Cardiovascular Flashcards
Thrombosis
is blood coagulation inside a vessel
Where can thrombosis occur
arterial circulation: high pressure, platelet rich
venous circulation: low pressure, fibrin rich
Normal bleeding time
2-9 minutes, 9-15 platlet dysfunction, 15+ critical
How to measure bleeding time
The time from the beginning of incision until the termination of bleeding is considered as the BT. A standard filter paper should be used every 30 seconds to draw off it until the blood completely stops
Arterial thrombosis-anatomy + symptoms
Coronary circulation- angina
Cerebral circulation- stroke syptoms
Peripheral circulation- pain in leg
Other territories- SMA- bellyache
Arterial thrombosis-etiology
Atherosclerosis
Inflammatory
Infective
Trauma
Tumours
Unknown- Platelet driven
Arterial thrombosis-Presentations
Myocardial infarction
CVA- cerebral vascular accident or stroke
Peripheral vascular disease
Others
Arterial thrombosis: treatment- coronary
Aspirin + other antiplatelets
Anticoagulants
Thrombolytic therapy: streptokinase tissue plasminogen activator
Reperfusion – Catheter directed treatments and stents
TPA generates plasmin, degrades fibrin- dissolve clots
Anticoagulants example and action
LMWH (low molecular weight heparins) and UFH (unfractionated heparin)- enhances antithrombin ability to inactive thrombin (factor IIa), factor Xa and factor IXa
Fondaparinux- inhibits factor Xa directly
Aspirin- thrombosis treatment
inhibits platelet function
Why is Fondaparinux used instead of heparin?
Rate of serious bleeding with Fondaparinux was much lower than with heparin because Fondaparinux has a lower half life
Arterial thrombosis: treatment- cerebral
Aspirin, other anti-platelets
Thrombolysis- Catheter directed treatments
Reperfusion
Why is heparin not used for strokes?
Limited efficacy and an increased risk of bleeding complications
Venous thrombosis-anatomy
Peripheral –Ileofemoral, femoro-popliteal
Other sites – Cerebral, Visceral
Fibrin driven
Venous thrombosis-diagnosis
Signs and symptoms-very non specific (specific= calf pain and chest pain/breathlessness)
Blood tests –D-dimer –sensitive but not specific- not used often for in patients
Imaging-usually required- ultrasound, or CT/MRI
Vichow’s triad
increased risk of vascular thrombosis- Hypercoagulability of blood, statis of flow+ Vessel wall injury/ Endothelial damage
What are the three components of Virchows triad?
intravascular vessel wall damage, stasis of flow, and the presence of a hypercoagulable state
Venous thrombosis-aetiology- Virchows triad blood flow
Immobilisation:
Surgery
Long haul flights
Trauma
Injury – physical, chemical
Venous thrombosis-aetiology- Virchows triad blood constituent
Mainly genetic
others:
Malignancy
Oestogens
Venous thrombosis-treatment
Heparin or LMWH
Warfarin
DOAC- main treatment for DVT
Endo-vascular- for longer clots in younger patients- clot destroyed or removed using catheter
Surgical- very rare
DOAC
direct oral anticoagulants
Warfarin action
Inhibits enzyme responsible for activating vitamin K, depletes body of functional vitamin K and reduce synthesis of vitamin K dependent factors clotting factors (10, 9, 7, 2)
When would the treatment of DVT be more aggressive?
DVT is very large, blocks major veins, or produces severe pain and swelling of the limb
Venous thrombosis-prevention
Mechanical or chemical thromboprophylaxis after risk assessment upon entrance to hospital
Also early mobilisation and good hydration
Heparin (UFH)
Given IV- typically continually
Binds to antithrombin and increases its activity
Indirect thrombin inhibitor
Short half life- good if you need to stop quickly ie for surgery
Aim APTT for heparin
activated partial thromboplastin time- ratio 1.8-2.8
Low molecular weight heparin
Smaller molecule, less variation in dose and renally excreted
Once daily, weight-adjusted dose given subcutaneously
Used for treatment and prophylaxis
Is HIT more common after LMWH or UFH?
LMWH is less likely than UFH to cause antibody generation and thus patients do not develop clinical HIT (Heparin‐induced thrombocytopenia)
Warfarin
Orally active
Prevents synthesis of active factors II, VII, IX and X
Antagonist of vitamin K
Long half life (36 hours)
Prolongs the prothrombin time
Problems with warfarin
Difficult to use,
Individual variation in dose
Need to monitor using INR (international normalised ratio, derived from prothrombin time)
NOAC / DOAC
Orally active
Directly acting on factor II or X
No blood tests or monitoring
Shorter half lives so bd or od
Used for extended thromboprophylasis and treatment of AF and DVT/PE
Not used in pregnancy
Whay are DOAC/NOAC not used in metal heart valves?
Shown to cause increase stroke rate
Fondaparineux
example of a Pentasaccharide so indirect Xa inhibitor
Pulmonary Embolism- symptoms
breathlessness, pleuritic chest pain
QT interval
Total duration of de/repolarization, QT interval increases when HR increases, Should be 0.35-0.45s
Pulmonary Embolism- signs
tachycardia, tachypnoea, pleural rub
Pulmonary Embolism vs DVT
PE and DVT have similar symptoms, risk factors and signs
Pulmonary Embolism- Differential diagnosis
Musculoskeletal, Infection, Malignancy, Pneumothorax, Cardiac, GI causes
Treatment PE
Supportive treatment
LMW Heparin
Oral warfarin for 6 months
DOAC/NOAC
Treat underlying cause
Prevention of PE
Anticoagulation
IVC filters- catches clot to prevent embolism to the lung
Pulmonary Embolism -Massive
Haemodynamic instability
Hypotension, cyanosis, severe dyspnoea, right heart strain/ failure
Rare
Pulmonary Embolism -Massive- treatment
Surgery
What is the commonest cause of vascular disease?
atherosclerosis
Pathophysiology for strokes
Atherosclerosis
Inflammatory
Vasospastic
Compression
Traumatic
Pro-thrombotic conditions
What happens to the plaque when we get an acute clinical complication?
plaque ruptures, it causes can causes ulceration
Thrombosis leading to ischemia (can become chronic)/necrosis (aneurysm development)
Plaque ulceration
acute thrombosis with occlusion, dislodging and peripheral embolism
Risk factors in PAD (peripheral arterial disease)?
Modifiable- Smoking
Hypertension
Diabetes
Hypercholesterolaemia
Non-Modifiable- age/sex
Acute ischemia in lower limbs
6Ps
Acute-embolus (AF, MI)
Acute on chronic-thrombus
Chronic ischemia in lower limbs
IC- intermittent claudication decreased mobility
Rest pain- end stage, constant pain
Tissue loss
Burgers test
6Ps for limb ischemia
pallor (unhealthy pale apperance), pain, paresthesia (abnormal sensation), paralysis, pulselessness, and poikilothermia
poikilothermia
inability to maintain a constant core temperature independent of ambient temperature
Burgers test-
Have the patient lie supine and raise the leg above the level of the head. If the sole of the foot becomes pale then the test is positive
Positive burgers test
sole of foot goes pale when raised above level of head while lying supine, suggests more severe ischaemia with distal limb artery involvement
What is the name of the circle consisting the arterial supply to brain?
Circle of willis- anterior MCA, ACA+ anterior choroidal artery
-posterior- vertebral artery, basilar, PCA
Ischaemic vs haemorrhagic stroke
Ischaemic 60%
Haemorrhagic 30%
Carotid Disease ( results from a blockage or narrowing of the carotid arteries)-50% of ischaemic strokes
In TIA/stroke is embolization or thrombosis more common?
Thrombosis is more common
True Aneurysms
True- involves all three layers of the arterial blood vessel wall, Weakening of the arterial wall leading to dilatation leading to outpouring
Commonest location is the infra-renal aorta
False aneurysms
False- caused by bleeding with in the artery wall
Mycotic aneurysm
Mycotic- weakness in wall relating to infection
What is the definition of an aneurysm?
bulging, weakened area in the wall of a blood vessel resulting in an abnormal widening or ballooning greater than 50% of the vessel’s normal diameter (width)
What information does a duplex ultrasound give you?
duplex ultrasound can show how blood flows to different parts of the body. It can also tell the width of a blood vessel and reveal any blockages
Duplex ultrasound
using high frequency sound waves to look at the speed of blood flow, and structure of the leg veins
What are the advantages of MRA over CTA?
MRA can be performed without a as harmful contrast agent and has no radiation, unlike CTA. Also, CTA relies on a working pumps (ie heart in good condition), where as MRA does not
Treatment for PAD- Risk factor modification
Antiplatelets
Statin
Stop smoking
Good control of BP
Good control of DM
ACE inhibitors?
exercise program
Invasive treatment for PAD –Lower Limbs
Endo-vascular:
Stenoses
Short occlusions
DEB- drug eluting balloon
DES- drug eluting stent
Bypass surgery using graft to bypass blockage: Better patency and limb salvage rates than DEB/DES, however higher morbidity and mortality
Intermittent claudication (IC)
lower extremity skeletal muscle pain that occurs during exercise due to insufficent O2 supply to meet demands of skeletal muscle
Should a patient with IC have exercise or angioplasty or surgery?
Exercise first as long as it not too severe
AAA Treatment- pros and cons
Endovascular: -ie stents
-Lower morbidity and mortality
-Life long surveillance
Open surgery: -Higher initial morbidity and mortality, chance of dying around surgery are higher, but lower long term morbidity and mortality after surgery
What is the current NICE recommendation for AAA repair open surgery or EVAR?
EVAR only for patients with hostile abdomens, medical comorbidities or anaesthetic risks that contra-indicate open surgery
Carotid Endarterectomy vs Endovascular stenting for AAA
Open surgery much more common than endovasuclar stenting
What prevents blood flowing distally?
Muscle contraction and valves
Pathophysiology of venous disease
Venous return
-Valves
-Muscle pump
Incompetence
Obstruction
Mixed
Where is the SFJ (sapheno-femoral junction) located?
4 patient fingerbreadths lateral and inferior to pubic tubercle on common side
Investigation for venous disease
Duplex- Gold standard
MRV- Pelvic
Venography- Pelvic
Treatment – Superficial Venous Disease
Lifestyle
Compression
Sclerotherapy
Endo-venous treatments
Surgical stripping
What is the current NICE recommendation for treatment of VVs (varicose veins)?
endothermal ablation- lasers
Treatment – Deep Venous Disease
Lifestyle
Compression
Stents
Valves
Greatest risk factor for coronary artery disease
age
Risk Factors For Atherosclerosis
Age
Tobacco Smoking
High Serum Cholesterol
Obesity
Diabetes
Hypertension
Family History- very strong predictor
Distribution of Atherosclerotic Plaques
Found within peripheral and coronary arteries
Focal distribution along the artery length
Atherosclerotic Plaques distribution governed by
haemodynamic factors- Changes in flow/turbulence (eg at bifurcations) cause the artery to alter endothelial cell function. Wall thickness is also changed leading to neointima. Altered gene expression in the key cell types is key.
Which of the following is not in artery walls
Tunica intima
Tunica media
Epithelial cells
Neutrophils
Epithelial cells- endothelial not epithelium
Atherosclerotic plaque structure
Lipid
Necrotic core
Connective tissue
Fibrous “cap”
Result of atherosclerotic plaque
Occlusion of the vessel lumen- resulting in a restriction of blood flow (angina)
“rupture”- thrombus formation – can be fatal
Response to Injury hypothesis of Atherosclerosis
-Initiated by an injury to the endothelial cells which leads to endothelial dysfunction.
-Signals sent to circulating leukocytes which then accumulate and migrate into the vessel wall.
-Inflammation ensues
Progression of Atherosclerosis
Fatty streaks
Intermediate Lesions
Fibrous Plaques/ Advanced Lesions
Plaque Rupture
Plaque erosion
Fatty streaks
Earliest lesion of atherosclerosis
Consist of aggregations of lipid–laden macrophages and T lymphocytes within the intimal layer of the vessel wall
Intermediate Lesions- layers
Lipid laden macrophages (foam cells)
Vascular smooth muscle cells
T lymphocytes
Adhesion and aggregation of platelets to vessel wall
Isolated pools of extracellular lipid
Fibrous Plaques or Advanced Lesions
Impedes blood flow
Prone to rupture
Fibrous cap made of ECM proteins including collagen (strength) and elastin (flexibility) laid down by SMC that overlies lipid core and necrotic debris
Contains: smooth muscle cells, macrophages and foam cells and T lymphocytes
Plaque Rupture
Fibrous cap has to be resorbed and redeposited in order to be maintained
If balance shifted eg in favour of inflammatory conditions (increased enzyme activity), the cap becomes weak and the plaque ruptures
Leads to thrombus (clot) formation and vessel occlusion
Plaque Erosion
Second most prevalent cause of coronary thrombosis
Small early lesions
plaque rupture vs plaque erosion
Ruptured plaque has a large lipid core with abundant inflammatory cells, red thrombus.
Eroded plaques have a small lipid core, disrupted endothelium, more fibrous tissue and a larger lumen, white thrombus.
Treatment of coronary artery disease
PCI - Percutaneous Coronary Intervention
More than 90% of patients require stent implantation
Restenosis was a major limitation, no longer though due to drug eluting stents
What are coronary stents used in patients today made of?
Plastic
Acute Coronary Syndromes
spectrum of acute cardiac conditions
from unstable angina to varying degrees of evolving
myocardial infarction (MI)
Rank degrees of MI from least to most severe
-Unstable angina- No ECG changes
-Non-Q wave MI
Non-ST-elevation M
-Q wave MI
ST elevation MI
Unstable angina
*Cardiac chest pain at rest
*Cardiac chest pain with crescendo pattern
*New onset or deterioration of previous angina
Diagnosis for unstable angina based on
history
ECG
troponin (no significant rise in
unstable angina)
treatment during an episode of stable anhinga
GTN spray
Stable angina
Chest pain caused by insufficient blood supply to myocardium and included by physical exertion or emotional stress
Prinzmetal angina
chest discomfort or pain at rest with ST segment elevation, seen on ECG
STEMI investigation
ST segment elevation, pathological Q waves after a few days, seen on ECG
Increased troponin levels
STEMI
complete occlusion of major CA, leads to full thickness damage of heart muscle
NSTEMI
partial occlusion of major CA or complete occlusion of minor CA, leads to partial thickness damage of the heart
NSTEMI investigation
ST depression +/ T wave inversion
Increased troponin levels
ST elevation on ECG
> 1mm of ST elevation (ST wave higher than PQ wave) in two contiguous leads on the 12 lead ECG
Non-Q wave vs Q MI
retrospectively, few days after MI
non-Q wave or Q-wave MI on the basis of whether new
pathological Q waves develop on the ECG
Non-Q wave MI on ECG
Poor R wave progression, ST elevation and biphasic
Q wave MI on ECG
Complete loss of R wave
Myocardial infarction- symptoms
Acute central chest pain, nausea, sweating, dyspnoea, SOB, palpitations, pallor
Dyspnoea
difficult or laboured breathing
Myocardial infarction- mortality
- Early mortality - 30% outside hospital
- 15% in hospital
- Late mortality - 5% first year
- 2-5% annually thereafte
Myocardial infarction- risk factors
higher age, DM, renal failure, ethnicity, smoking, HTN, obesity + sedentary lifestyle
MI differentials
Pericarditis, PE, myocarditis, GORD, aortic dissection
Myocardial infarction effect on cardiac muscles
Usually causes permanent heart muscle damage although
this may not be detectable in small MIs
Initial Management of STEMI
*Get in to hospital quickly – 999 call
*Paramedics – if ST elevation, contact primary PCI
centre for transfer for emergency coronary
angiography
*Take aspirin 300mg immediately
*Pain relief
MI treatment- MONA
Morphine, O2 (sats below 94%), Nitrates and Aspirin
Hospital management of STEMI after diagnosis
*Oxygen therapy only if hypoxic
*Pain relief – opiates/ nitrates
*Aspirin +/- platelet P2Y12 inhibitor
*Consider beta-blocker
*Consider other antianginal therapy
*Consider urgent coronary angiography e.g. if
troponin elevated or unstable angina refractory
to medical therapy
MI complications- Darth Vader
Death
Arrhythmia
Rupture
Tamponade
HF
Valve disease
Aneurysm
Dressler syndrome
Embolism
Recurrence regurgitation
ACS (acute coronary syndrome
Umbrella term that includes- STEMI, unstable angina + NSTEMI
Most common causes of ACS
MI due to atherothrombosis- type 1
Causes of type 2 MI
- Myocardial oxygen demand/supply mismatch
- coronary vasospasm without plaque rupture
*drug abuse (amphetamines, cocaine)
*dissection of the coronary artery related to defects of
the vessel connective tissue- more common in middle aged women
*thoracic aortic dissection
Causes of Myocardial oxygen demand/supply mismatch
sepsis, acute lung pathology, thyrotoxicosis,
pulmonary embolism, anaemia, haemorrhage or
other causes of hypotension/hypovolaemia –
underlying stable coronary artery disease may or
may not be a contributing factor
Tako-Tsubo cardiomyopathy (Stress-induced cardiomyopathy)
-May present as MI
-Often precipitated by acute stress such as extreme emotional distress in susceptible individuals
Tako-Tsubo cardiomyopathy (Stress-induced cardiomyopathy)- pathophysiology
Causes transient LV systolic dysfunction, typically ballooning of the left ventricular apex during systole that recovers over days or a few weeks with limited or no permanent damage
Troponin
Protein complex consisting of troponin C, troponin I and troponin T that regulates actin:myosin contraction
Troponin as markers of cardiac muscle injury
*Cardiac-specific isoforms of troponin T and troponin I are
highly sensitive markers for cardiac muscle injury
Diseases with positive troponin markers
- Gram-negative sepsis
- pulmonary embolism
- myocarditis
- heart failure
- tachyarrhythmias
- cytotoxic drugs
- vigorous exercise
Effect of aspirin on platelet inhibition
Irreversible inactivation of COX-1 (responsible for thromboxane production)
P2Y12
Plays role in amplification of platelet activation- e.g clopidogrel, prasugrel, and ticagrelor
P2Y12 inhibitors
Work by inhibiting P2Y12 action, so no platelet activation
Can have irreversible or reversible effect on platelets
Increase risk of bleeding so need to exclude serious bleeding prior to administration
Which is a more effective antiplatelet Prasugrel or clopidogrel?
Prasugrel is a more efficient prodrug than clopidogrel as some people do not metabolise clopidogrel into its active form due genetic changes
Prodrug
compound with little or no pharmacological activity that metabolizes inside the body and converts into a pharmacologically active drug compound
Common adverse effects of P2Y12 inhibitors
*Bleeding e.g. epistaxis, GI bleeds, haematuria
*Rash
*GI disturbance
Idiosyncratic adverse effects of ticagrelor (P2Y12 inhibitors)
*Dyspnoea requires switching to
prasugrel or clopidogrel
*Ventricular pauses: may resolve
GPIIb/IIIa antagonists
Only IV
Used in combination with aspirin and P2Y12 inhibitors for PCI
*Increase risk of major bleeding so used selectively
*Reducing use globally due to more effective oral
antiplatelet therapy
Percutaneous Coronary Intervention (PCI)
non-surgical procedure that uses a catheter to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque build up
Anticoagulants
- Target formation and/or activity of thrombin
*Inhibit both fibrin formation and platelet activation
Anti-anginal therapy for ACS
beta blocker, nitrates, calcium antagonist
Secondary prevention for ACS
statins, ACEI, beta blocker, other antihypertensive
therapy
When would you consider glycoprotein IIb/IIIa antagonists for STEMI
patient undergoing primary PCI
Heart failure patients-pharmacological
therapy
diuretic, ACEI, beta blocker, aldosterone antagonist
(spironolactone, epleronone)
Gold standard pharmacological
therapy in ACS
Aspirin and P2Y12 inhibitor combination (assuming no contraindications
and confirmed diagnosis)
ACS management- diagnosis
history, ECG, troponin +/- coronary angiography;
consider other diagnoses if uncertain
Check no active or recent life-threatening bleeding/severe anaemia
ACS management- ST elevation
arrange primary PCI (PPCI)
ACS management- initial antithrombotic therapy
dual antiplatelet therapy (DAPT) +
anticoagulant; may use GPIIb/IIIa antagonist for PPCI
Two types of cardiac myocytes
Atrio-ventricular conduction system – slightly faster conduction
General cardiac myocyte
Normal systolic ejection fraction
60-65%
Cardiac failure
Failure to transport blood out of hear
Cardiogenic shock
severe cardiac failure
Left sided cardiac failure
pulmonary congestion and then overload of right side
Right sided cardiac failure
venous hypertension and congestion
Diastolic cardiac failure (HFpEF)
Stiffer heart
Embryogenesis of the heart- origin
mesoderm
Paradoxical Embolism (PDE)
venous thrombus crosses an intracardiac defect (ie unclosed foramen ovale) from right to left into the arterial circulation, should have been logged in the heart or lungs
4 main features of Tetralogy of Fallot
- Pulmonary stenosis
- Ventricular septal defect
- Aorta overrides Ventricular septal defect
- Right ventricle hypertrophy
Tetralogy of Fallot- pulmonary stenosis
right ventricle blood is shunted into the left heart producing cyanosis from birth. Surgical correction- performed in first 2 years of life, progressive cardiac debility and risk of cerebral thrombosis increases with age
When is troponin releases?
After damage to myocytes
Why do you repeat troponin test?
comparing your levels over time can help determine the extent of the heart damage and prognosis
Pericarditis- Dressler syndrome
Delayed pericarditic reaction following infarction (2-10 weeks)
Common angina exacerbating factors- supply
Anaemia, hypoxemia
Common angina exacerbating factors- demand
Hypertension
Tachyarrhythmia
Valvular heart disease
Common angina exacerbating factors- environmental
cold weather, heavy meals, emotional stress
Myocardial ischemia - physiology
imbalance between the heart’s oxygen demand and supply, usually from an increase in demand (eg exercise) accompanied by limitation of supply:
1. Impairment of blood flow by proximal arterial stenosis
2. Increased distal resistance (left ventricular) hypertrophy
3. Reduced oxygen-carrying capacity of blood (anemia)
Common Non IHD causes of angina
Prinzmetal’s angina (coronary spasm)
Microvascular angina (Syndrome X)
Unstable angina (Crescendo angina)- gets worse, often mistake for heart attack
History: IHD
Personal details (demographics, identifiers)
Presenting complaint
History of PC + risk factors
Past medical history
Drug history, allergies
Family (1st degree mainly)/Social history
Systematic enquiry
Main Cardiac symptoms
Chest pain (tightness/ discomfort)
Breathlessness (at rest, have to sperate pulmonary from cardiac problems)
Factors pointing towards ischemic cardiac pain
Pain when exercise, elephant sitting on chest, front of chest
Chest pain: Differential diagnoses
Pericarditis/ myocarditis
Pulmonary embolism/ pleurisy
Chest infection/ pleurisy
Dissection of the aorta
Gastro-oesophageal (reflux, spasm, ulceration)
Musculo-skeletal (unlikely to be angina if after long period of exercise)
Psychological
Investigations of angina
Exercise testing, myoview scan, CT coronary angiography (best test but invasive), stress echo, perfusion MRI
Myoview scan
radioactive substance and x-ray used to create images which show blood flow to the heart muscle after stress and rest
Angina: drugs
Beta-blockers, Nitrate (dliates CA and vein), statin, aspirin, Ca channel blocker (reduce action of SMC, less O2 demand and cause vasodilation)
Beta blockers
Reduce HR and contracrility resulting lower CO so lower O2 demand on heart
β blockers: side-effects
Tiredness, nightmares, bradycardia, erectile dysfunction, cold hands and feet
β blockers: contra-indications
ASTHMATICS- Don’t give patients with asthma beta blockers
What class of drugs are Nitrates
Venodilators
Ca channel blockers
reduce action of SMC, less O2 demand and cause vasodilation
Main aspirin side effect
gastric ulceration
Statins
HMG CoA Reductase (enzyme involved in cholesterol synthesis) inhibitors, inhibits synthesis of cholesterol
Angina: treatment- first action drugs
Some combination of Aspirin, GTN, β Blocker, Statin
Angina: treatment- second action drugs
ACE inhibitor, long acting nitrate
Angina: treatment- invasive treatment
Revascularisation: PCI (percutaneous coronary intervention)/ CABG (open surgery)
Angina: treatment- last line drugs
Ca++ channel blocker
Potassium channel opener
Ivabradine
Pros of PCI (percutaneous coronary intervention)
Less invasive
Convenient
Repeatable
Acceptable
Cons of CABG (Coronary artery bypass graft)
Invasive
Risk of stroke, bleeding
Can’t do if frail, comorbid
One time treatment
Length of stay
Time for recovery
ECG
elctrocardiogram is a representation of the electrical events of the cardic cycle
Do electrical impulses that travel towards the electrode produce an upright or downwards deflection?
Towards=upright (positive) deflection
12 ECG leads
3 standard limb leads
3 augmented limb leads
6 precordial leads
Stannard Limb leads
I- RA to LA 0 degrees
II- RA to LL +60 degrees
III- LA to LL +120 degrees
Augmented limb leads
aVL- -30 degrees
aVR- -150 degrees
aVF- +90 degrees
Precordial leads measure
V1+V2= septal= RA+RV
V3+V4=anterior= anterior LV
V5+V6=lateral= lateral portion of LV
Stannard leads measure
I- lateral
II- inferior
III-Inferior
Augmented leads measure
aVR- none
aVL- lateral
aVF- inferior
P wave
Atrium depolarizing
Why is the a gap between P wave and QRS complex on normal ecg?
Delay in AV node, normally 0.12-0.2s
QRS complex
Ventricular depolarisation
T wave
Ventricular repolarisation
U wave
afterdepolarizations which follow repolarization, small round symmetrical and positive (same direction as T wave) in lead II, more prominent at slower HR
QT interval
Total duration of de/repolarization, QT interval increases when HR increases, Should be 0.35-0.45s
ECG rule 1- PR interval
PR interval should be 120-200 ms or 3-5 squares
ECG rule 2- QRS complex length
QRS<110ms, less than 3 squares
ECG rule 3- QRS direction
QRS complex should be dominating upright in leads I and II
ECG rule 4- QRS and T wave
QRS and T waves tend to have the same general direction in the limb leads
ECG rule 5- aVR
All waves are negative in lead aVR
ECG rule 6- R+S wave V1-6
R wave must grow from V1 to at least V4
S wave must grow from V1 to at least V3 and disappear in V6
ECG rule 7- ST segment and V1+V2
ST segment should start isoelectric expect in V1 and V2 where it may elevate
ECG rule 8- P wave direction
P wave should be upright in I, II and V2 to V6
ECG rule 9- Q wave
No Q wave (or very small one less than 0.04s) in I, II, V2 to V6
ECG rule 10- T wave direction
T wave must be upright in I, II, V2 to V6
Determining the HR using ECG
n=number of big boxes between 2 QRS complexes
Divide 300 by n (1500 if small boxes)
OR count number of beats in 10s (number of seconds per page) and *6
Quadrant approach- ECG
QRS complex in leads I and aVF, determine if they are predominantly +ive or -ive, shows normal axis or left/right deviation
Quadrant approach-
Lead aVF=+ive
Lead I= +ive
Normal axis
Quadrant approach-
Lead aVF=+ive
Lead I= -ive
RAD (right axis deviation)
Quadrant approach-
Lead aVF=-ive
Lead I= +ive
LAD (left axis deviation)
R bundle branch block- ECG
V1- RSR1- M pattern, slowed appearance on ECG
V6- QRS, normal
L bundle branch block- ECG
V1- W appearance
V6- M appearance
What does right/left axis deviation suggest
In themselves are rarely significant- minor dedications occur in tall, thin individuals (R) or short, fat individuals (L).
However, should alert you to look for other signs of R/L hypertrophy. Right axis deviation may suggest a pulmonary embolus. Left axis deviation can suggest a conduction defect.
Cardiomyopathy
primary heart muscle disease – often genetic
Hypertrophic cardiomyopathy (HCM)
caused by sarcomere protein gene mutations, ECG is abnormal, v large deflections and pronounced t waves as a result of thick wall
HCM symptoms
angina, dyspnoea, palpitations, dizzy spells or syncope
Dilated cardiomyopathy (DCM)
LV/RV or 4 chamber dilatation and dysfunction, often caused by cytoskeletal gene mutations
DCM symptoms
Similar to heart failure
Arrhythmogenic cardiomyopathy (ARVC/ALVC)
characterised by progressive fibrofatty replacement of the myocardium caused by desmosome gene mutations
Arrhythmogenic cardiomyopathy (ARVC/ALVC) main feature
Arrhythmia
True or false , not all cardiomyopathies carry an arrhythmic risk
False, All cardiomyopathies carry an arrhythmic risk
Inherited arrhythmia (channelopathy)
defects in ion (K+, NA+, Ca2+) channels caused by ion channel protein gene mutations
Channelopathies examples
long QT, short QT, Brugada and Catecholaminergic polymorphic ventricular tachycardia (CPVT)
Channelopathies impact on heart structure
Channelopathies have a structurally normal heart
Long QT syndrome
abnormal feature of the heart’s electrical system that can lead to a potentially life-threatening arrhythmia
Most likely cause of sudden cardiac death in young people
due to an inherited condition, likely a cardiomyopathy or ion channelopathy
Familial hypercholesterolaemia (FH)
Inherited abnormality of cholesterol metabolism, leads to serious premature coronary and other vascular disease
Mechanisms of BP control- Targets for therapy
CO + peripheral resistance
Systems to target- RAAS, SNS (noradrenaline), local vasoconstrictor/dilators mediators
Mechanisms of BP control- ACE inhibitors
Inhibits ACE, so inhibits conversion of angiotensin i > angiotensin ii
Angiotensin ii action
Increases action of SNS so increase peripheral resistance + CO, increase salt retention and vascular growth
ACE inhibitors- clinical indications
Hypertension, heart failure, diabetic
Most widely used ACE inhibitors
Ramipril, perindopril, enalapril, trandopril
ACE inhibitors- adverse effects
Relate to reduced angiotensin ii formation
Related to increased kinins- ACE also causes breakdown of bradykinin
ACEi Contraindications
History of angio-oedema (heredity, recurrent or from previous ACEi exposure)
Pregnant/ Breastfeeding women
Not as effective in patients of black African or Caribbean origin
Angiotensin II Receptor Blockers (ARB)- main clinical indications
Hypertension
Diabetic nephropathy
Heart failure (when ACE-I contraindicated)
Angiotensin II Receptor Blockers (ARB)- examples
Known as the -sartans, irbesartan, valsartan, losartan and candesartan
Angiotensin II Receptor Blockers (ARB)- adverse effects
Symptomatic hypotension (especially volume deplete patients)
Hyperkalaemia
Potential for renal dysfunction
Rash
Angio-oedema
ACE inhibitors- adverse effects- angiotensin ii formation
hypotension, acute renal failure- angiotensin ii constricts efferent arteriole, hyperkalaemia, teratogenic effects in pregnancy
ACE inhibitors- adverse effects- increased kinins
Cough, rash, anaphylactoid reactions
Calcium Channel Blockers (CCB)
Vasodilators, not Ca2+ antagonists
Calcium Channel Blockers (CCB)- Main clinical indications
Hypertension
Ischaemic heart disease (IHD) – angina
Arrhythmia (tachycardia
Most common type of CCB
AMLODIPINE
CCB- Dihydropyridines
drug ending in -dipine, Peripheral arterial vasodilators, Preferentially affect vascular SMC
CCB- Phenylalkylamines
Verapamil, main effects on heart- ive chronotopic+ -ive inotropic
CCB- Benzothiazepines
diltiazem, Intermediate heart/peripheral vascular effects
CCB causes of adverse effects
Due to peripheral vasodilatation (mainly dihydropyridines),
Due to negatively chronotropic effects (mainly verapamil/diltiazem),
Due to negatively inotropic effects (mainly verapamil)
CCB adverse effects- peripheral vasodilation
Dihydropyridines
Flushing, headache, oedema, palpitations
CCB adverse effects- negatively chronotropic effects
verapamil/diltiazem
Bradycardia
Atrioventricular block
CCB adverse effects- -ive chronotropic effects
Verapamil
Worsening of cardiac failure
What non CV side effect is common with verapmil vs other CCB
Constipation
Beta-adrenoceptor blockers (BB)- main clinical indications
Ischaemic heart disease (IHD) – angina
Heart failure
Arrhythmia
Hypertension
Cardioselective
used to imply β-1 selectivity however this is a misnomer given since up to 40% of cardiac β-adrenoceptors are β-2
Beta-adrenoceptor blockers (BB) adverse effects
Fatigue, headache, sleep disturbance/nightmares- as BB can cross Blood-brain barrier
Bradycardia, hypotension, cold peripheries
Erectile dysfunction-
Worsens Asthma (may be severe) or COPD
PVD – Claudication or Raynaud’s
Giving BB for heart failure
Heart failure – if given in standard dose or acutely- must be give in low dose and titrated
Diuretics classes and action on kidney
Thiazides and related drugs (distal tubule)
Loop diuretics (loop of Henle)
Potassium-sparing diuretics
Aldosterone antagonists
Diuretics main clinical indications
Hypertensin, heart failure
Main adverse effects of diuretics
Hypovolaemia+ Hypotension (mainly loop diuretics)
Low serum potassium (hypokalaemia)
Low serum sodium (hyponatraemia)
Low serum magnesium (hypomagnesaemia)
Low serum calcium (hypocalcaemia)
Raised uric acid (hyperuricaemia – gout)
Impaired glucose tolerance/Erectile dysfunction (mainly thiazides)
Anti-hypertensin drug for pregnant women
METHYLDOPA- Centrally acting
1st step anti-hypertensive for diabetics +/ <55
ACE-inhibitor or Angiotensin II receptor Blocker
1st step anti-hypertensive for >55 +/ Afro-Caribbean
CBB
Step 2 antihypertensive
ACE-I / ARB + CCB OR Thiazide like diuretic
Step 3 antihypertensive
ACE-I / ARB + CCB and Thiazide like diuretic
Step 4 antihypertensive
Resistant hypertension consider BB+ others
Types of heart failure
Heart failure due to left ventricular systolic dysfunction - LVSD
Heart failure with preserved ejection fraction (diastolic failure- issue with filling of heart) – HFPEF
Acute heart failure / Chronic heart failure
Acute vs Chronic heart failure
Acute- sudden heart attack
Chronic- develops slowly over weeks/months treated with pharmacology
Heart failure
complex clinical syndrome of symptoms and signs that suggest the efficiency of the heart as a pump is impaired, caused by structural or functional abnormalities of the heart
Most common causes of heart failure
Coronary artery disease
Treatment concept for chronic heart failure
Main benefit from vasodilator therapy via neurohumoral blockade (RAAS - SNS) and not from LV stimulants
Heart Failure- basic pharmacology
Symptomatic treatment of congestion- Diuretics
Disease influencing therapy-neurohumoral blockade
Inhibition of RAAS + SNS
Heart failure pharmacology- first line- triple therapy
Diuretic, ACE inhibitors and beta blocker therapy- Low dose and slow up titration
Sacubitril/Valsartan (Entresto) in Heart Failure
Sacubitril – neprilysin inhibitor (increases levels of natriuretic peptides, increases vasodilation)
Valsartan –angiotensin II blocker
SGLT2 Inhibitors + heart failure
1st used for DM, work by lower plasma glucose levels by blocking reabsorption of filtered glucose, which falls as plasma levels fall
Also found useful heart failure treatment
Nitrates
Arterial and venous dilators
Reduction of preload and afterload
Lower BP
Comes in tablet, spray (for angina pain) and IV (for emergency)
Nitrates main uses
Ischaemic heart disease (angina)
Heart failure
CAD- Chronic stable angina symptoms
Anginal chest pain
Predictable
Exertional
Infrequent
Stable
CAD- Unstable angina / acute coronary syndrome (NSTEMI) symptoms
Unpredictable
May be at rest
Frequent
Unstable
CAD- ST elevation Myocardial Infarction (STEMI) symptoms
Unpredictable
Rest pain
Persistent
Unstable
Chronic stable angina- pharmacology treatment
Antiplatelet therapy, Lipid-lowering therapy (statins), GTN spray for acute attack,
1st line treatment BB or CCB (switch then combined),
last line- long acting nitrate
Acute coronary syndromes (NSTEMI and STEMI)- pharmacology treatment
Pain relief: GTN spray, Opiates – diamorphine
Dual antiplatelet therapy
Antithrombin therapy
Consider Glycoprotein IIb IIIa inhibitor (high risk cases)
Background angina therapy: BB, long acting nitrate, CCB
Lipid lowering therapy: Statins
Therapy for LVSD/heart failure as required
Antiarrhythmic drugs- Vaughan Williams classification
Class I: Sodium channel blockers
Class II: BB
Class III: Prolong the action potential
Class IV: CCB, that act on heart
Antiarrhythmic drugs- digoxin
Cardiac glycoside- toxin so narrow therapeutic range
Inhibit Na/K pump
Enhances vagal tone
Increased ectopic activity
Increased force of contraction- due to increase Ca2+ in muscle from Na+/K+ pump failing
Antiarrhythmic drugs- digoxin uses
Used in atrial fibrillation (AF) to reduce ventricular rate response
Use in severe heart failure as positively inotropic
Antiarrhythmic drugs- Amiodarone
treats ventricular arrhythmias and atrial fibrillation
Anatomy of the Pericardium
2 continuous layer
Visceral single cell layer adherent to epicardium
Parietal layer- Fibrous
50 ml of serous fluid
What lies outside of the pericardium
Left atrium is mainly outside the pericardium
Great vessels and LV+RA+RV lie within
Cardiac tamponade
excessive fluid accumulates in the pericardium, in turn compressing the heart and restricting the filling of the cardiac chambers
Physiology of the pericardium
Mechanical function restrains the filling volume of the heart, initially stretchy but stiff at higher tension, so the pericardial sac has a small reserve volume
What happens when the small reserve volume of the pericardium is exceeded
If this volume is exceeded the pressure is translated to the cardiac chambers
Acute pericarditis
inflammatory pericardial syndrome with or without effusion
Pericardial fusion
a build-up of fluid between the layers of pericardium
Acute pericarditis- Aetiology Infectious
Viral (common)
Bacterial: Mycobacterium tuberculosis
other bacteria rare- very sick high mortality
Acute pericarditis- Aetiology Non- Infectious
Autoimmune (common):
Sjögren syndrome, rheumatoid arthritis, scleroderma,
systemic vasculitides
Neoplastic:
Secondary metastatic tumours (common, above all lung and breast cancer, lymphoma).
Metabolic:
Uraemia, myxoedema
Trauma- direct/indirect injury- often as a result of cardiac procedures
Acute pericarditis- Clinical presentation
Chest pain (sharp and pleuritic, doesn’t have heavy tight description like IHD)
Dyspnoea
Cough
Hiccups (phrenic)
Acute pericarditis- past medical history
Cancer, Rheumatological Dx, Pneumonia, Cardiac procedure (PCI, ablation), MI
Pericarditis- Clinical examination
Pericardial rub – pathognomonic, crunching snow
Sinus tachycardia
Fever
Signs of effusion (pulsus paradoxus, Kussmauls sign)
Pericardial friction rub
Grating, to-and-fro sound produced by friction of the heart against the pericardium. This sounds similar to sandpaper rubbed on wood
ECG - Pericarditis
Saddle shape ST wave
PR depression
No reciprocal changes
ECG- pericarditis vs STEMI
pericarditis differ from STEMI such as in pericarditis, ST elevations are concave in shape and T-wave inversions do not occur in the presence of ST elevations
Signs of taponade
Low blood pressure (hypotension). Bulging neck veins. Heartbeats that sound distant or muffled
Pericarditis- management
Sedentary activity until resolution of symptoms- only for athletes
NSAIDs and aspirin at very high doses
Colchicine (causes nausea and diarrhoea) reduces recurrence
Acute pericarditis recurrence
15-30% recurrence, Colchicine reduced recurrence rate by 50%
Most common types of valvular heart disease
Aortic Stenosis
Mitral regurgitation
Aortic Regurgitation
Mitral Stenosis
Normal Aortic Valve Area
3-4 cm2
Aortic Stenosis
Symptoms occur when valve area is 1/4th of normal
Aortic Stenosis- types
Valvular- commonest type- degenterative, rheumatic
Supravalvular
Subvalvular
Congenital cause of aortic stenosis
Bicuspid aortic valve- BAV, 0.5-2% of pop, 1st degree relative’s need screening
Pathophysiology of Aortic Stenosis
A pressure gradient develops between the left ventricle and the aorta. (increased afterload)
LV function initially maintained by compensatory pressure hypertrophy
When compensatory mechanisms exhausted, LV function declines
Presentation of Aortic Stenosis
Triad- scope, angina, dyspnoea
Syncope (exertional)- 15%
Angina: (increased myocardial oxygen demand; demand/supply mismatch) 35%
Dyspnoea (shortness of breath): on exertion due to heart failure (systolic and diastolic)-50%, occurs when servere
Sudden death <2%
Aortic stenosis- physical signs
Small vol, slow rising pulse- heart is struggling to eject blood
Heart sounds- soft or absent second heart sound- aortic valve not closing properly or at all
Ejection systolic murmur- crescendo-decrescendo- large gradient between LV and aorta
Natural history MR (mitral regulation)
The onset of symptoms is an indication of poor prognosis if left untreated
Investigation of aortic stenosis
Echocardiogram- LV size and function, gradient between aorta and LV (using Doppler probe) and aortic valve area (how much is it opening/closing)
Management of AS- general
Fastidious dental hygiene/ care- high risk of infection causing infective endocarditis
Consider IE prophylaxis in dental procedures- when high risk
Management of AS- medical
Limited role as mechanical problem, vasodilators are relatively contraindicated in severe AS
Management of AS- replacement
Aortic Valve Replacement:
Surgical
TAVI – Transcatheter Aortic Valve Implantation
TAVI (Transcatheter Aortic Valve Implantation)
Blow up balloon using catheter to crack open damaged aortic valve, damage aortic valve is withdrawn, new aortic valve is left behind
Indications for AS intervention
Any SYMPTOMATIC patient with severe AS (includes symptoms with exercise)
Any patient with decreasing ejection fraction
Any patient undergoing CABG with moderate or severe AS
Consider intervention if adverse features on exercise testing in asymptomatic patients with severe AS
Mitral Regurgitation
Backflow of blood from the LV to the LA during systole due to incompetent valve- mild MR seen in 80% of pop
MR- volume or pressure problem?
Volume overload problem
Primary vs Secondary MR
Primary MR- disease of leaflets
Secondary- normal valve architecture but impaired colures due to abnormal LV/LA geometry
Primary MR causes
Myxomatous degeneration (MVP)
Rheumatic heart disease
Infective Endocarditis
Secondary MR causes
dilated cardiomyopathy- too much tissue
Pathophysiology of MR
Pure Volume Overload
Compensatory Mechanisms: LA enlargement, LV hypertrophy and increased contractility
-Progressive left atrial dilation and right ventricular dysfunction due to pulmonary hypertension.
-Progressive left ventricular volume overload leads to dilatation and progressive heart failure
Physical signs and symptoms of MR
Auscultation: pansystolic murmur at the apex radiating to the axilla- intensity of murmur correlates with severity
Exertion Dyspnoea
HF
Natural History of MR
Once symptomatic, mortality sharply rises
Investigations in MR
ECG: LA enlargement, atrial fibrillation and LV hypertrophy with severe MR
CXR: LA enlargement, central pulmonary artery enlargement.
ECHO: Estimation of LA, LV size and function. Valve structure assessment
Management of MR- medications
Rate control for atrial fibrillation with beta-blockers, CCB, digoxin
Anticoagulation in atrial fibrillation and flutter
Nitrates / Diuretics in acute MR
Chronic HF Rx if chronic MR with CCF (congestive cardiac failure/ heart failure)
No indication for ‘prophylactic’ vasodilators such as ACEI, hydralazine
Management of MR- genral
Serial echocardiography
IE prophylaxis during dental procedure
Management of MR- surgery
Surgical replacement/repair, TEER- transcatheter edge to edge repair
Indications for surgery in severe MR
ANY Symptoms at rest or exercise (repair if feasible)
Asymptomatic:
If EF <60%, LVESD >40mm
If new onset atrial fibrillation/raised PAP >50 mmHg
Aortic Regurgitation
Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps
Aetiology of Chronic AR
Bicuspid aortic valve, Rheumatic- usually with AS
Infective endocarditis
Pathophysiology of AR
Combined pressure AND volume overload
Compensatory Mechanisms: LV dilation, LVH. Progressive dilation leads to heart failure
Physical Exam findings of AR
Wide pulse pressure due to high systolic pressure (due to increased pressure) and low diastolic pressure (leaking back into LV)
Auscultation- Diastolic blowing murmur at the left sternal border
Austin flint murmur (apex): Regurgitant jet impinges on anterior MVL causing it to vibrate
Systolic ejection murmur: due to increased flow across the aortic valve
Natural History of AR
Asymptomatic until 4th or 5th decade
Rate of Progression: 4-6% per year
Progressive Symptoms include:
- Dyspnoea: exertional, orthopnoea (when lying flat), and paroxysmal nocturnal dyspnoea (when sleeping)
Palpitations: due to increased force of contraction and ectopics
The Evaluation of AR
CXR: enlarged cardiac silhouette and aortic root enlargement
ECHO: Evaluation of the AV and aortic root with measurements of LV dimensions and function
Management of AR- general
IE prophylaxis
Serial Echocardiograms
Management of AR- medical
Vasodilators (ACEI’s potentially improve stroke volume and reduce regurgitation but indicated only in CCF or HTN
Management of AR- surgical
Definitive Treatment- aortic valve replacement/repair
(TAVI in exceptional cases only if unsuitable for SAVR- surgical aortic valve replacement)
AR- Indications for Surgery
ANY Symptoms at rest or exercise
Asymptomatic treatment if:
EF drops below 50% or LV becomes dilated > 50mm at end systole
Mitral Stenosis
Obstruction of LV inflow that prevents proper filling during diastole
normal MV area
4-6cm2
MS- MV area
Transmitral gradients and symptoms begin at areas less than 2 cm2
MS predominant cause
Rheumatic carditis
MS Pathophysiology
Progressive Dyspnea (SOB) (70%): LA dilation > pulmonary congestion
Increased Transmitral Pressures: Leads to LA enlargement and AF.
RHF symptoms: due to Pulmonary venous HTN
Haemoptysis (coughing up blood): due to rupture of bronchial vessels due to elevated pulmonary pressure
Physical Signs of MS
prominent “a” wave in jugular venous pulsations: Due to pulmonary hypertension and right ventricular hypertrophy
Signs of right-sided heart failure: in advanced disease
Mitral facies
Diastolic murmur: Low-pitched diastolic rumble most prominent at the apex
Management of MS
Identify patient early who might benefit from percutaneous mitral balloon valvotomy
Causes of hypertension
Often unspecific underlying cause
Screening limited to early onset (<30) with no RFs, hypertension resistant to 3 drugs or malignant hypertension
Significance of hypokalaemia with hypertension
Suggests hyperaldosteronism
Primary investigation with extreme high BP
Look at eyes for evidence of blood vessel damage- leakage of blood from vessels, swelling
Average BP response to one hypertensive with moderate hypertension
Systolic decrease by 8-10 mmHg
Diastolic decrease by 4-6 mmHg
White coat hypertension
Hypertension when you only see doctors, 1/4 of pop
Investigations for BP
Clinical measure
Unattended BP measure (Dr leaves room)
Home self measurement
Ambulatory BP measurement (over a 24 period)
Threshold for treatment
Low risk for CVD- 160/100mmHg
High risk for CVD- 140/90 mmHg
CVD risk calc using Qrisk3
Hypertension vs age
Hypertension strongly correlates with age, more common in male pre-menopause age, more common in females post-menopause
Hypertension symptom relief
Usually asymptomatic
Only symptomatic relief with treatment is headaches
Who needs hypertension treatment
Routine- <140/90 mmHg
Previous stroke/ heavy proteinuria/ CKD AND diabetes- <130/80 mmHg
Older patients- <150/90 mmHg- increased due to increased risk of falls due to lower BP when standing, need to measure older person BP when standing
No of drugs to control hypertension
1 drug- 39%
2 drug- 40%
3 drug- 16%
4 drug- 4%
4+ drugs- 1%
Main illness that HBP contributes to
Stroke, HF, dementia, PVD, renal failure, MI
Untreated HBP impact on life expectancy
Average 50 male with HBP- 5 years loss of life, 7 years loss of disease free life
Average benefit of HBP treatment
Gain 5 years of life expectancy
30% decrease in stroke risk
40% decrease in MI risk
Smoking effect on BP
On average smokers have lower BP as on average they are thinner
Lifestyle factors that influence BP
Weight, salt intake, exercise, alcohol intake
Main type of BP lowering medicine (action of drug)
BB (reduce renin release/cardic contractility), CCB, ACE inhibitors (block formation of angiotensin 2), diuretics (reduce circulating Na+)
Drug causes of increased BP
NSAIDs, SNRIs, corticosteroids, oestrogen containing oral contraceptives, stimulants, anti-anxiety drugs, anti-TNFs
Length of time for BP treatment
Treatment needed lifelong, treatment withdrawal leads to rebound in BP
Circumstances when BP lowering tablets should be stopped
During general anaesthesia, as it causes hypotension
Genetic transmission of congenital heart defects
Foetal recurrence
Background population- 1%
Father with Congen HD- 2.2%
Mother with Congen HD- 5.7%
Tetralogy of Fallot
Ventricular septal defect- shifts forward, obstructs pulmonary outflow track leads to pulmonary stenosis, hypertrophy of RV, overriding aorta
Tetralogy of Fallot - physiology
The stenosis of the RV outflow leads to the RV being at higher pressure than the left
Therefore blue blood passes from the RV to the LV
The patients are BLUE- wont survive an episode untreated
Tetralogy of Fallot – surgical repair
Mostly repaired before the age of 2, most do well, often get pulmonary valve regurgitation in adult life and require redo surgery and arrhythmias can occur
Ventricular septal defect (VSD)
Hole between high pressure LV and low pressure RV, common, treatment dependent on size of hole
Ventricular septal defect (VSD) - Physiology
High pressure LV
Low pressure RV
Blood flows from high pressure chamber to low pressure chamber
Therefore NOT blue
Increased blood flow through the lungs can lead to Eisenmenger’s syndrome (if large hole)
Eisenmengers syndrome
High pressure pulmonary blood flow
Eisenmengers syndrome- pathophysiology
High pressure pulmonary blood flow
Damages to delicate pulmonary vasculature
The resistance to blood flow through the lungs increases
The RV pressure increases
The shunt direction reverses
The patient becomes BLUE
Small Ventricular septal defect (VSD)
Can live normal lives without treatment
loud systolic murmur
higher risk of infection due to high velocity stripping lining of heart
Atrial septum defects (ASD)
Abnormal connection between atria, common, often presents in adulthood (if moderate/smaller)
Atrial septum defects (ASD) - Physiology
Slightly higher pressure in the LA than the RA
Shunt is left to right
Therefore NOT blue
Increased flow into right heart and lungs
Atrial septum defects (ASD) – clinical signs
Pulmonary flow murmur
Fixed split second heart sound (delayed closure of PV because more blood has to get out)
Big pulmonary arteries on CXR
Big heart on chest X ray
Closing Atrial septum defects (ASDs) techniques
Surgical
Percutaneous (key hole technique)
Earlier in life the better
Atrio-Ventricular Septal Defects- AVSD
Hole in centre of heart, Involves the ventricular septum, the atrial septum, the mitral and tricuspid valves, often associated with downs syndrome
AVSD - physiology- complete defect
Breathless as neonate
Poor weight gain
Poor feeding
Torrential pulmonary blood flow
Needs repair or PA band in infancy
Repair is surgically challenging
AVSD - physiology- partial defect
Can present in late adulthood
Presents like a small VSD / ASD
May be left alone if there is no right heart dilatation
Patent Ductus Arteriosus
Failure of ductus to close, leading to link between aorta and pulmonary artery, so increased blood flow in pulmonary vasculature
Patent Ductus Arteriosus- clinical signs
Continuous ‘machinery’ murmur
If large, big heart, breathless
Eisenmenger’s syndrome
Coarctation (narrowing) of the aorta
Narrowing of the aorta at the site of insertion of the ductus arteriosus
Coarctation of the aorta - physiology- severe
Complete or almost complete obstruction to aortic flow
Collapse with heart failure
Needs urgent repair
Coarctation of the aorta - physiology- mild
Presents with hypertension
Incidental murmur
Should be repaired to try to prevent problems in the long term
Coarctation repair
Surgical vs percutaneous repair
Subclavian flap repair, End to end repair, Coarctation angioplasty
Do congenital heart defects treatment end after childhood
No, should have regular check up throughout childhood
Bicuspid AV
Bicuspid not tricuspid AVs, common 1-2% of pop, more common in males
BAV aortopathy
BAV is usually associated with coarctation of aorta and ascending aortic dilation, some need protective surgery
Pulmonary Stenosis
Narrowing of the outflow of the right ventricle
Pulmonary stenosis physiology- severe
Right ventricular failure as neonate
Collapse
Poor pulmonary blood flow
RV hypertrophy
Tricuspid regurgitation
Pulmonary stenosis physiology- moderate/mild
Well tolerated for many years
RV hypertrophy
Pulmonary stenosis treatment
Balloon valvuloplasty
Open valvotomy
Open trans-annular patch
Shunt (to bypass the blockage)- rare
Fontan circulation
Only one useable ventricle, SVC to pulmonary artery as baby, IVC to pulmonary circulation, lead to passive venous return system
infective endocarditis (IE)
Infection of heart valve/s or other endocardial lined structures within the heart
infective endocarditis- Structures that can be infected
Septal defects, pacemaker leads, surgical patches ect
Treatment of infective endocarditis
Antibiotics/ antimicrobials- based on blood cultures, often don’t penetrate heart very well
May require cardiac surgery to remove the infectious material and/or repair the damage
Treatment of other complications (emboli, arrythmia, heart failure, etc)
Types of infective endocarditis
-Left sided native IE (mitral or aortic)
-Left sided prosthetic IE
-Right sided IE (rarely prosthetic as rare to have PV or TV replaced)
-Device related IE (pacemakers, defibrillators, with or without valve IE
-Prosthetic; Early (within year) or Late (after a year) post op
Infective endocarditis- risk factors
Abnormal valve; regurgitant or prosthetic valves are most likely to get infected.
Infectious material in the blood stream or directly onto the heart during surgery
Have had IE previously
Rheumatic heart disease
condition in which the heart valves have been permanently damaged by rheumatic fever- uncommon as rheumatic fever is more uncommon
Rheumatic fever
Very rare complication that can develop after a bacterial throat infection. It can cause painful joints and heart problems. Most people make a full recovery, but it can come back
The epidemiology of endocarditis
Historically- a disease of the young affected by rheumatic heart disease
Now- elderly
-iv drug users
-young with congenital HD
-anyone with prosthetic heart valves
IE Incidence
Rare, more common in males, PVE in the 1st post op year is 1-4%, after 1st year is 1%/year
Endocarditis presentation
New regurgitant heart murmur, embolic event s of unknown origin, sepsis of unknown origin, fever, many symptoms!!
IE Clinical presentation
Depends on site, organism, etc
Signs of systemic infection (fever, sweats, etc)
Embolisation; stroke, pulmonary embolus, bone infections, kidney dysfunction, myocardial infarction
Valve dysfunction; heart failure, arrythmia
IE Diagnosis: Modified Dukes Criteria
2 major criteria, 5 minor criteria
Definite IE- 2 major, 1 major+3 minor, 5 minor
Possible IE- 1 major, 1 major+1 minor, 3 minor
IE Diagnosis: Modified Dukes Criteria- major
Pathogen grown from blood cultures
Evidence of endocarditis on echo, or new valve leak
IE Diagnosis: Modified Dukes Criteria- minor
Predisposing factors
Fever
Vascular phenomena
Immune phenomena
Equivocal blood cultures
Echocardiography- Transthoracic echo (TTE)
Safe, non-invasive, no discomfort, often poor images so lower sensitivity
Echocardiography- Transoesophageal (TOE/TEE)
Excellent pictures but more invasive. Patients rarely want to have a second TOE. Generally safe but risk of perforation or aspiration.
IE- Peripheral stigmata
Petechiae 10 to 15%
Splinter haemorrhages
Osler’s nodes
Janeway lesions
Roth spots on fundoscopy
Petechiae
Macular petechial and embolic skin lesions
Splinter haemorrhages
Splinter haemorrhages found below finger nails
Osler nodes
Tender nodules in the digits of a patient with infective endocarditis
Janeway Lesions
Haemorrhages and nodules in the fingers of the patient with infective endocarditis.
Diagnosis of IE
Blood cultures (not always shown due to previous anti microbial therapy), raised CRP, ECG (ischemia or infarction, new appearance of heart block), TTE/TOE (detect vegetation)
C reactive protein
Protein that your liver makes, raised when there is inflammation on the body
IE treatment- When to operate
Antibiotics not working, complications to valve that needs replacing, need to remove infected devices
IE prevention
consider prophylaxis in high risk patients during dental procedures (prosthetic valves, previous IE, cyanotic heart disease)
Talk to the patient and the dentist!
ECG- Basic principles
Amplitude of deflection is related to mass of myocardium
* Width of deflection reflects speed of conduction
* Positive deflection is towards the lead/vector
ECG- Abnormalities of P wave- Low amplitude
-Atrial fibrosis, obesity, hyperkalaemia
ECG- Abnormalities of P wave- Alternative pacemaker foci
-Focal atrial tachycardias
-‘wandering pacemaker’
ECG- Abnormalities of P wave- High amplitude ‘Tall’
-Right atrial enlargement
ECG- Abnormalities of P wave- Broad notched ‘Bifid’
Left atrial enlargement
ECG- abnormalities of PR interval
Prolonged in disorders of AV node and specialised conducting tissue
ECG- QRS abnormalities- Broad QRS
-Ventricular conduction delay / BBB
Tall QRS complexes
ECG- QRS abnormalities- Tall QRS complexes
-Left ventricular hypertrophy (S wave in V1 and R wave in V5/V6 >35mm)
-Thin patient
ECG- QRS abnormalities- Small QRS complexes
-Obese patient
-Pericardial effusion
-Infiltrative cardiac disease
ECG- QRS normal
normally<120ms, Predominantly negative in V1, transitioning to postive by V6
ECG- PR interval normal
120-200ms
ECG- P wave normal
Normally <120 ms wide
Positive inferior leads
Positive in lead I
Negative in aVR
Biphasic in V1
ECG- QT interval normal
Corrected for heart rate (380 – 450ms)
ECG- QT interval abnormalities
Excessively rapid or slow repolarisation can be arrhythmogenic
“Long QT” or “Short QT” syndromes
Congenital, drugs, electrolyte disturbances
ECG- ST segment abnormalities
Normally isoelectric, Can be elevated in early repolarisation, myocardial infarction, pericarditis/myocarditis
ECG- T wave abnormalities
Direction of deflection usually similar to QRS (in limb leads), but in opposite direction in bundle branch block
Common tachycardias
Atrial fibrillation, Atrial Flutter
Supraventricular tachycardia
Focal atrial tachycardia
Ventricular tachycardia
Ventricular fibrillation
ECG- irregularly, irregular QRS complexes
AF- ECG
ECG- organised, saw shaped
Atrial flutter- ECG
Atrial fibrillation vs atrial flutter
In atrial fibrillation, the atria beat irregularly.
In atrial flutter, the atria beat regularly, but faster than usual and more often than the ventricles
Atrial fibrillation vs atrial flutter- ECG appearance
In atrial flutter, there is a “sawtooth” pattern on an ECG
In atrial fibrillation, the ECG test shows an irregular ventricular rate
Bradycardia causes
Conduction tissue fibrosis
Ischaemia
Inflammation/infiltrative disease
Drugs
AV conduction problems
1st degree AV block, second degree AV block (2 p wave :1 QRS), Third degree AV block
1st degree AV block
Abnormally slow conduction through the AV node, ECG- PR interval> 0.2s, without disruption of atrial to ventricular conduction
2nd degree heart block- Mobitz Type 1
PR interval gradually increases until AV node falls completely and no QRS wave is seen, then repeats
2nd degree heart block- Mobitz Type 2
Sudden unpredictable loss of AV conduction and loss of QRS with constant PR interval
3rd degree AV heart block
no electrical connection, V independent of A
ECG appearance- LBBB
WiLLiaM- V1= complex resembles W- deep downward deflection (dominant S wave)
-V6= complex resembles M- broad, notched or ‘M’ shaped R wave
Normal appearance of V1
QRS predominantly- -ive
Normal appearance of V6
QRS predominantly- +ive
Ischaemia ECG
T wave flattening inversion, ST segment depression
Infarction ECG
ST segment elevation, T wave normal
ECG- anterior wall affected
Leads- V2-4
Artery- LAD
ECG- Anteroseptal wall affected
Leads- V1-4
Arterty- LAD
ECG- anterolateral wall affected
Leads- I, aVL, V3-6
Artery- LAD, circumflex
ECG- inferior wall affected
Leads- II, III, aVF
Artery- RCA
ECG- lateral wall affected
Leads- I, aVL, V5-6
Artery- circumflex
ECG- Hyperkalaemia
Tall T waves, flattening of P waves, broadening of QRS… eventually ‘sine wave pattern’
ECG- Hypokalaemia
Flattening of T wave, QT prolongation
ECG- Hypercalcaemia`
QT shortening
ECG- hypocalcaemia
QT prolongation
ECG- saddle ST segment, depression of PR segment
Pericarditis
ECG- ST elevation in leads V2-V5 and aVL
Anterolateral MI
Ectopic heart beats
Extra beat out of sinus rhythm arising from ectopic regions of atria or ventricles
Complications of ectopic beats
High burden VE can cause heart failure
High burden AE can progress to AF
Ectopic beats symptomatic relief treatment
from reassurance/ BB
Ectopic beats- referral
-High burden ectopy (>5% of Heat beats, though risk prob not increased till >20% of Heart beats)
– Refractory to BB
– Structural heart disease
– Syncope
Atrial Fibrillation
Commonest sustained arrhythmia
Irregularly irregular pulse
Paroxysmal (self terminating) OR Persistent
Rapid firing- loss of A mechanical contraction
-irregular, often rapid, V response
AF treatment
Treat underlying cause
Rate control- BB (don’t use for asthmatics), CCB, digoxin
Acute sinus rhythm restoration- electrical/ pharmacological cardioversion
Maintain sinus rhythm- (Flecainide, Dronedarone, Sotalol, Amiodarone)
Permeant fix- pulmonary vein isolation, Catheter based AF therapy
AF complications
High stroke risk (use CHA2DS2-VASc), mitigate risk with anticoagulation (warfarin/ DOAC using ORBIT score) and balance bleeding risk
ECG- absent P waves, narrow QRS, tachycardia
Supraventricular tachycardia- SVT
SVT management
Advice on Valsalva manoeuvres
Can try beta blocker/CCB
Permeant cure- Catheter ablation AVNRT- invasive
ECG- no clear PR interval, slurred appearance (delta wave) of QRS
Accessory pathways- Congenital remnant muscle strands between atrium and ventricle
Wolff Parkinson white syndrome
Episodes of abnormally fast HR.
Caused by an extra electrical connection in the heart.
Congenital, although symptoms may not develop until later in life, episodes can be fatal
ECG-wolff parkinson white syndrome
short PR interval (<120 ms), prolonged QRS complex (>120 ms), and a QRS morphology consisting of a slurred delta wave
ECG- wide QRS complex- beyond 120 milliseconds — originating in the ventricles, tachycardia
ventricular tachycardia
Ventricular tachycardia causes
Diseased ventricles
-Myocardial infarction
-Cardiomyopathy
Electrical storm
3 or more sustained episodes of VT or VF, or appropriate ICD shocks during a 24-hour period
High risk/ poor prognosis
Electrical storm treatment
Correct underlying cause (electrolyte imbalance, ischaemia, infection, HF)
-BB, sedation
-amiodarone +/- lignocaine
-override pacing
-general anaesthesia/ Neuraxial blockade
– Catheter ablation
ECG- Tachycardias- narrow complex
SVT, AF/flutter
ECG- Tachycardias- broad complex
VT
SVT with BBB/preexcitation
Who is a higher risk of “silent MI”
Diabetics are at greater risk of having MI without chest pain, likely as a result of cardiac autonomic dysfunction
ECG- sinus tachycardia, RV strain (in V1,2,3), S1Q3T3
PE
S1Q3T3
presence of S wave in lead I and Q wave and inverted T wave in lead III, PE (not always shown, but characteristic)
Heart failure (HF)
An inability of the heart to deliver blood (and O2) at a rate commensurate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures
Causes of HF
-myocardial dysfunction
-Hypertension,
-alcohol excess,
-cardiomyopathy,
-valvular,
-endocardial,
-pericardial causes.
Commonest cause of HF
Myocardial dysfunction, typically as a result of IHD
Is HF usually curable?
No, typically it can only be treated, however if there is a modifiable cause (ie alcohol) it can be cured
The main phenotypes of HF
HF with reduced ejection fraction (HFrEF)- LV weak
HF with preserved ejection fraction (HFpEF)- LV stiff
Ejection fraction
% of blood that ejected from LV, women- 60-65%
men- 55-60%
Other phenotypes of HF
HF due to severe valvular heart disease (HF-VHD)
HF with pulmonary hypertension (HF-PH)
HF due to right ventricular systolic dysfunction (HF-RVSD)
HF- symptoms
Breathlessness
Tiredness
Cold peripheries
Leg swelling
Increased weight
HF- clinical signs
Tachycardia
Displaced apex beat
Raised JVP (Juglar venous pluse)
Added heart sounds and murmurs, 3rd H sound
Hepatomegaly, especially if pulsatile and tender
Peripheral and sacral oedema
Ascites
NYHA- class system
Class I: No limitation (Asymptomatic)
Class II: Slight limitation (mild HF)
Class III: Marked limitation (Symptomatically moderate HF)
Class IV: Inability to carry out any physical activity without discomfort (symptomatically severe HF)
Causes of acute decompensation of chronic heart failure
AMI
Uncorrected HBP
Obesity
Superimp. infection
AF & arrhythmias
Excess alcohol
Endocrine
-ve inotropes (Ca/beta)
NSAIDS
Treatment and Na+ noncompliance.
Lack of information given to patient about diet, medications, etc.
Treatment of HF
Diuretics, ACEI (not 1st line, not as effective in black people), aldosterone antagonists, BB (doesn’t have to be cardiac selective)
AF- ECG
ECG- irregularly, irregular QRS complexes
Atrial flutter- ECG
ECG- organised, saw shaped
Abnormally slow conduction through the AV node, ECG- PR interval> 0.2s, without disruption of atrial to ventricular conduction
1st degree AV block
PR interval gradually increases until AV node falls completely and no QRS wave is seen, then repeats
2nd degree heart block- Mobitz Type 1
Sudden unpredictable loss of AV conduction and loss of QRS with constant PR interval
2nd degree heart block- Mobitz Type 2
no electrical connection, V independent of A
3rd degree AV heart block
WiLLiaM- V1= complex resembles W- deep downward deflection (dominant S wave)
-V6= complex resembles M- broad, notched or ‘M’ shaped R wave
ECG appearance- LBBB
Leads- V2-4
Artery- LAD
ECG- anterior wall affected
Leads- V1-4
Arterty- LAD
ECG- Anteroseptal wall affected
Leads- I, aVL, V3-6
Artery- LAD, circumflex
ECG- anterolateral wall affected
Leads- II, III, aVF
Artery- RCA
ECG- inferior wall affected
Leads- I, aVL, V5-6
Artery- circumflex
ECG- lateral wall affected
Tall T waves, flattening of P waves, broadening of QRS… eventually ‘sine wave pattern’
ECG- Hyperkalaemia
Flattening of T wave, QT prolongation
ECG- Hypokalaemia
QT shortening
ECG- Hypercalcaemia`
QT prolongation
ECG- hypocalcaemia
Pericarditis
ECG- saddle ST segment, depression of PR segment
Anterolateral MI
ECG- ST elevation in leads V2-V5 and aVL
CHA2DS2-VASc
AF Stroke risk score
ORBIT
Bleeding Risk Score for Atrial Fibrillation predicts bleeding risk in patients on anticoagulation for afib
Supraventricular tachycardia- SVT
ECG- absent P waves, narrow QRS, tachycardia
short PR interval (<120 ms), prolonged QRS complex (>120 ms), and a QRS morphology consisting of a slurred delta wave
ECG-wolff parkinson white syndrome
Most common causes of heart failure
coronary heart disease (myocardial infarction), atrial fibrillation, valvular heart disease and hypertension
Cor pulmonale
alteration in the structure and function of the right ventricle caused by a primary disorder of the respiratory system resulting in pulmonary hypertension- type of RHF
Hypertension and heart failure
Prolonged hypertension promotes left ventricular hypertrophy which will eventually lead to heart failure
Restrictive Cardiomyopathy
Muscles of ventricles stiffen and can’t fill with blood
may be asymptomatic or present with symptoms of cardiac failure
Rarest type of Cardiomyopathy
Arrhythmogenic right ventricular cardiomyopathy/dysplasia
rare familial disorder that may cause ventricular tachycardia and sudden cardiac death in young, apparently healthy individuals
male predominance; first presentation often in adolescence
ECG- RBBB
QRS duration > 120ms
RSR’ pattern in V1-3 (“M-shaped” QRS complex)
Wide, slurred S wave in lateral leads (I, aVL, V5-6)
Right bundle branch block (RBBB) cause
normal variant, pulmonary embolism, cor pulmonale
Left bundle branch block (LBBB) cause
IHD, hypertension, cardiomyopathy, idiopathic fibrosis
ECG RBBB- MaRRoW=RBBB
broad QRS
‘M’- M pattern on V1
‘W’- sloped s wave in V5 (w)
ECG LBBB- WiLLiaM=LBBB
broad QRS
‘W’- W pattern in V1
‘M’- W pattern in V6
Prolonged QT syndrome
Seen on ECG
Causes by a congenital or acquired (certain medications, health conditions- hypothermia/ calcemia/ magensemia/ kalemia/ thyrodism)
Prolonged QT syndrome- compliactions
Torsades de pointes, VF, sudden death
Torsades de pointes
twisting of the points- Ventricles beat chaotically, causing ECG to appear twisted, heart pumps out less blood
If episode does not correct its self- VF can occur
Types of shock
Cardiogenic shock (due to heart problems)
Hypovolemic shock (caused by too little blood volume)
Anaphylactic shock (caused by allergic reaction)
Septic shock (due to infections)
Neurogenic shock (caused by damage to the nervous system)
Obstructive shock (caused by something outside of the heart which prevents the heart from pumping enough blood)
Shock
Life-threatening condition that occurs when the body is not getting enough blood flow. Lack of blood flow means the cells and organs do not get enough oxygen and nutrients to function properly
Atrioventricular nodal reentrant tachycardia (AVNRT)
Type of paroxysmal supraventricular tachycardia that results due to the presence of a re-entry circuit within or adjacent to the AV node
ECG- Atrioventricular nodal reentrant tachycardia (AVNRT)
heart rate between 140 and 280 beats per minute (bpm), and in the absence of aberrant conduction, a QRS complex of fewer than 120 millisecond
Murmurs of valvular disease- Systolic
Aortic stenosis, mitral regurgitation, mitral valve prolapse, tricuspid regurgitation
Murmurs of valvular disease- Diastolic
Aortic regurgitation, mitral stenosis
Murmurs of valvular disease- systolic ASMR
AS- Aortic stenosis
MR- Mitral regurgitation
Murmurs of valvular disease- Diastolic ARMS
AR- Aortic regurgitation
MS- Mitral stenosis
Rumbling mid-diastolic murmur with opening snap
Mitral stenosis
Pansystolic murmur radiating to left axilla
Mitral regurgitation
Ejection systolic murmur radiating to carotids and apex
Aortic Stenosis
Early diastolic murmur
Aortic regurgitation
Hypovolemic shock
Hypotension, tachycardia, weak thready pulse, cool, pale, moist skin- common after trauma
Decreased CO
Increased SVR
Cardiogenic shock
Hypotension, tachycardia, weak thready pulse, cool, pale, moist skin
Decreased CO
Increased SVR
Neurogenic shock
Hypotension, bradycardia, warm dry skin
Decreased CO, venous+ arterial vasodilation, loss sympathetic tone
Anaphylactic shock
Hypotension, tachycardia, cough, dyspnoea, pruritis, urticaria, restlessness, decreased LOC
Decreased CO
Decreased SVR
Septic shock
Hypotension, tachycardia, full bounding pulse, tachypnoea, decrease U/O, fever
Pink, warm, flushed skin
Decreased CO
Decreased SVR
First line hypertensive for <55
ACEi (angiotensin-II receptor antagonist if ACEi intolerant)
First line hypertensive for >55 or black
CCB or diuretic
2nd line hypertensive treatment
ACEi + CCB or ACEi or diuretic
3rd line hypertensive treatment
ACEi + CCB + diuretic
Hypertensives in pregnancy
ACEi + ARD are NOT used as they can cause fetotoxicity
ACEi contraindications
Absolute- Hypersensitivity reactions, pregnancy
Relative- Abnormal renal functions, aortic valve stenosis, hypovolemia
