopathies - Sepsis - End-stage heart failure - Extreme arrhytmias |
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How do the following parameters change in cardiogenic shock? - Blood volume - Stroke volume - Central venous pressure - Blood pressure - Heart rate |
In cardiogenic shock: - Blood volume is normal - Stroke volume decreases - Central venous pressure increases - Blood pressure decreases - Heart rate increases |
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What are the causes of distributive shock?
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The causes of distributive shock are: - Head trauma - Spinal lesion - Polytrauma - Anaphylaxis - Heat stroke - Acute pancreatitis - Sepsis (septic shock) |
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What characterizes the early "warm" phase of distributive shock?
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In the early "warm" phase of distributive shock will there be: - Extreme vasodilation causing low BP - Formation of arteriovenous shunts - No blood flow in capillaries - Damaged capillary endothelium - Fluid leaves the capillaries, causing oedema and lower plasma volume - Skin vasodilation gives warm skin |
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What characterizes the late "cold" phase of distributive shock?
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In the late "cold" phase of distributive shock will there be: - Decreased plasma volume and low BP activates vasoconstrictors - Vasoconstriction of the skin causes it to be cool and pallor - Abnormal distribution of blood |
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How do the following parameters change in the early phase of distributive shock? - Blood volume - Stroke volume - Central venous pressure - Blood pressure - Heart rate |
In the early phase of distributive shock: - Blood volume is normal - Stroke volume is normal - Central venous pressure is normal - Blood pressure decreases - Heart rate increases |
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How do the following parameters change in the late phase of distributive shock? - Blood volume - Stroke volume - Central venous pressure - Blood pressure - Heart rate |
In the late phase of distributive shock: - Blood volume decreased - Stroke volume decreased - Central venous pressure decreased - Blood pressure decreases - Heart rate increases |
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How is the brain affected in shock?
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The brain isn't really affected by shock, only in the very late stages, before death. |
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How is the coronary circulation affected in shock?
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The coronary circulation is auto-regulating, so it's only decreased in late phases of shock.
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How is the myocardium affected in shock?
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Circulating substances such as myocardial depressing factor (MDF), lysosomal enzymes and toxins decrease the myocardial contractility. Tachycardia compensates for low cardiac output, but this also reduces coronary perfusion of the myocardium. |
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How is the gastrointestinal tract affected in shock? (4 things)
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In shock will the absorption be impaired long before the secretion. Reduced absorption means fluid loss into the lumen, increase motility and diarrhoea. Later will ischaemia of the bowels cause hypomotility. The GI tract is more severely affected in elderly. Ischaemic bowel wall can allow bacteria to enter circulation. |
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How is the pancreas affected in shock?
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Hypoperfusion causes the pancreas to release protease enzymes and myocardial depressing factor (MDF), which decrease contractility in the myocardium.
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How is the liver affected in shock?
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Necrosis around the central veins occurs, releasing lysosomal enzymes. Bilirubin metabolism is impaired and can cause jaundice. The liver's ability to remove MDF diminishes. Liver failure occurs. |
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How is the kidney affected in shock?
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Both the cortical and medullary blood flow decreases significantly. Tubules will take hypoxic damage, causing filtrate to leak back into the circulation, causing oliguria and hyposthenuria. Nitrogen-containing compounds (urea) accumulates in blood, causing azotaemia (uraemia). Acute tubular nephropathy occurs. |
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How are the lungs affected in shock?
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Shock-lung occurs. Tachypnoea develops, causing dead-space ventilation and alveolar hypoventilation. Partial respiratory failure develops. Enzymes, free radicals and other molecules from the circulation cause local DIC. Endothelial damage causes exudate to leak out and cause pulmonary oedema. Breathing becomes more and more shallow, global respiratory failure and acute respiratory distress syndrome develops. |
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How is the pituitary affected in shock?
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Shock causes DIC inside the pituitary, which causes ischaemia and necrosis. Sheehan syndrome develops, where the pituitary doesn't produce hormones.
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How is the adipose tissue affected in shock?
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Adipose tissue receives no circulation in shock. Substances released from necrotic adipose tissue makes DIC worse.
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What is the maximum time a tissue can be ischaemic before reperfusion becomes dangerous?
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If a tissue is ischaemic for more than 15 minutes will reperfusion be harmful.
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For myocardial infarction must reperfusion occur within what time frame for best prognosis?
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For myocardial infarction must reperfusion occur within 3 hours to have the best prognosis.
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What's the normal coronary perfusion?
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The normal coronary perfusion is 80 mL/100g/min.
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What is characteristic for the oxygen extraction of the myocardium from the coronary circulation?
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The oxygen extraction is close to maximum, around 10-14 %.
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In which range of MAP is coronary blood flow autoregulated?
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Coronary blood flow is autoregulated between 60 and 150 mmHg.
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What does the Law of Laplace state?
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The Law of Laplace states that the ventricular wall tension is directly proportional to the pressure inside the ventricle and the radius of the lumen, and indirectly proportional to the thickness of the wall.
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What is coronary artery disease?
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Coronary artery disease is a disease caused by atherosclerotic plaques in the coronaries. It can cause acute coronary syndrome (like AMI) and chronic ischaemic heart disease.
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What is acute coronary syndrome?
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Acute coronary syndrome is an umbrella term for two diseases: - Acute myocardial infarction - Unstable angina |
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What is chronic ischaemic heart disease?
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Chronic ischaemic heart disease is an umbrella term for these conditions: - Stable angina - Silent myocardial ischaemia - Prinzmetal's angina - Mixed angina - Walk-through angina |
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At what time of the day does acute coronary syndrome most commonly occur?
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Acute coronary syndrome most commonly occurs in the morning.
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What causes the ST changes on the ECG in a myocardial infarct?
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Injured myocardial fibres are more electronegative than healthy, which produces a current of injury, which causes the ST changes on the ECG.
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What gives rise to the tall peaked T-wave on ECG in acute myocardial infarct?
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Necrotic cells release potassium, causing a local hyperkalaemia. This is what causes the tall, peaked T-wave.
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Which molecules are elevated in the blood after a myocardial infarction?
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- Creatine kinase - Troponin T - Troponin C - Myoglocin |
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What is percutaneous coronary intervention (PCI)?
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PCI is a procedure where a balloon catheter is inserted into the femoral artery and led to the occluded coronary. The balloon inflates and expands the lumen, and a stent is often placed.
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At what degree of coronary lumen occlusion does symptoms develop?
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Symptoms develop at around 70-75% coronary lumen occlusion.
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What is the cause of Prinzmetal's angina?
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Prinzmetal's angina is caused by a strong vasospasm of a subepicardial artery.
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What is the average cerebral blood flow?
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The cerebral blood flow is 700-800 mL/min or 60 mL/100g/min.
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What is the Roy-Sherrington principle?
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The Roy-Sherrington principle states that the brain can rearrange the cerebral circulation by controlling vasodilation and vasoconstriction. This principle plays an important role in autoregulation of cerebral circulation. |
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In what range of MAP is the cerebral circulation autoregulated?
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The cerebral circulation is autoregulated between 50 and 150 mmHg MAP.
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What can the consequence of increased cerebral perfusion be?
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The consequence of increased cerebral perfusion can be hydrostatic oedema causing increased intracranial pressure. |
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What can the consequence of decreased cerebral perfusion be?
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The consequence of decreased cerebral perfusion can be ischaemia or stroke.
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What are the common causes for regional ischaemic stroke?
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The common causes for regional ischaemic stroke are: - Atherosclerosis - Steal syndrome - Cerebral embolus |
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What are the common causes for global ischaemic stroke?
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The common causes for global ischaemic stroke are: - Adams-Stokes syndrome - 3rd degree AV block - Sinus arrest - Ventricular fibrillation - Very late phase of shock |
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What can cause vasogenic cerebral oedema?
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Vasogenic cerebral oedema is caused by an impairment of the blood-brain barrier, for example by: - Ischaemic stroke - Tumor |
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What can cause cytotoxic cerebral oedema?
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Cytotoxic cerebral oedema is caused by a metabolic disorder causing the Na+/K+ ATPase to fail, causing cells to swell. It can occur due to: - Ischaemia - Acidosis - Toxins - Hypoglycaemia - Hyperglycaemia - Uraemia |
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What can cause osmotic cerebral oedema?
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Osmotic cerebral oedema is caused by a change in the osmotic gradient, due to: - Water intoxication - Increased ADH (AVP) |
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What can cause hydrostatic cerebral oedema?
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Hydrostatic cerebral oedema is caused by a change in the hydrostatic pressure gradient. It can be caused by: - Hypertensive crisis (MAP above 150 mmHg) - A patient with chronic hypertension suddenly reducing their MAP to normal values |
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What is the normal blood pressure inside the pulmonary artery?
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The normal blood pressure in the pulmonary artery is 25/15 mmHg.
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How is the pulmonary vascular resistance compared to the total peripheral resistance?
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The pulmonary vascular resistance is five times lower than the total peripheral resistance (TPR).
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What is the pulmonary wedge pressure (PWP)? What's its normal value? What does an elevated PWP indicate?
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The pulmonary wedge pressure correlates with the pressure inside the left atrium. Its normal value is 5-12 mmHg. Elevated PWP indicates pulmonary congestion. |
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How will hypoxia affect the pulmonary blood pressure?
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Hypoxia causes vasoconstriction in the lungs. If the hypoxia is severe enough will there be pulmonary hypertension.
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What are the common causes of pulmonary hypertension due to vasoconstriction?
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The common causes of pulmonary hypertension due to vasoconstriction are: - High altitude - Sleep apnoea syndrome - COPD - V/Q mismatch |
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What are the common causes of pulmonary hypertension due to thromboembolism?
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The common causes of pulmonary hypertension due to thromboembolism are: - Emphysema - Lung fibrosis - Microembolism (DIC) |
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What are the common causes of pulmonary hypertension due to vein occlusion?
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The common causes of pulmonary hypertension due to vein occlusion are: - Backward left-sided heart failure |
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What are the consequences of pulmonary hypertension?
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The consequences of pulmonary hypertension: - Cor pulmonale - Inadequate left ventricular filling causing left-sided heart failure - Endothelial damage leading to atherosclerosis |
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What is the pathogenesis of renovascular hypertension?
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Renovascular hypertension develops when stenosis of the renal artery causes decreased renal blood flow, which activates the RAAS.
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What is the depressor system in the kidney, and where in the kidney is it located?
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The depressor system in the kidney can lower the blood pressure by secreting vasodilators. It is located in the kidney parenchyme. |
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What is the pathogenesis of renoparenchymal hypertension?
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Renoparenchymal hypertension develops when there is damage to the kidney parenchyme and therefore the depressor system.
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What is Conn syndrome?
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Conn syndrome, or primary hyperaldosteronism is a condition where the aldosterone levels are high. This causes hypertension.
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What is Cushing syndrome?
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Cushing syndrome is a condition where cortisol levels are high. It can cause hypertension by cortisol acting on mineralocorticoid receptors.
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What is adrenogenital syndrome?
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Adrenogenital syndrome is a condition where the adrenal glands undergo hyperplasia. Elevated levels of deoxycorticosterone causes hypertension.
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What is a pheochromocytoma?
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A pheochromocytoma is a cathecholamine-secreting tumor. It causes hypertension and can cause acute hypertensive crises.
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What is acromegaly?
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Acromegaly is a condition in which a pituitary tumor produces growth hormone. It causes hypertension.
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What is the mechanism for how acute heart failure causes pulmonary oedema?
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Acute heart failure causes cerebral hypoxia, which (by unknown mechanism) increases permeability in the pulmonary capillaries, causing oedema.
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