Cardiology 2 Flashcards

Question

What is autoimmune haemolytic anaemia?

Answer 1

* Antibody mediated destruction of RBCs * Divided into cold or warm depending on what temperature the antibodies bind to RBCs the best. * Warm: IgG binds to RBCs; Cold: IgM binds to RBCs. * Associated with Autoimmune conditions, infections and drugs * Causes extravascular haemolysis (warm) and extra/intravascular haemolysis (cold) * Warm: SLE, CLL, Drugs e.g. penicillin * Cold: M.pneumonia, EBV * Warm vs cold? Coombs test (normally direct)

Answer 2

* B12 is absorbed in the ileum bound to intrinsic factor (which made by parietal cells in the stomach) * Pernicious anaemia is an autoimmune reaction against intrinsic factor and parietal cells causing a B12 deficiency. Most common cause in the western world.

Answer 3

* Increased age * Vegan Diet (11% on a vegan diet) * Gastric surgery * Malabsorption * Drugs e.g. metformin

Answer 4

* Reduced levels of folic acid * RF: * Increasing age * Malabsorption * Pregnancy * Alcohol * Drugs: e.g. methotrexate, trimethoprim * Folate is absorbed in the jejunum

Answer 5

Characterised by the heart's inability to effectively fill and/or eject (pump) blood, caused by an underlying pathology commonly coronary artery disease or previous MI.

Answer 6

- Heart failure with reduced ejection fraction – HFrEF – where there is a pump dysfunction - Heart failure with preserved ejection fraction – HFpEF – due to a filling dysfunction

Answer 7

biventricular heart failure, left sided heart failure, right sided heart failure and cor pulmonale

Answer 8

uChange in function of the left ventricle resulting in decreased cardiac output, pulmonary congestion and decreased peripheral perfusion uCan be either with a reduced ejection fraction or preserved ejection fraction

Answer 9

- Coronary artery disease → decreases blood supply to cardiomyocytes → decreases contractile strength - Hypertension, aortic stenosis → ↑afterload → ↓stroke volume - Arrhythmias decrease ventricular filling and lead to ineffective contractions - Mitral or aortic regurgitation - Age, Obesity, Diabetes, Smoking, Ethansol, Illicit drug

Answer 10

- Underlying disease results in a decrease in the cardiac output results in backup of blood into left atrium, pushed back into pulmonary circulation → ↑pulmonary capillary pressure → pulmonary oedema → ↑gas exchange - RAAS activation due to ↓cardiac output. Angiotensin II production → systemic effects, increasing blood pressure, cardiac hypertrophy, decreased diuresis

Answer 11

Effects of compensation: ↑afterload, ↑LV workload, LV remodelling Pulmonary oedema Pulmonary haemorrhage (congested capillaries bursting) Cardiorenal syndrome Death

Answer 12

uLeft sided heart failure can present as uExertional dyspnoea and can be on rest uOrthopnoea uParoxysmal nocturnal dyspnoea (PND) uCough, restlessness uBibasal crackles on auscultation of lungs – pulmonary oedema uS3/S4 sound

Answer 13

- Change in function of the right ventricle leading to decreased delivery of blood to the pulmonary circulation and elevated venous pressure - ↑venous pressure leads to systolic volume overload - ↑Right ventricular workload → RV hypertrophy → ↓pumping ability **Caused** by left sided heart failure and the associated pulmonary oedema (most common cause). **Other causes** include RV infarct, bacterial endocarditis, pulmonary valve stenosis, cardiomyopathy.

Answer 14

- Peripheral pitting oedema - Fatigue/exercise intolerance – due to poor gas exchange - Hepatojugular reflux - Ascites - Hepatosplenomegaly - S3/S4 sounds

Answer 15

- Failure of left side of heart - Tricuspid regurgitation - Congestive hepatopathy – liver damage due to backup of blood - Cardiac cachexia – nausea, vomiting, anorexia, abdo pain - Eventual death

Answer 16

**Pulmonary Heart Disease** - Right heart failure secondary to pulmonary arterial hypertension - Right ventricular hypertrophy/dysfunction caused by pulmonary hypertension - Presents with signs and symptoms of right sided heart failure

Answer 17

- Elevated BNP/NT-pro-BNP – raised due to stretching of ventricular wall - Chest X-Ray - In Left Heart Failure & biventricular failure – cardiomegaly, pulmonary vascular congestion, Kerley B lines - Echocardiogram - ECG abnormalities – arrhythmias, tall QRS

Answer 18

- Beta blockers have an evidence base to reduce mortality. (e.g. bisoprolol) - ACE inhibitors (e.g. ramipril) and ARBs (e.g. candesartan) are also used - In fluid overload a loop diuretic can be prescribed e.g. furosemide

Answer 19

•If the dilated ventricle (as seen in systolic left sided HF) is able to maintain cardiac output by this means, the patient is said to be in **compensated heart failure**. However, ventricular dilation comes at the expense of increased wall tension and amplifies the oxygen requirements of an already-compromised myocardium. With time, the failing muscle is no longer able to propel sufficient blood to meet the needs of the body, and the patient develops **decompensated heart failure**.

Answer 20

Cardiomyopathy refers to diseases of the heart muscle. These diseases have many causes, signs and symptoms as well as treatments. In most cases, cardiomyopathy causes the heart muscle to become enlarged, thick or rigid.

Answer 21

* Hypertrophic Cardiomyopathy * Dilated Cardiomyopathy * Restrictive Cardiomyopathy * Arrhythmogenic Right Ventricular Cardiomyopathy * Takatsubo Cardiomyopathy

Answer 22

* When cardiomyopathy develops as a way to compensate for some other underlying disease like hypertension or valve disease its called secondary cardiomyopathy. * If it develops all by itself its called primary cardiomyopathy.

Answer 23

* Basics: When the walls of the heart become thick, heavy and hypercontractile, essentially the muscle grows a lot larger – and new sarcomeres are added in parallel * Usually LV is affected + muscle growth is asymmetrical meaning that the IV septum grows larger in comparison to the free wall and this causes 2 things: - Take up more room so less blood in the ventricle - More stiffness and less compliant and hence it cant stretch as much – cant fill as much leading to what type of HF?

Answer 24

* In some patient the LV outflow is blocked by the outgrowth of IV septum during **systole** – Increased blood velocity through smaller aortic valve and this pulls the **anterior** leaflet of the **mitral** valve towards the septum (VENTURI EFFECT) causing further obstruction * This is also referred to as **Hypertrophic Obstructive Cardiomyopathy** * Causes a **Cresendo-Decrecendo** Murmur (like AV valve stenosis) * Bifid Pulse from the mitral valve * S**4** Sound can be heard of atrial depolarization – pushing blood into a non-compliant ventricle during diastole

Answer 25

* Genetic: Autosomal Dominant: Missense mutation in the Beta Myosin Gene * Freidriches Ataxia: Autosomal Recessive * On Histology: Myocyte Disarray aka Myocytes organization is haywire

Answer 26

* Causes all **4 chambers to dilate** * New sarcomeres are added in series causes the muscles to become thin and there is less muscle present for contraction causing weak contractions * This causes reduced stroke volume and leads to **Systolic Heart Failure** * As chambers get larger they tend to stretch out the valves that separate the atrium and ventricles * This causes valves to not close all the way leading to regurgitation (Mitral and tricuspid: Holosystolic murmur) * Arrhythmia complication: stretching of conduction system

Answer 27

\> Primary : idiopathic: the most common cause \> inherited: either a familial genetic predisposition to DCM or a specific syndrome e.g. Duchenne muscular dystrophy, or haemochromatosis, sarcoidosis \> Myocarditis: e.g. Coxsackie B, HIV, diphtheria, Chagas disease(protozoan) \> Alcohol is toxigenic \> Drugs like chemotherapy: Daunorubicin and cocaine \> Wet beriberi decreases B1 \> Peripartum cardiomyopathy where DCM can develop in the 3rd trimester of pregnancy or in weeks following pregnancy probably because of of pregnancy associated hypertension.

Answer 28

* Is where the heart muscle is restricted meaning it becomes stiffer and less compliant * The muscles and size of ventricles stay about the same size or are maybe only slightly enlarged * When blood fills into restricted ventricles, the ventricles aren't allowed to expand.. because they cant stretch .. Less filling ... less pumped out causes diastolic HF

Answer 29

using ECG: smaller QRS complexes, low amplitude signals, Echo

Answer 30

Causes include amyloidosis, sarcoidosis, hemochromatosis, endocardial fibro elastosis (children), and Loeffler syndrome (endomyocardial fibrosis with an eosinophilic infiltrate and eosinophilia).

Answer 31

■ An aneurysm is a weakening/thinning of the arterial wall leading to a localized bulging. Definition of AAA: A permanent, localised dilatation in the wall of the abdominal aorta. **Cause**: Primarily from the loss of intima with loss of elastic fibres from the media

Answer 32

o Arterial disease - atherosclerosis - hypertension - diabetes - smokers oConnective tissue disorders - Marfan’s syndrome, Ehler-Danlos syndrome - Extracellular matrix becomes disrupted with changes in the balance of collagen and elastic fibres o Age – over 65 years o Male sex – 3 to 4 times more prevalent o Family history – especially in male first degree relatives

Answer 33

1) Asymptomatic pulsatile abdominal mass (normally diagnosed incidentally) 2) Detected during USS Routine Screening in men over age 65 3) Emergency (rupture) – Sudden onset, severe chest/abdominal pain that radiates to the back – Collapse – Hypotension with tachycardia – Profound anaemia

Answer 34

– History and examination - examination may identify a expansile, pulsating mass. – Ultrasound - To look at the diameter of the abdominal aorta. – (GOLD STANDARD) CT Angiography - Used preoperatively to check for renal artery involvement and for planning surgery.

Answer 35

o \<5.5 cm on ultrasound - Continued monitoring with ultrasounds o \>5.5 cm on ultrasound - Elective surgery to prevent rupture. o Emergency - Oxygen, 2 large-bore cannulas, fluid management (BP at 100mmHg to prevent dislodging a clot), surgical aneurysm repair **Prognosis:** 80% mortality for ruptured AAA

Answer 36

■ Clamping below the renal artery, then sewing a graft into the aneurysm sac ■ Endovascular Aneurysm Repair (EVAR) - less invasive endoscopic procedure whereby stents are inserted through the femoral artery

Answer 37

Definition: Blood escapes through the innermost tunica intima layer of the aorta wall, prising apart the media and creating a new lumen

Answer 38

- Acute severe tearing or ripping chest pain, radiating to the back - Weak or absent pulses - Systolic BP variation of \>20mmHg between the arms - Hypertension - Aortic regurgitation

Answer 39

Chest X-ray - Widened mediastinum CT Angiograph of Chest-Abdo-Pelvis (For STABLE patients) - False lumen

Answer 40

■ DEBAKEY Classification: * Type 1 - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally * Type 2 - originates in and is confined to the ascending aorta * Type 3 - originates in descending aorta, rarely extends proximally but will extend distally

Answer 41

DEBAKEY STANDFORD

Answer 42

* Type A - Involves the ascending aorta (+/- the descending aorta). 2/3rds of cases. * Type B - Involves only the descending aorta. 1/3rd of cases.

Answer 43

To prevent it becoming a AAA. * Type A - Surgery – open surgery or endovascular stent graft repair + control systolic at 100-120mmHg while waiting for intervention * Type B – If no complications, conservative management of bed rest + IV labetalol to reduce BP

Answer 44

Deep Vein Thrombosis ■ Deep venous thrombosis (DVT) affects the deep veins in the lower leg and the thigh, most commonly popliteal vein, femoral vein and iliac veins

Answer 45

* Obesity * Age * Smoking * female sex * family history * previous DVT and co-occurring conditions (pregnancy or pelvic tumour (causing venous stasis) * Malignancy * pelvic/lower limb orthopaedic surgery * thromboembolic disease (e.g. hypercoagulability)

Answer 46

1. Venous stasis: injury or inflammation, air travel 2. Endothelial damage: surgery, malignancy, trauma 3. Raised clotting factors: malignancy, congenital disease, drugs, thrombogenic state

Answer 47

o sudden-onset of localised pain o calf tenderness o Asymmetric swelling, redness and tight skin o superficial veins may be engorged o may be a low-grade pyrexia o Some patients are asymptomatic and collapse from a pulmonary embolism o variable oedema in and below the calf and Homan’s sign my be positive

Answer 48

o Wells’ Score to calculate risk of DVT o D-dimer testing - If it is negative- DVT is highly unlikely (High sensitivity) - If it is positive- it DOES NOT CONFIRM DVT (may be raised in patients with liver disease, rheumatoid disease, inflammation, cancer, trauma, pregnancy, recent surgery etc) o proximal duplex ultrasound o whole-leg ultrasound

Answer 49

§ Low-molecular-weight heparin (LMWH) is initially used § Subsequently converted to warfarin therapy - Warfarin is continued for 3–6 months after a first DVT but is needed lifelong after a second.

Answer 50

* Carotid Stenosis occurs when plaque (atherosclerosis) build up and narrow the carotid artery, reducing blood flow to the brain. The blockage increases your risk of stroke. * Occlusion or stenosis of the internal carotids is very serious and can lead to a CVA * Atherosclerosis occurs most commonly at the carotid artery bifurcation

Answer 51

1. Plaque deposits grows larger and larger, severely narrowing/completely occlude the artery à reduced blood flow to brain 2. Plaque deposits can roughen and deform artery wall à causes blood clots to form and block blood flow to brain 3. Plaque deposits rupture and tiny clots break away from repair, travel downstream to clog smaller arteries à blocks blood flow to brain

Answer 52

Older age PMHx of HTN PMHx of CVD Smoking Diabetes

Answer 53

o Asymptomatic o Cervical bruit o Focal neurological deficit lasting \>24hrs (i.e. stroke) o Focal neurological deficit lasting \<24hrs (i.e. TIA)

Answer 54

ABCD2 Prognostic Score: Clinical prediction rule used to determine the risk for stroke in the days following a transient ischemic attack

Answer 55

* BP, glucose, cholesterol, cross-match for blood * Duplex USS – for degree of stenosis * CT Angiography - defines arterial anatomy * MRI Angiography - identifies cerebral infarcts

Answer 56

Conservative and medical management for asymptomatic patients with less than 70% stenosis: - stop smoking - take aspirin and statin - control hypertension

Answer 57

Transient Ischaemic Attack ■ Definition: A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction. ■ aka ”mini-stroke” – TIAs have a sudden onset and may last from a few mins to 24hrs; most patients have complete resolution of symptoms and signs within 1hr

Answer 58

TIAs result when blood flow to the brain is temporarily interrupted and then restored.

Answer 59

Carotid Stenosis - Atrial fibrillation - Valvular disease

Answer 60

■ Sudden onset ■ Brief duration of symptoms (minutes to 24hrs max) ■ Patient/witness reports of focal neurological deficit - Dysphasia - Unilateral weakness or paralysis - Ataxia, vertigo or loss of balance - Sudden transient loss of vision in one eye

Answer 61

* Blood glucose * FBC and Platelet count * Prothrombin time, INR * Fasting lipid profile * CT Scan * (GOLD STANDARD) MRI of Head

Answer 62

* Arteriosclerosis= Atherosclerosis + Arteriolosclerosis * Multifactorial inflammatory disease of the tunica intima * Buildup of cholesterol plaques in the intima * Cholesterol +WBC * M\>F

Answer 63

: Abdo CramP: Abdominal artery\> Coronary\> Popliteal\> Carotid\> Circle of Willis

Answer 64

_Modifiable_ * Smoking * DM * HTN * Dyslipidemia * Alcohol _Nonmodifiable_ * FH * Age: M\>45, F\>55 * Postmenopausal females

Answer 65

* NO\> vasodilation via activation of eNOS -\> stimulation of guanylate cyclase and cGMP production-\> decreasing intracellular Ca2+ decreasing myocyte excitation and contraction. * LDL: transports cholesterol and Ca2+ INTO cell * HDL: transports cholesterol and Ca2+ OUT of cell * In ACS: Adenosine is released by ischaemic myocardium through A1 receptors-\>angina-\> PAIN

Answer 66

* Fatty streak is **thrombogenic**-\> platelets adhesion -\> PDGF, PGF, TGF-B secretion -\> SMC proliferation and migration of SMC from tunica media into tunica intima * SMC + macrophages secrete ECM ( elastin, collagen, proteoglycan)-\> form a wall around the fatty streak to prevent clotting-\> fibrous cap * LDL-\> calcium depostion * Endothelial cell injury prevents HDL from removing the calcium-\> **stiff fibrous cap**

Answer 67

* Endothelium becomes dysfunctional * Cause: Chronic stress due to smoking, high BP, hyperlipidemia * Chronic stress causes damage to the glycocalyx barrier which monitors the shear forces in the blood vessels * Permanent hyperglycaemia can destroy the glycocalyx. Regeneration takes 12 hrs. * Glycocalyx dysfunction-\> leaky vessel

Answer 68

**•Obstruction:** - 40% luminal obstruction: maximal flow during exercise maintained - \>50% -\> coronary ischemia - \> 70/75% lumen occluded prior to onset of symptoms -\> Downstream cellular injury/death * **Coronary arteries**-\> Angina+ ACS * **Internal carotid+ Middle cerebral-**\> Stroke + cerebral artery * **Mesenteric arteries**-\> acute/chronic mesenteric ischemia * **Popliteal artery**-\> peripheral ischemia ( gangrene + claudication) * **Renal artery**-\> Hypertension ( activation of RAAS) * **Weakening of vessel wall**-\> Abdominal aortic aneurysm below L2 ( no vaso vasorum) -\> hemorrhaging * **Thromboembolism, Cholesterol emboli**-\> livedo reticularis, AKI, gangrene

Answer 69

* Endothelial damage-\> LDL enters * Excess LDL-\> increases permeability of cells to enter the intimal layer-\> monocytes enter * Monocytes enter through diapedesis * LDL oxidizes and inactivates NO! * NO loses its vasoprotective effect **•-\> ACCUMULATION OF MACROPHAGES + oxLDL**

Answer 70

* oxLDL releases cholesterol * Monocytes engulf cholesterol-\> die off and form foam cells * Accumulation of foam cells-\> fatty streak

Answer 71

* BURST: * Foam cells undergo necrosis-\> release of MMPs * IFN-γ induces macrophage MMP expression-\> weakening of cap * IFN-γ inhibits VSMC proliferation and collagen synthesis-\> weakening of cap * Plaque rupture-\> exposure of underlying-\> thrombus formation

Answer 72

* Atheroma is formed * Grows * \*\*The thinner the fibrous cap, the higher risk of thrombus\*\*

Answer 73

•Bloods: - Lipid profile: TC, LDL, HDL, triglycerides - Fasting glucose - FBC - Creatinine - Myocardial damage markers: troponins, CK-MB ( ACS suspected) - Homocysteine - HbA1c - BNP - Thyroid fxn * ECG-\> ACS, underlying hypertrophy * Stress testing unless contraindicated * Echo-\> Valvular heart disease, HF * CT-\> extent of calcification * Coronary angiography

Answer 74

**_Lifestyle:_** * Smoking cessation * Weight loss **_Underlying comorbidity managed- HTN, DM_** •DM and renal disease treatment goal of BP\< 130/80 mmHg **_Medical:_** * Low dose aspirin, clopidogrel * Statin therapy

Answer 75

Coronary Artery Disease ## Footnote * Disease due to imbalance between myocardial oxygen demand and supply from coronary arteries * Reduced O2 supply to the heart is defined as myocardial ischemia-\> reduced ability of heart to contract * If prolonged ischemia -\> myocardial infarction

Answer 76

* Atherosclerosis\*\* * Coronary artery embolus: FAT BAT. Classic triad of fat emboli? * Vasculitis * Vasospasm * Aortic stenosis

Answer 77

Stable angina, Prinzmetal angina, ACS, sudden cardiac death

Answer 78

* Myocardial ischemia due to a plaque occluding \>75% of the coronary artery lumen. * Relieved by rest, nitroglycerin/GTN spray

Answer 79

* Deep/poorly localized pain * Squeezing/ crushing/suffocating retrosternal pain * Radiates to the arm, jaw, neck * SOB, nausea, vomiting, diaphoresis, fatigue, dizziness

Answer 80

•ECG normal, troponins normal, cardiac stress test +

Answer 81

TRUE- this is called a collateral circulation

Answer 82

1. Substernal chest discomfort 2. Provoked by exertion, stress 3. Relieved by GTN, rest * If all three met-\> typical angina * If 2-\> atypical angina * If 0,1-\> non-cardiac chest pain

Answer 83

* vasospasm of a large coronary artery * Transmural ischemia, rest pain, more prolonged than classic angina * ECG: ST elevation * Troponins normal * Women \<50

Answer 84

* Smoking * Electrolyte disturbance * Cocaine * Cold stimulation

Answer 85

Angina equivalent syndrome, syndrome X, silent ischemia, nocturnal

Answer 86

Acute Coronary Syndrome = plaque disrupted Involves: Unstable angina, NSTEMI, STEMI

Answer 87

* New- onset angina * Acute retrosternal chest pain * Dull/ squeezing/ crushing/ tightness * Radiation to neck, arm, shoulder, epigastrium * Dyspnea * Pallor * Nausea, vomiting * Diaphoresis * Dizziness, lightheadedness, syncope * Silent MI?

Answer 88

* Tachy/bradycardia * Hypotension * Raised JVP * Murmur due to arrhythmias * Cold extremities

Answer 89

Defined as 2 out of 3: 1. Unstable, ischaemic chest pain 2. Ischaemic ECG changes 3. Raised cardiac biomarkers

Answer 90

Digoxin is a type of medicine called a cardiac glycoside. It's used to control some heart problems, such as irregular heartbeats (arrhythmias) including atrial fibrillation. It can also help to manage the symptoms of heart failure, usually with other medicines. Digoxin is only available on prescription

Answer 91

* SAN: Usually RCA * AVN: Usually RCA * Bundle of His: RCA + branches of LAD * LBB: LAD. May have collaterals form RCA/LCX - Anterior fascicle: LAD - Posterior fascicle: RCA and may have septal branches of the LAD. •RBB: septal branches of LAD. May have collaterals form RCA/LCX

Answer 92

It shouldw be remembered that a new left bundle branch block (LBBB) may point towards Acute Coronary Syndrome

Answer 93

**Preload-** Volume of blood in ventricles at end of diastole (end diastolic pressure) **Afterload**- Resistance left venricle must overcome to circulate blood **End diastolic volume (EDV)-** amount of blood in the ventricle before contraction **Ejection systolic volume (ESV)-** amount of blood remaining in the heart after ejection

Answer 94

**•S1- Closure of the AV valves** * At end of phase 1/ beginning of phase 2 * ‘lub’ **•S2-Closure of SL valves** * At end of phase 3/ beginning of phase 4 * ‘dub’

Answer 95

**S3** * AKA ventricular gallop * Occurs just after S2 when the mitral valve opens, allowing for filling of left ventricle * In rapid ventricular filling * Sound is ONLY produced by a **large amount of blood (volume overload) striking overly compliant left ventricle** * Often a sign of systolic heart failure Eg: dilated cardiomyopathy **S4** * AKA atrial gallop * Occurs just before S1 when the atria contract to force blood into left ventricle * Sound is produced ONLY when **left ventricle is not complaint and atrial contraction forces against the wall** * Can be a sign of diastolic heart failure * Eg restrictive and hypertrophic cardiomyopathy •

Answer 96

AV valves close

Answer 97

* Stenosis = failure of the valve to open completely * Usually chronic and thus well-tolerated due to ventricular hypertrophy or atrial hypertrophy * Causes pressure overload * Diastolic HF: * As the heart fails to fill properly during diastole due to the decreased space in the ventricle

Answer 98

* Insufficiency or regurgitation = failure of a valve to close completely, thus causing reversed flow * Can be acute or chronic * Causes volume overload * Systolic HF: because the ventricles dilate, the walls thin out and there is no proper contraction

Answer 99

abnormal flow through diseased vavles typically produces abnormal heart sounds ## Footnote * Severe lesions can be palpated as thrills * Depending on the valve involved, murmurs are best heard at different locations on the chest wall

Answer 100

You look at 1) Timing- systolic or diastolic? 2) Shape? 3) Location? Radiation? 4) Pitch 5) Intensity-Grading?

Answer 101

* Refers to whether the murmur is systolic or diastolic * Systole occurs between S1 and S2 * Diastole occurs between S2 and S1

Answer 102

* A murmur is heard when the diseased valve interrupts the flow of blood during systole or diastole à therefore: * AV regurgitation or semilunar stenosis --\> **systolic murmur** * AV stenosis or semilunar regurgitation --\> **diastolic murmur**

Answer 103

Av doesnt close = AV reg SL doesnt open= SL stenosis

Answer 104

AV doesnt open= AV stenosis SL doesnt close = SL regurg

Answer 105

**Mid-systolic murmur (AKA ejection murmur)** * Begins just after S1 heart sound and stops before S2 heart sound * Therefore, S1 and S2 are distinctly audible **Holosystolic murmur** * Begins with immediately after S1 heart sounds and extends up to S2 * S1 and S2 are difficult or impossible to hear **Late systolic murmur** •Starts after S1 and may or may not extend up to S2

Answer 106

**Early diastolic** * Starts at the same time as S2 and ends before and ends before S1 * S1 will be distinctly audible and S2 may be difficult to hear **Mid-diastolic** * Starts after S2 and ends before S1 * Both S2 and S1 are distinctly audible **Late diastolic (AKA presystolic)** •Starts after S2 and extend up until S1

Answer 107

Shape refers to the change in intensity of the murmur over time: * Crescendo = progressively gets louder (increases in intensity) * Decrescendo = progressively gets quieter (decreases in intensity) * Crescendo-decrescendo = progressively get louder and then quieter - Has a “diamond shape” •Uniform = does not change in intensity

Answer 108

Location refers to where the murmur is usually heard best * 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 – midclavicular line, 5th intercostal space

Answer 109

Murmur will be high-pitched if there is a large pressure gradient across the pathological lesion •E.g. aortic stenosis à because there is usually a large pressure gradient between the left ventricular and aorta Murmur will be low-pitched because there is usually a small pressure gradient •E.g. mitral stenosis à because there is a lower pressure gradient between the left atrium and left ventricle during diastole

Answer 110

There are three main types: 1. Damage to collagen of the leaflets 2. Nodular calcification e.g. aortic valve stenosis 3. Fibrotic thickening (key feature in rheumatic heart disease)

Answer 111

What can cause problems? 1. Inflammation 2. Congenital HD 3. Underlying HD 4. Infections

Answer 112

•TTE (trans-thoracic echocardiogram) - Performed in 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, e.g. dobutamine * Catheterisation = angiogram is performed to assess the structure and function or coronary arteries

Answer 113

* Narrowing of the aortic valve * Causes obstruction of outflow of blood from LV through aorta * Can cause LV hypertrophy -\>LV HeartFailure-\> diastolic HF Causes * Mechanical wear and tear * Bicuspid valve * Rheumatic HD * Willams syndrome * Pagets disease (+hypercalcemia)

Answer 114

symptoms * Syncope * Angina pectoris * Dyspnoea Consequences 1. LV hypertrophy 2. Increased oxygen demand of the heart 3. Diastolic HF (doesn’t fill properly) 4. Reduced SV-\> Compensatory TachyC-\> Impaired coronary filling 5. Eventually RHF

Answer 115

What happens? * Incomplete closure of aortic valve * Causes backflow of blood from aorta to LV * Can cause LV dialation -\>LV HF-\> systolic HF Causes * Bacteria infection (infective endocarditis) * Chronic Inflammation * Aortic root dilation

Answer 116

Symptoms * Do not develop until LVF * Dyspnea on exertion * Orthopnea * Paroxysmal nocturnal dyspnea * Angina pectoris Consequences Acute -During diastole, blood flows back-\> Ventricular pressure increases-\> pressure transmits backwards into pulmonary circulation à pulmonary oedema and dyspnoea Chronic -Overtime, increased left ventricular end-diastolic volume à left ventricular dilation à LVF urgit

Answer 117

What happens? * Narrowing of mitral valve * obstruction of blood flow into the left ventricle * Can cause LA hypertrophy Causes * Rheumatic fever * Calcification * Carcinoid * Congenital

Answer 118

Symptoms * Dyspnea on exertion * Orthopnea * Paroxysmal nocturnal dyspnea * Pulmonary congestion * Later-\> symptoms of RHF Consequences 1. Incr volume and pressure in LA 2. Dilation of LA 3. Backflow of blood into pulmonary circulation 4. Pulmonary congestion, edema 5. Increased pulmonary pressure 6. Eventually RHF as it finds it harder to pump

Answer 119

What happens? * incomplete closure of the mitral valve * Leakage of blood from the left ventricle into the left atrium * Can cause LA dialation -\>LV HF-\> systolic HF Causes? * Mitral valve prolapse * Heart attack * LV heart failure * Rheumatic fever

Answer 120

Symptoms? * Palpitation * Dyspnoea * orthopnoea * Fatigue and lethargy * Pulmonary congestion * Later-\> symptoms of RHF Consequences Acute 1. No dilation of LA-\> LA pressure increases-\> incr in pulmonary pressure-\> pulmonary edema 2. Backflow of blood into pulmonary circulation Chronic 1. Eccentric hypertrophy 2. left atrial dilation as it is accommodated

Answer 121

**What happens?** * Incomplete closure of the pulmonary valve * backflow from the pulmonary artery to the right ventricle * Can cause LV hypertrophy -\>LV HF-\> diastolic HF **Causes?** Occurs secondary to pulmonary HTN Infective endocarditis Rheumatic endocarditis

Answer 122

**Symptoms** * Due to backed up blood * Distended neck veins * Swelling in ankles and feet * Hepatosplenomegaly **Consequences** 1. Blood flow back into RV 2. Increased volume of blood 3. Eccentric hypertrophy-\> RV dilation 4. Systolic RHF

Answer 123

**What happens?** * Incomplete closure of the tricuspid valve * Leakage of blood from the right ventricle into the right atrium * Can cause RA dilation -\>right sided HF due to the increase of volume and pressure **Causes?** * Pulmonary HTN * Heart attack * Congenital (ebstein abnormality) * Rheumatic fever

Answer 124

**Symptoms?** * Dyspnoea * Right-sided heart failure: * Distended neck veins * Swelling of ankles and feet * Hepatosplenomegaly * Ascites **Consequences** * Extra blood that flowed back into the atrium, flows back into the ventricle during diastole à increase in right ventricular pre-load * In order to deal with the extra work, the right ventricle becomes larger à eccentric ventricular hypertrophy * Eventually, the right ventricle might not be able to keep up à right sided-heart failure

Answer 125

**What happens?** * Narrowing of tricuspid valve * obstruction of blood flow into the right ventricle * Can cause RA hypertrophy **Causes** * Rheumatic fever

Answer 126

**Symptoms?** * dysphagia * Right sided heart failure * Distended neck veins * Swelling of ankles and feet * Hepatosplenomegaly **Consequences** 1. Incr volume and pressure in RA 2. hypertrophy of RA 3. Backflow of blood into systemic circulation (vena cava) 4. Right sided HF

Answer 127

**What happens?** * Narrowing of the pulmonary valve * Causes obstruction of outflow of blood from RV through pulmonary trunk * Can cause RV hypertrophy -\>RV HF-\> diastolic HF **Causes?** * Mechanical wear and tear * Rheumatic fever * Often congenital * Tetralogy of Fallot

Answer 128

**Symptoms** * Due to backed up blood Distended neck veins Swelling in ankles and feet Hepatosplenomegaly * Because blood cannot get to the lungs Cyanosis SOB and fatigue à especially during exercise **Consequences** 1. High pulmonary pressure 2. RV hypertrophy 3. Diastolic HF (doesn’t fill properly) 4. Blood gets backed up 5. Right HF

Answer 129

Diastolic Pressure+[1/3×(Systolic Pressure-Diastolic Pressure)] usually 93 mmHg MAP=Cardiac Output × Systemic Vascular Resistance Cardiac Output=Stroke Volume × Heart Rate

Answer 130

**Short term:** * Nervous System (baroreceptors) * Chemical (chemoreceptors) **Long term:** •Hormonal (RAAS)

Cardiology 2 Flashcards

(170 cards)