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421 Cards in this Set
- Front
- Back
- 3rd side (hint)
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What’s the difference between pacemaker and cardiac myocyte action potential? |
Back (Definition) |
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Formula for blood pressure? Changes in what factors will lead to change in BP? |
Blood pressure: cardiac output x peripheral resistance
Any changes in cardiac output, blood volume or peripheral resistance will lead to a change in BP |
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Short term blood pressure regulation mechanisms. Rapid response (seconds to minutes) |
Baroreceptor reflex: Regulates blood vessel diameter, heart rate, and contractility
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Where are baroreceptors found? |
They are stretch receptors found in: -carotid sinus = just above the bifurcation of external and internal carotids -aortic arch -and the walls of larger arteries |
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Describe the barorceptor reflex / baroreflex |
Baroreceptors detect increased blood pressure by stretch of arterial blood vessels. They carry this information up to the nucleus tractus and synapse. From there the impulses are sent up to the cardiovascular centre in the medulla The cardiovascular centre consists of two control centres: 1) Vasomotor control centre (which controls the diameter of blood vessels) 2) Cardiac control centre which has two parts. -cardiac accelerator (which increases heart rate & contractility) via sympathetic nerve fibres -cardiac decelerator (which decreases heart rate) via the parasympathetic fibres (NB: only sympathetic fibres affect contractility & diameter of blood vessels) |
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What happens short term when there’s high blood pressure? |
1) Stretch receptors detect the additional stretch and send impulses up to the cardiovascular centres via the vagus and glossopharyngeal nerve 2) The sympathetic action is inhibited (vasoconstriction of blood vessels is inhibited so arterioles dilate which decreases peripheral resistance. Veins also dilate, decreasing the rate of venous return to the heart thus decreasing preload/ diastolic filling of the heart leading to decreased cardiac output). Contractility & heart rate also decreases. 3) Parasympathetic action is activated: this slows down the heart rate 4) Combined affects of both result in decreases cardiac output. Since BP = CO x PR, and there’s a decrease in CO AND PR, blood pressure DECREASES. |
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What do different baroreceptors respond to? |
Respond more to CHANGING pressure rather than stationary pressure Carotid sinus: responds to an increase or decrease in arterial pressure Aortic arch: responds to increase in arterial pressure |
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What is the short term regulation in hypotension? |
The EXACT opposite of increased BP (decreases bp might occur due to rapid blood loss) Release of epinephrine and norepinephrine from the adrenal gland to enhance heart rate |
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What do chemoreceptors respond to CHANGES of? |
pCO2, pO2, pH |
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What are the two types of chemoreceptors, where are they found, and what do they respond to? |
Central and peripheral chemoreceptors Central chemoreceptors: found in medulla oblongata (ventrolateral surface) and they respond to changes in pH and CO2 Peripheral chemoreceptors: found in the aortic body (responds to changes in O2 and CO2) and carotid body (responds to changes in all 3) |
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How do chemoreceptor action work? |
A decrease in pO2 / pH or an increase in pCO2 stimulates the vasomotor centre This leads to an increase in cardiac output, heart rate, and vasoconstriction Therefore INCREASING bp (speeding the return of blood to the heart and lungs) |
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How does the RAAS system increase long term blood pressure? |
Angiotensin II is a powerful vasoconstrictor and is therefore capable of inducing hypertension Increased arterial pressure = decreased NaCl reabsorbed in the proximal tubule = more NaCl in the macula dense = decreased blood volume (this is called pressure natriuresis so basically the body increases sodium excretion when arterial blood pressure is high) |
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Some common vasodilators and vasoconstrictors |
Vasodilators: NO, bradykinin, prostacyclins, histamine, VIP, adrenaline (in skeletal muscles and liver) Vasoconstrictors: serotonin, endothelin, thromboxane, noradrenaline, angiotensin II, adrenaline (except in skeletal muscle and liver) |
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What are the different types of hypertension and what are their differences? |
Primary/ essential hypertension (90-95% of cases) -no identifiable cause -idiopathic -cause cannot be treated Secondary hypertension (5-10%) -result of underlying cause -suspected if patient is less than 40, hypertension that is resistant to treatment, has other symptoms too |
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Factors causing primary hypertension? |
GRADES 1. Issues in RAAS system (angiotensin may stimulate SNS centrally - patients respond to treatment with ACE inhibitors) 2. Genetic factors 3. Endothelial dysfunction (imbalance between vasodilators (NO) and vasoconstrictors (endothelin) leads to changes in endothelium) / hypertension can also lead to endothelial damage 4. Arterial stiffness (ageing causes thinning of arteries/ calcification. Can be caused by decreased vascular elasticity. Isolated systolic hypertension is common in elderly) 5. Dietary sodium and potassium 6. Issues with sympathetic NS (increased sensitivity to catecholamines) |
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Risk factors of primary hypertension |
Old age Obesity Heavy alcohol consumption Smoking African descent Sedentary lifestyle Family history Salt-heavy diet Social deprivation Anxiety and emotional stress |
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Causes of secondary hypertension: renal causes |
Chronic pyelonephritis Diabetic neuropathy: microalbuminuria or proteinuria Polycystic kidney disease: abdominal or flank mass, microscopic Haematuria Obstructive uropathy Renal cell carcinoma |
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Causes of hypertension: connective tissue disorders |
Scleroderma Systemic lupus erythematosus Polyarteritis nodosa |
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Causes of secondary hypertension: vascular disorders |
Coarctation of aorta: upper lump hypertension, significant difference in blood pressure between left and right Renal artery stenosis |
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Causes of secondary hypertension: drugs and substances |
Alcohol Cocaine and other substances Anti-depressants COCO, NSAIDS Corticosteroids Erythropoietin Liquorice |
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Causes of secondary hypertension: endocrine disorders |
Primary hyperaldosteronism (conn’s syndrome) MOST COMMON CAUSE OF HYPERTENSION Phaechromocytoma Cushing’s syndrome Acromegaly Hypothyroidism- increased diastolic BP Hyperthyroidism- increased systolic BP (increases systolic bp by decreasing systemic vascular resistance, increasing heart rate, raising cardiac output |
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Summary of the causes of secondary hypertension: |
Recent Renal Endocrine Coarction of aorta Estrogen (oral contraceptive) Neurological (raised ICP) Treatments (glucorticoids, NSAIDS) |
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What are the clinical symptoms of hypertension? |
Palpitations Angina Headache Blurred vision New neurology (eg. Limb weakness, paraesthesia) |
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Clinical signs of hypertension |
N CRAP New neurology Retinopathy Cardiomegaly Arrhythmias Proteinuria |
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How is hypertension diagnosed? |
NICE recommends the use of ambulatory BP measurements (ABPM) for the diagnosis of stage 1 and 2 hypertension. ABPM is a 24 hour evaluation of BP. Values should be checked in both arms to avoid white coat hypertension |
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How is hypertension staged |
Clinical bp ABPM Stage 1: >140/90 >135/85 Stage 2: > 160/100 >150/95 Stage 3: >180S/ 120D N/a Consider treatment for stage 1, definite treatment for stage 2, immediate referral to urgent care |
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What other investigations can be done for hypertension? |
12-lead ECG Urine dipstick Urine albumin: creatinine ratio Plasma glucose, electrolytes, creatinine eGFR (to exclude adrenal disease, CKD and diabetes) |
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Complications of hypertension |
PH SVC Stroke (increased risk of CVS events) QRISK3 score can help predict risk Vascular dementia Coronary heart disease Peripheral arterial disease Hypertensive retinopathy |
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What is hypertensive crisis? |
Systolic > 180 mmHg AND diastolic >120 mmHg Evidence of impending irreversible organ damage; commonly caused by patients with chronic hypertension who have stopped taking medication. Failure of normal auto regulation (confusion, drowsiness, chest pain, breathlessness) and bad prognosis |
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Hypertensive crisis can be divided into which two categories? |
Hypertensive urgency: no damage to end organs Hypertensive emergency: damage to end organs and symptoms (brain, lungs, heart, kidneys) |
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Hypertension management |
Step 1 Under the age of 55: ACE inhibitor or angiotensin 2 receptor blocker (ARB) Over the age of 55: calcium-channel blocker (CCB) Step 2 ACE inhibitor/ ARB + CCB Step 3 ACE Inhibitor/ ARB + CCB + Thiazide-like diuretic Step 4 Resistant hypertension: ACE inhibitor/ ARB + CCB + Thiazide-like diuretic + consider further diuretic 20,21 or alpha blockers or beta blockers 22. Seek expert advice |
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What is arteriosclerosis? |
Hardening & thickening of arterial wall Atherosclerosis is a form of arteriosclerosis |
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What is arteriolosclerosis? |
Hardening of small arteries/ arterioles |
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What is atherosclerosis? What can it be caused by? |
Hardening of medium/ large arteries caused by a build up of cholesterol plaques in the intima |
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What is an atheroma? |
Fibrous plaque |
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What are the common sites of arteriosclerosis? |
Most to least common: Abdominal Coronary Popliteal Carotid Circle of Willis |
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Stages of atheroma |
Back (Definition) |
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What is hypoxic hypoxia? |
Due to low O2 caused by pulmonary disease |
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What is anaemia hypoxia? Apart from anaemia what else causes this? |
Due to inadequate O2 delivery by Hb Caused by anaemia and CO poisoning |
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What might cause circulatory hypoxia or ischaema? |
Cardiogenic shock (whole body) and prolonged use of a tourniquet |
Cardiogenic shock is a life-threatening condition in which your heart suddenly can't pump enough blood to meet your body's needs. The condition is most often caused by a severe heart attack, but not everyone who has a heart attack has cardiogenic shock. Cardiogenic shock is rare. |
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What is histotoxic hypoxia? What might cause histotoxic hypoxia? |
Hypoxia that arises when tissues are unable to utilise O2 Eg. Cyanide poisoning |
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Which coronary artery is the coronary artery syndrome most likely to occur in? What is coronary artery disease? |
Left anterior descending artery Coronary artery disease develops when the major blood vessels that supply your heart become damaged or diseased. Cholesterol-containing deposits (plaques) in your coronary arteries and inflammation are usually to blame for coronary artery disease. The coronary arteries supply blood, oxygen and nutrients to your heart. A buildup of plaque can narrow these arteries, decreasing blood flow to your heart. Eventually, the reduced blood flow may cause chest pain (angina), shortness of breath, or other coronary artery disease signs and symptoms. A complete blockage can cause a heart attack. |
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Anatomy of the coronary arteries |
Front & back |
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What is angina? Aka angina pectoris? What is the classic presentation of angina? |
Chest pain or pressure due to lack of blood flow to the heart muscle causing ischaemia “Tearing chest pain” that can radiate to arm/ jaw/ neck
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What is stable angina? |
Chest pain that presents during physical activity when there’s an increased demand in O2. This happens because there’s a stable atherosclerotic plaque present in the coronary artery (70% of the lumen is blocked) so enough blood can get through to meet O2 demand at rest but during exercise or emotional stress when metabolic demand is high, not enough blood can get through causing subendocardial ischaemia (imagine the chest wall width ways, subendocardial is the area further from the epicardium, closest to the inside of the heart) . This causes DEMAND ISCHAEMIA but NO INFARCTION |
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What is unstable angina? |
The plaque ruptured + thrombus forms around ruptured plaque causing partial occlusion Pain occurs at rest or progresses rapidly over a short period of time This causes SUPPLY ISCHAEMIA + NO INFARCTION (Difference between unstable angina and MI is that unstable angina consist of ALIVE but ischaemic myocardium but MI consists of necrotic myocardium) |
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What is prinzmetal angina aka variant angina? |
No atherosclerotic plaque blocking the lumen, instead it’s caused by coronary artery vasospasm. The smooth muscles around the coronary artery randomly constricts. There is no correlation with stress or exercise. This reduces blood flow thus oxygen flow causing supply ischaemia This causes transmural ischaemia = ST elevation (Transmutation ischaemia = no oxygen to the entire myocardium not just subendocardium) |
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What conditions does acute coronary syndrome (ACS) consist of? |
Unstable angina NSTEMI STEMI |
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What is the area of the heart applied by the artery known as? |
Zone of perfusion |
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What happens in a myocardial infarction? |
A thrombotic ruptured plaque completely occluded the coronary artery causing the zone of perfusion to become ischaemic (muscle affected cannot contract properly now but this stage is reversible!!) After 20-40 mins the damage becomes irreversible + cells begin to die off. Zone of perfusion becomes zone of necrosis. |
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What are the two types of MI? |
NSTEMI STEMI |
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What is an NSTEMI? |
NSTEMI is a type of heart attack that does not have a ST segment elevation on an ECG or instead has a ST depression. NSTEMI is when during an MI the occlusion suddenly clears, and only the inner 1/3 of the heart (subendocardium) has undergone necrosis. Or alternatively if the atherosclerotic plaque PARTIALLY occludes the artery, not completely and allows some oxygenated blood to pass through and oxygenate tissues proximal to the plaque (hypoperfusion). In both circumstances, ischaemia and then necrosis if the inner 1/3 of the myocardium occurs. This is therefore also known as subendocardial infarction. |
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In an NSTEMI if the blockage suddenly lyses + breaks down what happens? |
The damage is limited to the inner 1/3 of myocardium (the innermost section of the heart). This is called SUBENDOCARDIAL INFARCTION and is characteristic of an NSTEMI |
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What’s a STEMI? |
(STEMI) occurs when a coronary artery becomes blocked (complete occlusion) by a blood clot, causing continued ischaemia. After 3-6 hrs the zone of necrosis extends through entire heart tissue causing TRANSMURAL ISCHAEMIA (characteristic of a STEMI) |
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What are possible complications of acute coronary syndrome/ Myocardial infarction? |
0-24 hours after MI: possible arrhythmias causing disrupted signals 1-3 days after: tissues may become inflamed causing pericarditis 3-14 days after: macrophages might invade, and start repair process by making connective tissue. This might cause myocardial rupture After two weeks: scarring may occur causing heart failure (bc that scared tissue is useless in helping to pump the heart so hypertrophy of cardio myocytes occur, in the long term causing heart failure) |
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How to diagnose an ACS? |
When there is irreversible damage to the heart tissues membranes are destroyed and enzymes + proteins from the tissues escape and enter blood. These markers are now used to indicate MI: Troponin I + T (most specific) Creatinine Kinase M+B (CK-MB) Myoglobin |
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When is troponin I + T released? When does it peak? How long does it last for? |
2-4 hours after infarction Peaks at 48 hours Lasts 7-10 days |
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What is CK-MB used to check? When is it released? When does it peak? How long does it last? |
To check for re-infarction Released 2-4 hours after MI Peaks at 24 hours Lasts 48 hours |
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When is myoglobin released? |
Earliest out of the three markers, and lasts around 48 hours |
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How to spot an NSTEMI from an ECG? |
ST depression Or T wave inversion |
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How to spot a STEMI in ECG? |
ST elevation |
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What are the different ECG leads called? |
I aVR V1 V4 II aVL V2 V5 III aVF V3 V6 |
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How are the different leads grouped together : what plane of the heart do they correspond with : which artery they affect? |
I + aVL + V5 + V6 = lateral = LCx or diagonal II + III + aVF = Inferior = RCA V1 + V2 = septal = LAD V3 + V4 = anterior = LAD |
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What is peripheral arterial disease caused by? |
Atherosclerosis and ischaemia |
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What is peripheral arterial disease and what is it caused by? |
Peripheral artery disease is a narrowing of the peripheral arteries serving the legs, stomach, arms and head. It is caused by atherosclerosis and ischaemia |
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What is chronic limb ischaemia? |
A condition where due to the presence of an atherosclerotic plaque there is a decrease in blood supply through the arteries supplying the legs meaning the tissues receive less O2 and become ischaemic |
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How do ischaemic tissues cause pain? |
Releases adenosine which causes pain = claudication/ limping Peripheral vascular/ artery disease is usually stable and doesn’t cause pain at rest. But increased walking/ exercise can increased demand for O2 this cause claudication/ pain |
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Depending on the location of pain in the lower limbs, it can be inferred what artery is affected. What arteries affect the following: -pain in hips and buttocks -pain in thighs -pain in upper 2/3 calf -pain in lower 1/3 calf -pain in foot |
-hips and buttocks: aorta + iliac -thighs: common + superficial femoral -upper 2/3 calf: popliteal -lower 1/3 calf: tibial -pain in foot: peroneal |
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What are other symptoms of chronic limb ischaemia apart from pain? |
-Elevation pallor: foot may turn pale when raised as gravity is against blood flow -Dependent rubor: foot might turn red when foot is tilted down as gravity is working with blood flow -Ulcer don’t heal normally As the plaque gets bigger: -Rest pain = continuous burning pain when the foot is elevated and relived when lowered -Gangrene |
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Signs of chronic limb ischaemia? |
Cold lower limb with dry skin + lack of hair Diminished or absent pulse sounds in the lower limb Possible AAA (abdominal aortic aneurysms) |
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Investigations for chronic limb ischaemia? |
Auscultation of iliac arteries of leg: bruit (whooshing sound) Doppler ultrasound (visualising blood flow) CT or MR angiogram Ankle-brachial index (ABI) = systolic BP of ankle/ systolic BP of arm: -normal = >0.9 -claudication = 0.4-0.9 -rest pain =0.2-0.4 -tissue loss =0-0.2 |
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What are the signs and symptoms of acute limb ischaemia? 6P’s |
Pain Pallor Paralysis Pulselessness Paraethesia Perishingly cold |
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What is chronic venous insufficiency? What defect does this cause to the veins? |
Chronic venous insufficiency (CVI) is when the downwards gravitational pull of blood causes veins walls to pull apart causing the valves to pull apart too. This leads to back flow of venous blood and eventual stasis. The extra blood over time causes these veins to become tortuous |
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What other diseases does chronic venous insufficiency cause? |
Varicose veins Deep vein thrombosis |
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What are collateral veins? |
Collateral veins are used as an alternate pathway to stop blood stagnation. They take the blood away from varicose veins back to the heart. Deep veins usually act as collateral veins but overtime they can also become enlarged + tortuous causing blood to pool (if this occurs over a long period of time = CHRONIC VENOUS INSUFFICIENCY). |
Varicose veins are twisted, enlarged veins. Any superficial vein may become varicosed, but the veins most commonly affected are those in your legs. That's because standing and walking upright increases the pressure in the veins of your lower body. |
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What vein are most commonly affected and become varicose veins? |
-superficial veins of legs (as they see higher pressures when standing rather than deep veins) -in the scrotum in men (varicocele). Warm stagnant blood can increase temperature in testicle eventually causing testicular atrophy -pooled blood in deep veins can also start to cause inflammatory reactions in vessels + surrounding tissues causing FIBROSIS + ULCERS |
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How can varicose veins be investigated for? |
Trendelenburg test = determines competency of valves in superficial and deep veins of legs in patients with varicose veins Doppler scans (more reliable) |
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What’s an ulcer? |
Unhealed sore or open wound due to destruction |
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What categories can ulcers by described using? |
Edge Depth Discharge: serous, serosanguinous, purulent Smell/ appearance Local or systematic Lymph node |
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What are the different possible edges of ulcers at what do they signify? |
Sloping edge/ healing ulcer / eg.venous stasis ulcer Punched-out edge/ arterial or neuropathic/ syphilitic gumma or ischaemic ulcer Undetermined edge/ infected/ tuberculous ulcer Rolled edge/ basal cell carcinoma Everted edge/ carcinomatous ulcer/ squamous cell carcinoma |
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The type of ulcer can be determined by the location of the ulcer. Where are venous, arterial, and neuropathic ulcers usually found? |
Venous: above medial and lateral malleolus Arterial (usually in pressure point, areas of low tissue perfusion): under heel, over toe joints, over malleoli Neuropathic (present on pressure points): over toe joints, under metatarsal, under heel, over malleoli |
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What are arterial ulcers? |
Ischaemic ulcers, they usually occur as a consequence of peripheral arterial disease. They occur in skin and tissues that are deprived of O2 (leading to necrosis and formation of an open wound) Lack of blood supply can result in minor scrapes or cuts failing to heal that also develop into ulcers |
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Signs of an arterial ulcer? |
Cold + pale leg Absent peripheral pulse, arterial bruits + loss of hair Delayed capillary refill |
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Characteristics of an arterial ulcer: |
Deeper + punched out Round + well-defined margins Black necrotic tissue Painful and patient gets temporary pain by hanging foot off bed Dry, think skin Reduced hair growth No bleeding |
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What is a venous ulcer? |
Venal valvular dysfunction results in stasis of blood causing an increase in venous pressure. This allows fluid and blood proteins to leak into surrounding tissues and overtime causing tiny capillaries to pinch shut. This leads to tissue ischaemia and then necrosis |
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Signs of a venous ulcer |
Varicose veins Oedema Brown discolouration of lower leg/ feet |
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Characteristics of a venous ulcer |
Shallow but large wound Irregular margins Base is normally red + large amount of exudate (haemosiderin staining (brown) + yellow exudate) Oozes blood Relatively painless |
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What is congenital heart disease? |
Congenital heart disease means a heart condition or defect that develops in the womb, before a baby is born |
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Examples of congenital heart diseases: |
Atrial septal defect Ventricular septal defect Atrioventricular septal defect Bicuspid aortic valve Coarction of aorta Ebstein’s anomaly Tetralogy of Fallot Transposition of great arteries |
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Describe normal atrial septal development |
1. A tissue called septum primum grows from the top of the heart toward the endocardial cushion (creating two chambers out of the atrium (right and left) 2. A hole appears near the top of this septum primum called ostium secondum 3. Another tissues called septum secondum grows from the top of the heart to the endocardial tissue, growing to the right of the septum primum 4. A small opening at the bottom of septum secondum is left open, this hole is called foramen ovale 5. This is now a make shift valve now which allows R to L shunting prenatally 6. At birth septum primum and septum secondum snap shut |
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What direction of blood flow does the foramen ovale provide? |
R to L shunt |
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What is atrial septal defect (ASD)? Which septum doesn’t grow enough for which ASD? |
Birth defect of the heart valve where there is a hole left in the septum that divides the atria (most commonly caused by the presence of ostium secondum, in which the septum secondum doesn’t grow enough during development so the hole remains open. You could also get a ostium primum ASD where septum primum doesn’t grow enough) This causes acyanotic defect (where oxygenated blood gets mixed with deoxygenated blood thus increasing O2 saturation in RA, RV, and PA. Extra blood also causes the delayed closure of the pulmonary valve) |
Acyonotic defect: it’s when the amount of oxygen in the body is not decreased |
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What is ASD cause associated with? |
Foetal alcohol syndrome 25% of Down syndrome cases have ostium primum ASD
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What is the pathophysiology of ASD? |
The L to R shunt loads more blood into the right heart causing pulmonary hypertension. |
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What are the clinical features of ASD? Systolic or diastolic murmur? Valvular heart sound? Which arrhythmias? |
Split S2 sound + systolic murmur (due to delayed closure of the pulmonary valve) Can result in: -Failure to thrive in children -Right sided heart failure -Arrhythmias (eg. atrial flutter) -Embolic events -Pulmonary hypertension |
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Potential complication of ASD? |
Paradoxical embolus (An emboli from DVT ends up passing through the right heart to the left through ASD and ends up in the brain causing a stroke) |
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Explain normal ventricular septal development |
Muscular ridge of tissue grows upwards from the apex of the heart and fuses with a thinner membranous region coming down from the endocardial cushions. If these don’t fuse then a hole is left in between. |
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What is a ventricular septal defect (VSD)? |
A hole in between the ventricles (Most common heart defect in babies but 30-40% close spontaneously so VSD is less common in adults) |
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What is VSD associated to be caused by? |
Foetal alcohol syndrome + Down’s syndrome + Trisomy 13 |
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What is the pathophysiology of VSD? |
Higher pressure on the left side of the heart than the right side causing a L to R shunt (acyanotic defect) However overtime the additional blood going to the lungs causes pulmonary hypertension to the point where pulmonary pressure > systemic pressure. When this happens blood flow is reversed and turns into a R to L shunt which is cyanotic (this is called eissenmenger syndrome) |
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What does the eissenmenger syndrome cause? |
A cyanosis defect = decreased O2 to tissues Pulmonary hypertension becomes greater than systematic blood pressure so it becomes a left to right shunt instead causing a cyanotic defect |
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What are the clinical features of a VSD? |
Pansystolic murmur (associated with smaller VSDs, as the pressure equalised in large VSD the murmur is softer) Systolic thrill with parasternal heave Signs of pulmonary hypertension Cyanosis |
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What is an atrioventricular septal defect? |
Deficiency of AV septum due to abnormal or inadequate fusion of superior and inferior endocardial cushions Can be complete or incomplete |
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Complete AVSD? |
A large hole in the centre of the heart allowing communication between all 4 chambers (one common AV valve) |
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Incomplete AVSD? |
Only has some defects (Has both tricuspid and bicuspid valve) |
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What are the clinical features of AVSD? |
Pansystolic murmur (due to AV regurgitation) Breathing problems Pounding heart Weak pulse Cyanosis Poor feeding + slow weight gain Fatigue Peripheral oedema and ascites |
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Potential complications of AVSD? |
Arrhythmias Congestive HF Pulmonary hypertension |
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What is bicuspid aortic valve? What gene is it associated with? What can is a complication of it? |
Aortic valve with 2 leaflet instead of 3 Associated with NOTCH1 gene Males > females Can cause aortic regurgitation or stenosis |
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What is coarctation of aorta (CoA)? |
Narrowing of the aorta There’s three different types |
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What are the 3 types of CoA? |
Pre-ductal coarctation (most common) Ductal coarctation Post-ductal coarctation |
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What is pre-ductal coarctation? When does it occur? What is it associated with? |
Coarctation comes AFTER aortic arch but BEFORE patent ductus arteriosus This is known as infant coarctation (occurs during foetal development) Associated with Turners syndrome (where only 1 X chromosome is inherited in females) |
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Pathophysiology of pre-ductal coarctation |
Normally the left heart & aorta would have much higher pressure than the right heart and pulmonary artery. However due to the coarctation, although there’s still high pressure upstream of coarctation, there is now much lower pressure downstream of coarctation (lower pressure in aorta than PA) So blood moves from PA into patent ductus arteriosus and into the aorta (thoracic aorta). This blood is deoxygenated blood though and is pumped into lower extremities. It causes CYANOSIS at birth (blue/ purple lower extremities in babies) |
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What is ductal coarctation? |
At insertion of ductus arteriosus Usually appears when ductus arteriosus closes |
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When does Post ductal coarctation occur? |
Occurs after ligamentum arteriosum No patent ductus arteriosus + no mixing of oxygenated and deoxygenated blood |
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Pathophysiology of post-ductal coarctation? |
There is a higher pressure before the coarctation than after = causing upstream and downstream issues |
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What are the upstream issues of a post-ductal coarctation? |
Increased blood flow into aortic branches leading to increased BP in upper extremities and head (this causes increased cerebral blood flow + increased risk of berry aneurysms; most common type of brain aneurysm) Aortal and aortic valve dilation (this causes pressure + increased risk of aortic dissection) |
Aortic dissection : Aortic dissection (AD) occurs when an injury to the innermost layer of the aorta allows blood to flow between the layers of the aortic wall, forcing the layers apart. In most cases, this is associated with a sudden onset of severe chest or back pain, often described as "tearing" in character. |
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Downstream issues of post-ductal coarctation |
Decreased blood flow to the lower extremities (because of reduced bp) Reduced perfusion to kidneys, causes RAAS activation, causing hypertension (headaches and nosebleeds) Severe narrowing causing formation of collateral circulation involving the pericapsular and intercostal arteries |
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What does the reduced bp (downstream issue) caused by post-ductal coarctation lead to in the lower limbs? |
weak pulse claudication (due to reduced BP) cold legs (due to reduced flow) |
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What is the consequence of collateral circulation of the intercostal arteries? |
Anterior intercostal arteries and the first two posterior intercostal arteries are supplied by the aorta BEFORE coarctation so the BP in them is very high. Posterior arteries 3 and below are all supplied by the aorta AFTER coarctation so BP is very low. These anterior and posterior arteries anastomose in the middle and the high blood pressure from the anterior arteries causes the posterior arteries to dilate in order to accommodate the blood flowing into them. They dilate so much that when the heart beats, the posterior arteries pulsate and rub against the ribs causing RIB NOTCHING (mainly affects ribs 3-4; no reversed flow in ribs 1-2 so no rib notching there) |
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Clinical features of post-ductal coarctation? |
Radio-femoral delay Radio-radial delay (if coarctation is before subclavian) Mid-systolic murmur Vascular murmur (bruits) |
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What investigations should be done for post-ductal coarctation? |
CXR dilated aorta at the site of coarctation (shaped like a 3) ECG CT or MRI Blood pressure in legs is lower than arms Femoral pulse is felt AFTER radial pulse (normally it’s the other way around) |
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What is ebstein’s anomaly? |
Septal and posterior leaflets of tricuspid valve are displaced into apex of RV This causes ‘arterialisation’ of right ventricle (large RA and small RV bc part of the RV basically becomes RA) Occurs due to the valve not separating normally from ventricular myocardium during development |
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What’s the the clinical features of ebstein’s anomaly? |
S3 and S4 sounds Widely split S1 and S2 sound Systolic murmur of tricuspid regurgitation Cyanosis due to patent foramen ovale Right atrial hypertrophy Right ventricular conduction defect |
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What is tetralogy of Fallot? ToF |
4 things: -pulmonary artery stenosis: blood can’t get through to lungs very well thus leads to... -right ventricular hypertrophy (in order to compensate and push blood through the ventricle) -ventricular septal defect (usually accompanies the pulmonary stenosis and hypertrophy. Usually a VSD would grant a L to R shunt but because of the very high pressure in the RV, deoxygenated blood acc ends up going from R to L. This causes cyanosis) -overriding aorta (it can be right under the VSD shunt? The position of it is just abnormal) |
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What are the clinical features of tetralogy of Fallot? |
Babies often exhibit symptoms of cyanotic spells = “tet spells” Patients may have a pansystolic murmur |
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Walk through a cyanotic spell |
Normal > increased O2 demand when the baby movies around a lot> heart pumps more deoxygenated blood > CYANOSIS > baby squats down > kinks femoral arteries > increased vascular resistance > so increase systemic pressure > pressure in L is greater than R > shunt reversed > back to normal |
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What are the great arteries? |
Aorta and pulmonary arteries |
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What is transposition of great arteries (TGA)? |
Can exists as complete/ dextro transposition of great arteries The two great arteries swap locations - this means the blood on the right side never gets oxygenated and blood in left never gets deoxygenated |
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Why does dextrose TGA not exhibit symptoms in the foetal heart? What is the only way to really survive TGA? |
Because the foetus is reliant on the maternal circulation and shunts so doesn’t use its own lungs However after birth, the baby has to use its own lungs Dextro-TGA can be fatal unless there is a way to mix the pulmonary and systemic circulation (patent foramen ovale, PDA, VSD) System is very insufficient as tissues don’t receive enough O2. Babies must be supplied with prostaglandin E to keep the PDA open |
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What is complete or dextrose transposition of great arteries (TGA)? |
The two great arteries swap locations - this means the blood on the right side never gets oxygenated and blood in left never gets deoxygenated |
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What happens if the shunts are large enough in d-TGA? |
Symptoms are not noticed but will eventually lead congestive HF This will happen because of eventual right ventricular hypertrophy due to higher pressures (right ventricle is sending blood up the aorta to the body) and left ventricular atrophy due to lower pressures (left ventricle is only sending blood to lungs) |
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What is congenitally corrected or levo-TGA? |
Right and left ventricle swap places with the AV valves Circulation is preserved Acyanotic and no obvious symptoms at birth However tricuspid valve and the RV are built for lower pressure so causes RV hypertrophy and tricuspid valve will be stretched during regurgitation eventually just leading to heart failure |
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What is cardiomyopathy? |
A problem with heart muscles |
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What are the different types of cardiomyopathy? |
Dilated (most common) Hypertrophic Restrictive Arrhythmogenic |
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What happens to the sarcomeres during systole and dystole? |
During dystole sarcomeres lengthen causing the ventricles to relax (the more blood that fills in (preload)= more the sarcomeres stretch = more tension the sarcomeres hold = and the greater the stroke volume is) During systole the sarcomere shorten and cause the ventricles to contract |
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What’s the difference between concentric and eccentric hypertrophy? |
Concentric hypertrophy is associated with increased left ventricular wall thickness whereas eccentric hypertrophy is characterized by dilatation of the left ventricular chamber; however, there occurs a general increase in the overall size of cardiomyocytes under both conditions |
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What is dilated cardiomyopathy? |
Left ventricular hypertrophy (new sarcomeres are added in series making the heart bigger length ways but not width) so the chambers of the heart grow larger (dilate). This leaves the walls of the chambers thin compared to chambers size with less muscle to use for contraction. So think + less muscle = weaker contractions = less blood is pumped out of the heart (lower stroke volume). This causes the patients to develop biventricular congestive heart failure (type of systolic heart failure bc contractions occur during systole) As chambers get wider, the tricuspid & mitral valves are stretched out so they start regurgitating blood (mitral & tricuspid valve regurgitation) Occurs due to eccentric hypertrophy |
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What are the causes of dilated cardiomyopathy? |
Idiopathic Genetic: Duchenne muscular dystrophy (DMD), haemochromatosis Alcohol abuse Ischaemic heart disease Wet beriberi |
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What is wet beriberi? |
Thiamine deficiency |
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What infection might cause dilated cardiomyopathy? |
Coxsackievirus |
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What is the pathophysiology of dilated cardiomyopathy? |
1.Walls become thinner compared to the large chamber size 2. Heart muscle is weaker so cannot pump effectively 3. Weaker contraction = reduced stroke volume 4. SYSTOLIC HEART FAILURE As the chamber gets larger, the valves are more stretched out causing mitral and tricuspid regurgitation |
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What are the clinical features of dilated cardiomyopathy? |
Chest pain Fatigue Dyspnoea S3 sound Holosystolic murmer Arrhythmias Signs of heart failure |
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How to investigate for dilated cardiomyopathy? |
ECHO cardiogram ECG CXR |
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What is hypertrophic cardiomyopathy? |
Increased ventricular wall thickness without an obvious cause Causes due to concentric hypertrophy |
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What happens in hypertrophic cardiomyopathy? |
Myocardium becomes thick, heavy and hypercontractile The wall width = less than 15mm or 13mm of familial Most common cause of sudden cardiac arrest (heart stops beating) |
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What part of the heart does hypertrophic cardiomyopathy usually affect? |
Usually affects Left Ventricle |
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What are the causes of hypertrophic cardiomyopathy? What is it associated with? |
Autosomal mutation of myosin binding protein C and beta-myosin heavy chain (most common) Associated with people who have Friedrich’s ataxia (neurodegenerative condition) |
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What is the pathophysiology of hypertrophic cardiomyopathy? What murmur does it cause? |
1. Myocardium in LV is much bigger and a lot more stiffer (less elastic) both of which leads to less room for blood in LV 2. Therefore there is less filling of the ventricles during diastole 3. So less blood is pumped out and STROKE VOLUME is lower 4. DIASTOLIC HEART FAILURE 5. Because the myocardium is so thick, the tissues may become ischaemic (this is responsible for the fast arrhythmias) and may lead to sudden death (especially in young athletes) If there is muscle growth of the IV septum, it blocks the outflow tract (route to aorta) and also draws the anterior leaflet of the mitral valve inwards so there’s greater obstruction. This causes a crescendo-decrescendo murmur |
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What are the clinical features of hypertrophic cardiomyopathy? |
Chest pain Syncope Arrhythmia Dyspnoea S4 sound Pansystolic murmer due to mitral regurgitation Bifid pulse Sudden cardiac death |
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How to investigate for hypertrophic cardiomyopathy? What to look out for in the ECG specifically? |
ECHO cardiogram ECG = tall QRS complexes in ventricular hypertrophy Genetic analysis |
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What is restrictive cardiomyopathy? |
Walls of the heart are rigid (but not thick) Heart is restricted from stretching and filling with blood properly Less blood is pumped = DIASTOLIC HEART FAILURE |
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What’s the the causes of restrictive cardiomyopathy? |
Amyloidosis Sarcoidosis Endocardial fibroelastosis Haemochromatosis |
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Clinical features of restrictive cardiomyopathy? |
Signs of heart failure S4 sound |
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How to investigate for restrictive cardiomyopathy? |
ECHO cardiogram ECG CXR |
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What is arrhymogenic cardiomyopathy? |
Inherited condition, predominantly affects the RV Autosomal dominant mutation in the genes coding for desmosomes Fatty replacement of myocytes causing dilation Leads to ventricular arrhythmias |
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Clinical features of arrthymogenic cardiomyopathy? |
Ventricular arrhythmias Syncope Sudden cardiac death |
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What is heart failure? |
When the heart fails because it’s unable to meet the demands of the body because it cannot pump enough blood |
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What are the two different types of heart failure? |
Systolic heart failure = ventricles cannot pump enough blood Diastolic heart failure = ventricles cannot full up properly |
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Equation for ejection fraction: |
Stroke Volume / End-diastolic volume |
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Cardiac output equation: |
Stroke Volume x Heart Rate |
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What happens to stroke volume, end diastolic volume, and ejection fraction in systolic heart failure? |
Stroke Volume: ⬇️ End diastolic volume: same THEREFORE: Ejection Fraction ⬇️ |
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What ejection fraction is considered normal, borderline, and heart failure? |
Normal: 50-70% Borderline: 40-50% Heart Failure: <40% |
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What happens in diastolic heart failure? What happens to Ejection fraction? |
End diastolic volume decreased because ventricles cannot fill up properly, thus stroke volume decreases too As BOTH decrease, ejection fraction is PRESERVED |
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What is Frank Sterling Law? |
As end diastolic volume increases, stroke volume will also increase |
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Types of heart failure? |
1. Left-sided systolic heart failure 2. Left-sided diastolic heart failure 3. Right-sided heart failure |
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What are the three main causes of systolic left-sided heart failure? |
Ischaemia (MOST COMMON) Long-standing hypertension Dilated cardiomyopathy (All these damage myocardium which leads to weakened ventricular contractions) |
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How does ischaemia lead to left-sided heart failure? |
Atherosclerosis causes ischaemia which damages the myocardium. Less powerful contractions. |
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How does long standing hypertension cause left-sided heart failure? |
Causes CONCENTRIC left ventricular hypertrophy As there is more muscle = there is increased demand for O2 + compression of coronary arteries by the extra muscle so even less blood is delivered to myocardium. More demand of oxygen and reduced supply via blood causes muscles to weaken leading to systolic heart failure |
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How does dilated cardiomyopathy cause left-sided heart failure? |
The left ventricle dilates in order to fill up the ventricle with more preload = so contraction strength is greater (frank-starling) This works for a bit but overtime muscles around the ventricles become way too thin and thus weak. They struggle to contract all the blood out so cause systolic heart failure |
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What are the 4 main causes of left-sided diastolic heart failure? |
1. Long standing hypertension 2. Restrictive cardiomyopathy/ hypertrophic cardiomyopathy 3. Less blood to kidney activates RAAS 4. Aortic stenosis (overall ventricles do not fill properly due to less space in the heart or stiffness) |
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How does long standing hypertension cause left-sided diastolic heart failure? |
Causes concentric hypertrophy which reduces filling space So there’s less space for blood So causes diastolic heart failure
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How does restrictive cardiomyopathy cause left-sided diastolic heart failure? |
The muscle is still and less compliant so accommodates less blood |
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How does less blood entering the kidneys leading to RAAS activation cause left-sides diastolic heart failure? |
RAAS activation causes fluid retention. This initially helps because according to FRANK STARLING LAW, increases preload = increased contraction strength. More preload requires more forceful contractions which the heart can’t keep up with. Overtime large amounts of fluid leaks out of vessels and then builds up in surrounding spaces
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What are the problems with left-sided heart failure? |
Blood cannot be pumped forward so it backs up into the lungs causing pulmonary oedema Blood gets more and more backed up overtime All the way into the right side of the heart causing RIGHT SIDED HEART FAILURE |
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What’s the the clinical symptoms of pulmonary oedema caused by left sided heart failure? |
Dyspnoea and Orthopnea Crackles Coughing up pink frothy sputum Capillaries in the lung can also rupture causing haemosiderin macrophages (these are also known as heart failure cells!!!) |
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What are the three main causes of right sided heart failure? |
1. Pressure in pulmonary artery due to left heart failure 2. Cor pulmonale 3. Atrial septal defect (L-R shunt) |
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How might pressure in pulmonary artery due to LHF cause right sided heart failure? |
Harder to pump blood which causes right ventricular hypertrophy |
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How does cor pulmonale cause right-sided heart failure? |
Hypoxia causes pulmonary arteriolar vasoconstriction This increases pulmonary BP causing right ventricular hypertrophy |
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How might an atrial septal defect cause right sided heart failure? |
Right ventricular hypertrophy occurs due to the increased pressure This causes ischaemia and low end diastolic volume of the left side of the heart (this is true for ALL of the previous hypertrophic heart failures) |
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What problems might right-sided heart failure cause? |
Left heart failure causes fluid to build up in the lungs and right sided heart failure causes fluid to build up in the body causing: Raised JVP Hepatosplenomegaly (which might cause cirrhosis and ascites) Pitting oedema |
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What are the clinical features of heart failure? |
Nocturia Fatigue Tachycardia and arrhythmias S3 sound (systolic) and S4 sound (diastolic) Pulsus alternans = strong pulse followed by a weak pulse Pulmonary oedema = bi-basal crepitations |
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How is the neuro-hormonal system activated? |
Activated in response to myocardial injury which causes reduced cardiac output and reduced arterial pressure, however this compensatory mechanism ultimately cause the progression of heart failure |
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What 4 things happen when the neuro-hormonal system is activated? COMPENSATION FOR HEART FAILURE |
RAAS is activated Sympathetic Nervous System is activated Natriuretic Peptides are released ADH release |
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Pathophysiology of RAAS compensation in heart failure |
Activated in response to decreased renal perfusion due to low cardiac output. Angiotensin 2 binds to AT1 receptor leading to vasoconstriction causing: -Increasing bp -sympathetic tone -aldosterone -sodium -fibrosis |
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How does sympathetic nervous system help during heart failure? |
Releases catecholeamines which increase the heart rate and contractility Causing more hypertrophy, fibrosis and remodelling |
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What is compensation & decompensation in heart failure? |
Compensation: the body attempts to increase the cardiac output by either increasing the stroke volume or the heart rate. (SV x HR =CO) This is done through RAAS activation or SNS activation. This causes more blood to enter the heart, so stroke volume is greater and thus the heart contracts harder. However this harder contractions require more oxygen and blood but the cardiac cells aren’t getting that = so they start to die off. This is when the natriuretic peptides save the day, they oppose the SNS and RAAS and maintain the cardiac output even when the stroke volume is reduced. |
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What do natriuretic peptides do? |
Vasodilation Reduce bp Reduce sympathetic NS tone Reduce aldosterone levels Natriuresis Diuresis Antifibrolotic effects |
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What is ANP? |
Atrial natriuretic peptide is a peptide hormone secreted from the atrial myocytes in response to increased Atrial volume. ANP inhibits reabsorption of Na+ and water in the PCT and collecting ducts and causes naturesis. It also inhibits secretion of ADH and aldosterone. |
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What is BNP? |
Brain natriuretic peptide or ventricular natriuretic peptide is a hormone secreted by the cardiomyocytes in the heart ventricles in response to increased ventricular volume due to increased blood volume (BNP has x10 less affinity than ANP) |
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What is the function of ANP and BNP? |
Decrease systemic vascular resistance Decrease central venous pressure Increase natriuresis (sodium excretion by the kidneys) |
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What investigations can be done to check for heart failure? |
Bloods: elevated BNP / Elevated ANP/ hyponatremia or reduced sodium levels / ECG CXR (boot shaped heart suggest RV hypertrophy) Trans-thoracic ECHO (TTE) GOLD STANDARD (checks for the atrial and ventricular size, LV ejection fraction, and diastolic dilation |
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What is endocarditis? |
Inflammation of the inner layer of the heart (endocardium) |
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What is infective endocarditis? |
Infection of the endocardial surface of the heart including of valvular structures, chordae tendinae etc |
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What is non-bacterial thrombotic endocarditis (NBTE)? What part of the endocardium is commonly affected? |
Non-infective endocarditis Formation of sterile platelet + fibrin on cardiac valves and adjacent endocardium (valves are commonly affected as they are the site of turbulent blood flow. This is devoid of infection or bacteria!!) Happens due to trauma, circulating immune complexes, vasculitis, hypercoagulable state |
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What are the risk factors of endocarditis? |
Prostatic valve Congenital heart defects Rheumatic heart disease IV drug abuse |
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What are the acute causes of endocarditis? |
Staph. aureus (most common) Group A haemolytic streptococci Strep. Pneumonia Neisseria gonorrhoea |
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Subacute causes of endocarditis? |
Viridans streptococci (most common) Non-enterococcal group D streptococci Enterococci |
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Pathophysiology of endocarditis? |
Turbulence of blood flow damages the endocardial lining exposing the inner layers (collagen and tissue factor) Platelets stick to this and form a thrombus = NBTE Bacteria sticks to the thrombus causing inflammation |
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What are the clinical features of endocarditis? |
FROGS JN Fever Roth’s spot Osler’s notes Glomerulonephritis Splinter haemorrhages
Janeway lesions New murmur (depending on the valve affected)
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Investigations for endocarditis? |
bacteraemia FBC- positive for anaemia/ leukocytosis ECG CXR |
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What criteria is used to diagnose endocarditis? |
Duke criteria |
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Front (Term) |
1. Pericardial cavity 2. Endocardium 3. Myocardium 4. Fibrous pericardium 5. Parietal layer of serous pericardium 6. Epicardium (visceral layer of serous pericardium) |
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What is pericarditis? What is the pericardium usually perfused and innervated by? |
Inflammation of the pericardium. Haemorrhagic exudate in the pericardial cavity released by visceral pericardium Internal mammary arteries and innervated by phrenic nerve |
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What are the causes of pericarditis? |
Viral infection (most common): coxsackievarius Bacterial infection; mainly TB Idiopathic |
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What is the pathophysiology of pericarditis? |
1. Fluid and immune cells move into the pericardial tissue = tissue becomes thicker 2. Pericardial effusion develops as the serous pericardium cannot remove the fluid as quickly as it comes in 3. If a lot of fluid collects, the pericardium starts pushing pressure on the heart and prevents it from stretching out or relaxing between contractions 4. This can lead to cardiac tamponade (cardiac chambers can’t fill properly with blood leading to decreased CO) 5. If the inflammation persists, it can cause fibrosis of the serous pericardium which makes it become stiff . This is called constructive pericarditis 6. Overtime it becomes harder for the heart to expand and relax and overtime this reduces stroke volume and to compensate the heart rate increases. |
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What are the clinical features of pericarditis? |
Fever Chest pain: worse on heavy breathing and better when sitting up and leaning forward Large pericardial effusion: reduced heart sounds, reduced CP- shortness of breath, low blood pressure, light-headedness |
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Investigations for pericarditis? What will you hear in auscultation? What will you see on CXR? |
Auscultation: friction rub (caused by the serous layers rubbing against each other) ECG CXR: water bottle sign ECHO |
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Label the cardiac skeleton |
Back (Definition) |
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When do AV valves close? |
During ventricular contraction |
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When do semilunar valves close? |
At the beginning of ventricular relaxation (diastole) |
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What is preload? What conditions is it increased in? |
Volume of blood in ventricles at the end of diastole (end diastolic pressure) Increased in: Hypervolemia Regurgitation of cardiac valves Heart failure |
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What is afterload? What causes increased afterload |
Resistance left ventricle must overcome to circulate blood Increased in hypertension and vasoconstriction (Increased afterload = increased cardiac workout) |
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What is end diastolic volume (EDV)? |
Amount of blood in the ventricles before contraction |
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What is end systolic volume (ESV)? |
Amount of blood remaining in the heart after ejection |
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Cardiac cycle |
Back (Definition) |
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What is the first heart sound called and what creates it? |
S1 sound Results from closing of the mitral and tricuspid valves (Mitral valve closure = M1 and Tricuspid valve closure = T1) M1 closing is louder than T1 due to higher pressure in the left side of the heart so makes up the main component of the S1 sound |
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What is the second heart sound and what is it produced by? |
S2 sound Produced by the closure of aortic and pulmonary valves Aortic valve closure = A2 and Pulmonary valve closure = P2 A2 is louder than P2 due to higher pressure on the left side of the heart thus A2 makes up the main component of S2 sound |
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What is the third heart sound and what causes it? |
S3 sound aka ventricular gallop Occurs just after S2 when the mitral valve opens, allowing for possible filling of left ventricle Sound is ONLY produced by a large amount of blood striking overly complaint left ventricle Often a sign of systolic heart failure or volume overload |
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What is the fourth heart sound and what causes it? |
S4 sound aka atrial gallop Occurs just before S1 when the atria contracts and forces blood into left ventricle Sound is produced ONLY when left ventricle is a bit stiff and atrial contraction forces blood through AV valves Can be a sign of diastolic heart failure(hypertrophy) a sign of pressure overload or hypertension |
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What is the definition of murmer? |
Abnormal flow through diseased valves typically producing abnormal heart sounds |
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Severe lesions can be palpated as what? |
Thrills |
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What 4 factors help define what murmur you’re hearing? |
Timing Shape Location Pitch |
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What does the timing of the murmur tell us? |
Refers to whether the murmur is systolic or diastolic Systolic murmurs occur between S1 and S2 (between AV valve closure and semilunar valve closure) Diastolic murmurs occur between S2 and S1 (between semilunar valve closure and AV valve closure) |
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What happens to the different heart valves during systole and diastole? |
During systole AV valve closed and Semilunar valve opens Vice versa for diastole |
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When is a murmur heard? |
When the diseased valve interrupts the flow of blood during systole or diastole. Therefore: AV regurgitation or semilunar valve stenosis = systolic murmur AV stenosis or semilunar valve regurgitation =diastolic murmur |
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What are the 3 classifications of a systolic murmur? |
Mid-systolic murmur (ejection murmur): S1 and S2 and distinctively audible bc it begins after S1 sound and terminates before S2 sound Holosystolic murmur: S1 and S2 are almost impossible to hear bc it begins after S1 sound and extends upto S2 sound Late systolic murmur starts after S1 and may or may not extend upto S2 |
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What are the 3 classifications of diastolic murmurs? |
Early diastolic: S1 will be distinctively audible but S2 might be difficult to hear bc it starts at the same time as S2 and ends before S1 Mid-diastolic: both S2 and S1 are distinctively audible bc murmur starts after S2 and ends before S1 Late diastolic: starts after S2 and extends up to S1 |
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What does the shape of a murmur refer to and what are the different shapes? |
Refers to the change in intensity of the murmur over time: Crescendo = progressively gets louder Decrescendo = progressively gets quieter Crescendo-decrescendo = progressively gets louder then quieter (has a diamond shape) Uniform = does not change in intensity |
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Which murmur is associated with which valvular heart disease? |
Crescendo-decrescendo murmur: semilunar stenosis Holosystolic murmur: AV regurgitation Early diastolic or decrescendo murmur: semilunar regurgitation Mid-late diastolic murmur: AV stenosis |
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What does the location of murmurs tell us? |
(Location usually refers to where the murmur is best heard) Aortic valve: right sternal edge, 2nd intercostal space Pulmonary valve: left sternal edge, 2nd intercostal space Tricuspid valve: left sternal edge, 4th/5th intercostal space Mitral valve: mid clavicular line, 5th intercostal space |
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What can you learn from the pitch of a murmur? |
Murmur will be high pitched is there is a large pressure gradient across the pathological lesion (eg. Aortic stenosis bc there’s usually a large pressure gradient between left ventricle and aorta) Murmur will be low pitched when there’s a small pressure gradient (eg. Mitral stenosis bc there’s a lower pressure gradient between the left atrium and left ventricle during diastole) |
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What is stenosis? What is regurgitation? |
Stenosis: failure of the valve to open completely (usually chronic and thus well-tolerated due to ventricular hypertrophy or atrial dilation). Causes pressure overload. Regurgitation or insufficiency: failure of a valve to close completely, thus causing reversed flow (can be acute or chronic). Causes volume overload. |
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What are the 3 main mechanisms for valvular heart disease? |
1. Damage to collagen that weakens the leaflets eg. Mitral valve prolapse 2. Nodular calcification beginning in interstitial cells eg. Aortic valve stenosis 3. Fibrotic thickening (key feature in rheumatic heart disease) |
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What is rheumatic fever? What pathogen causes rheumatic fever? |
Inflammatory disease than can involve the heart, brain and joints Usually develops 2-4 weeks after an infection of the throat by streptococcal pyrogenes bacterium (if the infection is left untreated, it causes rheumatic fever) |
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What is the mechanism causing rheumatic fever? |
Production of antibodies against a persons own tissues Due to genetic reasons some people are more exposed to bacteria than others thus they’re more at risk of getting rheumatic fever and valvular disease |
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What investigations can be done for valvular disease? |
TTE (trans-thoracic echocardiogram): performed on all patients TOE (trans-oesophageal echocardiogram): performed in 20% of patients Stress echocardiogram = performed when the patient is exercising or by giving drugs to increase the heart rate eg. Dobutamine Catheterisation: angiogram is performed to assess the structure and function of coronary arteries |
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Cause of aortic stenosis? |
Mechanical stress overtime Bicuspid valve Chronic rheumatic fever |
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What murmur is heard in aortic stenosis? |
Crescendo-decrescendo systolic ejection |
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What are the other cardiac signs of aortic stenosis? |
Heaving apex with non-displaced beat Soft S2 sound Systolic thrill Ejection click Slow narrowing pulse Gallivardin phenomenon |
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What is the cause of aortic regurgitation? |
Aortic dilation Infective endocarditis Rheumatic fever |
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What murmur is heard in aortic regurgitation? |
Diastolic decrescendo murmur |
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What are other cardiac signs of aortic regurgitation? |
Widening pulse pressure S3 sound Austin-flint murmur |
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Mitral stenosis cause? |
Rheumatic fever |
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Mitral stenosis murmur? |
Delayed diastolic decrescendo |
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Other cardiac signs of mitral stenosis? |
Loud S1 Opening snap Palpitations Small pulse (AF) Malar flush |
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Mitral regurgitation causes? |
Mitral valve prolapse Ischaemic heart disease Rheumatic fever |
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Mitral regurgitation murmur? |
Holosystolic murmur |
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Other cardiac signs of mitral regurgitation? |
Pulsus paradoxus (exaggerated fall in bp when patient breaths in) Soft S1 and S3 Laterally displaced apex heart beat |
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Pulmonary valve stenosis cause? |
Congenital Mechanical stress over time |
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Pulmonary stenosis murmur? |
Crescendo-decrescendo systolic ejection |
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Other cardiac signs of pulmonary stenosis? |
Ejection click |
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Cause of pulmonary regurgitation? |
Pulmonary hypertension Infective endocarditis Rheumatic endocarditis |
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Pulmonary regurgitation murmur? |
Diastolic decrescendo |
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Other cardiac signs of pulmonary regurgitation? |
Graham-Steel murmur |
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Tricuspid valve stenosis cause? |
Rheumatic fever |
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Tricuspid stenosis murmur? |
Delayed diastolic decrescendo |
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Other cardiac signs of tricuspid stenosis? |
Opening snap |
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Tricuspid valve regurgitation causes? |
Pulmonary hypertension Rheumatic fever Heart attack |
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Tricuspid valve regurgitation murmur? |
Holosystolic |
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Other cardiac signs of tricuspid regurgitation? |
Loud P2 Carvallo’s sign (murmur gets louder with inspiration) Right ventricular heave |
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What is the definition of anaemia? |
Decrease in the volume % of RBC in the blood resulting in a Hb level of: -Less than 130g/L in men -Less than 120g/L in women (So you’re either losing blood too quickly or not making it fast enough) |
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What is the main symptom of anaemia? What are the 3 general causes why anaemia develops? |
Chronic, constant, unexplained fatigue -deficient erythropoiesis -excessive haemolysis -haemorrhage |
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What are three different types of anaemia? |
Microcytic = less than 80fL MCV Normocytic =80-100fL MCV Macrocytic = more than 100fL MCV |
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What are the systematic symptoms of anaemia? |
Eyes: yellowing Skin: pale, cold, yellowy Respiratory: shortness of breath Muscular: weakness Intestinal: changed stool colour Central: fatigue, dizziness, fainting(only in severe) Low blood pressure Heart: palpitations, rapid heart rate, chest pain, angina, heart attach (last 3 in severe) Spleen: enlargement |
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What are the 3 types of microcytic anaemia? |
Develops due to insufficient haemoglobin being available for erythropoiesis in the bone marrow. Therefore additional cell devisions occur in order to produce smaller RBC’s with sufficient haemoglobin concentrations: Fe3+ deficiency Thalassaemia Sidero-blastic |
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Two causes of normocytic anaemia? |
Haemorrhage Chronic disease |
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2 types of Macrocytic anaemia? |
B12 deficiency Folate deficiency |
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What is blood composed of? |
Plasma (55%) like water, protein and solutes Formed elements (45%) like erythrocytes, leukocytes, thrombocytes |
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What is ferritin? |
An intracellular protein that stores iron and releases it in a controlled manner |
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Hypochromic and hyperchromic ? |
Hypo= pale RBC = low Hb Hyper= bright red RBC =high Hb |
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What is mean corpuscular volume (MCV) |
lab volume that measures the average size and volume of RBC |
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What is MCH? |
Value that refers to the average quantity of Hb present in a single RBC |
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What is serum iron? |
Amount of circulating iron that is bound to transferrin (90%) and serum ferritin (10%) |
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What is total iron binding capacity? (TIBC) aka transferrin iron binding capacity? |
The amount of transferrin in your blood that is available to attach to the iron |
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What is transferrin? |
Protein produced in the liver that transports iron through the blood plasma = regulates the absorption of iron into the blood |
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Phase 1: atrial contraction |
1. Depolarisation of the SAN causes atrial depolarisation (P wave on ECG/ p wave is EVERYTHING up till Q) 2. Atrial depolarisation causes atrial systole, as the atria contract they exert pressure in the blood within which forces blood through open AV valves into the ventricles 3. The end of atrial systole is also the end of ventricular diastole (relaxation) |
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Phase 2: isovolumetric ventricular contraction |
1. As ventricular systole begins, the pressure inside the ventricles rises which causes the AV valves close shut producing the S1 sound 2. There pressure inside the ventricles is high enough to shut the AV valves but not yet high enough to open the semi-lunar valves. So the ventricles contract within a closed space. This phase is known as isovolumetric contraction because no blood is ejected and the volume of blood in the ventricles is unchanged This is represented by the QRS complex on an ECG (QRS HAPPENS BECAUSE OF VENTRICULAR DEPOLARISATION NOT VENTRICULAR CONTRACTION) |
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Phase 3: Rapid ventricular ejection |
Rapid ventricular ejection starts when the ventricular pressures exceeds the aortic and pulmonary pressures. The semi-lunar valves open and blood is ejected out of the ventricles This is represented by the flat line between S and T-wave (the period between ventricular depolarisation and ventricular repolarisation) (THIS IS THE VENTRICLES ACTUALLY CONTRACTING) |
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Phase 4: reduced ejection |
Ventricular pressures start to fall and the force of ventricular ejection is reduced When the aortic and pulmonary pressure becomes higher than the ventricular pressure, the semi-lunar valves snap shut, marking the end of systole and beginning of diastole This is represented by the T wave |
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Phase 5: isovolumetric relaxation |
The first part of diastole As the ventricles relax, the pressure in the aorta becomes greater than the pressure in the ventricles and blood in the aorta begins to back flow. This backflip causes the aortic valve to fill with blood and snap shut. This is S2 sound. With all valves closed, ventricular pressure drops rapidly but volume remains unchanged Simultaneously the atria is being filled with blood and the atrial pressure rise slowly Represented by flat like after T wave |
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Phase 6: rapid ventricular filling |
When ventricular pressure drops below atrial pressure, the AV valves open and the blood flows down the atria passively into the ventricles The atria then contracts and cycle repeats itself |
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F D B C B |
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What are the 12 ECG leads? |
Chest leads: V1 septal view V2 septal view V3 anterior view V4 anterior view V5 lateral view V6 lateral view Limb leads: Lead I lateral view (RA to LA) Lead II inferior view (RA to LL) Lead III inferior view (LA to LL) Lead IV = used to earth the patient aVR lateral view (LA+LL to RA) aVL lateral view (RA+LL to LA) aVF inferior view (RA+LA to LL) |
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Basics of the shape of an ECG |
-electrical activity TOWARDS lead = positive deflection -electrical activity away from lead = negative deflection -heigh of deflection represents the amount of electrical activity flowing in that direction |
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What do you need to make a lead? |
A positive and negative electrode |
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Why do we prefer lead two? |
Depolarisation of the heart occurs in lead II which is why we use this lead the most when interpreting ECG All 3 leads will be positive (as all leads travels from a negative to a positive electrode) but lead II will be the MOST positive It also faces the direction where most depolarisation will occur (left ventricle) |
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What is the normal cardiac axis range? |
-30• to +90 |
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What is the area covered by left axis deviation and right axis deviation? |
Left axis: -30 to -50 Right axis: 90• to 180• |
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How to tell if there’s right or left axis deviation? |
Right axis deviation: Looking at lead I and II QRS complexes are aRRiving towards each other Left axis deviation= QRS complexes are Leaving each other Extreme axis deviation = -90 and 180 |
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Causes of right axis deviation? |
Right ventricular overload due to COPD or PE |
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Causes of left axis deviation? |
Inferior infarct |
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Explain QRS complex in terms of ECG |
Q-wave: left bundle branch depolarises a tiny bit before the right bundle branch and it depolarises the intra-ventricular septum, where the wave of depolarisation moves slightly away from the viewing electrode (slight negative deflection on ECG) R-wave: depolarisation of ventricular cells which occurs from inner to outer layers S-wave: depolarisation of ventricular muscle moves upwards from the apex via purkinje fibres (away from the electrode so it shows as negative deflection) |
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Describe T-wave in terms of ECG |
Represents ventricular repolarisation Double negative effect makes the T-wave a positive deflection on ECG. Repolarisation makes the membrane potential more negative (1st negative) and here the repolarisation occurs from outside layers inwards moving AWAY from the positive electrode (2nd negative) |
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How to read an ECG? |
5 large squares = 1 second One large square = 0.2 seconds |
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How to calculate regular and irregular heart rhythm from an ECG? |
Regular: 1. Count the number of large squares present within the R-R interval (from one R to the other R) 2. Divide 300 by this number to calculate the heart rate Irregular: 1. Calculate the number of complexes in the rhythm strip (each rhythm strip is normally 10 seconds long) 2. Multiply the number of complexes by 6 (giving the average number of complexes in one minute) |
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What is value for tachycardia and bradycardia? |
Tachy: greater than 100 bpm Brady: less than 60 bpm |
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What’s the 3 types of heart rhythms? |
Regular Regularly irregular Irregularly irregular |
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What does the cardiac axis describe? |
The overall direction of electrical spread within the heart |
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What to check for in an ECG in regards to P-waves? |
Are P waves present? Are they followed by a QRS complex? Do they look normal? Check duration, direction and shape |
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What to check for if P waves are absent? What does a sawtooth p wave/ a chaotic baseline/ and a flatline represent? |
Atrial activity -Is there a sawtooth baseline? Flutter waves = atrial flutter -is there a chaotic baseline? Fibrillation waves = atrial fibrillation -is it flat line? No atrial activity = asystole (no contraction) |
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What can you tell from the PR interval on an ECG? |
A normal PR internal = 3-5 small squares Short PR-interval: -P wave is originating from somewhere closer to the AV node so conduction takes less time (SAN is not in a fixed place and some people’s atria are smaller) -Atrial impulse is getting to the ventricle by a faster shortcut instead of conducting slowly across the atrial wall. This is an accessory pathway and can be associated with a delta wave Prolonged PR-interval: -suggests the presence of an atrioventricular block (AV block) |
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What is a delta wave? |
Associated with Wolff Parkinson white syndrome; basically the slurred upstroke of the QRS complex |
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What can the QRS complex tell you in an ECG? |
Width: narrow vs broad: narrow is normal Height: tall complexes imply ventricular hypertrophy or can be bc patient is tall and slim Morphology: -delta waves = early ventricular activity -Q waves = single Q waves can be normal - J point segment = J point is where S wave joins the ST segment, this point can be elevated resulting in the ST segment also being raised. Might look like ST elevation so can be confusing and scary. Mostly in under 50’s |
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What to look for/ what can you tell from the ST segment of an ECG? |
In healthy individuals there should be NO elevation or depression, just a straight line ST elevation: significant when it’s greater than 1 small square in 2 or more contiguous (next to each other) leads or more than 2 small squares in 2 or more chest leads ST depression: greater than half a small square in 2 or more contiguous leads |
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What does ST elevation and depression indicate? |
ST elevation: most commonly caused by acute-full thickness myocardial infarction ST depression: Indicates myocardial ischaemia |
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What can we learn from the WT interval? |
Abnormally short of less than 350ms Prolonged if 440ms in men and 400ms in women Can be due to antipsychotic and antiemetic drugs |
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What are the different types of T-waves? |
Back (Definition) |
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When are inverted T waves normal? |
In V1 and inversion in aVR is a normal variant |
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When do abnormal T waves like Tall tented T waves occur? |
Hyperkalaemia and hyper acute STEMI |
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When do inverted T waves occur? (Not in V1 and aVR) |
Non-specific sign of a lot of conditions: Ischaemia Bundle-branch blocks PE Left ventricular hypertrophy in lateral leads Hypertrophic cardiomyopathy General illness |
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When do biphasic T waves occur? (They have 2 peaks) |
Can be indicative of ischamia and hypokalaemia |
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When do flat T waves occur? |
Non specific sign that can represent ischaemia or electrolyte imbalance |
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What are U waves? |
Uncommon finding It’s a half a small square deflection after the T wave best seen in V2 or V3 These become larger the slower the bradycardia Can be seen in hypokalaemia |
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What is an arrhythmia? |
Abnormal heart rhythm caused by abnormal electrical impulses in the heart. Caused by disturbances in: -rate -rhythm -impulse formation -impulse conduction |
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What are some SAN (impulse formation) disorders and impulse conduction disorders? |
Impulse formation disorders? -disorder in automaticity : SAN is enhanced or suppressed eg. catecholamines, hypoxia, drugs, ACh -Trigger activity: caused by cations loading into the cell causing depolarisation. This can occur due to ischaemia (cells undergo changes that make it a pacemaker), long open Ca2+ and K+ channels Disorders of impulse conduction: -Blocks -Re-entry |
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What is the re-entry impulse conduction disorder? |
In a re-entrant circle, an impulse is conducted again and again around the circle independently of the SAN Normally, by the time the impulse travels to the start, the area is in a refractory period (so another impulse is not conducted) |
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What are the causes of re-entry in arrhythmia? |
1. Pathway around the circle is longer eg. Dilated heart 2. Slower velocity of conduction, eg. Due to blockage of purkinje, ischaemia of muscle or hyperkalaemia 3. Refractory period of muscle is shortened eg. In response to drugs (epinephrine) or after repetitive electrical stimulation (Basically the idea is that normally by the time the impulse gets back to the beginning the myocytes are still in refractory period so you can’t kickstart a new action potential so it just ends there but say you’ve got a dilated heart, by the time the action potential gets back to the beginning the myocytes have already gone through the refractory period and are ready to have another action potential therefore you get a re-entry circuit. Sans with slower velocity of conduction, because if it’s moving slower by the time it gets to the beginning it’s ready to kick off again) |
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What are the types of arrhythmias and what problem causes it? |
1. P wave (upright in lead II and inverted in aVR) = problem in atria 2. PR interval = problem in AVN 3. QRS complex = problem with ventricular (depolarising) 4. ST segment =pause before repolarisation 5. T wave = problem with ventricular repolarisation 6. QT internal = problem with depolarisation and repolarisation |
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What are sinus arrhythmias? |
Dysfunction of SAN (disorder of automaticity) |
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What are the three types of sinus arrhythmias? |
Sinus respiratory arrhythmias Sinus bradycardia Sinus tachycardia (Anything ‘sinus’ is regular. So the heartbeat is regular it’s just too fast or too slow) |
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What is sinus respiratory arrhythmias? |
Normal changes in rhythm during deep respiration -occurs in healthy, young people -variation in P-P intervals Inspiration decrease Vagal tone (Vagal tone refers to activity of the vagus nerve) which INCREASES heart rate Expiration restores vagal tone and decreases heart rate |
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What is sinus bradycardia? |
Heart rate less than 60bpm due to decreased activity in SAN |
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What’s the the causes of sinus bradycardia? |
Hypothermia Dysfunction of SAN (sick sinus syndrome = degeneration of SAN in elderly) Anorexia Hypothyroidism Normal in athletes Inferior wall myocardial infarction |
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What is sinus tachycardia? What can prolonged sinus tachycardia lead to? |
Heart rate greater than 100 bpm due to increased activity in SAN Prolonged tachycardia can tire the ventricles out and eventually lead to heart failure + blood stasis > further clot formation and emboli |
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What are the causes of sinus tachycardia? |
Increases in body temperature Acute heart failure Acute MI Pulmonary embolism Overwhelming activation of sympathetic NS Blood loss Exercise Anxiety Thyrotoxicosis Hypotension |
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Depending on how many irritated zones there are present in the atria, what two types of atrial tachycardia can occur? |
Focal: discharge from a single ectopic focus in atrium Multi-focal: discharge from multiple ectopic foci in atrium |
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What ECG changes occur in atrial tachycardia? |
Tachycardia Regular and irregular rhythm Narrow QRS complex Different P waves |
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What is atrial flutter and what causes it? |
Caused by a single re-entry circuit in the right atrium Atria receive organised electrical signals Flutter waves are seen “sawtooth pattern” on P waves (best seen on leads II, III and aVF |
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What is atrial fibrillation on an ecg? What causes it? |
Caused by multiple re-entrant circuit Irregular chaotic waves in both atria Atria recieve disorganised signals ‘Twitching of atria’ Atrial rate is very high (>350) Very common Blood is delivered less effectively to tissues (leads to blood stasis and increased risk of clots which can lead to so many problems) |
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What are AV blocks? |
Kind of similar to a bundle branch block. Bundle branch block Is a block in the left and right bundle branches but an AV block is a block in the bundle of hiss or the AVN. AV block leads to delayed conduction or blockage of impulses from atria to ventricles = longer PR interval (Normal PR interval = 0.12-0.2 s (3-5 small squares) |
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What are AV blocks caused by? |
Problems in the AVN -ischaemia, compression or inflammation Eg. CAD, acute rheumatic disease, toxicity, electrolyte disturbance, acute MI |
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What are the different types of AV blocks and what are their characteristic ECG? |
1st degree (not really a block more of a non-progressive but longer than normal PR interval) 2nd degree MOBITZ I (progressive lengthening of PR interval until a beat is dropped) 2nd degree MOBITZ II (fixed PR interval with randomly dropped QRS complexes. This one is dangerous!!) 3rd degree (No relationship between P waves and QRS complexes, happens since there’s a complete block of signals signal so cardiomyocytes become their own pacemakers and the atria and ventricles contract asynchronously. Lyme disease can cause this!!) |
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What are bundle branch blocks? |
In normal ECG: positive deflection of QRS complex in V1 and negative deflection of QRS complex in V6 Left bundle branch block: -left bundle branch is blocked -depolarisation from the right to the left via impulses -left ventricular depolarisation causes a second wave Right bundle branch block: Right bundle branch is blocked Depolarisation occurs from the left to the right Right ventricular repolarisation causes a second wave |
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What is asystole? |
Absence of ventricular contraction -aka cardiac flat line -p waves may be present but there is no ventricular activity -can be inducted during cardiac surgeries with a bypass machine -treated with cpr |
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What is ventricular tachycardia? Does this cause hypertension or hypotension? |
Originates in the ventricles due to an underlying cardiac cause Can be monomorphic or polymorphic Clinical features: chest pain, palpitations, hypotension, and syncope Fatal if not treated |
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What is ventricular fibrillation? |
Most serious Fatal if not stopped in 1-3 minutes No coordinated contractions between all of the ventricular muscles ECG changes: chaotic rate, chaotic irregular rhythm, no P waves, no QRS Unconsciousness occurs within 4 to 5 seconds due to lack of blood flow to the brain Irretrievable death of tissues begins to occur throughout the body with a few minutes |
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What is long QT syndrome? What can potentially cause this? |
If QT is long then ventricular polarisation is going on for too long and repolarisation is being delayed -dysfunctional depolarisation: calcium channels are open for too long -dysfunctional repolarisation: K+ channels are not functioning properly -can be caused by anti-arrhythmics Normally asymptotic until it progresses to Torsades de pointed and arrhythmias ECG changes: long QT > 0.4s |
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What is Torsades de pointes? What is it caused by? What can it progress to? |
-‘twisting of the points’ -complication of long QT syndrome -especially caused by low magnesium and low K+ -characterised by a gradual change in amplitude and twisting of the QRS complexes around the isoelectric line -dangerous as it can progress into Ventricular fibrillation |
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What is demand ischaemia? |
Demand ischemia is another type of heart attack for which blockages in the arteries may not be present. It occurs when a patient’s heart needs more oxygen than is available in the body’s supply. It may occur in patients with infection, anemia, or tachyarrhythmias (abnormally fast heart rates). Blood tests will show the presence of enzymes that indicate damage to the heart muscle.
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How to treat a STEMI? |
Thrombolytics (clot busters) Angioplasty with catheters A stent– a metal, mesh tube – is often inserted at the same time to permanently prop the cleared artery open to allow blood to flow through. |
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You suspect patient is having a heart attack but there’s no ST elevation. How to test whether it’s an NSTEMI or not? |
Patients will test positively for a protein called troponin in their blood that is released from the heart muscle when it is damaged. In NSTEMI heart attacks, it is likely that any coronary artery blockages are partial or temporary. |
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You suspect patient is having a heart attack but there’s no ST elevation. How to test whether it’s an NSTEMI or not? |
Patients will test positively for a protein called troponin in their blood that is released from the heart muscle when it is damaged. In NSTEMI heart attacks, it is likely that any coronary artery blockages are partial or temporary. |
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How is an NSTEMI treated? |
Treatment for an NSTEMI heart attack consists of medication and evaluation for whether a blockage is present that should be treated with medication only, cleared through angioplasty or treated with cardiac bypass graft surgery. |
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How to assess the damage after a heart attack? |
Echocardiogram (is an ultrasound of the heart) |
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What’s an angiogram? |
An angiogram is an X-ray procedure that can be both diagnostic and therapeutic. It is considered the gold standard for evaluating blockages in the arterial system. An angiogram detects blockages using X-rays taken during the injection of a contrast agent (iodine dye). |
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What is a coronary artery spasm? |
A coronary artery spasm is when the artery wall tightens and blood flow through the artery is restricted – potentially leading to chest pain, or blood flow is cut off all together – causing a heart attack. Coronary artery spasm comes and goes. Because there may not be a build-up of plaque or a blood clot in the artery, a coronary artery spasm may not be discovered by an imaging test called an angiogram that is typically performed to check arteries for blockages. |
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How to treat a coronary heart spasm? |
Treatment for a coronary artery spasm consists of medications such as nitrates and calcium channel blockers. |
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How is prinzmetal angina treated? |
This form of angina is treated with drugs that reverse or inhibit coronary vasospasm. These drugs include calcium-channel blockers and nitrodilators. These drugs also reduce oxygen demand to further improve the oxygen supply/demand ratio. |
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What kind of ischaemia are all three angina associated with? |
All three forms of angina are associated with a reduction in the oxygen supply/demand ratio. |
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What are cardiopulmonary baroreceptors, where are the found, and describe their action |
Low pressure baroreceptors responsible for regulation of blood volume. They are found in the right heart and pulmonary arteries and veins. When blood volume in the heart increases, they fire increased signals to the cardiovascular centres via the vagus nerve. This causes the heart rate to increases thus the CO to increases (increases HR bc it wants to get rid of the blood faster?) Increases CO = more blood reaches the kidneys so more water & sodium can be excreted at the kidneys in an attempt to lower blood volume (this is known brainbridge reflex) Signals are also sent to hypothalamus reducing its production of ADH, so more water can be excreted via the kidneys. ANP is also released from the cardiopulmonary baroreceptors which dilate the renal arteries allowing more blood to reach the kidneys faster. ANP also inhibits the reabsorption of water & sodium. All these are reversed in low blood volume. |
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What are the 3 triggers of the RAAS cycle? What receptor? |
1) triggered in response to low Na+ at macula densa (DCT) 2) decrease in stretch of baroreceptors in afferent arteriole 3) sympathetic stimulation of the juxtaglomerular cells in afferent arteriole via B1 adrenoreceptors |
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Describe what happens when RAAS cycle is triggered in low bp? |
1) JXG cells release renin and liver releases angiotensinogen 2) renin cleaves the angiotensiongen and produces angiotensin 1 3) ACE enzyme produced by the vascular endothelial cells in the lungs then converts angiotensin 1 into angiotensin 2 |
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What is the action of angiotensin 2 and how does this increase BP? |
1) arteriole vasoconstriction 2) increased Na+ in kidneys (water will follow, increasing blood volume) 3) ADH release from hypothalamus 4) SNS releases noradrenaline 5) adrenal cortex releases aldosterone |
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What are the risk factors of atherosclerosis? |
Hypertension Diabetes mellitus Smoking High levels of LDL / HDL Age Family history African descent |
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Compare stable, unstable, and vasospastic angina: |
ALL ARE REVERSIBLE (MI isn’t) Stable and unstable cause a ST depression on an ECG (bc only subendocardium is ischaemic) Vasospastic causes ST-elevation because it’s TRANSMURAL ischaemia All angina can be treated with NITROGLYCERIN (vasodilator) but vasospastic also responds to CCB |
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What are 5 aetiologies of heart failure? |
Ischaemic heart disease Valvular heart disease Hypertension Cardiomyopathy Constructive pericardial disease (tamponade) |
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What is heart failure with reduced ejection fraction and heart failure with preserved ejection fraction? |
<40% = SYSTOLIC HEART FAILURE reduced ejection fraction; develops due to LV systolic dysfunction resulting in decreased stroke volume (eccentric hypertrophy and LV fibrosis) >50% DIASTOLIC HEART FAILURE preserved ejection fraction; develops due to reduced LV compliance resulting in decreased end diastolic volume, therefore EF is still maintained (concentric hypertrophy) |
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Noradrenaline triggers which receptors on the heart to cause what? |
B1 receptors on nodal cells : increase heart rate & contractility A1/ A2 receptors to increase vasoconstriction |
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How should heart failure be managed? |
Loop diuretics (furosemide) Ace inhibitors (benazepril) Aldosterone antagonists (spironolactone) |
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JVP? |
Since there’s no valve between the right atria and superior vena cava, the pressure in the jugular vein will reflect the the pressure changes in the right atrium. So increased atrial pressure = increased JVP |
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What is thalassemia? |
Autosomal recessive disorder that causes decreased globin production resulting in abnormal haemoglobin |
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What causes iron deficiency anaemia? |
Decreased iron uptake (in diet) Malabsorption (surgery/ coeliacs/ achlorhydria) Increased iron loss (GI bleeding ulcers/ IBD/cancer) or menorrhagia (heavy periods) Increased iron requirement (pregnancy/ infancy) Leads to less RBC’s and defective production of mitochondrial enzymes |
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Specific symptoms of iron deficiency anaemia? |
Koilonychia (abnormally thin nails which aren’t curved and have become flat) Hair loss PICA (wanting to eat non food things?) Plummer Vinson syndrome |
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What is sideroblastic anaemia? Mutations in what gene causes sideroblastic anaemia? |
Characterised by inability to produce protoporphyrin (which usually binds with iron to produce haem) causing an accumulation of iron in sideroblasts (nucleated RBC prescursor) Causes: -congenital: X-linked, mutations in delta-ALA-synthetase gene -acquired: alcoholism (most common), vitamin B6 deficiency |
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What would a peripheral blood smear in sideroblastic anaemia show? |
Pappenheimer bodies |
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What is thalassemia and what causes it? |
Abnormality in Hb production due to mutations in the 4 alpha genes or the 2 beta genes Alpha genes: problems with synthesis 1. Silent 2. Mild anaemia 3. Severe anaemia 4. Fatal Beta genes: point mutations 1. Major = asymptomatic or general anaemia symptoms 2. Symptoms develop within 3-6 months (jaundice, chipmunk face, haematochromatosis) |
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Normocytic anaemia and it’s causes? |
Aplastic anaemia: inability of bone marrow to produce haematopoietic stem cells resulting in pancytopenia (deficiency in all 3 blood cell lineage) Anaemia of chronic disease: inflammatory cytokines (iL-6) decrease bone marrow sensitivity to erythropoietin and down regulate iron release into the blood Fluid overload(hypervolemia): excess Na+/ fluid intake or increase in blood plasma during pregnancy decreases RBC concentration in blood Sickle cell anaemia: autosomal recessive inheritance causes production of abnormal HbS resulting in ‘suckling’ of RBC in low O2 partial pressure. Deformed RBC’s are more prone to haemolysis resulting in anaemia Active blood loss (haemorrhaging) |
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What is macrocytic anaemia? |
B12 and folate deficiencies resulting in an inability to synthesise new bases to form DNA Fewer cell divisions of haemoglobinised RBC and therefore there is larger MCV |
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Macrocytic anaemia can either be Megaloblastic or normoblastic. What does this mean? What causes each of the anaemia? |
Megaloblastic: large immature RBC eg. In B12 and folate deficiency Normoblastic: normal sized RBC eg. In liver disease, pregnancy, hyperthyroidism |
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Causes of B12 deficiency |
Pernicious anaemia (most common): -autoimmune reaction that destroys gastric parietal cells Gastric parietal cell destruction by: -Crohn’s -coeliac -short bowel syndrome |
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What causes folate deficiency? |
Increased demand (pregnancy) Decreases dietary intake Reduced adsorption (alcohol & drugs) |
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What are the clinical features of macrocytic anaemia? |
Normal anaemia symptoms Glossitis (B12 deficiency) Atherosclerosis Pancytopenia: bleeding, recurrent infection anaemia Folic acid deficiency in pregnancy causes neural tube abnormalities B12 deficiency can cause neuropsychiatric symptoms B12 REQUIRES INTRINSIC FACTOR RELEASED BY GASTRIC PARIETAL CELLS TO BE ABSORBED |
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What is polycythemia? |
Hb levels increase greater than a normal amount 1. Increase in RBC = true polycythemia 2. Reduction is plasma volume = relative |
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What are causes of polycythemia? |
Primary: inappropriate overproduction of RBC (bone marrow problem) Secondary: inappropriate increase in RBC caused by external factors like (smoking, renal hypoxia, sleep apnoea) |
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Complications of polycythemia? |
Budd-chiari syndrome (blood clots in liver) Arterial thrombosis Hepatosplenomegaly |
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What is leukaemia? |
Blood cancer Begins in the bone marrow + results in increased number of abnormal blood cells. These cells are not fully developed (blast or leukaemia cells) |
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What are the different types of leukaemia? |
Lymphoblastic: cancerous change in bone marrow cells that form lymphocytes. Acute is most common in children and chronic is most common in adults Myeloid: cancerous change myeloid cells of bone marrow cells (form RBC, WBC apart from lymphocytes, and Platelets) |
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What is Acute and chronic myeloid leukaemia associated with? |
AML: with Down syndrome CML: with Philadelphia chromosome |
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Clinical features of leukaemia? |
Anaemia due to low RBC Prolonged bleeding and bruising due to low platelets Increased infections due to low WBC Weakness and weight loss Bone pain |
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What is lymphoma? What are the two types? |
A cancer of the lymphatic system (esp lymphocytes) including lymph nodes There’s two types: -Hodgkins lymphoma (determined by the presence of Reed-Sternberg cells) -non Hodgkins (more common) |
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Clinical features and diagnosis of lymphoma? |
Painless lymphadenopathy B symptoms = night sweats, fever, weight loss, pruritis Diagnosis: Blood smear: Reed-sternberg (“owl eyes”) |
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What is multiple myeloma? What are the clinical features? |
Cancer of plasma cells CRAB Hyper Calcaemia Renal dysfunction Anaemia Bone disease |
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Multiple myeloma diagnosis: what proteins in urine? What patter on skull? |
FBC: anaemia U&Es: renal failure Ca2+ high Skill XR: pepper pot skull Urine: bence-Jones proteins |
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What is thrombocytosis? |
Too many platelets Primary: essential thrombosis Secondary: reactive thrombosis (if it’s caused by an underlying condition) |
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What is thrombocytopenia? What are the causes of this? |
Low platelet count Reduced production: myelodysplastic syndrome sepsis Increased destruction: HELLP syndrome (haemolysis, elevated liver and low platelet) and DIC (disseminated intravascular coagulation) |
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What is intravascular coagulation (DIC)? |
A condition in which blood clots form throughout the body, blocking small blood vessels |
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Look over year 1 cardio notes for anatomy of the conduction system & cardiac cycle & action potential of cardiomyocytes & pacemaker cells |
Pls 🥺 |
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Look over atherosclerosis & plaque formation from first year |
🥺 |
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Phase 7: Reduced ventricular filling aka diastasis |
Ventricles get 90% of the blood in phase 6&7 thus those phases are called passive ventricular filling They only get 10% from the atrial contraction of the next cardiac cycle (phase 1) |
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Supraventricular vs ventricular arrhythmias? |
Supravertricular: very narrow QRS bc conduction is happening very fast and there’s a problem in bundle of his or above it Ventricular: wide QRS bc of slower depolarisation |
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Which symptom is accepted as increasing the risk of sudden cardiac death in patients with hypertrophic cardiomyopathy? |
Syncope |
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Which valvular disease would a blood pressure of 163/58 be consistent with? |
Aortic regurgitation |
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Which phase does the 3rd sound correspond with? |
Rapid ventricular filling (not atrial contraction) |
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Which valvular abnormality is associated with pulmonary artery pressures and large A waves in the JVP? |
Tricuspid stenosis |
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A patient has a coronary plaque. The fibrous cap has been eroded and the lipid core is exposed to the bloodflow. On top of the plaque there is a platelet clot forming that almost occludes the artery but from time to time bits of the thrombus break off keeping the lumen patent. What condition is compatible with the above picture? |
Non-STEMI |
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Which phase of the ECG corresponds to the beginning of the rapid passive ventricular filling? |
The ST segment |
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Which ion channel is open during the plateau phase of the action potential in cardiac myocytes side |
Voltage gated calcium channel |
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Which ion channel or pump remove calcium from cardiac myocytes to the extracellular space? |
Sodium/ calcium exchanger |
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Which ion channel plays the most important part in repolarising cardiac myocytes? |
Voltage gated potassium channels (delayed rectifier) |
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Which channel causes the rapid upstroke of the action potential in cardiac myocytes? |
Voltage gated sodium channel |
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Which channel is blocked by local anaesthetics? |
Voltage gated sodium channels |
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Which channel is blocked by drugs causing pharmacologically acquired long QT syndrome? |
A voltage gated potassium channel (delayed rectifier) |
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Which medication inhibits the sodium potassium chloride carrier in the thick ascending limb of the loop of Henley? |
Furosemide |
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Angiotensin 2 leads to which one? Vasoconstriction of the afferent or efferent arteriole? |
Efferent |
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Which drug slows the heart rate by acting on beta receptors of the heart. In patients with heart failure this medication has an evidence-base to reduce mortality too. What is it? |
Bisoprolol |
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What is marfan’s dissection? What gene causes it? |
Inherited disorder of the fibrillin (FBN1) gene which encodes for the connective tissue protein fibrillin-1. This connective tissue disorder leads to abnormalities in aortic wall causing progressive aortic dilation thus increasing the risk of acute aortic dissection |
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What is cardiac tamponade? |
When blood or excess pericardial fluid/ exudate fills the pericardial space, putting increased pressure on the heart. This prevents the LV from expanding properly. |
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Clinical features of cardiac tamponade? |
-pulsus paradoxus (decrease in bp during inspiration) -hypotension -elevated JVP -diminished heart sounds -pericardial friction rub |
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What are the phases of a cardio myocytes action potential? |
Phase 4- Resting phase Phase 0- Depolarisation Phase 1- Early repolarisation Phase 2- Plateau phase Phase 3- Repolarisation |
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What happens in phase 0 of a cardio myocytes action potential? |
1. Action potential from SA node/ neighbouring cardiomyocyte causes fast Na+ channels to open 2. Some Na+ enter the cell, raising the TMP 3. At -70mV threshold, lots more Na+ channels open causing influx of Na+ 4. When the TMP is around - 40mV, L-type Ca2+ channels, beginning the steady influx of Ca2+ into the cell down the concentration gradient (The depolarisation of a cardio myocytes is caused by the sodium influx not calcium. The calcium influx causes the contraction not depolarisation) 5. TMP depolarises to over 0mV 6. Na+ channels close |
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What happens in phase 1? |
Voltage gated Na+ channels close Transient outward K+ channels open and efflux of K+ decreases the TMP as there is more K+ moving out than Ca+ in. These channels then close. |
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What happens in phase 2 of the cardiac myocytes action potential? |
Steady influx of Ca2+ from L-type Ca2+ channels (slow) balances K+ efflux to create a plateau to maintain the action potential Myocardium contraction occurs |
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What happens in phase 3 of a cardiac myocytes action potential? |
L-type Ca2+ channels are inactivated Delayed rectifier K+ channels open to bring the TMP back to resting |
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What happens in phase 4 of a cardiac myocytes action potential? |
Resting membrane potential is ~80mV Na+/K+ pump is active at resting membrane potential. Resting membrane is more permeable to K+ Action potential from a neighbouring cell causes the TMP to rise |
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What happens in the refractory period following a action potential? |
Na+ channels inactivate during repolarisation, creating an absolute refractory period, where the myocyte is insensitive to new waves of excitation Once the current begins recovering from inactivation, the myocyte progresses to relative refractory period, where it is possible to elicit a small response but not one that progresses The refractory period is longer in a cardiac muscle than a skeletal muscle This prevents from tetanus from occurs and ensures that each contraction is followed by enough time so that the heart chamber can refill before the next contraction |
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Describe the action potential in a pacemaker cells |
PHASE 4: RESTING HCN channels mediate a spontaneous ‘funny current’ that is activated when there is hyperpolarisation (~60mV) When the funny current is generated, there is spontaneous K+ efflux and Na+ influx – Na+ >>> K+ and there fore there is depolarisation When TMP = -55mV, T-type Ca2+ channels open and continue slow depolarisation to the threshold PHASE 0: DEPOLARISATION TMP = -40mV = threshold potential for pacemaker cells L-type calcium channels open and depolarise cells (PHASE 2: PLATEAU Slow L-type Ca2+ channels start to close) PHASE 3: REPOLARISATION Delayed rectifier K+ channels cause K+ efflux that repolarises the cell |
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How does nervous activity change the pacemaker current? |
Nervous impulses from the autonomic nervous system and hormones (such as adrenaline) can change the timing and the strength of each heartbeat – BUT THEY DO NOT CHANGE THE RHYTHM Increase in sympathetic impulses causes the phase 4 of the action potential to steepen – reaches threshold faster Also increases the Na+ influx decreasing the time to reach threshold + increases the rate of action potentials firing Increase in parasympathetic stimulation does the opposite as it releases ACh which decreases the slope of phase 4 |
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A boot shaped heart on cxr would suggest what? |
RV hypertrophy |
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High yield facts for cardiac cycle |
1) Atrial Contraction: occurs at the end of diastole/ represented by P-Wave/ S4 sound 2) Isovolumetric Ventricular contraction: Beginning of systole/ S1 sound/ Represented by QRS 3) Rapid Ejection: S-T segment 4) Reduced Ejection: T wave/ marks the beginning of ventricular repolarisation 5) Isovolumetric relaxation: S2 sound/ marks beginning of diastole/ ventricles generate negative pressure) 6) Rapid Ventricular Filling: AV valves open/ S3 sound Both these are the flatline between t-wave and p- wave 7) Reduced Ventricular Filling |
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Blood Vessel for Bypass |
Radial Artery Great Saphenous Vein Internal Thoracic Artery |
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How is the plateau phase prolonged? |
Na+/Ca2+ exchanger moves Ca2+ out for 3Na+ ions to help prolong the plateau phase |
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