Cardiovascular Flashcards
What is the ECG?
Electrocardiography - A representation of the electrical events of the cardiac cycle
What can ECG identify?
- Arrhythmias
- Myocardial ischaemia and infarction
- Pericarditis
- Chamber hypertrophy
- Electrolyte disturbances (i.e. hyperkalemia or hypokalemia)
- Drug toxicity (i.e. digoxin and drugs which prolong the QT interval)
What is the SA node? + what is the normal heart rate?
the dominant pacemaker with an intrinsic rate of 60-100 bpm
(NORMAL HEART RATE) - the fastest depolarising tissue
what is the AV node?
back-up pacemaker with an intrinsic rate of 40-60 bpm
Ventricular cells?
back-up pacemaker with an intrinsic rate of 20-45 bpm
Impulse conduction pathway?
Sinoatrial node → AV node → Bundle of His → Bundle branches →
Purkinje fibres
P wave
atrial depolarisation - seen in every lead apart from aVR
PR interval
time taken for atria to depolarise and electrical activation to get
through AV node
QRS complex
ventricular depolarisation, still called QRS even if Q and/or S
are missing depending on what lead you are looking at
ST segment
interval between depolarisation & repolarisation
T wave
ventricular repolarisation
Tachycardia
increased heart rate
Bradycardia
decreased heart rate
Dextrocardia
heart on right side of chest instead of left
Acute anterolateral myocardial infarction
ST segments are raised in
anterior (V3 - V4) and lateral (V5-V6) leads
Acute inferior MI
ST segments are raised in inferior (II, III, aVF) leads
Atrial repolarisation?
usually not evident on an ECG since it occurs at
the same time as the QRS complex so is hidden
On a 25mm/sec ECG
- Horizontally: • One small box = 0.04s/40ms • One large box = 0.20s - Vertically: • One large box = 0.5mV
Left ventricle
palpated in the 5th left intercostal space and mid-clavicular
line, responsible for the apex beat
Stroke volume
The volume of blood ejected from each ventricle during systole
Cardiac output
The volume of blood each ventricle pumps as a function of time
(liters per minute):
• Cardiac output (L/min) = Stroke volume (L) x Heart rate (BPM)
Total peripheral resistance
The total resistance to flow in systemic blood
vessels from beginning of aorta to vena cava - arterioles provide the most
resistance
Preload
the volume of blood in the left ventricle which stretches the cardiac
myocytes before left ventricular contraction - how much blood is in the
ventricles before it pumps (end-diastolic volume). When veins dilate it results in
a decrease in preload (since by dilating veins the venous return decreases).
Afterload
the pressure the left ventricle must overcome to eject blood during
contraction - dilate arteries = decrease in afterload
Contractility
force of contraction and the change in fibre length - how hard
the heart pumps. When muscle contracts myofibrils stay the same length but
the sarcomere shortens - force of heart contraction that is independent of
sarcomere length
Elasticity
myocardial ability to recover normal shape after systolic stress
Diastolic dispensibilty
the pressure required to fill the ventricle to the same
diastolic volume
Compliance
how easily the heart chamber expands when filled with blood
volume
Starlings law
Force of contrition is proportional to the end diastolic length of
cardiac muscle fibre - the more ventricle fills the harder it contracts
At rest the cardiac muscle
not at optimal length. Below optimal length means
the force of contraction is decreased - inefficient
↑ venous return
= ↑ end diastolic volume = ↑ preload = ↑ sarcomere
stretch = ↑ force of contraction thus = ↑ stroke volume and force of
contractions
Standing
decreases venous return due to gravity thus, cardiac output decreases, which causes a drop in blood pressure, stimulating baroreceptors to increase blood pressure
HEART SOUNDS:
- S1
- mitral and tricuspid valve closure
- S2
- aortic and pulmonary valve closure
- S3
- in early diastole during rapid ventricular filling, normal in children and pregnant women, associated with mitral regurgitation and heart failure
- S4
- ‘Gallop’, in late diastole, produced by blood being forced into a stiff
hypertrophic ventricle - associated with left ventricular hypertrophy
commonly develop atherosclerosis
Circumflex, Left anterior descending (LAD) and right coronary arteries
Risk factors for atherosclerosis:
- Age - increases with age
- Tobacco smoking - leads to endothelium erosion
- High serum cholesterol
- Obesity - since more pericardial fat and thus increase in inflammation
- Diabetes - hyperglycaemia damages endothelium
- Hypertension
- Family history
Distribution of atherosclerosis plaques:
- Found within peripheral and coronary arteries
- Focal distribution along the artery length
Structure of an atherosclerotic plaque:
- A complex lesion consisting of: • Lipid • Necrotic core • Connective tissue • Fibrous “cap” - Eventually the plaque will either occlude the vessel lumen resulting in a restriction of blood flow (ANGINA), or it may rupture (thrombus formation and subsequent death)
Atherosclerosis formation: 1
- Initiated by an injury to the endothelial cells which leads to endothelial dysfunction
- Once initiated, chemoattractants (chemicals that attract leukocytes) are
released from endothelium to attract leukocytes which then accumulate and
migrate into the vessel wall - Chemoattractants are released from site of injury and a concentration-
gradient is produced - Inflammatory cytokines found in plaques:
• IL-1 - KEY ONE
• IL-6
• IFN - gamma - Fatty streaks:
• Earliest lesion of atherosclerosis
• Appear at a very early age (less than 10)
• Consist of aggregations of lipid-laden macrophages and T lymphocytes
within the intimal layer of the vessel wall
Atherosclerosis formation: 2
- Intermediate lesions:
• Composed of layers of: - Lipid laden macrophages (foam cells - macrophages that have
taken up lots of lipids) - Vascular smooth muscle cells
- T lymphocytes
• There is adhesion and aggregation of platelets to the vessel wall
(aspirin inhibits platelet aggregation) - Fibrous plaques/advanced lesions:
• Impede blood flow
• Prone to rupture
• Covered by dense fibrous cap made of extracellular matrix proteins
including collagen (strength) and elastin (flexibility) laid down by smooth
muscle cells that overly lipid core and necrotic debris
• May be calcified
• Contains: - Smooth muscle cells
- Macrophages and foam cells (lipid laden macrophages)
- T lymphocytes
- Red cells
• Plaque is filled with fibrin
Atherosclerosis formation: - Plaque rupture:
- Plaque rupture:
• Plaque is constantly growing and receding
• The fibrous cap needs to be resorbed and redeposited in order to be
maintained
• If balance shifts e.g. in favour of inflammatory conditions (increased
enzyme activity) then the cap becomes weak and the plaque ruptures
• Basement membrane, collagen and necrotic tissue exposure as well as
haemorrhage of vessel within the plaque
• Thrombus (clot) formation and subsequent vessel occlusion
Angina
is chest pain or discomfort as a result of reversible myocardial ischaemia
This usually implies narrowing of one or more of the coronary arteries
Tends to be exacerbated by exertion and relieved by rest
• Types:
- Stable angina:
• Induced by effort and relieved by rest
• Types:
- Unstable (crescendo) angina:
• Angina of recent onset (less than 24hrs) or
• Deterioration in previously stable angina, with symptoms frequently
occurring at rest
• Angina of increasing frequency or severity, occurs on minimal
exertion or even at rest - form of acute coronary syndrome
• Types:
- Prinzmetal’s angina:
• Caused by coronary artery spasm (rare)
• Epidemiology:
- Myocardial ischaemia resulting in angina occurs when there is a mismatch
between blood supply and metabolic demand - this can occur due to:
• Atheroma/stenosis of coronary arteries thereby impairing blood flow -
most common cause
• Valvular disease
• Aortic stenosis
• Arrhythmia
• Anaemia - thus less O2 can be transported - Ischaemic metabolites including adenosine, stimulate nerve endings and
produce pain - More common in men
Risk factors for angina
- Smoking
- Sedentary lifestyle
- Obesity
- Hypertension
- Diabetes mellitus
- Family history
- Genetics
- Age
- Hypercholesterolaemia
Pathophysiology:
That of atherosclerosis develops
narrowing of coronary arteries that results
in ischaemia and thus pain i.e. angina
Angina - Initiation:
• Endothelial dysfunction and injury around sites of sheer and damage with subsequent lipid accumulation at sites of impaired endothelial
barrier
• Local cellular proliferation and incorporation of oxidise lipoproteins occurs
• Mural thrombi on surface and subsequent healing and repeat of cycle
Angina - Adaption:
• As plaque progresses to 50% of vascular lumen size the vessel can no
longer compensate by re-modelling and becomes narrowed
• This drives variable cell turnover within the plaque with new matrix
surfaces and degradation of matrix
• May progress to unstable plaque
Angina - Clinical stage:
• The plaque continues to encroach upon the lumen and runs the risk of
haemorrhage or exposure of tissue HLA-DR antigens which might
stimulate T cell accumulation
• This drives an inflammatory reaction against part of the plaque contents
• Complications develop including ulceration, fissuring, calcification and
aneurysm change
Angina - - Pathological stages:
• Fatty streak:
- These show macrophages filled with abundant lipid (foam cells)
- Also smooth muscle cells with fat
• Intimal cell mass:
- These are collections of muscle cells and connective tissue
without lipid - “cushions”
• The atheromatous plaque:
- Characterised by distorted endothelial surface containing
lymphocytes, macrophages, smooth muscle cells and a variably
complete endothelial surface
- There is local necrotic and fatty matter with scattered lipid rich
macrophages
- Evidence of local haemorrhage may be seen with iron deposition
and calcification
- Complicated plaques are those which show calcification and mural
thrombus - making them vulnerable to rupture
• Complications of plaque rupture:
- Acute occlusion due to thrombus
- Chronic narrowing of vessel lumen with healing of the local
thrombus
- Aneurysm change
- Embolism of thrombus +/- plaque lipid content
• Clinical presentation Angina:
- Central chest tightness or heaviness
- Provoked by exertion, especially after meal or in the cold windy weather or by
anger or excitement - Relieved by rest or GTN spray
- Pain may radiate to one or both arms, the neck, jaw or teeth
- May be dyspnoea, nausea, sweatiness and faintness
- Scoring:
• 1. Have, central, tight, radiation to arms, jaw & neck
• 2. Precipitated by exertion
• 3. Relieved by rest or spray GTN
• 3/3 = Typical angina
• 2/3 = Atypical pain
• 1/3 = Non-anginal pain
• Differential diagnosis Angina:
- Pericarditis/myocarditis
- Pulmonary embolism
- Chest infection
- Dissection of the aorta
- GORD
• Diagnosis Angina: - 12 lead ECG:
- Often normal
- May show ST depression
- Flat or inverted T waves
- Look for signs of past MI
• Diagnosis Angina: - Treadmill test/Exercise ECG:
• Put ECG on patient, then make them run on treadmill uphill - trying to
induce ischaemia
• Monitor how long patient is able to exercise for
• If you see ST segment depression then this is a sign of late-stage
ischaemia
• Many patients unsuitable e.g. can’t walk, very unfit, young females and
bundle branch block
• Diagnosis Angina:- CT Scan Calcium scoring:
• CT the heart and if there is atherosclerosis in the arteries then the
calcium will light up white - if there is significant calcium then this would
indicate angina
• Diagnosis Angina:- SPECT/myoview:
• Radio-labelled tracer injected into patient
• Its taken up by the coronary arteries where there is good blood supply -
this will light up
• Where there is little blood supply these areas will not light up
• If there is no light after exercise then this is indicative of myocardial ischaemia
• Diagnosis Angina:- Cardiac catheterisation
//Angina
Treatment Angina: - Modify risk factors:
- Stop smoking
- Encourage exercise
- Weight loss
• Treatment angina : - Treat underlying conditions
//angina
• Treatment angina : - Pharmacological: • Aspirin:
- Antiplatelet effect (inhibits platelet aggregation) in coronary arteries
thereby avoiding platelet thrombosis - To reduce events
- E.g. salicylate
- COX inhibitor - reduces prostaglandin synthesis including
thromboxane A2 resulting in reduced platelet aggregation - Side effects - gastric ulceration
• Treatment angina : - Pharmacological: • Statins:
- HMG-CoA reductase inhibitors - reduces cholesterol produced by
liver - Reduce events and LDL-cholesterol
- Anti-atherosclerotic
• Treatment angina : - Pharmacological: • Betablockers - 1st line antianginal:
- Reduce force of contraction of heart
- E.g. Bisoprolol and atenolol
- Act on B1 receptors in the heart as part of the adrenergic
sympathetic pathway - B1 activation → Gs → cAMP to ATP → contraction
- Reduces:
• Heart rate (negatively chronotropic)
• Left ventricle contractility (negatively inotropic)
• Cardiac output - Side effects; tiredness, nightmares, bradycardia, erectile
dysfunction and cold hands and feet - DO NOT GIVE in asthma, heart failure/heart block, hypotension and bradyarrhythmias
• Treatment angina : - Pharmacological: • Glyceryl Trinitrate (GTN) spray - 1st line antianginal:
- Nitrate that is a venodilator
- Dilates systemic veins thereby reducing venous return to right
heart - Reduces preload
- Thus reduces work of heart and O2 demand
- Also dilates coronary arteries
- Side effect: profuse headache immediately after use
• Treatment angina : - Pharmacological: • Ca2+ channel antagonists/blocker:
- Primary arterodilators
- Dilates systemic arteries resulting in BP drop
- Thus reduces afterload on the heart
- Thus less energy required to produce same cardiac output
- Thus less work on heart and O2 demand
- E.g. verapamil
• Treatment angina : - Revascularisation:
• To restore patent coronary artery and increase flow reserve
• Done when medication fails (most) or when high risk disease is
identified
• Percutaneuos Coronary Intervention (PCI):
- Dilating coronary atheromatous obstructions by inflating balloon
within it
- Insert balloon and stent, inflate balloon and remove it, stent
persists and keeps artery patent
- Expanding plaque = make artery bigger
- Pros; less invasive, convenient, short recovery & repeatable
- Cons; risk of stent thrombosis, not good for complex disease
• Coronary Artery Bypass Graft (CABG):
- Left Internal Mammary Artery (LIMA) used to bypass proximal
stenosis (narrowing) in Left Anterior Descending (LAD) coronary
artery
- Pros; good prognosis, deals with complex disease
- Cons; invasive, risk of stroke or bleeding, one time treatment and
need to stay in hospital - long recovery
- ACUTE CORONARY SYNDROME: • Umbrella term that includes: - ST-elevation myocardial infarction (STEMI):
- Develop a complete occlusion of a MAJOR coronary artery previously affected by atherosclerosis
- This causes full thickness damage of heart muscle
- Can usually be diagnosed on ECG at presentation
- Will produce a pathological Q wave some time after MI so also known as Q-wave infarction
- ACUTE CORONARY SYNDROME: • Umbrella term that includes: - Unstable (crescendo) angina (UA):
• Angina of recent onset (less than 24hrs) or
• Cardiac chest pain with crescendo pattern
• Deterioration in previously stable angina, with symptoms frequently
occurring at rest
• Angina of increasing frequency or severity, occurs on minimal
exertion or even at rest - form of acute coronary syndrome
- ACUTE CORONARY SYNDROME: • Umbrella term that includes:- Non-ST-elevation myocardial infarction (NSTEMI):
• Occurs by developing a complete occlusion of a MINOR or a partial
occlusion of a major coronary artery previously affected by
atherosclerosis
• Is a retrospective diagnosis made after troponin results and
sometimes other investigation results are available
• This causes partial thickness damage of heart muscle
• Also known as a Non-Q wave infarction will see ST depression and/
or T wave inversion
- ACUTE CORONARY SYNDROME: • Umbrella term that includes: The difference between a UA and a NSTEMI
in a NSTEMI there is
occluding thrombus which leads to myocardial necrosis and a rise in
serum troponin or creatine kinase-MB (CK-MB)
Myocardial infarction
occurs when cardiac myocytes die due to myocardial
ischaemia
• Type 1 MI:
- Spontaneous MI with ischaemia due to a primary coronary event e.g. plaque erosion/rupture, fissuring or dissection
• Type 2 MI:
- MI secondary to ischaemia due to increased O2 demand or
decreased supply such as in coronary spasm, coronary
embolism, anaemia, arrhythmias, hypertension or
hypotension
• Type 3,4,5 MI:
- MI due to sudden cardiac death, related to PCI and related to CABG respectively
Risk factors of ACS:
- Age
- Male
- Family history of Ischaemic Heart Disease (IHD) - MI in first degree relative
below 55 - Smoking
- Hypertension, diabetes mellitus, hyperlipidaemia
- Obesity & sedentary lifestyle
Pathophysiology of ACS:
- Rupture or erosion of the fibrous cap of a coronary artery plaque
- Leading to platelet aggregation and adhesion, localised thrombosis,
vasoconstriction and distal thrombus embolisation - The presence of a rich lipid pool within the plaque and a thin, fibrous cap is
associated with an increased risk of rupture - Thrombus formation and the vasoconstriction produced by platelet release
of serotonin and thromboxane A2 result in myocardial ischaemia due to
reduction of coronary blood flow - Fatty streak → Fibrotic plaque → Atherosclerotic plaque → Plaque rupture/
fissure and thrombosis → MI or Ischaemic stroke or Critical leg ischaemia
or Sudden CVS death - In unstable angina the plaque has a necrotic centre and ulcerated cap and
the thrombus results in PARTIAL OCCLUSION - In myocardial infarction the plaque also has a necrotic centre but the
thrombus results in TOTAL OCCLUSION
Clinical presentation of ACS:
- Unstable angina: • Chest pain; new onset, at rest with crescendo pattern • Breathlessness • Pleuritic pain • Indigestion - New onset angina - Recent destabilisation of pre-existing angina with moderate or severe limitations of daily activities - Acute central chest pain, lasting more than 20 minutes, associated with: • Sweating • Nausea and vomiting • Dyspnoea • Fatigue • Shortness of breath • Palpitations - May present without chest pain (silent infarct) e.g. in elderly or diabetics - Distress and anxiety - Pallor - Increased pulse and reduced BP - Reduced 4th heart sound - May be signs of heart failure (increase in jugular venous pressure) - Tachy/bradycardia - Peripheral oedema
Differential diagnosis: ACS
- Angina
- Pericarditis
- Myocarditis
- Aortic dissection
- Pulmonary embolism
- Oesophageal reflux/spasm
• Diagnosis: ACS - 12 lead ECG:
• Can be normal
• ST depression and T-wave inversion (this tends to occur hours/days
after) (NSTEMI) are highly suggestive of an ACS, particularly if
associated with anginal chest pain
• Can get hyperacute (tall) T waves
• With a STEMI, complete occlusion of a coronary vessel will result in a
persistent ST-elevation, hyperacute (tall) T waves or new left bundle
branch block pattern - may see pathological Q waves a few days after
MI (sign of previous MI)
• Diagnosis: ACS- Biochemical markers:
• Troponin (T & I):
- T & I are the most sensitive and specific markers of myocardial
necrosis
- Serum levels increase within 3-12 hours from the onset of chest
pain and peak at 24-48 hours
- They then fall back to normal over 5-14 days
- Can act as prognostic indicator to determine mortality risk and
define which patients may benefit from aggressive medical therapy
and early coronary revascularisation
• CK-MB:
- CK-MB can be used as a marker for myocyte death - but has low
accuracy since it can be present in the serum of normal
individuals and in patients with significant skeletal muscle damage
- However it can be used to determine re-infarction as levels drop
back to normal after 36-72 hours
• Myoglobin:
- Becomes elevated very early in MI but the test has poor specificity
since myoglobin is present in skeletal muscle
• Diagnosis: ACS - CXR:
• Look for cardiomegaly, pulmonary oedema or a widened mediastinum
(aortic rupture)
• Treatment: ACS
- Pain relief: • GTN spray • IV opioid - Anti-emetic - Oxygen: • Aim for 94-98% saturation • 88-92% for those with COPD
• Treatment: ACS - Antiplatelets:
• Atheromatous plaque rupture results in platelets being exposed to ADP/ThromboxaneA2/ adrenaline/thrombin/collagen tissue factor
• This results in platelet activation/aggregation via IIb/IIIa glycoproteins binding to fibrinogen (enables platelets to adhere to each other = aggregation)
• Then thrombin (already present in surroundings) is able to enzymatically convert fibrinogen to fibrin (insoluble) resulting in the formation of a fibrin
mesh over platelet plug and the formation of a thrombotic clot
• Aspirin (oral):
- COX1-inhibitor = blocks formation of thromboxane A2 thus
prevents platelet aggregation
• P2Y12 inhibitors (oral):
- Inhibit ADP-dependant activation of IIb/IIIa glycoproteins thereby preventing amplification response of platelet aggregation
- Can be used if allergic to aspirin
- Can also be used alongside aspirin as a dual anti-platelet therapy
- E.g. Clopidogrel, Prasugrel & Ticagrelor
- Side effects: neutropenia (low neutrophils), thrombocytopenia (low platelets) and INCREASED RISK OF BLEEDING
- AVOID if CABG planned
• Glycoprotein IIb/IIIa antagonists (IV):
- Only IV available
- Used in combination with aspirin and oral P2Y12 inhibitors in patients with ACS undergoing Percutaneous Coronary Intervention (PCI)
- INCREASES RISK OF MAJOR BLEEDING
- E.g. Abciximab, Tirofiban and Eptifbatide
• Treatment: ACS
- Beta blockers (IV & oral): • E.g. Atenolol (IV then oral) or Metoprolol (IV then oral) • Side effects: Avoid with asthma, heart failure, hypotension and bradyarrhythmias - Statins (oral): • HMG-CoA reductase inhibitors • E.g. Simvastatin, Pravastatin and Atorvastin - ACE inhibitors (oral): • E.g. Ramipril and Lisonopril • Monitor renal function - Coronary revascularisation: • PCI • CABG - high risk mortality in high risk groups e.g. recent MI - Risk factor modification: • Stop smoking • Lose weight and exercise daily • Healthy diet • Treat hypertension & diabetes • Low fat diet with statins
- ACUTE MYOCARDIAL INFARCTION:
• Necrosis of cardiac tissue (myocyte death) due to prolonged myocardial ischaemia due to COMPLETE occlusion of artery by thrombus
• Two types of MI:
- ST elevation MI (STEMI):
• Develop a complete occlusion of a MAJOR coronary artery previously affected by atherosclerosis
• This causes full thickness damage of heart muscle
• Usually diagnosed on ECG at presentation
• Tall T waves
• ST elevation and subsequent pathological Q wave
• May present as new left bundle branch block (LBBB) on ECG
• COMPLETE - Non ST elevation MI (NSTEMI) or Non-Q infarction:
• Occurs by developing a complete occlusion of a MINOR or a partial
occlusion of a major coronary artery previously affected by
atherosclerosis
• This causes partial thickness damage of heart muscle
• A RETROSPECTIVE diagnosis made after troponin results and
sometimes other investigation results are available
• ST depression/T wave inversion
• STEMI is the most common medical emergency
• Risk factors of MI:
- Age
- Male
- History of premature coronary heart disease
- Premature menopause
- Diabetes mellitus
- Smoking
- Hypertension
- Hyperlipidaemia
- Obesity and sedentary lifestyle
- Diabetes mellitus
- Family history of Ischaemic Heart Disease (IHD) - MI in first degree relative
below 55
• Pathophysiology of MI:
- Rupture or erosion of vulnerable fibrous cap of coronary artery atheromatous plaque
- This results in platelet aggregation, adhesion, local thrombosis, vasoconstriction and DISTAL THROMBUS EMBOLISATION resulting in PROLONGED COMPLETE ARTERIAL OCCLUSION resulting in myocardial
necrosis within 15-30 minutes in a STEMI (since major artery occluded fully) - STEMI:
• The sub-endocardial myocardium is initially affected but, continued ischaemia, the infarct zone extends through the sub-epicardial myocardium, producing a transmural Q wave MI
• Early reperfusion may salvage regions of the myocardium - reducing future mortality and morbidity
• Clinical presentation of MI:
- Any patient presenting with severe chest pain lasting more than 20 minutes
may be suffering from an MI - Chest pain:
• Severe central ongoing pain, lasting more than 20 minutes
• Pain may radiate to the left arm, jaw or neck
• Pain DOES NOT usually respond to sublingual GTN spray - opiate
analgesia is required
• Pain described as substernal pressure, squeezing, aching, burning or
even sharp pain
• Associated with; sweating, nausea, vomiting, dyspnoea, fatigue and/or
palpitations - Breathlessness
- Fatigue
- Distress and anxiety
- Pale, clammy and marked sweating
- Significant hypotension (low BP)
- Bradycardia or tachycardia
• Differential diagnosis of MI:
- Stable angina, unstable angina, NSTEMI, pneumonia, pneumothorax, oesophageal spasm, GORD, acute gastritis, pancreatitis and MSK chest pain
• Diagnosis: - STEMI
- Diagnosed on presentation
- ST elevation
- Tall T waves
- L bundle branch block (LBBB)
- T wave inversion and pathological Q waves follow
• Diagnosis: - NSTEMI
- Diagnosis is retrospective made after troponin results etc.
- ST depression and T wave inversion
• Diagnosis MI: - ECG
• Performed on admission to A & E
• Continuous monitoring required due to high likelihood of significant
cardiac arrhythmias
ECG changes confined to leads that FACE INFARCTION
Anterior - ST elevation V1-3 Inferior - St elevation II, III, AVF Lateral - I, AVF V5-6 Posterior - ST depression V1-3 Dominant R wave ST elevation V5-6 Subendocardial - any
• Evolution of STEMI on ECG:
- After the first few minutes, the T waves
become tall, pointed and upright, and there is
ST segment elevation - After the first few hours, the T waves invert, the R-wave voltage decreases and Q waves develop
- After a few days, the ST segment returns to normal
- After weeks or months, the T wave may return to upright but the Q WAVE REMAINS
• Diagnosis MI:
- Troponin I or T increased
- Myoglobin increased
- Transthoracic echocardiography (TTE) may be helpful to confirm MI, as
wall-motion abnormalities are detected early in STEMI
• Treatment MI:
- Pre-hospital:
- Aspirin 300mg chewable
- GTN (sublingual)
- Morphine
• Treatment MI:
- Hospital:
- IV morphine
- Oxygen if their sats are below 95% or are breathless
- Beta-blocker - Atenolol
- P2Y12 inhibitor - Clopidogrel
• Treatment MI:
- Coronary revascularisation:
• PCI:
- Presented to all patients who present with an acute STEMI who can be
transferred to a primary PCI centre WITHIN 120 MINUTES of first
medical contact
- If not possible then give patient fibrinolysis and then transfer to PCI
centre after infusion
• CABG
• Treatment MI:
- Fibrinolysis - enhance the breakdown of occlusive thromboses by the activation of plasminogen to form plasmin - Risk factor modification: • Stop smoking • Lose weight and exercise daily • Healthy diet • Treat hypertension & diabetes • Low fat diet with statins - Secondary prevention: • Statins • Aspirin long term • Warfarin if large MI • o blockers • ACE inhibitors
- COMPLICATIONS OF MYOCARDIAL INFARCTION:
• Sudden death - often within hours often due to ventricular fibrillation
• Arrhythmias - in the first few days due to electrical instability following infarction,
pump failure and excessive sympathetic stimulation
• Persistent pain - 12 hours-few days after due to progressive myocardial necrosis
• Heart failure:
- When cardiac output is insufficient to meet the bodies metabolic demands
- Due to ventricular dysfunction following muscle necrosis also resulting in
arrhythmias
• Mitral incompetence - can happen in the first few days or occur later. Due to
myocardial scarring preventing valve closure
• Pericarditis - due to transmural infarct resulting in inflammation of pericardium,
more common in STEMI
• Cardiac rupture:
- Early rupture - the result of shearing between mobile and immobile
myocardium
- Late rupture - due to weakening of wall following muscle necrosis and acute
inflammation
• Ventricular aneurysm - due to stretching of newly formed collagenous scar tissue
- CARDIAC FAILURE:
• The inability of the heart to deliver blood and thus O2 at a rate that is commensurate with the requirement of metabolising tissue of the body
• Is a syndrome and not a diagnosis on its own
• Can result from any structural or functional cardiac disorder that impairs the hearts ability to function and meet the demands of supplying sufficient oxygen
and nutrients to the metabolising body
• Risk factors of cardiac failure:
- 65 and older
- African descent
- Men (due to lack of protective effect provided by oestrogen resulting in the early onset of IHD in men
- Obesity
- People who have had an MI
Pathophysiology cardiac failure:
- When the heart begins to fail, there are many systems involved that initiate physiological COMPENSATORY CHANGES that try to maintain cardiac output and peripheral perfusion in order to negate the effects of the heart failure
- However as heart failure progresses, these mechanisms are overwhelmed
and become pathophysiological also known as DECOMPENSATION
Pathophysiology cardiac failure: • Venous return (preload):
- Myocardial failure leads to a reduction of the volume of blood ejected with each heart beat, and an increase in the volume of blood remaining after systole
- This increased diastolic (or preload - the volume of blood in the ventricle before contraction) volume stretches the myocardial fibres and, as Starling’s law of the heart says, myocardial contraction is restored since the stretching of myocardial fibres will increase its force of contraction
- However, in heart failure, the failing myocardium actually doesn’t contract as much in response to increased preload meaning cardiac output cannot be maintained and may decrease
Pathophysiology cardiac failure:• Outflow resistance (afterload):
- Outflow resistance (afterload) is the load or resistance against which the ventricle contracts
- It is made up of:
• Pulmonary and systemic resistance
• Physical characteristics of the vessel walls
• The volume of blood that is ejected - When there is an increase in afterload there is a increase in end-diastolic volume and a decrease in stroke volume and thus a DECREASE in cardiac output
- This results in a increase of end-diastolic volume and dilatation of the ventricle itself (the more the ventricle is dilated the harder it must work i.e. the more resistance there is to contract against) which then further exacerbates the problem of afterload
Pathophysiology cardiac failure:• Sympathetic system activation:
- When baroreceptors (located in the arterial wall of the aorta, carotid and in the heart walls and major veins) detect a drop in arterial pressure or an increase in venous pressure (due to back flow of blood) they stimulate sympathetic activation
- This increases the force of contraction (positively inotropic) of the heart (which increases stroke volume) as well as heart rate - both resulting in an increase in cardiac output
- However in heart failure there is chronic sympathetic activation which results in the receptors being acted on by the sympathetic system to down regulate resulting in their being less receptor to act on meaning the effect of sympathetic activation is diminished and cardiac output stops increasing in response to sympathetic
activation
Pathophysiology cardiac failure:• Renin-Angiotensin System:
- Reduced cardiac output leads to diminished renal perfusion,thereby activating the renin-angiotensin system whereby; angiotensinogen is converted to angiotensin I under the action of renin, angiotensin I is then converted to angiotensin II under the act
of angiotensin converting enzyme (ACE), angiotensin II then stimulates the release of aldosterone from the adrenal cortex above the kidneys - This results in increased Na+ reabsorption and thus water reabsorption as well as the release of ADH which stimulates water retention
- This results in the increased volume of the blood which in turn increases blood pressure and thus venous pressure which in turn increases pre-load thereby increasing the stretching of the heart and thus force of contraction and thus stroke volume and thus
cardiac output - However, with increased force of contraction the cardiac myocytes require more energy and thus more blood however in heart failure (which is most commonly caused by ischaemic heart disease) there will be no increase in blood and thus the cardiac myocytes will die resulting in a decrease in force of contraction and thus a decrease in stroke volume and a decrease in cardiac output
- Classification of heart failure:• Systolic versus diastolic failure: - Systolic:
- Inability of the ventricle to contract normally resulting in a decrease in cardiac output
- Caused by ischaemic heart disease, myocardial infarction and cardiomyopathy (disease of heart muscle thus impairing function)
- Classification of heart failure:• Systolic versus diastolic failure: - Diastolic:
• Inability of the ventricles to relax and fill fully thereby
decreasing stroke volume and decreasing cardiac output
• Caused by hypertrophy (due to chronic hypertension which results in increased blood pressure thereby increasing afterload so heart pumps against more resistance and thus cardiac myocytes grow bigger to compensate for this) of ventricles resulting in there being less space for blood to fill in and thus decreased cardiac output
• Also caused by aortic stenosis (the narrowing of the aortic valve) which also increases afterload and thus decreases cardiac output
- Classification of heart failure:• Acute vs chronic heart failure:- Acute:
• Often used exclusively to mean new onset or decompensation of chromic heart failure characterised by pulmonary and/or peripheral oedema with or without signs of peripheral hypotension
- Classification of heart failure:• Acute vs chronic heart failure:- Chronic:
- Develops slowly
* Venous congestion is common but arterial pressure is well maintained until very late
• Clinical presentation of heart failure:
- Three cardinal symptoms are; shortness of breath, fatigue & ankle swelling but these are non-specific!
- Dyspnoea especially when lying flat (orthopnoea)
- Cold peripheries
- Raised jugular venous pressure (JVP)
- Murmurs and displaced apex beat
- Cyanosis
- Hypotension
- Peripheral or pulmonary oedema due to back flow resulting from the decreased cardiac output
- Tachycardia
- Third & fourth heart sounds
- Ascites
- Bi-basal crackles
- Use New York Heart Association (NYHA) classification for the assessment of the severity of symptoms:
• Class I: No limitation (asymptomatic) - exercise = no fatigue, dyspnoea or palpitation
• Class II: Slight limitation (mild HF (heart failure)) - comfortable at rest, normal activity = fatigue, dyspnoea and palpitations
• Class III: Marked limitation (moderate HF) - comfortable at rest, gentle activity = fatigue, dyspnoea & palpitations
• Class IV: Inability to carry out any physical activity without discomfort (severe HF) - symptoms occur at rest
• Diagnosis of heart failure:
- Blood tests:
• Brain natriuretic peptide (BNP): - Secreted by ventricles in response to increase myocardial wall
stress - Increased in patients with heart failure
- Levels correlate with ventricular wall stress and the severity of
heart failure
• FBC, U&E’s and liver biochemistry - CXR:
• Alveolar oedema
• Cardiomegaly
• Dilated upper lobe vessels of lungs
• Effusions (pleural) - ECG:
• Shows underlying causes; ischaemia, left ventricular hypertrophy in
hypertension or arrhythmia
• If ECG and BNP normal then heart failure is unlikely
• If both abnormal then go to echocardiogram - Echocardiography:
• Assess cardiac chamber dimension
• Look for regional wall motion abnormalities, valvular disease and
cardiomyopathies
• Look for sign of MI
• Treatment of heart failure:
- Lifestyle changes:
• Avoid large meals, lose weight, stop smoking, exercise, vaccination - Diuretics:
• Promote sodium and thus water loss thereby reducing ventricular filling pressure (preload) decreasing systemic and pulmonary congestion
• Generally provide symptomatic relief
• Loop diuretic - furosemide
• Thiazide diuretic - bendroflumethiazide (inhibit sodium reabsorption in
the distal convoluted tubule)
• Aldosterone antagonist (thereby inhibiting ADH release resulting in
water loss) - spirolactone & epelerone - note with these beware of renal
impairment and hyperkalaemia - ACE inhibitors:
• Ramipril, enalipril, captopril
• Side effects: cough (since inhibit ACE and thus the breakdown of
substance P and bradykinin which results in cough), hypotension,
hyperkalaemia and renal dysfunction
• If cough is a problem then can give angiotensin receptor blockers (not
as effective as ACE-inhibitors) e.g. canderstan or valsartan
• Treatment of heart failure:
- Beta-blockers: • Bisoprolol, nebivolol, carvedilol • Start at low dose and titrate upwards • DO NOT GIVE TO ASTHMATICS - Digoxin - Inotropes - Revascularisation: • When some viable myocardium remains • Illicit PCI stenting - Surgery to repair: • Mitral valve repair, aortic or mitral valve replacement - Heart transplant in young people - Cardiac resynchronisation - improve the coordination of the atria and ventricles
- MITRAL VALVE
• Mitral valve is on the left side and is also known as the tricuspid valve, it separates the left atrium from the left ventricle
MITRAL STENOSIS:
- Obstruction of left ventricle inflow that prevents proper filling during diastole
- Mitral valve has 2 cusps
Epidemiology of Mitral STENOSIS:
- Normal mitral valve area is 4-6cm2, symptoms begin at areas less than 2cm2
- Most common cause of mitral stenosis is rheumatic heart disease
secondary to rheumatic fever due to infection with group A beta-haemolytic
streptococcus e.g. Streptococcus Pyogenes - The condition is more common in men than women
- Inflammation due to rheumatic fever leads to commissural fusion and a
reduction in mitral valve orifice area, causing the characteristic doming
pattern seen on echocardiography - Over many years, the condition progresses to valve thickening, cusp fusion,
calcium deposition, a severely narrowed (stenotic) valve orifice and
progressive immobility of the valve cusps - Prevalence and incidence is decreasing due to a reduction of rheumatic
heart disease - Other causes include:
• Infective endocarditis (3.3%)
• Mitral annular calcification (2.7%) - rarely leads to mitral stenosis if extensive, particularly in elderly patients and those with end-stage renal
disease
Risk factors of Mitral STENOSIS:
- History of rheumatic fever
- Untreated streptococcus infections
Pathophysiology of mitral stenosis:
- Thickening and immobility of the valve leads to obstruction of blood flow
from the left atrium to the left ventricle - In order for sufficient cardiac output to be maintained, the left atrial pressure
increases and left atrial hypertrophy and dilatation occur - Consequently pulmonary venous, pulmonary arterial and right heart
pressures also increase - The increase in pulmonary capillary pressure is followed by the development
of pulmonary oedema - this is seen particularly when atrial fibrillation occurs,
due to the elevation of left atrial pressure and dilatation, with tachycardia
and loss of coordinated atrial contraction - This is partially countered by alveolar and capillary thickening and
pulmonary arterial vasoconstriction (reactive pulmonary hypertension) - Pulmonary hypertension leads to right ventricular hypertrophy, dilatation
and failure with subsequent tricuspid regurgitation
• Clinical presentation mitral stenosis:
- Usually there are no symptoms until the valve orifice is moderately stenosed
i.e. area is less than 2cm2 - This usually doesn’t occur until several decades after the first attack of
rheumatic fever - Progressive dyspnoea - due to left atrial dilation resulting in pulmonary
congestion (reduced emptying), which is worse with; exercise, fever,
tachycardia and pregnancy - Haemoptysis - due to rupture of bronchial vessels due to the elevated
pulmonary pressure - Right heart failure - due to the development of pulmonary hypertension with
symptoms of weakness, fatigue and abdominal or lower limb swelling - Atrial fibrillation - due to left atrium dilation giving rise to palpitations
- Systemic emboli - due to atrial fibrillation, most commonly in the cerebral vessels
• Clinical presentation mitral stenosis:
- Prominent “a” wave in jugular venous pulsations - due to pulmonary
hypertension and right ventricular hypertrophy - Mitral facies/malar flush - bilateral, cyanotic or dusky pink discolouration
over the upper cheeks - pinkish-purple patches on the cheeks due to
vasoconstriction in response to diminished cardiac output - Heart sounds:
• Diastolic murmur (heard when blood flows over a valve): - Low-pitched diastolic rumble most prominent at the apex
- Heard best with patient lying on the left side in held expiration
• Loud opening S1 snap: heard at apex when leaflets are still mobile:
- Due to the abrupt halt in leaflet motion in early diastole, after a
rapid initial opening, due to fusion at the leaflet tips
- As the valve cusps become more immobile, the loud first heart
sound softens and the opening snap disappears
• The more severe the stenosis, the longer the diastolic murmur and the
closer the opening snap is to S2 (second heart sound)
• Diagnosis mitral stenosis:
- CXR: • Left atrial enlargement • Pulmonary oedema/congestion • Occasionally calcified mitral valve - ECG: • Atrial fibrillation • Left atrial enlargement - Echocardiogram: • GOLD STANDARD for diagnosis • Assess mitral valve mobility, gradient and mitral valve area
• Treatment of :
- Mitral stenosis is a mechanical problem and medical therapy does not
prevent progression - Beta-blockers e.g. Atenolol and digoxin which control heart rate and thus
prolong diastole for improved diastolic filling - Diuretics for fluid overload e.g. Furosemide
- Percutaneous mitral balloon valvotomy:
• Catheter is inserted into the right atrium vie the femoral vein under local
anaesthesia
• The interatrial septum is then punctured and the catheter advanced into
the left atrium and across the mitral valve
• The balloon is inflated and puts pressure on valve thereby separating
the leaflets thereby increasing the size of the mitral valve opening thus
enabling more blood to flow from left atrium into left ventricle - Mitral valve replacement
- MITRAL REGURGITATION:
• Backflow of blood from the left ventricle to the left atrium during systole
• Mild physiological mitral regurgitation (MR) is seen in 80% of normal
individuals
• Epidemiology MITRAL REGURGITATION:
- Occurs due to abnormalities of the valve
leaflets, chordae tendinae, papillary muscles or left ventricle - Most frequent cause is myxomatous degeneration (MVP) (weakening of the chordae tendinae) - resulting in a floppy mitral valve that prolapses (mitral valve prolapse)
- Other causes include:
• Ischaemic mitral valve
• Rheumatic heart disease
• Infective endocarditis
• Papillary muscle dysfunction/rupture
• Dilated cardiomyopathy
• Risk factors of MITRAL REGURGITATION:
- Associated with females
- Lower BMI
- Advanced age
- Renal dysfunction
- Prior MI
Pathophysiology MITRAL REGURGITATION:
- Regurgitation into the left atrium produces left atrial dilatation but little
increase in left atrial pressure if the regurgitation is longstanding, since the
regurgitant flow is accommodated by the large left atrium - Pure volume overload due to leakage of blood into left atrium during systole
- Compensatory mechanisms: Left arterial enlargement, left ventricle
hypertrophy (since left ventricle must put in same effort to pump less blood(due to regurgitation) so needs to pump harder to maintain cardiac output and
thus hypertrophy to increase stroke volume) and increases contractility:
• Progressive left atrial dilatation and right ventricular dysfunction due to
pulmonary hypertension
• Progressive left ventricular volume overload leads to dilatation and
progressive heart failure
Clinical presentation of MITRAL REGURGITATION:
- Auscultation:
• Soft S1 and a pan systolic murmur at the apex radiating to the axilla
• Prominent third extra heart sound (S3) in congestive heart failure/left
atrium overload
• In chronic mitral regurgitation, the intensity of the murmur does not
correlate with the severity - Exertion dysponea i.e. exercise intolerant
- Dysponea develop because of pulmonary venous hypertension that arises as
a direct result of the mitral regurgitation and secondarily as a consequence
of left ventricular failure - Fatigue and lethargy due to reduced cardiac output
- Increased stroke volume is felt as a palpitation
- Symptoms of right heart failure and eventually lead to congestive cardiac
failure - Heart failure may coincide with increased haemodynamic burden e.g in
pregnancy, infection or atrial fibrillation
• Natural history of MITRAL REGURGITATION:
- Compensatory phase: 10-15 years
- Once patients ejection fraction becomes less than 60% and/or becomes
symptomatic then mortality rises sharply - Severe mitral regurgitation has a 5%/year mortality rate
• Diagnosis: MITRAL REGURGITATION
- ECG:
• May show left atrial enlargement, atrial fibrillation and left ventricle
hypertrophy in severe MR
• But not diagnostic - CXR:
• Left atrial enlargement and central pulmonary artery enlargement - Echocardiogram:
• Estimation of left atrium and left ventricle size and function
• Also gives valve structure assessment
• Transoesophageal is very helpful
Treatment: MITRAL REGURGITATION
- Medications:
• Vasodilators such as ACE-inhibitors e.g. Ramipril or Hydralazine
(smooth muscle relaxer)
• Heart rate control for atrial fibrillation with Beta blockers (Atenolol),
Calcium channel blockers and digoxin
• Anticoagulation in atrial fibrillation and flutter
• Diuretics for fluid overload e.g. Furosemide - Serial echocardiography:
• Mild: 2-3 years
• Moderate: 1-2 years
• Severe: 6-12 months
- Indications for surgery: • Any symptoms at rest or exercise then initiate repair if feasible • Asymptomatic: - If ejection fraction is less than 60% - If new onset atrial fibrillation
AORTIC VALVE
- Aortic valve is located on the left side of the heart and separates the left
ventricle from the aorta - Aortic valve has 3 cusps
- It is one of the two semilunar valves of the heart, the other being the
pulmonary valve
AORTIC STENOSIS:
• Narrowing of the aortic valve resulting in obstruction to the left ventricular
stroke volume, leading to symptoms of chest pain, breathlessness, syncope
and fatigue
