Cardiovascular Flashcards
What are the 7 risk factors for atherosclerosis?
Age Smoking High serum cholesterol Obesity Diabetes Hypertension Family history
Where are atherosclerotic plaques found?
Peripheral or coronary arteries - Focal distribution along the artery length
What harm-dynamic factors govern atherosclerotic plaque distribution
Changes In flow and turbulence ie. at bifurcations causes artery to adjust wall thickness leading to neointima development
Describe the structural components of a atherosclerotic plaque
Lipid Necrotic core Connective tissue Fibrous cap lymphocytes
What happens if the atherosclerotic plaque occludes a vessel lumen
Restricts blood Flow (Angina)
What happens if an atherosclerotic plaque ruptures
Thrombus formation and death
What initiates the formation of an atherosclerotic plaque?
Injury to endothelial cells leading to endothelial dysfunction - this causes signals to be sent to circulating leukocytes which accumulate and migrate into vessel wall
What stimuli cause inflammation in the arterial wall?
- LDL passing in and out of arterial wall in excess, accumulate in arterial wall and undergo oxidation and glyceration
- Endothelial dysfunction in response to injury hypothesis
What is the role of chemoattractants in the formation of atherosclerotic plaque?
Once released from the endothelium, They attract leukocytes through chemotaxis - concentration gradient is created which drives the movement of cells
Which inflammatory cytokines can be found in atherosclerotic plaques
IL-1 IL-6 IL-8 IFN-y (Proinflammatory agent) TGF-B Monocyte Chemoattractive Protein-1
What are the 4 stages of atherosclerosis?
- Fatty streak formation
- Intermediate lesion
- Fibrous plaque or advanced lesion
- Plaque rupture
At what age do fatty streaks begin to form
<10 years
What does a fatty streak consist of?
Aggregations of lipid laden macrophages and T lymphocytes within the intimal layer of the vessel wall
What are the layers of an intermediate lesion
Foam cells Vascular smooth muscle cells T-lymphocytes Adhesion and aggregation of platelets to vessel wall Isolated pools of extracellular lipid
What are the 4 steps of the adhesion cascade
- Capture
- Rolling - slows cell down for adherence
- Adhesion
- Transmigration
What mediates the capture and rolling stage of the adhesion cascade?
Selectins
What mediates the adhesion and transmigration stages of the adhesion cascade
Integrins and chemoattractants
What are the main concerns with fibrous plaques and advanced lesions?
They made impede blood flow or be prone to rupture
Which cells secrete the fibrous cap that covers fibrous plaques
Smooth muscle cells that overlie the lipid core and the necrotic debris
What does a fibrous plaque contain?
Smooth muscle cells, macrophages, foam cells and T-lymphocytes
What does the dense fibrous cap on a fibrous plaque contain
ECM proteins including collagen (Strength) and elastin (Flexibility)
What occurs in order for a plaque to rupture
If the balance is shifted in favour of inflammatory conditions such as increased enzyme activity that causes the cap to become weak hence the cap ruptures
What is the result of plaque rupture?
Thrombus formation and vessel occlusion
What is the treatment for coronary artery disease?
Percutaneous coronary intervention
What is the main issue with percutaneous coronary intervention?
Restenosis - artery becomes blocked again once the stent is removed
Name 2 drugs used to prevent restenosis following percutaneous coronary intervention
Paclitaxel
Sirolimus
Name three drugs used in the treatment of atherosclerosis
Aspirin - anti platelet
Clopidogrel/Ticagreclor
Statins - reduce cholesterol synthesis
What is atherosclerosis
Hardened plaque in the intimal of an artery - inflammatory process
What can an atherosclerotic plaque cause
- Heart attack
- Stroke
- Gangrene
Which histological layer of an artery may be thinned by an atheromatous plaque
Media
Define angina
Angina is a type of IHD - symptom of O2 supply and demand mismatch to the heart experienced on exertion
What are the 4 types of angina
Stable (Induced by effort)
Unstable (Occurs at rest)
Prinzmetal’s (Occurs during rest due to coronary spasm)
Microvascular
What are 5 possible causes of angina
- Narrowed coronary artery (Atherosclerosis)
- Increased distal resistance
- Reduced O2 carrying capacity (Anaemia)
- coronary artery spasm
- Thrombosis
What are 5 modifiable risk factors for angina
- Hypertension
- Smoking
- Diabetes
- Hyperlipidaemia
- Obesity/sedentary lifestyle
Give three non-modifiable risk factors for angina
- Increasing Age
- Gender (Male bias)
- Family history/Genetics
Describe the pathophysiology of angina that results from atherosclerosis
On exertion there is an increased demand for O2 - coronary blood blood obstructed by atherosclerotic plaque –> Myocardial ischaemia –> Angina
Describe the pathophysiology of angina from anaemia
On exertion there is increased O2 demand - in someone with anaemia there is reduced O2 transport –> Myocardial ischaemia –> Angina
How do blood vessels try and compensate for increased myocardial demand during exercise
When demand increases, during exercise, microvascular resistance drops so flow increases
Why are the blood vessels unable to compensate for increased myocardial demand in someone with CV disease
In CV disease, epicardial resistance is high meaning microvascular resistance has to fall at rest to supply myocardial demand at rest. When the person exercises the microvascular resistance cannot drop more so Flow cant increase to meet metabolic demand = angina
How can angina be reversed?
Resting - reduces myocardial demand
What three factors can limit blood supply
- Impairment of blood flow by proximal arterial stenosis
- Increased distal resistance
- Reduced oxygen carrying capacity of the blood
How would you describe the chest pain in angina
Crushing central chest pain
Heavy and tight
Patient will often make a fist shape to describe the pain
Give 5 symptoms of angina
- Crushing central chest pain
- Pain relieved with rest or GTN
- Pain precipitated by exercise, emotion and temperature
- Pain may radiate to the arms, neck or jaw
- Breathlessness/Nausea/sweating/faintness
If someone comes claiming chest pain, what characteristics about the pain do you want to determine? (OPQRST)
Onset Position (Site) Quality (Nature/character) Relationship (With exertion/meals/posture) Radiation (Anywhere on upper body) Relieving or aggrevating factors Severity Timing Treatment (Does GTN work immediately)
What conditions would someone with angina most frequently experience symptoms
Cold weather
heavy meals
Emotional stress
What is the differential diagnosis for angina
Pericarditis/myocarditis Pleural effusion PE/Pleurisy Pneumonia Pneumothorax GORD Dissection of the aorta Musculoskeletal Psychological
What investigations would you do for someone you think might have angina
- ECG - usually normal (Consider exercise ECG)
- Stress Echo (Pictures of heart following dobutamine administration)
- Perfusion MRI
- CT coronary angiogram
What might an ECG on someone with angina show
ST depression
Flat inverted T waves
What lifestyle changes should someone with angina make?
Stop smoking
Weight loss
Increase exercise
Healthy diet (Increase fruit, veg and oily fish)
What treatments may be used in the secondary prevention of angina
- Aspirin
- ACEi
- Statins
- Antihypertensives
What three anti-anginal treatments may be used in the treatment of symptomatic angina
- GTN spray
- Beta blocker (Atenolol)
- Calcium channel blocker (Verapamil, amlodipine)
Describe the action of beta blockers in the treatment of angina
Antagonise sympathetic activity so decrease chrontropic (HR) and inotropic (Contractility) heart effects leading to decreased cardiac output and decreased O2 demand
What are the side effects of beta blockers
Bronchospasm Cold fingers Bradycardia Tiredness Erectile dysfunction
In which individuals are beta blockers contraindicated
Asthmatics
Heart failure
Hypotension
Bradyarrhythmias
Describe the action of nitrates in the treatment of angina
GTN spray is a venodilator –> Reduces venous return –> Reduced preload –> Reduced myocardial work and demand
Describe the action of calcium channel blockers in the treatment of angina
Arteriodilators –> Cause reduced BP –> Reduced after load –> Reduced myocardial demand
Name 2 drugs that might be used in someone with angina or in someone at risk of angina to improve their prognosis
Aspirin
Statins
Describe the action of aspirin
Irreversibly inhibits COX-1 reducing thromboxane A2 synthesis which reduces platelet aggregation
What is a side effect of aspirin
Gastric irritation
What is the effect of statins
HMG CoA inhibitors which reduces cholesterol production by the liver
Define revascularisation
Restore patent coronary arteries and increase flow
Name 2 types of revascularisation
Percutaneous Coronary Intervention (PCI)
Coronary Artery Bypass Graft (CABG)
Which artery and which veins are commonly used in CABG
Internal mammary artery (To supply LAD) Saphenous Vein (To supply RCA)
Give 2 advantages and 1 disadvantage of PCI
Less invasive
Convenient and acceptable
High risk of restenosis
Give 1 advantages and 2 disadvantage of CABG
Good prognosis after surgery
Very invasive
Long recovery time
What are acute coronary syndromes
ACS encompasses a spectrum of acute cardiac conditions including unstable angina evolving to MI (STEMI and Non STEMI)
What is the most common cause of ACS
Rupture of an atherosclerotic plaque and subsequent arterial thrombosis
What are the uncommon causes of ACS
Coronary vasospasm
Drug abuse
Coronary artery dissection
Describe the pathophysiology of ACS
Atherosclerosis –> Plaque rupture –> Platelet aggregation –> Thrombosis formation –> Ischaemia and infarction –> Necrosis of cells –> Permanent heart muscle damage and ACS
What is a type 1 MI
Spontaneous MI with ischaemia due to plaque rupture
What is a type 2 MI
Secondary to ischaemia due to increased O2 demand
What causes an STEMI to develop
Complete occlusion of a major coronary artery
What causes a Non STEMI
Developing complete occlusion of a minor or partial coronary artery
Why do you see increase serum troponin in NSTEMI and STEMI
Occluding thrombus causes necrosis of cells and myocardial damage - Troponin is sensitive marker for cardiac muscle injury so is significantly raised to reflect this
What is the issue with looking at troponin for MI
It is not specific for acute coronary syndromes
What are three signs of unstable angina
- Cardiac chest pain at rest
- Cardiac chest pain with crescendo patterns
- No significant rise in troponin
What are 6 symptoms of an MI
- Unremitting and severe central chest pain
- Pain occurs at rest
- sweating
- Breathlessness
- Nausea
- Vomiting
- 1/3 occur in bed at night
What are 5 potential complications of MI
- HF
- Rupture of infarcted ventricle
- Rupture of inter ventricular septum
- Mitral regurgitation
- Arrhythmias
- Heart block
- Pericarditis
What are three non modifiable risk factors for MI
Gender (Male)
Age (Older)
Family history
What are the modifiable risk factors for MI
- Smoking
- Obesity
- Hyperlipidaemia
- Diabetes
- Hypertension
- Sendentary lifestyle
- Stress
What are the signs of an MI
Distress Pallor Anxiety Brady/tachycardia High/low BP 4th heart sounds HF sounds
What is the differential diagnosis for MI
Pericarditis Stable angina Aortic dissection GORD Pneumothorax MSK pain
What investigations would you do on someone you suspect to have ACS
- ECG
- Blood tests
- Chest x-ray (Cardiomegaly, pulmonary oedema, wide mediastinum)
What might an ECG of someone with unstable angina show
Might be normal or show some T wave inversion and ST depression
What might the ECG of someone with NSTEMI show
T wave inversion
ST depression
No Q waves
What might the ECG of someone with a STEMI show
ST elevation
Tall T waves
Q waves
T wave inversion
What would the troponin levels be like in someone with unstable angina
Normal
What would serum troponin levels be like in someone with STEMI/NSTEMI
Significantly raised
In what other conditions might you see in raised troponin
- gram negative sepsis
- Pulmonary embolism
- Myocarditis
- Heart failure
- Arrhythmias
Other than troponin, what other bloods tests might you do
FBC
U/Es
Glucose
Lipids
Describe the initial management of ACS
- Call 999
- if STEMI then paramedics should call PCI centre for transfer
- Aspirin 300mg
- Pain relief (Morphine)
- Oxygen if hypoxic
- Nitrates
What is the hospital management for a STEMI
- ECG
- O2
- IV access for bloods
- brief assessment
- Antiplatelet
- Analgesics
- Anti-ischaemic (GTN, Beta-blocker)
- Low molecular weight heparin
- Primary PCI or thrombolysis
What is the treatment of choice for STEMI
PCI
What is the function of P2Y12
Amplifies platelet aggregation
What are three side effects of P2Y12 inhibitors
Bleeding
Rash
GI disturbance
Describe the secondary prevention therapy for people having a STEMI
- Aspirin
- Clopidogrel (P2Y12 inhibitor)
- Statins
- Beta blocker
- ACE Inhibitor
- Modification of risk factors
What is dual anti-platelet therapy
Aspirin + Clopidogrel
What are the complications of surgical intervention for MI
LV dysfunction leading to HF, arrhythmia, pericarditis, ventricular wall thrombus, DVT and PE
What factors affect the response to clopidogrel
Dose Age Weight Disease (Diabetes + CKD) Drug interactions (Omeprazole) CYP2C19 loss of function alleles
ECG - What is the J point
Where the QRS complex becomes the ST segment
ECG - What is the normal axis of the QRS complex
-30 degrees to + 90 degrees
ECG - what does the P wave represent
Atrial depolarisation
ECG - How long should the pR interval be?
120-200ms
ECG - what might a long PR interval indicate
Heart block
ECG - How long should the QT interval be
0.35-0.45s
ECG - what does the QRS complex represent
Ventricular depolarisation
ECG - What does the T wave represent
Ventricular repolarisation
ECG - where would you place lead I
From the right arm to the left arm with the positive electrode on the left arm (Axis = 0 degrees)
ECG - where would you place lead II
From the right arm to the left leg with positive electro on the left leg (Axis 60 degrees)
ECG - where would you place lead III
From the left arm to the left leg with the positive electrode on the left leg (Axis 120 degrees)
ECG - where would you place lead avF
Halfway between the right arm and left arm to the left leg with the positive electrode at the left leg (Axis 90 degrees)
ECG - Where would you place lead avL
From halfway between the right arm and the left leg to the left arm with the positive electrode at the left arm (Axis 30 degrees)
ECG where would you place lead avR
From halfway between the left arm and the left leg to the right arm with the positive electrode being at the right arm 9Axis 150degrees)
What is the dominant pacemaker of the heart
SAN (60-100bpm)
Ho many seconds should the QRS complex be
Less than 110ms
In which leads would you expect QRS complex to be upright
Leads 1 and 2
In which leads are all wave negative
AVR
In which leads must the R wave grow
V1-4
in which leads must the S wave grow
From chest leads V1-3. Disappears in V6
In which leads should T waves and P waves be upright
Leads 1,2, V2-V6
What might tall pointed P waves on an ECG suggest
Right atrial enlargement
What might notched M shaped P waves on an ECG suggest (Bifid P waves)
Left atrial enlargement
Give 3 signs of abnormal T waves
- Symmetrical
- Tall and peaked
- Biphasic or inverted
What happens to the QT interval when HR increases
QT interval decreases
What are the symptoms of DVT
Non specific symptoms Pain Swelling Tenderness Warmth Discolouration
What investigations might be done in order to diagnose a DVT
- Ultrasound compression
(If vein won’t compress then it is full of clot) - D-dimer (Looks for fibrin breakdown products) - if normal you can exclude DVT - If positive it doesn’t confirm DVT diagnosis (need to go on to do the ultrasound)
What is the treatment for DVT
- Low molecular weight heparin
- Oral warfarin
- Compression socks
- Treat the underlying cause (Malignancy and thrombosis)
What are the 2 types of thrombosis
Spontaneous
Provoked
What are the 5 risk factors for DVT
- Surgery, immobility, leg fracture
- oral contraceptive pill, Hormone replacement therapy
- Long haul flights
- Genetic disposition (Thrombophillia)
- Pregnancy
How can DVTs be prevented
- Hydration
- Early mobilisation
- Compression stockings
- Foot pumps
- Low molecular weight heparin
Which individuals are at low risk of thromboprophylaxis
- <40 years
- Surgery <30mins
- Early mobilisation and hydration
- No chemical
Which individuals are at high risk of thromboprophylaxis
- Hip and knee surgery
2. Prolonged immobility
What might be a consequence of a dislodged DVT
Pulmonary embolism
How would you describe an arterial thrombosis
Platelet rich - white thrombus
How would you describe a venous thrombosis
Fibrin rich - red thrombus
What are the potential consequences of DVT that breaks off an blocks a pulmonary artery
Hypotension, cyanosis, severe dyspnoea, right sided heart failure
What is the differential diagnosis of PE
Musculoskeletal, infection, malignancy, pneumothorax, cardiac, gastro
What are the symptoms of PE
Breathlessness
pLeuritic chest pain
What are the signs of PE
Tachycardia
Tachypnoea
Pleural rub
What are the investigations for someone suspected to have a PE
CXR (Normal)
ECG (Sinus tachycardia)
Blood gases (Type 1 respiratory failure)
Mainly done to rule out other causes
What further investigations may be carried out in someone suspected of having a PE
D-dimer
Ventilation perfusion scan
Spiral CT
What is the treatment for PE
Low molecular weight heparin or oral warfarin
Direct oral anticoagulants
Treat the underlying cause
What are the preventative measures for PE
Early mobilisation
Mechanical with stockings
Chemical = LMWH
How does warfarin work
Prevents the synthesis of active clotting factors II, VII, IX and X leading to anti-coagulation
What is warfarin an antagonist of
Vitamin K
Why is warfarin difficult to use
Lots of interactions
Difficult to get into therapeutic range
needs constant monitoring
Define thrombosis
Blood coagulation inside a vessel
What are the 3 potential consequences of an arterial thrombus
- Myocardial infarction
- Stroke
- Peripheral vascular disease ie gangrene
What are the risk factors for atherosclerosis which is a precursor for arterial thrombosis
Smoking Diabetes Hypertension Hyperlipidaemia Obesity Stress/Type A personality
What are the causes of Venous thrombosis
Circumstantial Surgery Imobilisation Oestrogens malignancy Long haul flights Genetic Acquired
What is the treatment for venous thrombus
LMWH
Oral warfarin for 3-6 months
DOAC for 3-6months
What is a psychosocial factor
Factors influencing psychological responses to the social environment and pathophysiological changes
What are the 4 psychosocial factors that increase CHD
- Type A personality (Hostile, competitive, impatient - identify with questionnaires)
- Depression/Anxiety (Measure with MMPI)
- Psychosocial work (More than 11hours per day, high demand with low control)
- Lack of social support
What can doctors do for those with CHD risk
- Observe behaviour patterns
- identify depression/anxiety
- Ask questions from assessment tools
- Ask about occupation
- Liaise with social support services
- Vascular screening
- Risk reduction through promoting healthier lifestyles
- Qrisk2 score
How much fluid is in the pericardial space?
50ml
What is the function of the serous fluid between the visceral and parietal pericardium
Acts as a lubricant so to allow smooth movement of the heart inside the pericardium
What is the function of the pericardium
It restrains the filling volume of the heart
Define pericarditis
Inflammatory pericardial syndrome with or without effusion
What are the causes of pericarditis
Viral (Enterovirus, Herpesviruses) Bacterial (TB, Staph) Autoimmune (Sjorgens, RA) Neoplastic Metabolic (Uraemia, hypothyroidism) Trauma and iatrogenic Idiopathic
How can acute pericarditis be clinically diagnosed?
Need 2 of the following
- Chest pain
- Friction rub
- ECG changes
- Pericardial effusion
Give 5 symptoms of pericarditis
- Central chest pain
- Dyspnoea
- Cough
- Hiccups
- Skin rash
- Viral prodrome
Describe the properties of pericarditis chest pain
Relieved by sitting forward Worse when lying down Severe Sharp Pleuritic Rapid onset
Why might someone with pericarditis have hiccups
Irritation of the phrenic nerve
What are the differential diagnoses for pericarditis
Pneumonia, pleural effusion, PE, GORD, MI, GI inflammation, aortic dissection, pneumothorax, pancreatitis, peritonitis
What investigations might you do on someone with pericarditis
- ECG
- CXR
- Bloods (FBC, ESR, CRP)
- Echocardiogram
What might an ECG look like in someone with acute pericarditis
PR depression seen in most leads
Saddle shaped concave ST elevation
What is the treatment for pericarditis
- Sedntary lifestyle until symptoms resolve
- Ibuprofren
- Colchicine (Anti-inflammatory)
- Immunosuppressants
What is pericardial effusion
Collection of fluid within the potential space of the serous pericardial sac
What can be the effect of large fluid collection in the pericardial sac
Causes ventricular filling to be compromised leading to cardiac tamponade
What are the symptoms of pericardial effusion
- Soft distant heart sounds
- Apex beat obscured
- Raised jugular venous pressure
- Dyspnoea
- Bronchial breathing
- Signs of tamponade
What are the symptoms of cardiac tamponade
- High pulse with low Bp
- High jugular venous pressure
- Muffled 1st and second heart sounds
- Kussmauls sign (Raised jugular venous pressure and increased vein distension during inspiration
- Pulsus paradoxus
What is pulsus paradoxes
Exaggeration of normal variation in the pulse pressure seen with inspiration such that there is a drop in systolic blood pressure
What investigations are used in the Diagnosis of pleural effusion
- CXR
- ECG
- low voltage QRS
- Sinus tachycardia - Echocardiogram (Echo free zone surrounding the heart)
What investigations are used in the diagnosis of pleural effusion
- CXR
- Becks triad
- ECG
- Low voltage QRS - Echocardiogram
- echo free zone around the heart
- Late diastolic collapse of right atrium
What is Becks triad
Falling blood pressure
Rising jugular venous pressure
Muffled heart sounds
What is the treatment of pleural effusion
Treat underlying cause
Most resolve spontaneously
May re-accumulate due to malignancy which requires pericardial fenestration
what is the treatment for cardiac tamponade
Urgent drainage via pericardiocentesis to drain the fluid and relieve the pressure on the heart
What is constrictive pericarditis
Where the pericardium becomes thick, fibrous and calcified due to TB, bacterial infection and rheumatic heart disease
This causes the pericardium to become inelastic and interfere with diastolic filling of the heart
What are the symptoms of constrictive pericarditis
Kussmauls sign Pulsus Paradoxus Diffuse heart sounds Ascites Oedema RHF Atrial dilatations
How would you diagnose constrictive pericarditis
CXR
- small heart with or without pericardial calcification
ECG
- Low voltage QRS
Echocardiogram
- Thickened, calcified pericardium
- Small ventricular cavities with normal wall thickness
What is the treatment for constrictive pericarditis
Complete resection of the pericardium
Why do we treat hypertension
Because it is an important preventable cause of premature morbidity and mortality
Hypertension is a major risk factor for what conditions?
Stroke MI HF Chronic renal disease Cognitive decline Premature death Atrial fibrillation
What is the criteria for a diagnosis of hypertension
Clinic BP of 140/90 mmHg or higher
What are individuals with suspected hypertension offered to monitor their blood pressure
Ambulatory blood pressure monitoring to confirm the diagnosis of hypertension
What are the clinic and ambulatory criteria for stage 1 hypertension
clinic = 140/90 Am = 135/85
What are the clinic and ambulatory criteria for stage 2 hypertension
clinic = 160/100 Am = 150/95
What are the diagnostic criteria for severe hypertension
Systolic 180
Diastolic 110
What are the treatment options for primary hypertension
- Lifestyle modification
2. Antihypertensive drug therapy
Who is likely to develop secondary hypertension
Young individuals
Individuals who are resistant to treatment
Those showing symptoms and signs of the secondary underlying cause (Kidneys, adrenal glands, renal artery stenosis)
Who is offered hypertensive treatment?
People aged over the age of 80 with stage 1 hypertension who have one or more of the following
- Target organ damage
- Established CVD
- Renal disease
- Diabetes
- A 10 year cardiovascular risk of 20% or greater
Offer antihypertensive treatment to people of any age with stage 2 hypertension
What is the BP target for someone under the age of 80
<140/90 for clinic
<135/85 for ambulatory
What is the BP target for someone over the age of 80
<150/90 f0r clinic
<145/85 for ambulatory
What are the mechanisms of blood pressure control
- Cardiac output and peripheral resistance of circulation
- Interplay between renin-angiotensin-aldosterone and sympathetic nervous system (Drop in Bp causes noradrenaline release causing vasoconstriction and increased contractility of the heart and increase PR, CO and BP)
- Local vascular vasoconstrictor and vasodilator mediators
What is the driver of chronic hypertension
Peripheral resistance
Describe the renin-angiotensin-aldosterone system
Angiotensinogen converted by renin to angiotensin I.
Ang I converted to Ang II by ACE
What are the effects of angiotensin II
Vascular hypertrophy and hyperplasia
Aldosterone release leading to sodium reabsorption
Vasoconstriction leading to increased peripheral
resistance and cardiac output
Activates sympathetic nervous system leading to increased noradrenaline
What are the effects of sympathetic NS on RAAS, CO and peripheral resistance
Noradrenaline causes renin release
Noradrenaline causes increases peripheral resistance and cardiac output
Noradrenaline is a vasoconstrictor
What are the main clinical indications for the use of ACEi
Hypertension
Heart failure
Diabetic nephropathy
Give 4 examples of ACEi
End in 'pril' Ramipril Perindopril Enalapril Trandolapril
What are the adverse effects of ACEi related to decreased ANG II formation
Relate to decreased ANG II formation
- Hypotension
- Acute renal failure because ANG II helps to perfuse the glomerulus by constricting the artery leaving the kidney
- Hyperkalaemia (Due to blocking aldosterone)
- Teratogenic effects in pregnancy
Why do you get increased bradykinin production with ACEi
Because ACE is a non specific enzyme that converts bradykinin into inactive peptides so if you block ACE then you increase the amount of circulating bradykinin
What are the adverse effects of ACEi associated with increased kinin formation
Persistent dry cough
Rash
Anaphylactoid reactions due to increased bradykinin
How do angiotensin II receptor blockers work?
Any ANG II produced is blocked from binding to the AT-1 receptor
What are the main clinical indications for angiotensin II receptor blockers
Hypertension
Diabetic nephropathy
Heart failure (When ACE-I contraindicated)
Name some examples of angiotensin II receptor blocker drugs
End in ‘sartan’
Candesartan Losartan Valsartan Irbesartan Telmisartan
What are the main adverse effects of angiotensin II receptor blockers
Symptomatic hypotension (Especially in volume depleted patients) Hyperkalaemia Potential for renal dysfunction Rash Angio-oedema Contraindicated in pregnancy GENERALLY WELL TOLERATED
What are the main clinical indications for calcium channel blockers
Hypertension
Ischaemic heart disease (Angina)
Arrhythmias (Tachycardia)
Name some examples of calcium channel blockers
End in 'pine' Amlodipine Nifedipine Felodipine Lacidipine Diltiazem Verapamil
What is the action of calcium channel blockers
To block L-type calcium channels
What are the three different categories of calcium channel blocker
- Dihydropyridines = nifedipine, amlodipine, felodipine, lacidipine
- Phenylalkylamines = verapamil
- Benzothiazepines = Diltiazem
Where do dihydropyridine calcium channel blockers preferentially act and what is their M.O.A?
Preferentially affect the vascular smooth muscle where they act as arteriolar vasodilators as calcium plays an important role in vasoconstriction
Where do Phenylalkylamines calcium channel blockers preferentially act and what is their MOA
Mainly affect heart calcium channels and are negatively chronotropic (Reduce HR) and negatively ionotropic (Reduce force of contraction
Verapamil
Where do benzodiazepine calcium channel blockers preferentially act and what is their mechanism of action
Intermediate heart and peripheral vascular effects
Arteriole vasodilator and -ve chrono and ionotropic
Diltiazem
What adverse effects are associated with dihydropyridines calcium channel blockers
Due to peripheral vasodilation
- Flushing
- Headache
- Oedema
- Palpitations
What adverse effects are associated with verapamil an diltiazem calcium channel blockers
Due to the negative chronotropic effects
- Bradycardia
- Atrioventricular block
What adverse effects are associated with verapamil
Due to the negative ionotropic effects
Worsening of cardiac failure
bradycardia
Constipation
What are the main clinical indications for the use of beta-blockers
Ischaemic heart disease (Angina)
Heart failure
Arrhythmia
Hypertension
Name some examples of beta blockers
Bisoprosol Atenolol Propanolol Carvediol Metoprolol Nadolol
Which beta blockers are B1 selective
Metoprolol
Bisoprolol
Which beta blocker is non selective
Propranolol
Nadolol
Carvediol
What are the adverse effects of beta blockers
Fatigue Headache Sleep disturbance Bradycardia Hypotension Cold peripheries Erectile dysfunction Worsening of Asthma (Bronchospasm), PVD, HF
How do diuretics work
Increase urine and salt excretion so useful in diseases of congestion
What are the main clinical uses of diuretics
Hypertension
Heart failure
What are the 4 classes of diuretic
Thiazides
Loop diuretics
Potassium sparring diuretics
Aldosterone antagonists
Where do thiazide drugs work and name some examples
Distal tubule
Bendroflumethiazide
Hydrochloromethiazide
Clorthalidone
Where do loop diuretics work and name some examples
Loop of henle
Furosemide (Blocks NKCC2)
Bumetanide
Name some examples of potassium sparing diuretics
Spironolactone
Eplerenone
AMiloride
Triameterine
What are the adverse effects of diuretics
Hypotension Hypovolaemia Hypokalaemia Hyponatraemia hypomagnesaemia hypocalcaemia Raised uric acid (Gout) Erectile dysfunction Impaired glucose tolerance
Name three other antihypertensive medications
A1 adrenoceptor blockers (Doxazosin)
Centrally acting antihypertensives (Moxonidine/methyldopa (Used in pregnancy)
Direct renin inhibitors (Aliskiren)
What is the front line antihypertensive treatment for individuals under 55 years
ACE inhibitor or ANG II receptor blocker
What is the front line treatment for over 55’s or afro-caribbean of any age
Calcium channel blocker
What is the second treatment combination for hypertension
ACE-I/ARB + CCB
What is the third line treatment combination for hypertension
ACE-I/ARB + CCB + Thiazide diuretic
What is the treatment options for resistant hypertension
Spironolactone
High dose thiazide diuretic
Alpha blocker
Beta blocker
Define heart failure
Complex clinical syndrome of symptoms and signs that suggest the efficiency of the heart as a pump is impaired
What is the most common cause of heart disease
Coronary artery disease
What is the symptomatic treatment option for HF
Diuretics to treat the congestion - usually loop diuretics such as furosemide
What are the disease influencing treatment options for HF
Inhibition of RAAS (ACEi or ARBs
Inhibition of sympathetic nervous system (Beta blockers
Why is it important to titrate medication doses in patients with heart failure
Because patients are still reliant on the RAAS and sympathetic nervous system to maintain their hearts
What are the alternative treatment options for HF patients who are ACE-I intolerant
Aldosterone antagonists such as spirolactone and diparalone
Neprilysin inhibitor
Hydralazine/nitrate combination
Digoxin or ivabradine
Why are neprilysin inhibitors used in the treatment of HF
Naturietic peptides cause you to lose salt and fluid but these are broken down by neprilysin so inhibit it and you potentiate the effects of neprilysin
What are the 2 types of cardiac natriuretic peptides
Atrial natriuretic peptide (Atria)
Brain natriuretic peptide (Ventricles)
What causes natriuretic peptides to be released
Stretching of the atrial and ventricular muscle cells
Raised atrial or ventricular pressure
Volume overload
What are the main physiological effects of natriuretic peptides
Increase sodium excretion and water excretion
Relax the vascular smooth muscle
Increase vascular permeability
Inhibit the release of aldosterone, ANG II or ADH
Name an example of a neprilysin inhibitor
Sacubitril
What is entresto
A combination of sacubitril and valsartan
What is the physiological effect of nitrate medication
Arterial and venous dilators
Reduce the preload and after load and lower BP
What are the main clinical uses of nitrates
IHD (Angina)
Heart failure
Name some examples of nitrate medication
Isosorbide mononitrate (Long acting)
GTN spray
GTN Infusion
What are the main adverse effects of Nitrates
Headache
GTN syncope
What are the treatment options for chronic stable angina
- Anti-platelet (Aspirin or clopidogrel)
- Statins (Atorvastatin)
- GTN spray for acute attack
- Beta blocker or calcium channel blocker
What are the treatment options for acute coronary syndrome (STEMI and NSTEMI)
- Pain relief (GTN and opioids)
- Dual anti platelet therapy (Aspirin + Ticagrelor)
- Antithrombin (Fondaparinux)
- Glycoprotein IIb IIIa inhibitor
- Background angina therapy (Beta blocker, CCB)
- Lipid lowering therapy (statins)
- Surgical (PCI or CABG)
Describe class I anti-arrhythmic drugs
Sodium channel blockers used for tachycardia arrhythmias
1a = lengthen the duration of action potential for atrial arrhythmias
1b = Shortens or has no effect on action potential duration for ventricular arrhythmias
1c = no effect on action potential but promotes greater sodium current depression
Give an example of class I 1a anti-arrhythmic drug
Disopyramide
Quinidine
Procainamide
Give an example of Class I 1b anti-arrhythmic drug
Lidocaine
Mexilitene
Give an example of class I 1c anti-arrhythmic drug
Flecainide
Propafenone
Describe class II anti-arrhythmic drugs and give some examples
Beta-adrenoceptor antagonists
Propanolol, nadolol, carvedilol (Non-selective)
Bisoprolol, metoprolol (B1 selective)
Describe class III anti-arrhythmic drugs and give some examples
Prolong the action potential as they are potassium channel blockers so they block repolarisation
Amiodarone
Sotalol
Describe class IV anti-arrhythmic drugs
Calcium channel blockers such as verapamil, dilitiazem
What is digoxin and how does it work
Cardiac glycoside that inhibits the Na+/K+ pump
What are the main effects of digoxin on the heart
Bradycardia
Slow of atrioventricular conduction
Increased ectopic activity
Increased force of contraction
What are the main side effects of digoxin
Nausea, vomiting, diarrhoea, confusion
In what diseases is digoxin clinically indicated
Atrial fibrillation and severe heart failure
Define cardiomyopathy
Group of diseases of the myocardium that affect the mechanical and electrical functions of the heart
What are the 4 types of cardiomyopathy
- Hypertrophic (Muscle is thickened)
- Dilated (Heart chambers are dilated)
- Restricted
- Arrhythmogenic (Heart structure abnormality leads to rhythm disturbance)
What are the risk factors of a cardiomyopathy
Family history High blood pressure Obesity Diabetes Previous MI
What is hypertrophic cardiomyopathy
Ventricular hypertrophy/thickening of the muscle (Septal hypertrophy) - leads to a smaller ventricular cavity
How many people have a hypertrophic cardiomyopathy
1 in 500
What is the inheritance pattern of hypertrophic cardiomyopathy
Autosomal dominant - familial
What is the pathophysiology of hypertrophic cardiomyopathy
Caused by sarcomeric protein gene mutations leading to hypertrophic non-compliant vesicles that impair diastolic filling and result in reduced SV and CO
Also disarray of cardiac myocytes which affects cinduction
What are the symptoms of a hypertrophic cardiomyopathy
Angina and chest pain Dyspnoea Exertional syncope Sudden death S4 jerky pulse Double apex beat ESM
What are the signs of hypertrophic cardiomyopathy
Jerky carotid pulse
Ejection systolic murmur
Double apex beat
S4
What 4 investigations would you carry out in someone you believe to have hypertrophic cardiomyopathy
ECG - LVH and deep Q waves
Echocardiogram (MR SAM ASH)
- Mitral Regurgitation
- Systolic anterior motion
- Asymmetrical hypertrophy
What would the ECG of someone with hypertrophic cardiomyopathy show
Left ventricular hypertrophy with progressive T wave inversion and deep Q waves
What would the echocardiogram of someone with hypertrophic cardiomyopathy show
(MR SAM ASH)
Ventricular hypertrophy with small left ventricle
Mitral regurgitation
Systolic anterior motion
Asymmetrical hypertrophy
What is the treatment for hypertrophic cardiomyopathy
- -ve inotropes ie. B-blockers (Atenolol) and CCB (Verapamil)
- Amiodarone (Anti-arrhythmic)
- Septal myomectomy
What is a dilated cardiomyopathy
Where the left ventricle has become dilated so it contracts poorly and has thin muscle
Poorly generated contractile force leads to progressive dilatation of the heart
What is the inheritance pattern of dilated cardiomyopathy
Autosomal dominant - familial
What is the pathophysiology of dilated cardiomyopathy
Cytoskeletal gene mutations
What are the other causes of dilated cardiomyopathy (DILATES)
Dystrophy Infection (Myocarditis) Late pregnancy Autoimmune SS Toxins (EtOH) Endo = Thyrotoxicosis
What are the symptoms of dilated cardimyopathy
Arrhythmias dyspnoea fatigue HF Thromboembolism
What are the signs of dilated cardiomyopathy
Increased jugular venous pressure
Decreased blood pressure
S3 gallop
Displaced Apex beat
What investigations would you conduct in someone suspected to have dilated cardiomyopathy
CXR (Cardiomegaly, Pulomonary oedema)
ECG (Tachycardia, T wave inversion)
ECHO (Globally dilated heart with decreased ejection fraction)
Cathether and biopsy (Myocardial fibre disarray)
What are the treamtne options for dilated cardiomyopathy
Bed rest
Diuretics, ACEi, digoxin for the HF
What is restrictive cardiomyopathy
Poor dilation of the heart restricts the hearts ability to take on blood and pass it to the rest of the body due to a rigid myocardium
What are the causes of restrictive cardiomyopathy (MiSSHAPEN
Sarcoid Systemic Sclerosis Haemochromatosis Amyloidosis Primary end-myocardial fibrosis Eosinophilia Neoplasia
What is the clinical presentation of restive cardiomyopathy
Dyspnoea Fatigue Embolic symptoms Elevated jugular venous pressure Hepatic enlargement Third and fourth heart sounds
What investigations would yo carry out in someone with restrictive cardiomyopathy
CXR, ECHO and ECG are abnormal but non specific so carry out cardiac catheterisation
What is the treatment for restrictive cardiomyopathy
No treatment with poor prognosis
Consider transplant
What is arrhythmogenic cardiomyopathy
Progressive genetic cardiomyopathy characterised by progressive fatty and fibrous replacement of ventricular myocardium
What is the inheritance pattern of arrhythmogenic cardiomyopathy
Autosomal dominant but in incomplete penetrance it can be recessive
What is the pathophysiology of arrhythmogenic cardiomyopathy
Desmosome (Holds cardiac cells together) gene mutation
What is the clinical presentation of arrhythmogenic cardiomyopathy
Cardiac cells are not held as closely together due to desmosome mutation leading to arrhythmias
Syncope
What investigations would you conduct in an individual you suspect to have arrhythmogenic cardiomyopathy
ECG may show T wave inversion, be abnormal for right ventricle and show epsilon waves
ECHO may be normal but in advanced disease might show right ventricular dilatation
Genetic testing
What is the treatment for arrhythmogenic cardiomyopathy
Beta blockers for patients with non life-threatening symptoms
Amiodarone for patients with more severe symptoms
What is Naxos disease
Fibro-fatty infiltration of the heart and ventricular arrhythmias
What is the clinical presentation of Naxos disease
Plantar keratoderma due to cell separation
Wooley hair
Recessive disease
What is a channelopathy
Inherited arrhythmia caused by ion channel protein gene mutations usually related to K+,Na+ and Ca2+
Name some examples of channelopathies
Long QT Short QT Brugada Catecholamingeric polymorphic ventricular tachycardia Wolff Parkinson White
What may channelopathies lead to?
Sudden arrhythmic death syndrome
What is the clinical presentation of channelopathies
Structurally normal heart but recurrent syncopes
What is familial hypercholesterolaemia
Inherited abnormality of cholesterol metabolism due to mutation in the LDL receptor which normally removes cholesterol from the circulation - causes 100x increase in risk of heart attack
What are the clinical manifestations of hypercholesterolaemia
Lipid seen in the hands and the eyes
Name some aorto-vascular syndromes
Marfan
Loeys-dietz
Ehler danlos
What is the pathophysiology of sort-vascular syndromes
Abnormalities in fibrillar which is densely located at the base of the aorta making that area more susceptible to rupture
What is the clinical presentation of patients with aortovascular syndromes
Tall and lanky with arm span wider than height
Changes in palate and height
Can develop aortic aneurysm
What is heart failure
When cardiac output is inadequate to deliver blood and O2 at a rate that meets the requirements of metabolising tissue in the body despite adequate filling pressures
What is the pathophysiology of compensated heart failure
- Starling effect causes the heart to dilate to enhance contractility
- This leads to remodelling mainly hypertrophy
- RAAS and ANP/BNP release
- Sympathetic activation
What is the pathophysiology of decompensated heart failure
- Progressive dilatation leads t impaired contractility
- Hypertrophy leads to myocardial ischaemia
- Activation of RAAS leads to Na+ and H2O retention and increased venous pressure which leads to oedema
- Sympathetic excess leads to increased afterload and decreased cardiac output
What is systolic cardiac failure
Impaired contraction
What is diastolic cardiac failure
Impaired filling
What are the risk factors for heart failure
65 or older African Descent Men Obesity Previous MI
What are the causes of right sided HF
LVF
Cor Pulmonale
Tricuspid or pulmonary valve disease
What are the symptoms of right sided heart failure
Anorexia and nausea
What are the signs of right sided heart failure
Increased jugular vein pressure and distension
Hepatomegaly and splenomegaly
Pitting oedema
Ascites (Fluid build up in the peritoneal space)
What are the 4 main causes of left sided heart failure
- Ischaemic heart disease
- Dilated cardiomyopathy
- Sustained hypertension
- Restrictive and hypertrophic cardiomyopathy
- Mitral and aortic valve disease
What are the symptoms of left sided heart failure
Fatigue
Exertional dyspnoea
Orthopnoea (Difficulty breathing when lying down)
Nocturnal cough (with pink frothy sputum)
Wt loss and muscle wasting
What are the signs of left sided heart failure
Cold peripheries Cyanosis Cardiomegaly S3 and tachycardia Wheeze Displaced apex beat
Define acute heart failure
New onset or decompensation of chronic
Peripheral or pulmonary oedema
Evidence of peripheral hypo perfusion
Define chronic heart failure
Develops slowly
Venous congestion common
Outline the New York Heart Associated classification of heart failure
- No limitation of activity (asymptomatic)
- Comfortable at rest by dyspnoea on ordinary activity
- Marked limitation of normal activity
- Dyspnoea at rest and activity
What investigations would you carry out in an individual excepted to have heart failure
- Bloods - looks for natriuretic peptide
- CXR
- ECG
- ECHO
What would you expect to see in the bloods of someone with heart failure
BNP secreted from the ventricles in response to increased pressure and myocardial stretch so BNP marker of heart failure
When analysis a CXR of a heart failure patient, what are you looking for
Alveolar shadows Karley B lines Cardiomegaly Upper lobe divisions Pleural effusions Fluid in fissures
What might the ECG of someone with HF suggest
Ischaemia
Hypertrophy of LA/LV
What would you expect to see on the ECHO of someone with HF
Ejection fraction normally 60%
Hypertrophy
What is the primary prevention for HF
Stop smoking decrease salt intake Optimise weight Aspirin Statins
What is the specific front line treatment for heart failure
ACEi/ARB + Diuretic + Beta blocker
via neurohumoral blockade (RAAS-SNS)
What is the second treatment for heart failure
Spironolactone
ACEi+ ARB
Vasodilators (Hydralazine)
What is the third line treatment option for heart failure
Digoxin
Cardiac resynchronisation therapy (Pacemaker)
What are the 5 causes of heart failure
- Comment is IHD
- Hypertension
- Cardiomyopathy
- Excessive alcohol
- Obesity
Briefly describe the pathophysiology of heart failure
When the heart fails, compensatory mechanisms attempt to maintain CO but as HF progresses these mechanism become exhausted and become pathophysiological
What are the compensatory mechanisms in HF
- Sympathetic system
- RAAS
- Natriuretic peptides
- Ventricular dilation
- Ventricular hypertrophy
Explain how the sympathetic system is compensatory in heart failure and give one disadvantage of sympathetic activation.
The sympathetic system improves ventricular function by increasing HR and contractility = CO maintained.
BUT it also causes arteriolar constriction which increases after load and so myocardial work
Explain how RAAS is compensatory in heart failure and give one disadvantage of RAAS activation.
Reduced CO leads to reduced renal perfusion; this activates RAAS. There is increased fluid retention and so increased preload.
BUT it also causes arteriolar constriction which increases after load and so myocardial work.
Give 3 properties of natriuretic peptides that make them compensatory in heart failure
- Diuretic.
- Hypotensive.
- Vasodilators.
What are the 3 cardinal symptoms of HF?
- Shortness of breath.
- Fatigue.
- Peripheral oedema
What is primary hypertension
When the cause is unknown (95% of cases)
What is secondary hypertension
When the cause is known
What is stage 1 hypertension
Clinic BP >140/90
AM BP >135/85
What is stage 2 hypertension
Clinic BP >160/100
AM BP > 150/90
What is severe hypertension
Clinic BP >180/110
What is malignant hypertension
Clinic BP >180/110 + papilloedema and or retinal haemorrhage
What are the causes of hypertension (remember PREDICTION)
Primary (95%)
Renal (Glomerularnephritis, PCKD)
Endo (Cushing’s, Conns, Phaeo, acromegaly
Drugs (Cocaine, NSAIDs, Amphetamines, alcohol, oral contraceptive pill
Intra-cranial pressure increase
CoA
Toxaemia of pregnancy
increased viscosity
Overload with fluid
Neurogenic
What is the end organ damage caused by hypertension (remember CANER)
Cardiac (IHD, LVH –> CCF, AR, MR)
Aortic (Aneurysm, dissection)
Neuro (Encephalopathy, CVA)
Eyes (hypertensive retinopathy)
Renal (Proteinuria)
What investigations would you carry out in a patient you expected to be hypertensive
24hr ambulatory BPM
Urine (Haematuria, ALB: creatine ratio, protein)
Bloods (FBC, U+E, eGFR, glucose)
ECG
Calculate 10yr CV risk
Echo for LVH
Fundoscopy for retinal haemorrhage or papilloedema
What lifestyle interventions are important in the treatment of hypertension
Increase exercise Decrease smoking Decrease alcohol Decrease salt Decrease caffeine
What are the indications for commencing the pharmacological management of hypertension
<80 years with stage 1 hypertension
(End organ damage or CV risk of >20%)
Anyone with stage II
Anyone with severe/malignant hypertension
What are the blood pressure targets following pharmacological management
Under 80 = <140/90
Over 80 = <150/90
What is the 1st line anti-hypertensive treatment for someone under the age of 55
ACEi/ARB
What is the 1st line anti-hypertensive treatment for someone over the age of 55 or are black
CCB or thiazide diruretic
What is the second line treatment for hypertension
ACEI/ARB + CCB
What is the third line treatment for hypertension
ACEi/ARB + CCB + Diuretic
What is the treatment options for someone with resistant hypertension
ACEi + CCB + Diuretic + Beta blocker
What is cor pulmonate
RV hypertrophy and dilatation due to pulmonary hypertension
Name 5 conditions that hypertension is a major risk factor for
- MI
- Stroke
- Heat failure
- Chronic renal disease
- Dementia
Will anti-hypertensives make someone feel better?
Anti-hypertensives won’t necessarily make someone feel better as there are few symptoms associated with high BP although headache symptoms may improve.
Name 4 valvular heart diseases
- Aortic stensis
- Aortic regurgitation
- Mitral regutgitation
- Mitral stenosis
Briefly describe aortic stenosis
A disease where the aortic orifice is restricted so the LV cannot eject blood properly in systole leading to pressure overload
What are the causes of aortic stenosis
- Senile calcification
- Congenital bicuspid valve
- Rheumatic fever
Describe the pathophysiology of aortic stenosis
Aortic orifice is restricted so the pressure gradient between the LV and aorta increases. This increases afterload and leads to subsequent ventricular hypertrophy and ischaemia - this culminates in LVF
When does aortic stenosis become symptomatic
when the valve is 1/3 its normal size
What are the three main symptoms of aortic stenosis
Angina
Dyspnoea
Syncope
What are three signs of aortic stenosis
Slow rising carotid pulse with decreased pulse amplitude
Narrow pulse pressure
Soft or absent S2 heart sound
Crescendo-decrescendo ejection systolic murmur
What are the investigations to carry out in someone with suspected aortic stenosis
Bloods ECG - LVH CXR - LVH and calcified AV Echo and doppler (Thickened calcified cusps, pressure gradient >40, jet velocity >4 and valve area >1) Cardiac catheterisation
What is the definition of severe aortic stenosis
Pressure gradient >40mmHg
Jet velocity >4m/s
Valve area <1cm2
What is the management for someone with aortic stenosis
- Ensure good dental hygiene
- Infective endocarditis prophylaxis
- Aortic valve replacement or trans catheter aortic valve implantation
Who should be offered aortic valve replacement
Severe symptomatic patients with AS
Severe asymptomatic AS with decreasing ejection fraction
Severe AS undergoing CABG
What is aortic regurgitation
Aortic valve is not competent and blood leads back into the LV during diastole due to caption of aortic cusps
What are the causes of aortic regurgitation
- infective endocarditis
- Aortic dissection (Type A)
- Congenital bicuspid aortic valve
- Connective tissue disease such as Marfans or Ehler’s Danlos
Describe the pathophysiology of aortic regurgitation
Pressure and volume overload in the LV leads to compensatory LV dilatation and LVH - LVF
What are 3 symptoms of aortic regurgitation
- Exertional dyspnoea
- Orthopnoea
- Angina
- Palpitations
- Syncope
What are the signs of aortic regurgitation
- Collapsing pulse (Corrigans sign)
- Wide pulse pressure
- Displaced apex beat
- Ejection diastolic murmur
- Soft/Absent S2 heart sounds
What investigations might you carry out in someone with suspected aortic regurgitation
ECG - LVH
CXR (Cardiomegaly, dilated ascending aorta, pulmonary oedema)
ECHO (Aortic structure and function and evidence of infective endocarditis
What are the management options for someone with aortic regurgitation
IE prophylaxis. Vasodilators e.g. ACEi. Regular echo’s to monitor progression. Surgery if symptomatic.
What is mitral stenosis
Obstruction of LV inflow that prevents proper filling from the LA during diastole
What are the causes of mitral stenosis
- Rheumatic heart disease
- Prosthetic valve
- Congenital
- Infective endocarditis
- Calcification
Describe the pathophysiology of Mitral stenosis
- LA dilation = pulomonary congestion
- Increased transmitral pressure = LA enlargement and AF
- Pulmonary venous hypertension causes RHF symptoms
Give 3 symptoms of mitral stenosis
Dyspnoea
Haemoptysis
Fatigue
Chest pain
What are the signs of mitral stenosis
- Malar flush
- a wave in jugular venous pulsations
- Diastolic murmur
- Loud 1st heart sound
What investigations might you do in seomone with mitral stenosis
- ECG - atrial fib and LA enlargement
- CXR - LA enlargement, mitral calcification, pulmonary oedema
- ECHO and Doppler
What is the diagnostic criteria for severe mitral stenosis
Valve orifice <1cm2
Pressure gradient >10mmHg
Pulmonary artery systolic presssure >50mmHg
What is the management for mitral stenosis
in AF rate control e.g. beta blockers/CCB. Anticoagulation if AF. Balloon valvuloplasty or valve replacement. IE prophylaxis.
Why does medication not work for mitral and aortic stenosis?
The problem is mechanical and so medical therapy does not prevent progression.
What is mitral regurgitation
Backflow of blood from the left ventricle to the LA during systole leading to LV volume overload
What are the causes of mitral regurgitation
- Mitral valve prolapse
- Rheumatic heart disease
- Infective endocarditis
4
Annular calcification
What is the pathophysiology of mitral regurgitation
LV volume overload leading to compensatory LA enlargement, LVH and increased contractility.- progressive LV volume overload leads to dilatation and progressive HF
What are the symptoms mitral regurgitation
- Dyspnoea on exertion
- AF
- Pulmonary congestion
What are the signs of mitral regurgitations
- Pansystolic murmur
- Soft 1st heart sound
- 3rd heart sound
4, displaced apex beat
What investigations for Mitral regurgitation
Bloods
CXR
ECHO
ECG
What is the management of mitral regurgitation
Rate control for AF e.g. beta blockers. Anticoagulation for AF. Diuretics for fluid overload. IE prophylaxis. If symptomatic = surgery.
What is infective endocarditis
Cardiac valves and endocardial lined structures develop vegetations composed of bacteria
What are the risk factors for infective endocarditis
Abnormal valve regurgitation
Prosthetic valves
Dental caries
Post-Op wounds
Rheumatic fever
What are the different types of IE
- Left side native
- Left side prosthetic
- Right sided
- Device related IE
What is infective endocarditis commonly caused by
Staphylococcus aureus
Pseudomonas Aeruginosa
Streptococcus viridian’s (Dental problems)
Describe the epidemiology of infective endocarditis
Now a disease of
- Elderly
- Young drug abusers
- Young with congenital heart defects
- Anyone with prosthetic heart valves
What are the clinical signs of infective endocarditis
Signs of sepsis (Fever, sweats, wt loss, clubbing, splenomegaly
Immune complex lesions
(Vasculitis, Roth spots, splinter haemorrhages, oslers nodes, janeway lesions
Which diagnostic criteria is used to diagnose infective endocarditis
Duke criteria
Describe the duke criteria
2 major criteria
(i) +ve blood culture
(ii) Endocardium involved (+ve echo or new valvular regurgitation
5 Minor criteria
- Predisposition
- Fever
- Vascular phenomena
- Immune phenomena
- Equivocal blood cultures
Definitive IE = 2 major/ 1 major + 3minor or 5 minor
What are Roth spots
Boat shaped retinal haemorrhages
What are janeway lesions
Painless Palmer macule
What are Osler’s nodes
Painful purple maculae’s on finger pulps
What investigations might you carry out in someone with suspected IE
Bloods - normochromic, normcytic anaemia
ECG - AV block
Urine = microhaematuria
Echo
(i) Transthoracic detects vegetation >2mm
(ii) Transoesophageal is more sensitive
What is the treatment for IE
Antimicrobials IV for around 6 weeks
When do you consider surgery for infective endocarditis
Heart failure
Emboli
Valve obstruction
Prosthetic valve
What is an arrhythmia
Abnormality of cardiac rhythm
What do arrhythmias causes
Sudden death Syncope HF Chest pain Dizziness Palpitations Can be asymptomatic
What are the two types of arrhythmia
Bradycardia
Tachycardia
Define bradycardia
HR low
<60
What are the causes of bradycardia
DIVISION
Drugs
- antiarrhythmics
- B-blockers
- CCB
- Digoxin
Ischaemia (Inferior infarct)
Vagal hypertonia (Athlete)
Infection (IE, RF)
Sick sinus syndrome
Infiltration (Dilated cardiomyopathy)
O = Hypothermia, thyroid and kalaemia
Neurogenic
What are the two types of bradycardia
Sinus node disease
AVN/Distal conduction problems (Heart block)
Define tachycardia
HR fast
>100
What are the two types of tachycardia
Supraventricular tachycardias
Ventricular tachycardias
What is the treatment for bradycardia
If asymptomatic and HR >40 then not required
If <40bpm then treat the underlying cause
Medical options = atropine and isoprenaline or pacing
What is heart block
AVN blockage leading to bradycardia
What is 1st degree heart Blok
Delayed AV contraction leading to a fixed prolonged PR interval
What is second degree heart block
When some contractions from the atria fail to pass through the AVN and reach the ventricles so there are more P waves than QRS waves
What is third degree heart block
Atrial contractions do not pass through the AVN so Atrial and ventricle rhythms are independent
What are the causes of heart block
Coronary Artery Disease
Cardiomyopathy
Conducting tissue fibrosis
What are narrow complex tachycardias
Supraventricular tachycardias
Rate >100bpm
QRS width <120ms
What are the 4 types of supraventricular tachycardia
Sinus Tachycardia Atrial - flutter - fibrillation - tachycardia
AV nodal re-entry tachycardia
AV re-entry tachycardia
What is sinus tachycardia
When there is excessive activation of the SAN leading to shortened RR intervals
What are the causes of sinus tachycardia
Exercise
Fever
Thyrotoxicosis
What are the risk factors for SVT
MI
Rheumatic heart disease
Pericarditis
What are the causes of SVT
Drugs Alcohol Smoking Congenital WPW MI
What are the symptoms of SVT
Paroxymal attacks, palpitations
Syncope
tachycardia
What features would you see on an ECG of someone with AV nodal re=entry tachycardia
P wave absent or immediately before or after QRS
Normal QRS
What would you seen on the ECG of someone with AV re-entry tachycardia
P waves between QRS complexes
QRS narrow or wide
What ECG features would you see with atrial tachycardia
Abnormal shaped P waves
Normal QRS
Rate >150bpm
What ECG features would you see in atrial flutter
Saw toothed baseline as atria contract
narrow QRS
What ECG features would you seen in atrial fibrillation
No P waves
Irregularly irregular QRS
What is atrial fibrillation
Chaotic irregular atrial rhythm
What is the heart rate in atrial tachycardia
125-250
What is the heart rate in atrial flutter
250-350
What is the heart rate in atrial fibrillation
350+
What are the causes of atrial fibrillation
IHD Rheumatic heart disease Thyrotoxicosis Hypertension Mitral valve stenosis Alcohol PE Post OP
What are the symptoms of atrial fibrillation
Asymptomatic Chest pain Palpitations Dyspnoea Faintness Syncope
What are the signs of atrial fibrillation
Irregularly irregular pulse
Pulse deficit
How do we manage atrial fibrillation
CCB
BB
Digoxin for rate control
Cardioversion for rhythm control
What is the definition of broad complex tachycardias
Rate >100bmp
QRS width >120ms
What are the causes of ventricular tachycardia
Infraction Myocarditis QT interval increases Valve abnormality Iatrogenic (Digoxin, antiarrhytmics) Cardiomyopathy Hypokalaemia
What ECG features do you see in ventricular tachycardia
No p waves
Broad regular QRS
No T waves
What ECG features do you see in Ventricular fibrillation
Shapeless rapid oscillations with no organised complexes
What ECG features do you see in WPW
Accessory conducting bundle
Short PR interval
Slurred upstroke of QRS called delta wave
What ECG features do you seen in hyperkalaemia
Tall tented T waves
Widened QRS
Absent P waves
What ECG features do you see in hypokalaemia
Small T waves
ST depression
Prolonged QT interval
What ECG features do you see in pericarditis
PR depression and saddle shaped ST elevation
What ECG features do you see in hypercalcaemia
QT shortening
What ECG features do you see in hypocalcaemia
QT lengthening
Define shock.
When the cardiovascular system is unable to provide adequate substrate for aerobic cellular respiration.
Give 7 signs/symptoms of shock.
- Pale.
- Sweaty.
- Cold.
- Pulse is weak and rapid.
- Reduced urine output.
- Confusion.
- Weakness/collapse.
What can cause hypovolemic shock?
- Loss of blood e.g. acute GI bleeding, trauma, post-op, splenic rupture.
- Loss of fluid e.g. dehydration, burns, vomiting, pancreatitis.
Classification of shock: describe the vital signs in class 1 e.g. blood loss, pulse, blood pressure, pulse pressure, respiratory rate and urine output.
- 15% blood loss.
- Pulse < 100 bpm.
- Blood pressure - normal.
- Pulse pressure - normal.
- Respiratory rate: 14 - 20.
- Urine output > 30ml/h.
Classification of shock: describe the vital signs in class 2 e.g. blood loss, pulse, blood pressure, pulse pressure, respiratory rate and urine output.
- 15-30% blood loss.
- Pulse > 100 bpm.
- Blood pressure - normal.
- Pulse pressure - decreased.
- Respiratory rate: 20 - 30.
- Urine output: 20 - 30ml/h.
Classification of shock: describe the vital signs in class 3 e.g. blood loss, pulse, blood pressure, pulse pressure, respiratory rate and urine output.
- 30-40% blood loss.
- Pulse > 120 bpm.
- Blood pressure - decreased.
- Pulse pressure - decreased.
- Respiratory rate: 30 - 40.
- Urine output: 5 - 15ml/h.
What can cause cardiogenic shock?
- Cardiac tamponade.
- Pulmonary embolism.
- Acute MI.
- Fluid overload.
What is septic shock?
A systemic inflammatory response associated with an infection (bacterial endotoxins).
What is anaphylactic shock?
An intense allergic reaction associated with massive histamine release = haemodynamic collapse. The patient may be breathless, wheezy and have a rash.
What is the treatment for anaphylactic shock?
Adrenaline and supportive therapy e.g. O2 delivery, fluid replacement.
What is VSD?
An abnormal connection between the two ventricles.
Would a baby born with VSD be cyanotic?
No. There is a higher pressure in the LV than the RV and so blood is shunted from the left to right meaning there is an increased amount of blood going to the lungs; not cyanotic.
Give 4 clinical signs of a large VSD.
- High pulmonary blood flow.
- Breathless, poor feeding, failure to thrive.
- Increased respiratory rate,
- Tachycardia.
- Requires surgical repair.
What syndrome might VSD lead on to?
Eisenmengers syndrome.
Infective endocarditis
Briefly describe the physiology of Eisenmengers syndrome.
High pressure pulmonary blood flow damages pulmonary vasculature -> there is increased resistance to blood flow (pulmonary hypertension) -> RV pressure increases -> shunt direction reverses (RV to LV) -> CYANOSIS!
What are the risks associated with Eisenmengers syndrome?
- Risk of death.
- Endocarditis.
- Stroke.
What are the causes of VSD
Congenital
Acquired post MI
What is the clinical presentation of a small VSD
Loud systolic murmur
Systolic thrill
What is the treatment for VSD
Surgical closure is symptomatic
What might you see on CXR for a small VSD and a large VSD
Small = mild pulmonary plethora
Large = cardiomegaly and marked pulmonary plethora
What is ASD?
An abnormal connection between the two atria; it is fairly common.
Would a baby born with ASD be cyanotic?
No. There is a higher pressure in the LA than the RA and so blood is shunted from the left to right, therefore not cyanotic. - blood flow increased to the right heart and the lungs
Give 5 clinical signs of a large ASD.
- Significant increase in blood flow through the right heart and lungs - pulmonary flow murmur.
- Enlarged pulmonary arteries.
- Right heart dilatation.
- SOBOE.
- Increased chest infection.
- Delayed pulmonary valve closure
- Pulmonary hypertension
What are the complications of ASD
Paradoxical emboli
Eisenmenger’s syndrome
What would you see on the CXR of someone with ASD
Cardiomegaly and pulmonary plethora
Treatment of ASD
Surgical
What is ASVD
Atrio-ventricular septal defects. Basically a hole in the very centre of the heart.
What heart structures are involved in an ASVD
Ventricular septum
Atrial septum
Mitral valve
Tricuspid valve
Give 2 clinical signs of AVSD.
- Breathless.
- Poor feeding and poor weight gain
- Torrential pulmonary flow
What is PDA?
Patent ductus arteriosus.
Give 4 clinical signs of PDA.
- Torrential flow from the aorta to the pulmonary arteries can lead to pulmonary hypertension and RHF.
- Breathless.
- Poor feeding, failure to thrive.
- Risk of endocarditis.
What is the treatment of PDA
Surgical/percutaneous
Local anaesthetic and venous approach
Indomethacin that decreases prostaglandin 2 levels
Describe the pathophysiology behind coarctation of the aorta.
Excessive sclerosing that normally closes the ductus arteriosus extends into the aortic wall leading to narrowing.
What are the signs of aortic coarctation
Weak femoral pulse
Hypertension in right arm
Systolic murmur/ bruit heard over left scapula
What are the complications of aortic coarctation
HF
Aneurysm
Hypertension
What is the treatment for aortic coarctation
Balloon dilation and stenting
Subclavian flap repair
Coarctation angioplasty
What is pulmonary stenosis?
Narrowing of the RV outflow tract.
What are the symptoms of pulmonary stenosis
RVF
RVH
Collapse
Poor pulmonary blood flow
Treatment of pulmonary stenosis
Balloon valuloplasty
Open valvotomoy
Shunt
Name 3 congenital heart defects that are not cyanotic.
- VSD.
- ASD.
- PDA.
Name a congenital heart defect that is cyanotic.
Tetralogy of Fallot.
Right to left shunt.
What are the issues with a bicuspid aortic valve
Develop stenosis more quickly
Degenerate quicker
Develop regurgitation quicker
What is tetralogy of Fallot
Abnormal separation of trunks arterioles into aorta and pulmonary arteries
- VSD
- Pulmonary stenosis
- RVH
- Overriding aorta
What is the presentation of tetralogy of fallot in children and adults
Children - cyanotic episodes, clubbing
Adults - Asympto, cyanosis
What is the treatment for tetralogy of fallot
Surgical (usually before a year)
Closure of the VSD and correction of the pulmonary stenosis
Where do supra-ventricular tachycardia’s arise from?
They arise from the atria or atrio-ventricular junction.
Do supra-ventricular tachycardia’s have narrow or broad QRS complexes?
Supraventricular tachycardias are often associated with narrow complexes.
Where do ventricular tachycardia’s arise from?
The ventricles.
Do ventricular tachycardia’s have narrow or broad QRS complexes?
Ventricular tachycardias are often associated with broad complexes.
What pathophysiological mechanism can cause atrial flutter?
The re-entry mechanism - there is blockage of the normal circuit. Another pathway forms, takes a different course and re-enters the circuit -> tachycardia.
What is the commonest supra-ventricular tachycardia?
AV node re-entry tachycardia (AVNRT).
Do you see P waves in AVNRT?
No - the P waves are within the QRS complex.
Give 4 symptoms of AVNRT.
- Sudden onset/offset palpitations.
- Neck pulsation.
- Chest pain.
- Shortness of breath.
Describe the acute treatment of AVNRT.
Acute treatment: vagal manoeuvre and adenosine.
What drugs might you give to someone to suppress future episodes of AVNRT?
Beta blockers, CCB, flecainide.
Describe the pathophysiology of accessory pathway arrhythmias.
Congenital muscle strands connect the atria and ventricles - accessory pathway. This can result in pre-excitation of ventricles.
Describe the pathophysiology of focal atrial tachycardia.
Another area of the atrium becomes more autonomic than the sinus node and so sinus node function is taken over -> focal atrial tachycardia.
What might you see on an ECG taken from someone with focal atrial tachycardia.
Abnormal P waves appear before a normal QRS.
What is the treatment for ventricular tachycardia in an urgent situation?
DC cardioversion.
What is the long term treatment for ventricular tachycardia in high risk patients?
Implantable defibrillator.
What are ectopic beats?
Very common, generally benign arrhythmias caused by premature discharge. The patient may complain of symptoms of ‘skipped beats’.
Give 3 causes of long QT syndrome.
- Congenital.
- Electrolyte disturbances e.g. hypokalaemia and hypocalcaemia.
- A variety of drugs.
Give 2 signs of long QT syndrome.
- Palpitations.
2. Syncope.
Give 4 causes of sinus bradycardia.
- Ischaemia.
- Fibrosis of the atrium.
- Inflammation.
- Drugs.
Types of second degree AV block: describe Mobitz type 1.
PR interval gradually increases until AV node fails and no QRS is seen.
Types of second degree AV block: describe Mobitz type 2.
There is a sudden unpredictable loss of AV conduction and so loss of QRS. PR interval is constant but every nth QRS complex is missing.
What are the complications of atherosclerotic plaques
Haemorrhage Plaque rupture/fissures Overlying thrombosis Dissection Aneurysm
What is the proper name for arterial debris
Embolism
What is the proper name for arterial narrowing
stenosis
What is the proper name for arterial blockage
Occlusion
What is the pathology of an aortic aneurysm
Degradation of the elastic lamina leading to permanent >50% dilatation of the aorta
What are the causes of aortic aneurysm
Atherosclerotic and collagen diseases (Marfans and vascular Ehlers danlos
Risk factors for aortic aneurysm
Smoking, High BP, atherosclerosis, family Hx, COPD and sedentary lifestyle
What are the symptoms of an abdominal aortic aneurysm
Asymptomatic may be some abdominal/back pain
What are the symptoms of a thoracic aortic aneurysm
Chest and neck pain, compression symptoms
What happens when an aortic aneurysm ruptures
Hypotension, collapse and death
Investigations for aortic aneurysm
Abdominal ultrasound
What is the management of an aortic aneurysm
Surgery or supportive stent implant
- Open aneurysm repair
- Endovascular aneurysm repair
What is the pathophysiology of aortic dissection
Tear in the aortic intima –> High blood pressure into the aortic wall forms a haematoma which separates the intimal from the adventitia creating a false lumen
What are the risk factors for aortic dissection
Atherosclerosis, high BP, cocaine, aortic aneurysm and smoking
What are the symptoms of an initial aortic tear
Sudden severe chest pain, pulse loss and diastolic murmur
What are the later symptoms of aortic dissection
Aortic branch occlusion
What investigations would you do for someone with suspected aortic dissection
ECG and CXR
What is the treatment for aortic dissection
Stenting
Surgery if the dissection is progressing
What is the treatment for peripheral vascular disease
Clopidogrel
What is the pathophysiology of peripheral vascular disease
Atherosclerosis –> Stenosis of peripheral arteries
Partial blockage of leg or peripheral vessels by atherosclerotic plaque and resulting thrombus resulting in insufficient t perfusion of lower limb resulting in lower limb ischamia
What are the symptoms of peripheral vascular disease
Critical leg ischaemia (Rest pain, ulceration, gangrene)
Acute limb ischaemia (Pain, pale, paralysis, paraesthesia, perishing cold, pulseless)
Carotid artery disease (Stroke and TIA)
Abdominal aortic aneurysm (Asymptomatic until rupture occurs)
What diagnostic test confirms peripheral vascular disease
Doppler ultrasonography
What is the treatment of peripheral vascular disease
Modify risk factos
- Exercise and weight control
- Control (Hypertension, hyperlipidaemia, diabetes, anti platelet, smoking cessation)
Revascularisation for critical ischaemia
Amputation
Saddle shaped and PR depression are associated with what condition
Pericarditis
Tall tented T waves and pathological Q waves are associated with what condition
Hyperkalaemia
ST elevation is associated with what condition
STEMI
Absent P waves is associated with what condition
Atrial fibrillation
ST depression is associated with which condition
Angina
Pain when lying down but alleviated by leaning forward is associated with what condition
Acute pericarditis pain
Early diastolic murmur is associated with what condition
Mitral stenosis
Early systolic click murmur is associated with what condition
Mitral valve stenosis
Ejection systolic crescendo decrescendo murmur is associated with what condition
Aortic stenosis
Pansytolic murmur is associated with what condition
Mitral regurgitation
increasing cGMP and reducing intracellular Ca2+ is the Mechanism for which drug class
Calcium channel blockers
Inhibition of COX and thromboxane A2 is the mechanism for which drug class
NSAIDs
Inhibition of vitamin K production is the mechanism for which drug class
Warfarin
Inhibition of thrombin and factor Xa is the mechanism of which drug class
heparin
In infective endocarditis, which of the following is not seen on the hands Roth spots Janeway lesions Oslar nodes Splinter haemorrhage Clubbing
Roth spots
What is the diagnostic test for HF
BNP as levels increase when you have ventricular dysfunction
What compound is responsible for the cough associated with ACE inhibitors
Bradykinin
