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Core Conditions > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

MI (NSTEMI) Definition

A
  • Acute ischaemic event causing myocyte necrosis
  • Initial ECG may show ischaemic changes such as ST depressions, T-wave inversions or transient ST elevations – may also be normal or show non-specific changes
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2
Q

how common is an MI (NSTEMI)

A

• CVD is the number one cause of death worldwide

affects mainly men

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3
Q

causes of an MI (NSTEMI)

A

• Result of an acute imbalance between myocardial oxygen demand and supply, most commonly due to a reduction in myocardial perfusion
• Several different sequences of events that may lead to an NSTEMI:
- Plaque rupture with superimposed non-occlusive thrombus or embolic events leading to coronary vascular obstruction  MOST COMMON CAUSE
- Dynamic obstruction, such as in vasospasm
- Progressive luminal narrowing (i.e. chronic arterial narrowing from restenosis)
- Inflammatory mechanisms i.e. vasculitis
- Extrinsic factors leading to poor coronary perfusion (such as hypotension, hypovolaemia or hypoxia)

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4
Q

Risk factors for an MI (NSTEMI)

A
  • Atherosclerosis
  • Diabetes
  • Smoking
  • Dyslipidaemia
  • Age >65yrs
  • HBP
  • Cocaine use
  • Depression
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5
Q

Symptoms/ signs for an MI (NSTEMI)

A
  • Presence of risk factors
  • Chest pain  tightness, heaviness, aching, burning, pressure or squeezing – pain is most often retrosternal and can often radiate to the left arm, lower jaw, neck etc
  • Diaphoresis – sweating to an unusual degree
  • Abdo pain
  • HBP
  • N&V and SOB
  • Physical exertion
  • Diabetics may not have chest pain
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6
Q

DDx for MI (NSTEMI)

A
  • STEMI
  • Aortic dissection
  • PE
  • Peptic ulcer disease
  • Acute pericarditis
  • Oesophageal spasm
  • Costochrondritis
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7
Q

Investigation for MI (NSTEMI)

A

• 1st LINE:

  • ECG: non-specific ST-T wave changes or ischaemic changes
  • TRIAL OF SUBLINGUAL GLYCERYL TRINITRATE: ongoing pain
  • CARDIAC TROPONIN: test is more specific than CK-MB or myoglobin and is the best marker for msk injury and small MI - >99th percentile of normal
  • CK: >99th percentile of normal
  • CK-MB: - >99th percentile of normal
  • FBCs, U&E’s, Serum Creatinine, LFTs, blood glucose
  • CXR: may show pulmonary oedema
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8
Q

Management for MI (NSTEMI)

A

• 1st LINE:

  • MONA – morphine, oxygen (only if <94% sats), nitrates (GTN), aspirin
  • Aspirin: orally
  • If aspirin-intolerant  clopidogrel
  • Give oxygen if O2 sats below 90%
  • PLUS: beta-blocker, calcium-channel blocker, glyceryl trinitrate
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9
Q

prognosis and complications for MI (NSTEMI)

A
  • CVD responsible for about 30% of UK deaths

- Cardiac arrhythmias, depression, CHF, cardiogenic shock

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10
Q

definition of MI (STEMI)

A
  • Myocardial cell death that occurs because of a prolonged mismatch between perfusion and demand
  • Usually caused by occlusion in the coronary arteries
  • ST-elevation MI is suspected when a patient presents with persistnet ST-segment elevation in 2 or more anatomically contiguous ECG leads in the context of a consistent clinical history
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11
Q

How common is MI (STEMI)

A
  • CVD responsible for about 30% of UK deaths

- MIs are 3 times more likely in men than women

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12
Q

causes of MI (STEMI)

A
  • Atherosclerotic plaques form gradually over years
  • They begin with the accumulation of low-density lipoprotein cholesterol and saturated fat in the intima (inner layer) of blood vessels
  • Followed by the adhesion of leukocytes t the endothelium, then diapedesis and entry into intima where they accumulate lipids and become foam cells – rich source of proinflammaotry mediators  FATTY STREAK
  • Subsequent evolution involves migration of smooth muscle cells from the media, and their proliferation and deposition of extracellular matrix including proteoglycans, interstitial collagen and elastin fibres – some of the smooth muscle cells in advanced plaques exhibit apoptosis – plaques often develop calcification spots as they evolve  eventually causes arterial occlusion and stenosis
  • STEMI typically occurs after abrupt and catastrophic disruption of a cholesterol-laden plaque - this results in exposure of substances that promote platelet activation and aggregation, thrombin generation, and thrombus formation, causing interruption of blood flow
  •  If the occlusion is severe and persistent, myocardial cell necrosis follows
  • On interruption of blood flow in the coronary artery, the zone of myocardium supplied by that vessel immediately loses its ability to shorten and perform contractile work
  • Early hyperkinesis of the non-infarcted zones occurs, probably as a result of acute compensatory mechanisms including increased sympathetic activity and Frank-Starling mechanism
  • As necrotic myocytes slip past each other, the infarction zone thins and elongates, especially in anterior infarction, leading to infarction expansion
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13
Q

risk factors for MI (STEMI)

A
  • Hypertension
  • Smoking
  • Diabetes
  • Obesity
  • Metabolic syndrome
  • Physical inactivity
  • Dyslipidaemia
  • Renal insufficiency
  • Established coronary artery disease
  • Fx of premature coronary artery disease
  • Cocaine use
  • Male sex
  • Advanced age
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14
Q

symptoms/signs for MI (STEMI)

A
  • Chest pain - diabetics may not have chest pain
  • Dyspnoea
  • Pallor
  • Diaphoresis – common feature associated with MI due to high sympathetic output
  • Nausea
  • Vomiting
  • Dizziness
  • Weakness
  • Tachycardia
  • Additional heart sounds  audible S3 or S4 on cardiac exam indicates poor cardiac muscle compliance of the infarcted muscle
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15
Q

DDx for MI (STEMI)

A
  • Unstable angina
  • NSTEMI
  • Aortic dissection
  • PE
  • Pneumothorax
  • Pneumonia
  • Pericarditis
  • Myocarditis
  • GORD
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16
Q

Investigations for MI (STEMI)

A

• 1ST LINE:

  • ECG: if ECG shows ST-segment elevation, the patient should be urgently assessed for reperfusion therapy
  • CARDIAC BIOMARKERS: elevated troponin
  • GLUCOSE: hyperglycaemia is common in the setting of acute MI, with or without a history of diabetes – normal or elevated levels
  • U&E’s: determines if any disturbances that may need management are present – may be abnormal
  • SERUM LIPIDS: cholesterol levels may be lowered by high catecholamine levels produced by the MI in its early phases – need ot be repeated in 30-60 days – normal or elevated levels
  • CXR: widened mediastinum suggests aortic dissection, pulmonary oedema indicates impaired cardiac function
  • CORONARY ANGIOGRAM: presence of thrombus with occlusion of the artery
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17
Q

Management for MI (STEMI)

A 
•	1ST LINE:
-	ASPIRIN: orally
o	Give oxygen if O2 sats below 90%
o	If ongoing chest pain  give morphine
•	If unstable  revascularisation (PCI) or coronary artery bypass graft (CABG)
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18
Q

Prognosis or complications for MI (STEMI)

A

Prognosis - about 15% who have an acute MI will die from it

complications - sinus bradycardia, complete heart block with anterior MI, recurrent chest pain

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19
Q

Acute Coronary Syndrome definition

A
  • Refers to a spectrum of acute MI or infarction
  • Divivded into three clinical categories according to the presence or absence of STEMI, NSTEMI and unstable angina
  • Syndrome which describes decreased blood fow in the coronary arteries such that part of the heart muscle is unable to function properly or dies
  • Depending on the tests this can go from: ECG  ST-elevation or no ST-elevation, unstable angina from cardiac markers if pos, neg it is MI and either NSTEMI or STEMI
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20
Q

Angina (Stable) definition

A
  • SHID and low-risk unstable angina are most commonly caused by atheromatous plaques in the coronary arteries that obstruct blood flow
  • Anginal symptoms are a clinical manifestation of ischaemia
  • Key contributory factors to progression of atheromatous disease include smoking, hypertension, hyperlipidaemia, diabetes and obesity
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21
Q

how common is Angina (Stable)

A

prevalence is unclear

higher in males than females

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22
Q

causes of Angina (Stable)

A
  • Atheromatous plaque leading to obstruction of coronary blood flow is the most common cause
  • Damage to the aterial wall produces an inflammatory response and the development of atheromatous plaques
  • Exposure of the arterial endothelium to low-density lipoproteins results in the expression of adhesion molecules that allow leukocytes to stick to the arterial wall
  • Upon entry into the artery wall, blood monocytes begin to scavenge lipids and become foam cells
  • Macrophage foam cells release additional cytokines and effector molecules that stimulate smooth muscle migration from the arterial media into the intima, as well as smooth muscle cell proliferation
  • In this process, the initial fatty deposition of lipoprotein in the arterial intima develops ito atherosclerotic plaques
  • Ischaemic symptoms may result from obstruction of blood flow due to atherosclerotic plaques or when a clot or vasospasm is superimposed on less severe plaques
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23
Q

risk factors for Angina (Stable)

A
  • Advancing age
  • Smoking
  • Hypertension
  • Elevated LDL cholesterol
  • Isolated low HDL cholesterol
  • Diabetes
  • Inactivity
  • Obesity
  • Male
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24
Q

symptoms/signs of Angina (Stable)

A
  • Presence of risk factors
  • Typical angina symptoms – chest pressure or squeezing lasting several minutes, provoked by exercise or emotional stress and relieved by res or GTN
  • Atypical angina symtpoms – chest discomfort with only 2 characteristics of typical angina
  • Features of low-risk unstable angina include pain from exertion lasting less than 20 minutes, pain not rapidly increasing and normal/unchanged ECG
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25
Q

DDx of Angina (Stable)

A
  • PE
  • Pericarditis
  • Aortic dissection
  • Pneumothorax
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26
Q

Investigations for Angina (Stable)

A
  • Lymph node examination
  • If unexplained  consider a very urgent FBC
  • In people >40, with supraclavicular lymphadenopathy or persistent cervical lymphadenopathy, consider an urgent chest X-ray
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27
Q

Management of Angina (Stable)

A

• 1st LINE:

  • CALCIUM CHANNEL BLOCKER OR BETA BLOCKER FIRST LINE
  • LIFESTYLE EDUCATION
  • ANTIPLATELET THERAPY: aspirin or clopidogrel
  • ANTI-ANGINAL THERAPY: bisoprolol
  • STATIN: atorvastatin
  • ANTIHYPERTENSIVE: bisoprolol
  • Acute  give GTN – careful with phosphodiesterase inhibitors (contraindicated)
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28
Q

Prognosis and complications of Angina (Stable)

A

prognosis - patients can expect a reduction in angina symptoms

complications - chronic heart failure, MI, stroke, depression

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29
Q

Angina (Unstable) Definition

A

• ACS that is defined by the absence of biochemical evidence of myocardial change

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30
Q

how common is Angina (Unstable)

A

CVD is the number one cause of death globally for men and women

affects mainly adults

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31
Q

causes of Angina (Unstable)

A
  • CAD is the underlying cause in nearly all pts with acute MI
  • Most common cause of UA is due to CA narrowing caused by a thrombus that develops on a disrupted atherosclerotic plaque and is usually non-occlusive
  • Less common cause is intense vasospasm of a CA (variant or Prinzmetal’s angina) – intense vasospasm is caused by vascular smooth muscle or by endothelial dysfunction
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32
Q

risk factors for Angina (Unstable)

A
  • Female
  • Personal history of CAD
  • Increased age
  • Fx of CAD
  • Hypertension
  • Smoking
  • Diabetes
  • Hyperlipidaemia
  • PVD
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33
Q

Symptoms of Angina (Unstable)

A
  • Presence of risk factors
  • Increasing frequency of chest pain – pain occurs daily or several times a day
  • Increasing severity of chest pain – decreasing levels of activity needed to trigger chest pain and may occur at rest
  • Retrosternal chest pain radiating to jaw, arm or neck – retrosternal pressure or heaviness radiating to the jaw, arm or neck that is relieved or improved by nitrates
  • Dyspnoea
  • Fourth heart sound (S4)
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34
Q

signs of Angina (Unstable)

A

• 3 key symptoms:
- Constricting discomfort in the front of the chest, in the neck, shoulders, jaw, or arms
- Precipitated by physical exertion
- Relieved by rest or GTN within about 5 minutes
• Typical angina has all 3, atypical have 2/3, people with non-anginal chest pain have one or none of the 3 features.

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35
Q

DDx of Angina (Unstable)

A
  • Stable angina
  • STEMI/NSTEMI
  • CHF
  • Chest wall pain
  • Pericarditis
  • Myocarditis
  • Aortic dissection
  • PE
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36
Q

Investigations for Angina (Unstable)

A

• 1st LINE:

  • ECG: may be normal or have transient ST segment depression or T-wave inversion
  • CARDIAC BIOMARKERS: not elevated
  • FBC: normal
  • ELECTROLYTES AND RENAL FUNCTION: normal
  • BLOOD SUGAR: normal, elevated in the presence of diabetes
  • LIPID PROFILE: increased
  • COAGULATION: normal
  • CXR: pulmonary oedema
  • CORONARY ANGIOGRAPHY: gold standard for assessing the presence and severity of CAD, and allows concurrent tx with angioplasty and stenting
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37
Q

Management for Angina (Unstable)

A

• 1st LINE:

  • PRESUMED CARDIAC CHEST PAIN: oxygen, nitrates (GTN) and morphine
  • CONFIRMED UNSTABLE ANGINA: antiplatelet therapy  aspirin (without stenting), clopidogrel (with stenting), + statin + beta blocker + ACEi
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38
Q

Prognosis and complications for Angina (Unstable)

A

Prognosis - dependant on cause

complications - Bleeding, thrombocytopenia, CHF, ventricular arrhythmias

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39
Q

AF definition

A
  • Supraventricular tachyarrhythmia
  • Characterised by uncoordinated atrial activity on the surface ECG, with fibrillatory waves of varying shape, amplituds and timing associated with an irregularly irregular ventricular response when AV conduction is intact
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40
Q

how common is AF

A
  • 0.5-1% prevalence

* Elderly patients, higher prevalence in men than women 1.5:1 M:F

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41
Q

Causes of AF

A
  • AF is usually associated with anatomically and histologically abnormal atria as a result of underlying heart disease
  • Dilation of the atria with fibrosis and inflammation causes a difference in refractory periods within the atrial tissue and promotes electrical re-entry that results in AF
  • Presence of rapidly firing foci, typicall in the pulmonary veins, may trigger AF and this is sutained by firbillatory conduction or multiple re-entrant circuits
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42
Q

risk factors of AF

A
  • Hypertension
  • CAF
  • CHF
  • Advancing age
  • Diabetes
  • Rheumatic valvular disease
  • Alcohol abuse
  • Male sex
  • Presence of other arrhythmias
  • Smoking
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43
Q

symptoms/ signs of AF

A
  • Presence of risk factors
  • Palpitations
  • Tachycardia
  • Irregular pulse
  • Stroke – complication of AF
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44
Q

DDx of AF

A
  • AF with variable AV conduction
  • Multifocal atrial tachycardia
  • Atrial tachycardia with variable AV conduction
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45
Q

Investigations of AF

A

• 1ST LINE:

  • ECG: absent P-waves, presence of fibrillatory waves that vary in size, shape and timing, irregularly irregular QRS complexes
  • THYROID PROFILE: suppressed TSH if hyperthyroidism  thyrotoxicosis may present with AF
  • ECHOCARDIOGRAM: may have valvular regurgitation or stenosis, left ventricular or atrial enlargement, peak right ventricular pressure (pulmonary HTN), left ventricular wall thickness and function
  • SERUM UREA AND ELECTROLYTES (INCLUDING SERUM MAGNESIUM): may be normal, may be abnormal with renal dysfunction
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46
Q

management of AF

A

• 1st LINE:
- ANTICOAGULATION OR ANTIPLATELET THERAPY: warfarin
o + rate control: bisoprolol/propranolol (1st), digoxin/dilitazem (2nd)

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47
Q

Prognosis and complications of AF

A

Prognosis - depends on several factors
complications - stroke, hypotension, heart failure, exacerbation of reactive airway disease associated with beta-blocker therapy

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48
Q

Essential Hypertension definition

A

• Defined as BP >140/90mmHg with no secondary cause identified

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49
Q

how common is Essential Hypertension

A
  • 1 billion people are hypertensive

- mainly adults, mainly men

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50
Q

causes of Essential Hypertension

A
  • BP = CO x PVD  affected by preload, contractility, vessel hypertrophy and peripheral constriction
  • Pathology associated with and the perpetuation of the hypertensive state involves structural changes, remodelling and hypertrophy in resistance arterioles
  • Changes have been associated with the early and progressive development of small vessel atherosclerosis which is probably the cause of end-organ damage seen in advanced hypertension
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51
Q

risk factors of Essential Hypertension

A
  • Obesity
  • Aerobic exercise <3 times/week
  • Moderate/high alcohol intake
  • Metabolic syndrome
  • Diabetes
  • Black ancestry
  • Age >60 years
  • Fx of hypertension or coronary artery disease
  • Sleep apnoea
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52
Q

symptoms/signs of Essential Hypertension

A
  • Presence of risk factors
  • Blood pressure over 140/90mmHg
  • Retinopathy
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53
Q

DDx of Essential Hypertension

A
  • Drug-induced  NSAIDs, oral contraceptive pill, immunosupressants, erythropoietin
  • CKD
  • Renal artery stenosis
  • Aortic coarctation
  • Hypothyroidism
  • Hyperthyroidism
  • Hyperparathyroidism
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54
Q

Investigations of Essential Hypertension

A

• 1st LINE:

  • ECG: may show evidence of left ventricular hypertrophy or old infarction
  • FASTING METABOLIC PANEL WITH ESTIMATED GFR: may show renal insufficiency, hyperglycaemia, hypokalaemia, hyperuricaemia or hypercalcaemia
  • LIPID PANEL: may show high LDL, low HDL, or high triglycerides
  • URINALYSIS: may show proteinuria
  • Hb: anaemia or polycythaemia suggests secondary cause or complication
  • TSH: high or low if thyroid dysfunction
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55
Q

Management of Essential Hypertension

A

• 1st LINE:
- Step 1:
o Younger than 55  ACE inhibitor
o Older than 55 or black of any age  calcium channel blocker or thiazide-type diuretic
- Step 2: ACEi + calcium channel blocker or ACEi + thiazide-type diuretic (indapamide)
- Step 3: ACEi + calcium channel blocker + thiazide-type diuretic
- Step 4: Step 3+ a further diuretic therapy or α-blocker or β blocker - consider seeking specialist advice

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56
Q

Prognosis and complications of Essential Hypertension

A

prognosis - good when treated

complications - CAD, LVF, cerebrovascular accident, CHF, retinopathy

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57
Q

DVT definition

A
  • Development of a blood clot in a major deeo vein in the leg, thigh, pelvis or abdomen, which may result in impaired venous blood flow and consequent leg swelling and pain
  • Venous thrombosis may also occur in the upper extremities or in more unusual sites such as the portal, mesenteric, ovarian and retinal veins as well as the veins and venous sinuses of the brain
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58
Q

how common is DVT

A

1 in every 1000 adults

affects frequent flyers, obese people, higher in black people

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59
Q

causes of DVT

A
  • Most blood clots that develop in the deep venous system of the leg begin to form just above and behind a venous valve
  • Clots often resolve spontaneously but when the propagation of the trhombus does occur it expands and grows proximally and across the lumen of the vein
  • A clot might occlude the entire lumen, but it is more commonly located on one peripheral aspect of the lumen
  • Many DVTs arise in the calf veins and propagate proximally
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60
Q

risk factors of DVT

A
  • Medical hospitalisation within the past 2 months
  • Major surgery within 3 months
  • Active cancer
  • Severe or lower-extremity trauma
  • Increasing age
  • Pregnancy
  • Factor V leiden
  • Protein C, S or antithrombin deficiency
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61
Q

symptoms / signs of DVT

A
  • Calf swelling
  • Localised pain along deep venous system
  • Asymmetric oedema – worse on leg with suspected DVT
  • Prominent superficial veins
  • Worsening pain when bending the foot
  • Leg cramping at night
62
Q

DDx of DVT

A
  • Cellulitis
  • Claf muscle tear/Achilles tendon tear
  • Calf muscle haematoma
  • Large or ruptured popliteal cyst (bakers cysts)
63
Q

Investigations of DVT

A

• 1ST LINE:
- WELLS SCORE:
o Clinical signs and symptoms of DVT +3
o PE is number 1 diagnosis or equally likely +3
o Heart rate >100 +1.5
o Immbolization at least 3 days OR surgery in the previous 4 weeks +1.5
o Previous, obectively diagnosed PE or DVT +1.5
o Haemoptysis +1
o Malignancy with treatment within 6 months ot palliative +1
- QUANTITATIVE D-DIMER LEVEL: normal (DVT excluded if wells score <2); elevated (proceed to imaging)
- PROXIMAL DUPLEX ULTRASOUND: abnormal  inability to fully compress lume of vein using ultrasound transducer, reduced or absent spontaneous flo, lack of repsitatory variation, intraluminal echoes, colour flow patency abnormalities, normal  all vein segments fully compressible, non-diagnostic
- WHOLE-LEG ULTRASOUND: same as proximal duplex
- U&E’s: baseline values
- LFTs: baseline values
- FBC: baseline values

64
Q

management of DVT

A

• 1st LINE:

  • LMWH: heparin
    • anticoagulation: rivaroxaban
65
Q

prognosis and complications of DVT

A

prognosis - good when Tx

complications - PE, bleeding during urial treatment, post-thrombotic syndrome

66
Q

Left Ventricular Failure (CHF) Definition

A
  • Heart is unable to generate a cardiac output sufficient to meet the demands of the body without increasing diastolic pressure
  • Can result from any cardiac disease that compromises ventricular systolic or diatolic function or both
67
Q

How common is Left Ventricular Failure (CHF)

A

1-2%

affects mainly adults

68
Q

causes of Left Ventricular Failure (CHF)

A

• Heart failure represents a complex syndrome in which an initial myocardial insult results in the over-expression of multiple peptides with different short and long-term effects on the cardiovascular system

69
Q

risk factors of Left Ventricular Failure (CHF)

A
  • MI
  • Diabetes
  • Dyslipidaemia
  • Old age
  • Male
  • Hypertension
  • Left ventricular dysfunction
  • Cocaine abuse
  • Exposure to cardiotoxic agents
  • LVF
  • Renal insufficiency
  • Valvular heart disease
  • Sleep apnoea
  • Elevated homocysteine
70
Q

symptoms of Left Ventricular Failure (CHF)

A
  • Presence of risk factors
  • Dyspnoea – most common symptom of left-sided heart failure
  • Neck vein distention
  • S3 gallop
  • Cardiomegaly
  • Hepatojugular reflux
  • Rales
  • Orthopnoea and paroxysmal nocturnal dyspnoea
  • Nocturia
  • Night cough
  • Signs of pleural effusion - bilateral
  • Ankle oedema
  • PND – paroxysmal nocturnal dyspnoea
71
Q

signs of Left Ventricular Failure (CHF)

A
  • Tachycardia (rate over 100)
  • Laterally displaced apex beat, heart murmurs, and third and fourth heart sounds (gallop rhythm)
  • Hypertension
  • Raised JVP
  • Enlarged liver (due to engorgement), respiratory signs such as tachypnoea, basal crepitation’s, and pleural effusions
  • Dependent oedema, ascites
  • Obesity.
72
Q

DDx of Left Ventricular Failure (CHF)

A
  • Ageing/physical inactivity
  • Pneumonia
  • PE
  • Cirrhosis
  • Nephrotic syndrome
  • Venus stasis
  • DVT
73
Q

Investigations of Left Ventricular Failure (CHF)

A

• 1st LINE:

  • CXR: abnormal, bilateral or right sided pleural effusion indicates CHF
  • TRANSTHORACIC ECHOCARDIOGRAM: systolic HF: depressed and dilated left and/or right ventricle with low ejection fraction, diastolic HF: LVEF normal but LVH and abnormal diastolic filling patterns
  • ECG: evidence of underlying CAD, left ventricular hypertrophy, or atrial enlargement, may be conduction abnormalities and abnormal ARS duration
  • FBC, Serum Electrolytes, Serum Creatinine, Blood glucose, LFTs, TFTs
74
Q

Management of Left Ventricular Failure (CHF)

A

• 1st LINE:

- ACEi + beta blocker + diuretic

75
Q

Prognosis and complications of Left Ventricular Failure (CHF)

A

prognosis - dependant on cause

complications - pleural effusion, acute decompensation of CHF, acute renal failure

76
Q

mitral stenosis definition

A

• Narrowing of the mitral valve orifice, usually caused by rheumatic valvulitis producing fusion of the valve commissures and thickening of the valve leaflets

77
Q

how common is mitral stenosis

A
  • most cases are caused by rheumatic fever
  • 2 per 100,000 people
  • affects primarily women who develop it - 3x more than men
78
Q

causes of mitral stenosis

A
  • As the valve orifice becomes reduced in mitral stenosis, flow between the left atrium and left ventricle is progressively impeded and pressure in the left atrium remains higher than that of the left ventricle
  • By restricting flow = 1. Increased left atrial pressure is referred ot lungs, where it leads to congestion nd the symptoms associated with it 2. Restricted orifice limits filling of the LV thereby limiting CO  producing symptoms mimicking LHF
79
Q

risk factors for mitral stenosis

A
  • Streptococcal infection
  • Female
  • Serotogenic medications e.g. fenfluramine and dexfenfluramine
  • SLE
  • Amyloidosis
  • Bronchial carcinoid syndrome
80
Q

symptoms/ signs for mitral stenosis

A
  • Presence of risk factors
  • Hx of RF
  • Dyspnoea – due to pulmonary congestion
  • Orthopnoea – due to increased LA pressure
  • Opening snap on auscultation
  • Diastolic murmur –low-pictched, rumbling mid-diastolic murmur at apex
  • Loud P2 – sign of pulmonary hypertension and/or right VF
  • Neck vein distension
  • Paroxysmal nocturnal dyspnoea
  • Haemoptysis
  • Hoarseness
  • Peripheral oedema
  • Ascites
  • Loud S1
  • Left parasternal heave
81
Q

DDx for mitral stenosis

A
  • Left atrial myxoma

* Unexplained AF

82
Q

Investigations for mitral stenosis

A

• 1st LINE:

  • ECG: non-specific test is performed at baseline and again if there is a change in pts rhythm  AF, left atrial enlargement, RVF
  • CXR: test ordered at baseline  double right heart border indicating an enlarged left atrium, prominent pulmonary artery, Kerley B lines
  • TRANS-THORACIC ECHOCARDIOGRAPHY: definitive test to confirm the diagnosis and to quantitate the severity of the disease  hockey stick-shaped mitral deformity
83
Q

Management for mitral stenosis

A

• 1st LINE:

  • PREGNANT: diuretics e.g. furosemide
  • BALLOON VALVOTOMY: with very severe disease (valve area <1.0cm^2)
  • Otherwise no tx is needed
84
Q

Prognosis and complications for mitral stenosis

A

prognosis - excellent prognosis when Tx

complications - AF, stroke, warfarin induced haemorrhage

85
Q

Mitral regurgitation definition

A
  • Commonest valve lesion
  • Mitral valve apparatus consists of anterior and posterior leaflets, chordae tendineae, anterolateral and posteromedial papillar muscles and mitral annulus
  • Any aberrations of the mitral valve apparatus, due to mechanical, traumatic, infectious degenerative, congenital or metabolic cause may lead to MR
86
Q

how common is mitral regurgitation

A
  • more than 5 million people worldwide

- unknown

87
Q

causes of mitral regurgitation

A
  • Typical causes of acute MR include IE, ischaemic papillary muscle dysfunction or rupture, acute RF and acute dilation of the left ventricle due to myocarditis or ischaemia
  • Common causes of chronic MR include those above but also myxomatous degeneration of the mitral leaflets or chordae tendineae, mitral valve prolapse and mitral annular enlargement
  • Chronic MR can be mild or moderate and can be asymptomatic for many years, howeverm with progression of the disease to severe, eccentric cardiac hypertrophy occurs, which leads to elongation of the myocardial fibres and increased LV end-diastolic volume
  • Compensatory mechanism that allows an increase in total stroke volume to maintain adequate CO
  • Additionally, both LV and LA enlargement will accommodate the regurgitant volume at a lower filling pressure which prevents pulmonary congestion
  • Eventually, prolonged volume overload leads to LV dysfunction and increased LV end-systolic diameter
88
Q

risk factors of mitral regurgitation

A
  • Mitral valve prolapse
  • Hx of rheumatic heart disease
  • IE
  • Hx of cardiac trauma, MI, congenital heart disease, IHD, ventricular systolic dysfunction
  • Anorectic/dopaminergic drugs
89
Q

symptoms of mitral regurgitation

A
  • Presence of risk factors
  • Dyspnoea on exertion
  • Decreased exercise tolerance
  • Lower extremity oedema
  • Holosystolic murmur
  • Fatigue
  • Displaced point of maximal impulse – indicates severe and chronic MR
90
Q

DDx of mitral regurgitation

A
  • ACS
  • IE
  • Mitral stenosis
  • Aortic stenosis
  • Aortic or pulmonary valve disease
  • Atrial myxoma
91
Q

Investigations of mitral regurgitation

A

• 1st LINE:

  • TRANSTHORACIC ECHO: presence and severity of MR, other structural and flow abnormalities
  • ECG: may show underlying arrhythmia or prior infarction
92
Q

management of mitral regurgitation

A

• 1st LINE:

  • ACUTE OR SEVERE CHRONIC: annuloplasty or mechanical valve and anticoagulation or bioprostheses (SURGERY)
  • IF ASYMPTOMATIC: ACEi and beta-blockers
93
Q

prognosis or complications

A

Prognosis - unclear

complications - AF, pulmonary hypertension, postoperative stroke, prosthesis stenosis, LV dysfunction and CHF

94
Q

Aortic Stenosis Definition

A
  • Obstruction of blood flow across the aortic valve due to pathological narrowing
  • Progressive disease that presents after a long subclinical period
95
Q

how common is Aortic stenosis

A

• AS is the most common valvular disease in the US and Europe and is the second most frequent cause for cardiac surgery
affects mainly older patients

96
Q

causes of aortic stenosis

A
  • Calcification of the normal trileaflet valves is the most common cause of AS i adults
  • Calcific aortic disease represents a spectrum ranging from aortic sclerosis (defined ad leaflet thickening without obstruction) to severe AS
  • Congenitally bicuspid valves account for the majority of the remainder of cases –pts with coarctation of the aorta and turners syndrome have a higher incidence of bicuspid valves
  • In rheumatic disease, an autoinflammatory reaction is triggered by prior strep infection that targets the valvular endothelium leading to inflammation and eventually calcification
97
Q

risk factors for aortic stenosis

A
  • Age over 60
  • Congenitally bicuspid aortic valve
  • Rheumatic heart disease
  • CKD
  • Radiotherapy
  • High LDL cholesterol
  • Hyperlipoproteinaemia
98
Q

symptoms of aortic stenosis

A
  • Presence of risk factors
  • Dyspnoea – shortness of breath on exertion
  • Chest pain – develop exertional chest pain (angina)
  • Ejection systolic murmur – loudest at the right upper sternal border
  • S2 diminished and single – aortic valve closure is delayed and often coincides with pulmonic valve closure, producing a single second heart sound
  • Carotid parvus et tardus – carotid upstroke is frequently delayed and diminished in severe AS, often obsent in older pts with less compliant vasculature
99
Q

signs of aortic stenosis

A
  • Paradoxicallysplit S2 – with more severe stenosis, aortic valve closure may become so delayed that it follows pulmonic valve closure during expiration producing the paradoxically split S2, mayt be accentuated by left bundle branch block
  • Gallavardin’s phenomenon – a musical quality, holosystolic murmur is present at the apex of the heart that occurs in older pts with calcific AS which may mimic mitral regurgitation
  • Bleeding – develop an acquired von Willebrand deficiency that predisposes to bleeding and is caused by turbulent flow across the stenotic valve
100
Q

DDx of aortic stenosis

A
  • Aortic sclerosis
  • IHD
  • Hypertrophic cardiomyopathy (HCM)
101
Q

Investigations of aortic stenosis

A

• 1st LINE:

  • TRANSTHORACIC ECHO (INC DOPPLER): elevated aortic pressure gradient; measurement of valve area and LVEF, best test for the initial diagnosis and subsequent evaluation of AS
  • ECG: may demonstrate LVF and absent Q waves, AV block, hemiblock or bundle branch block
102
Q

Management of aortic stenosis

A

• 1st LINE:

  • UNSTABLE: medical therapy or balloon valvuloplasty  i.e. beta blockers/vasopressors
  • STABLE: surgical aortic valve replacement
103
Q

prognosis and complications of aortic stenosis

A

prognosis - varies
complications - CHF, sudden cardiac death in symptomatic patients or asymptomatic pts, infection of prosthetic valve, re-stenosis, valve dehiscence

104
Q

Aortic regurgitation definition

A
  • Diastolic leakage of blood from the aorta into the LV
  • It occurs due to inadequate coaptation of valve leaflets resulting from either intrinsic valve disease or dilation of the aortic root
  • It can remain asymptomatic for decades before pts present with irreversible myocardial damage
105
Q

how common is aortic regurgitation

A
  • not as common as aortic stenosis and MR

- 13% in men and 8.5% in women

106
Q

causes of aortic stenosis

A

• ACUTE:
- End-diastolic pressure in LV rises sharply
- Heart tries to compensate by increasing the HR and increasing the contractility (Starling’s law) to keep up with the increased preload, but this is insufficient to maintain the normal stroke volume and fails
• CHRONIC:
- Both the LV volume and pressure overload
- An increase in LV volume and pressure causes an increase in wall tension
- According to Laplace’slaw, wall tension is directly proportional to the product of cavity pressure and radius, and inversely proportional to wall thickness
- To compensate for the increased wall tension, the heart wall undergoes hypertrophy
- Both concentric and eccentric hypertrophy can occur but most are eccentric – sarcomeres are laid down in series – results from volume overload, concentric – sarcoemeres replicate in parallel – results from pressure overload from increased systolic pressure to nromalise the end-systolic stress
- Systolic hypertension occurs secondary to increased stroke volume, which combines both regurgitant and forwards stroke volume
- The volume overload, which is directly related to the severity of the leak, results in an increase in LV end-diastolic volume
- End-diastolic pressure remains normal due to an increase in ventricular compliance resulting from increased cavity size

107
Q

risk factors of aortic regurgitation

A
  • Bicuspid aortic valve
  • RF
  • Endocarditis
  • Marfan’s syndrome and related connective tissue disease
  • Aortitis
108
Q

symptoms/ signs of aortic regurgitation

A
  • Presence of risk factors
  • Diastolic murmur – absence of diastolic murmur significantly reduces the likelihood of AR
  • Dyspnoea – caused by pulmonary oedema in acute AR
  • Fatigue, weakness, orthopnoea, paroxysmal nocturnal dyspnoea
  • Pallor, mottled extremities, rapid and faint peripheral pulse, jugular venous distension – due to cardiogenic shock
  • Basal lung crepitations
  • Altered mental status
  • Soft S1
  • Soft or absent A2
  • Collapsing (water hammer or Corrigan’s) pulse
  • Cyanosis
  • Displaced, hyperdynamic apical impulse
  • Systolic thrill – may be palpable over the base of the heart or suprasternal notch due to increased stroke volume
109
Q

DDx of aortic regurgitation

A
  • MR
  • Mitral stenosis
  • Aortic stenosis
  • Pulmonary regurgitation
110
Q

Investigations of aortic regurgitation

A

• 1st LINE:

  • ECG: may show non-specific ST-T wave changes, left axis deviation, or conduction abnormalities
  • CXR: may show cardiomegaly
  • ECHOCARDIOGRAM: visualisation of the origin of regurgitant jet and its width, detection of cause of aortic valve pathology
  • COLOUR-FLOW DOPPLER: one of the most specific and sensitive techniques used to judge the severity of the regurgitant flow by using the ratio of proximal jet width
111
Q

Management of aortic regurgitation

A

• 1st LINE:

  • ACUTE: inotropes + vasodilators + urgent aortic valve replacement/repair  dopamine, nitroprusside and aortic valve replacement
  • CHRONIC: aortic vale replacement or transcatheter aortic valve implantation
112
Q

prognosis and complications of aortic regurgitation

A

prognosis - mortality is low (<0.4% per year)

complications - operative mortality, CHF, arrhythmias, IE, sudden death

113
Q

right ventricular failure definition

A

• Complex syndrome in which the ability of the heart to maintain the circulation of blood is impaired because of structural or functional impairment of ventricular filling or ejection

114
Q

how common is right ventricular failure

A
  • 1/35 people

- higher in males than females, elderly

115
Q

causes of Right Ventricular Failure

A
  • RHF: RV infarct, pulmonary hypertension, PE, cor pulmonale, COPD, severe bradycardia or tachycardia, pericardial disease (constrictive)
  • OTHER CAUSES: IHD, cardiomyopathy (dilated), hypertension
116
Q

Risk Factors of Right Ventricular Failure

A
  • AF
  • Diabetes
  • Fx of heart failure or suddent cardiac death
117
Q

symptoms of Right Ventricular Failure

A
  • Presence of risk factors
  • Dyspnoea – breathlessness on exertion
  • Orthopnoea – breathlessness on lying falt
  • Nocturnal cough or waking from sleep (PND)
  • Fluid retention – ankle swelling, bloated feeling, abdominal swelling or weight gain
  • Fatigue, decreased exercise tolerance or increased recovery time after exercise
  • Light headedness or hx of syncope
118
Q

signs of Right Ventricular Failure

A
  • Tachycardia
  • Laterally displaced apex beat, heart murmurs and third and fourth heart sounds (gallop rhthym)
  • Hypertension
  • Raised JVP
  • Enlarged liver (due to engorgement)
  • Respiratory signs such as tachypnoea, basal crepitations and pleural effusions
  • Oedema, ascites, obesity
119
Q

DDx for Right Ventricular failure

A
  • COPD, asthma, PE, lung cancer, axiety
  • Nephrotic syndromes
  • Thyroid disease
  • Bilateral renal artery stenosis
120
Q

Investigations of Right Ventricular failure

A

• 1st LINE:

  • ECHOCARDIOGRAPHY: allows assessment of ventricular systolic and diastolic function  shows regional wall motion abnormalities and may reveal the aetiology of HF
  • NO PRIOR MI: measure naturitic peptide level
  • 12-LEAD ECG
  • CXR, FBCs, U&E’s, HbA1c, TFTs, LFTs, fasting lipids  helps to exclude diagnoses
121
Q

management of Right Ventricular Failure

A

• 1st LINE:

  • CONFIRMED HF WITH REDUCED EF: loop diuretic (furosemide) -> titrate the dose up to deal with the fluid overload, ACEi and betablocker -> only start one drug at a time, antiplatelet or statin therapy  if needed
  • CONFIRMED HF WITH PRESERVED EF: : loop diuretic (furosemide), antiplatelet or statin therapy  if needed
122
Q

prognosis and complications of Right Ventricular Failure

A

Prognosis - Patients can expect a reduction in angina symptoms

complications - chronic heart failure, MI

123
Q

Valvular heart disease Definition

A
  • SHID and low-risk unstable angina are most commonly caused by atheromatous plaques in the coronary arteries that obstruct blood flow
  • Anginal symptoms are a clinical manifestation of ischaemia
  • Key contributory factors to progression of atheromatous disease include smoking, hypertension, hyperlipidaemia, diabetes and obesity
124
Q

How common is valvular heart disease

A
  • prevalence is unclear

- higher in males than females

125
Q

causes of valvular heart disease

A
  • Atheromatous plaque leading to obstruction of coronary blood flow is the most common cause
  • Damage to the aterial wall produces an inflammatory response and the development of atheromatous plaques
  • Exposure of the arterial endothelium to low-density lipoproteins results in the expression of adhesion molecules that allow leukocytes to stick to the arterial wall
  • Upon entry into the artery wall, blood monocytes begin to scavenge lipids and become foam cells
  • Macrophage foam cells release additional cytokines and effector molecules that stimulate smooth muscle migration from the arterial media into the intima, as well as smooth muscle cell proliferation
  • In this process, the initial fatty deposition of lipoprotein in the arterial intima develops ito atherosclerotic plaques
  • Ischaemic symptoms may result from obstruction of blood flow due to atherosclerotic plaques or when a clot or vasospasm is superimposed on less severe plaques
126
Q

risk factors for valvular heart disease

A
  • Advancing age
  • Smoking
  • Hypertension
  • Elevated LDL cholesterol
  • Isolated low HDL cholesterol
  • Diabetes
  • Inactivity
  • Obesity
  • Male
127
Q

symptoms / signs of valvular heart disease

A
  • Presence of risk factors
  • Typical angina symptoms – chest pressure or squeezing lasting several minutes, provoked by exercise or emotional stress and relieved by res or GTN
  • Atypical angina symtpoms – chest discomfort with only 2 characteristics of typical angina
  • Features of low-risk unstable angina include pain from exertion lasting less than 20 minutes, pain not rapidly increasing and normal/unchanged ECG
128
Q

DDx of valvular heart disease

A
  • PE
  • Pericarditis
  • Aortic dissection
  • Pneumothorax
129
Q

Investigations of valvular heart disease

A
  • Lymph node examination
  • If unexplained  consider a very urgent FBC
  • In people >40, with supraclavicular lymphadenopathy or persistent cervical lymphadenopathy, consider an urgent chest X-ray
130
Q

management of valvular heart disease

A

• 1st LINE:

  • CALCIUM CHANNEL BLOCKER OR BETA BLOCKER FIRST LINE
  • LIFESTYLE EDUCATION
  • ANTIPLATELET THERAPY: aspirin or clopidogrel
  • ANTI-ANGINAL THERAPY: bisoprolol
  • STATIN: atorvastatin
  • ANTIHYPERTENSIVE: bisoprolol
  • Acute  give GTN – careful with phosphodiesterase inhibitors (contraindicated)
131
Q

prognosis and complications of valvular heart disease

A

Prognosis - patients can expect a reduction in angina symptoms

complications - chronic heart failure, MI, stroke, depression

132
Q

Infective endocarditis definition

A

• Infection involving the endocardial surface of the heart, including the valvular structures, the chordae tendineae, sites of septal defects or the mural endocardium

133
Q

how common is infective endocarditis

A
  • 10-15K cases in the US each yr

- Half of pts are over 60

134
Q

causes of infective endocarditis

A
  • IE typically develops on the valvular surfaces of the heart, which have sustained endothelial damage secondary to turbulent blood flow
  • As a result, platelets and fibrin adhere to the underlying collagen surface and create a prothrombotic milieu
  • Bacteraemia leads to colonisation of the thrombus and perpetuates further fibrin deposition and platelet aggregation, which develops into a mature infected vegetation
  • Acute IE is associated with more virulent organisms, classically staph aureus
  • Thrombus is formed by the offending organism and S aureus may invade endothelial cells and increase the expression of adhesion molecules as well prothrombotic factors
135
Q

risk factors of infective endocarditis

A
  • Prior hx of IE
  • Presence of artificial prosthetic heart valves
  • Certain types of congenital heart disease
  • Post-heart transplant (pts who develop a cardiac valvulopathy)
136
Q

symptoms of infective endocarditis

A
  • Fiever/chills
  • Night sweats, malaise, fatigue, anorexia, weight loss, myalgias
  • Weakness
  • Arthralgias
  • Headache
  • SOB
137
Q

signs of infective endocarditis

A
  • Roth spots – immune complex deposition in blood vessels producing a vasculitis and petechial haemorrhages in the skin, under the nails and in the retinae
  • Osler’s nodes – tender subcutaneous nodules in the fingers
  • Janeway lesions – painless erythematous mavules on the palms
138
Q

DDx of infective endocarditis

A
  • RF
  • Atrial myxoma
  • Libman-sacks endocarditis
  • Non-bacterial thrombotic endocarditis
139
Q

Investigations of infective endocarditis

A

• 1st LINE:

  • FBC: anaemia, leucocytosis
  • SERUM CHEMISTRY PANEL WITH GLUCOSE: normal or elevated urea
  • URINALYSIS: RBC casts, WBC casts, proteinuria, pyuria
  • BLOOD CULTURES: bacteraemia, fungaemia
  • ECG: prolonged PR interval, non-specfic ST/T wave abnormalities, AV block
  • ECHOCARDIOGRAM: valvular, mobile vegetations
140
Q

management of infective endocarditis

A

1st LINE:

- BETA-LACTAM + GENTAMICIN, OR VANCOMYCIN +/- GENTAMICIN: benzylpenicillin

141
Q

complications of infective endocarditis

A

• CHF, systemic embolization, valvular rupture or fistula

142
Q

Postural Hypotension (Orthostatic Hypotension)

A
  • Fall in systolic blood pressure of at least 20mmHg (at least 30mmHg in pts with hypertension) and/or a fall in diastolic BP of at least 10mmHg within 3 minutes of standing
  • It becomes clinically significant if it is accompanied by symptoms of cerebral hypoperfusion, which can lead to syncope and falls
143
Q

how common is postural Hypotension (Orthostatic Hypotension)

A
  • 11-16% prevalence

- greater in older people

144
Q

causes of postural Hypotension (Orthostatic Hypotension)

A
  • When an otherwise healthy person stands, about 700mL of blood pools in the leg veins and the lower abdominal veins
  • Venous return to the heart decreases, resulting in a transient decline in CO
  • This leads to baroreflex-mediated sympathetic activation with an increase in cardiac stroke volume and peripheral vasoconstriction, as well as parasympathetic withdrawal with an increase in HR
  • These rapid haemodynamic hcnages prevent BP from falling
  • Failure of these mechanisms causes orthostatic hypotension
  • Cerebral blood flow normally remains constant throughout a wide range of blood pressure by autoregulation, but the mechanism is overwhelmed when systolic BP is around 50mmHg at brain level (about 70mmHg at cardiac level when a person is standing), leading to light-headedness and syncope
145
Q

risk factors for postural Hypotension (Orthostatic Hypotension)

A
  • Fraility and physical deconditioning
  • Medications that impair sympathetic tone
  • Volume depletin
  • Autonomic neuropathy (e.g. diabetes mellitus)
  • Parkinson’s
  • Lew-body dementia
146
Q

symptoms/signs for postural Hypotension (Orthostatic Hypotension)

A
  • Presence of risk factors
  • Postural light-headedness, syncope, and other symptoms of cerebral hypoperfusion – visual changes, weakness, fatigue, trouble concentrating and pain across the neck and shoulders are symptoms of cerebral hypoperfusion
  • Parkinsonian features
  • Cerebellar ataxia
  • Weight loss
  • Resting tachycardia or impair heart rate variation
  • Abnormal GI motility
  • Erectile dysfunction and lack of ejaculation
  • Anhidrosis, heat intolerance, dry skin, focal hyperhidrosis
147
Q

DDx for postural Hypotension (Orthostatic Hypotension)

A
  • Neurally mediated (vasovagal) syncope
  • Vertigo
  • Non-specific falls in older people
  • Psychogenic syncope (pseudo-syncope)
148
Q

Investigations for postural Hypotension (Orthostatic Hypotension)

A

• 1st LINE:
- POSTURE TEST: BP should be measure supine or sitting and after standing for 3 minutes, systolic BP falls >20mmHg (30 in pts with hypertension) and diasyolic BP falls >10mmHg within 3 minutes of standing upright

149
Q

Management for postural Hypotension (Orthostatic Hypotension)

A

• 1st LINE:
- ELMINATE AGGRAVATING FACTORS AND INSTITUTE LIFESTYLE CHANGES: medications that incude or aggravate orthostatic hypotension (e.g. amitriptyline and other antidepressants, diuretics and other antihypertensive agents, alpha-blockers, sildenafil and other phosphodiesterase-5-inhibitors) should be carefully revied and eliminated if appropriate

150
Q

Prognosis or complications for postural Hypotension (Orthostatic Hypotension)

A

prognosis - dependant on cause

complications - falls, supine hypertension

Core Conditions (13 decks)

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