Cardiovascular Lecture ILO’s Flashcards
Mean Arterial Blood Pressure =
Cardiac Output x Total Peripheral Resistance
Describe the pathological process that leads to hypertension:
Risk Factors for ATHEROMA
A - Arterial Hypertension
T- Tobacco
H- Hereditary (Familliar Hypercholesterolaemia)
E- Endocrine (diabetes, hypothyroidism, postmenopausal oestrogen deficiency)
R- Reduced physical activity
O- Obesity
M- Male gender
A- Age
Common sites: Aorta, Coronary, Carotid, Cerebral, Renal, Iliac, femoral, popliteal and intestinal arteries.
Complications of atheroma
Developed atheroma can lead to thrombosis or aneurysm
Expansion of intima reduces the size of the vessel lumen
Reduced perfusion can lead to transient or permanent ischaemia.
• Coronary arteries -> angina
• Leg arteries -> intermittent claudication
• Mesenteric arteries -> ischaemic colitis
• Cerebral and vertebral arteries -> cerebrovascular events
• Severe ischaemia from partially occluded vessels can cause infarction
Describe the key factors that contribute to BP regulation
• Circulatory volume (therefore stroke volume)
• Force of ventricular contraction
• Elasticity of arteries
• Peripheral resistance
Describe the role played by arterial baroreceptors and atrial stretch receptors
Atrial stretch
When venous return is raised (e.g. in the case of increased circulatory volume):
Atrial myocytes release atrial natriuretic peptide (ANP), which is a vasodilator and
1. Promotes Na+ excretion – H20 follows
2. Inhibits secretion of ADH (antidiuretic
hormone or vasopressin)
Describe the circumstances in which hypotension or hypertension may arise
Stress
Hormonal Factors
Type 2 Diabetes
Shock
Orthostatic (postural) hypotension
Dehydration
Arrhythmias
Shock (from severe infection, stroke, anaphylaxis, major trauma, or heart attack)
Describe the role of the renin angio tensin aldosterone and other hormonal systems play in longer term regulation of blood pressure
• Renin-Angiotensin- Aldosterone System
Renin is released from cells in the walls of the afferent arterioles of kidney glomeruli.
It is released in response to lowered kidney perfusion pressures caused by, amongst other things, lowered BP.
Renin acts on a protein called angiotensinogen (gen – erates angiotensin) and cleaves this precursor at specific sites to form angiotensin I (which is inactive)
Angiotensin converting Enzyme (ACE) then converts angiotensin 1 to angiotensin 2
Angiotensin 2:
Potent vasoconstrictor
Stimulates ADH production
Activates aldosterone secretion (increases sodium production)
• Adrenaline
(Shifts the blood from one place to another)
Released from the adrenal medulla in response to lowered BP.
Does two things:
1. Speeds heart rate and force of ventricular contraction.
2. Dilates the skeletal muscle and constricts splanchnic vascular beds.
Therefore: increases cardiac output and systolic BP, but often has little effect on mean arterial BP
• Antidiuretic hormone
(ADH, vasopressin)
Released from the posterior part of the pituitary in response to decreased blood pressure and increased plasma osmolality. Release is slowed by ethanol/alcohol
Two mechanisms of action:
Promotes reabsorption of water in the kidney
Constricts blood vessels if present at a high enough concentration.
Thus, ADH increases SV and TPR, keeping BP up
• Atrial natriuretic peptide (ANP) (decreases blood pressure)
Released from the atria in response to stretch by increased blood volume.
Three mechanisms of action:
1. Promotes sodium (and thus water) excretion in the kidney.
2. Inhibits ADH and aldosterone secretion. 1. Acts as a vasodilator.
4. Can slow renin release.
Thus, ANP lowers SV and TPR, keeping BP down
Describe the different types of muscle.
Smooth, skeletal and cardiac.
Skeletal:
Connected to bone, striated, voluntary, high power, usually relaxed, different fibres for different energy systems, fatigue, multi nucleated, cells fees together
Cardiac:
Striated, Involuntary, High power, Pump (cyclic), uninucleated, non fatiguing
Smooth:
Location hollow organs, Smooth, Involuntary, Low power, Usually contracted
Explain the sliding filament theory:
• Calcium ions diffuse into myofibrils from sarcoplasmic reticulum
• Ca2+ cause movement of tropomyosin on actin
• This movement causes exposure of the myosin head binding sites on the actin
• Myosin heads attach to binding sites on actin forming actinomyosin bridges
• Hydrolysis f ATP on myosin heads causes them to nod
• Nodding pulls actin molecules over the myosin
• Attachment of a new ATP to each myosin head causes myosin heads to detach from actin sites and separates it from actin, returning to its original shape
Describe an action potential within a neurone:
• Voltage gated sodium channels open and sodium diffuse into the axon
• This reverse potential difference across axon membrane to +40 mV (depolarisation)
• Voltage gated sodium channels close and voltage gated potassium channels open, potassium diffuses into the axon reversing the potential difference across the membrane as the axon becomes more negative (repolarisation)
• Potassium channels remain open and the membrane become hyperpolarised (-90mv, below resting potential)
• The sodium potassium pump re establish resting potential
Describe how a resting potential is established within a neurone:
• 3 sodium out
• 2 potassium in
• Via sodium potassium pump
• In axon cell membrane
• Per ATP
• Membrane impermeable to sodium ions (all sodium ion channels closed)
• Some potassium channels open
• Potassium moves back out down electrochemical gradient
• Overall uneven disruption of ions resulting in more negative -70mv resting potential in the neurone
Describe how an action potential is carried across a cholinergic synapse
• Action potential arrives at the pre synaptic knob and causes voltage gated calcium ions to diffuse in to the neurone
• This causes synaptic vesicles to move to the pre synaptic membrane and release acetylcholine into the synaptic cleft
• Acetly choline diffuses across the synapse and binds to receptors on the post synaptic membrane
• This causes voltage gated sodium channels to open and sodium diffuses into the post synaptic neurone
• If enough sodium enters, an action potential will be generated
• Acetyl choline is broken down by cholinesterase and products are taken up by pre synaptic membrane.
P Wave
Depolarisation of atria
Right atrial activation begins first
Relatively little muscle
Small amplitude
Normal P waves may have a slight notch
P-R Interval
•Time for conduction through AV node, Bundle of His, Purkinje fibres
•Time from onset of atrial depolarisation to onset of ventricular depolarisation
•Measured from start of P wave to 1st deflection of QRS complex (irrespective of whether the QRS complex begins with a Q wave or an R wave)
•Duration 0.12 – 0.20 s (3small squares to 5small squares)
If prolonged- AV node problem eg heart block
QRS Complex
0.08-0.12s (3ss)
Problem with impulses in ventricles if abnormal
● Ventricular Depolarisation
● Large muscle mass of LV results in
QRS predominantly representing LV
Definitions
Q Wave: Any initial negative deflection
R Wave: Any positive deflection
S Wave: Any negative deflection after R
Normal Values
QRS Duration: < 120 ms
R wave height variable
S wave depth < 30 mm
Q waves:
•Normal Q waves can be found in leads facing the left ventricle (I, II, aVL, V5, V6 )
•Occasionally occur in lead III
•< 2 mm in depth ( two small squares)
•< 40 ms in duration (one small square)
ST Segment:
• QRS complex ends at J Point
• ST Segment: J Point to start of T Wave
• End of ventricular depolarisation to beginning of
repolarisation. Muscle is depolarised and is contracting -
isoelectric ≠ inactive!
• Usually level ± 1 mm from baseline - may slope slightly upwards
QT Interval
0.36 - 0.45/0.47s men/female
If prolonged could be ventricular tachycardia
Total time for depolarisation & repolarisation of the ventricles
T and U Wave
T Wave
• Ventricular repolarisation
• Asymmetrical
• Rarely exceeds 10 mm
U Wave
• Small deflection after T Wave
• Many ECGs have no discernable U Wave
How to work out heart rate on an ECG?
300/ RR interval (in big squares)
Which part of the heart does V1 - V6 measure on an ECG?
V1 - V2 Septum
V3 - V4 Anterior
V5 - V6 Lateral
What is the difference between stable and unstable angina?
Stable- predicted by exercise/ change in temp
Relived by GTN spray
Unstable- sudden deterioration in angina symptoms
No ST elevation or raised troponin levels
What is the difference between a STEMI and NSTEMI
STEMI- Complete blockage by thrombus
ST Elevation
Plaque ruptures leading to thrombosis
Myocardial ischemia with irreversible necrosis
NSTEMI- narrowing of the arteries
Myocardial necrosis present
Risk of progressing to STEMI
Describe the two methods of reperfusion therapy:
Primary PCI- putting in a wire through the femoral artery high blasts away thrombus
Thrombolysis
Secondary prevention of CAD
Low dose aspirin - decrease risk of death by 25%
Statins
Smoking
Diet and weight modifications
Limit alcohol
Increased exercise
Control diabetes/ alcohol
Describe the secondary prevention medical management after an MI (6A’s)
Aspirin - 75 mg once daily
Another antiplatelets eg clopidogrel or ticagrelor (low risk of bleeding) for up to 12 months
Atorvastatin - 80mg once daily
ACE Inhibitors (eg ramipril titrated as tolerated to 10mg once daily)
Atenolol or other beta blocker (bisnoprolol) titrated as high as tolerated
Aldosterone antagonist for those with clinical heart failure (ie eplerenone titrated to 50mg once daily)
NICE guidelines for stable angina:
Either a beta blocker or a calcium channel blocker first line
If the symptoms are not adequately controlled (or cannot tolerate) consider switching to an alternative or use a combination of the first two
If the patients symptoms are not adequately controlled by one or a combination then consider a third line – long acting nitrate, ivabradine or ranolazine
If in combination with a beta blocker – not verapamil or diltiazem
Only if patient cannot tolerate calcium channel blockers or beta blockers should monotherapy with nitrate, ivabradine or ranolazine be offered.
Triple therapy should be considered whilst awaiting revascularisation
Management of NSTEMI/ Unstable angina:
Sub lingual GTN or IV nitrates § Morphine
Oral Beta Blockers
Aspirin
Ticagrelor / Clopidogrel § ACE inhibitor
Statin
Fondaparinux
Acute NSTEMI treatment:
B- Beta blockers unless contraindicated
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative)
M – Morphine titrated to control pain
A – Anticoagulant: Low Molecular Weight Heparin (LMWH) at treatment dose (e.g. enoxaparin 1mg/kg twice daily for 2-8 days)
N – Nitrates (e.g. GTN) to relieve coronary artery spasm
O - oxygen only if their oxygen saturations are dropping (i.e. <95%).
Initial treatment for MI:
§ Pain relief & antiplatelets
§ Diamorphine / Morphine
§ Oxygen
§ Sublingual GTNitrate or IV
§ Aspirin
§ Cyclizine or metoclopramide
§ Thrombolysis with or without heparin
§ IV beta blockers, IV nitrates (if suitable)
§ Aspirin , ACE inhibitors , oral beta blockers . Lipid lowering agents, dual antiplatelets
§ Angiography as needed , revascularisation as needed
Chest Pain consultation
SOCRATES
• Site: Where exactly is the pain?
• Onset: When did it start, was it constant/intermittent, gradual/ sudden?
• Character: What is the pain like e.g. sharp, burning, tight?
• Radiation: Does it radiate/move anywhere?
• Associations: Is there anything else associated with the pain, e.g. sweating, vomiting.
• Time course: Does it follow any time pattern, how long did it last? • Exacerbating / relieving factors: Does anything make it better or
worse?
• Severity: How severe is the pain, consider using the 1-10 scale?
What is an aortic dissection and how is it diagnosed?
Aortic dissection/ intra-mural haematoma
Tear between intima and media in the aorta due to high pressure environment.
Often described as a tearing pain and often the worst pain they have experienced in their life time.
The pain may radiate from the chest to the back and sometimes to the abdomen.
Often has a sudden onset and can be associated with syncope and sudden collapse.
Chest X ray often shows widened aortic arch.
Can be diagnosed by contrast CT, aortic MRI or transoesophageal echocardiography
• CT scan is the most commonly used due to its high diagnostic accuracy and widespread availability.
• MRI can be used and is considered to be the gold standard but due to poor availability often not used.
How is aortic dissection treated?
TYPE A dissection (ascending aorta) MORE COMMON
Surgery as medication to lower blood pressure has poor response rate.
Surgery involves root repair / grafting.
TYPE B dissection (descending aorta)
Type B dissection/haematomas (descending aorta) are usually managed medically (surgery doesn’t affect overall outcomes)
• Emergency treatment is with rapid titratable beta-blockade with labetalol most commonly used.
• Aggressive blood lowering medication is then used using standard combinations of antihypertensive mediation and following the ACD antihypertensive management Rule.
• Some patients appear to benefit from subsequent aortic endovascular repair (stenting )
What is pericarditis?
• Pericarditis is an inflammation of the membrane surrounding the heart called the pericardium.
• Characteristic changes are visible in the ECG. Similar ST elevation but different to STEMI changes.
• Viral and bacterial infections may sometimes be the cause of the inflammation.
The chest pain of pericarditis however is aggravated by deep breathing and influenced by changes in body position.
• The pain eases for example when the breath is held or if the patient leans forward.
• Frequently pericarditis mistaken for MI as has similar Signs & Symptoms and similar but different ST elevation on the ECG.
What is the treatment for pericarditis and how does it sound?
NSAIDS - ibroprofen
PPI omeprazole
Pericardiocentris (needle in heart t drain fluid if patient is unstable)
Friction rub is how it sounds
What is myocarditis?
Involves infection of the heart causing inflammation to the myocardium.
Often due to infection by common virus (parvovirus B19) and other less common infections such as Lyme disease.
Often recent history of viral infection including fever, rash diarrhoea, sore throat and joint pain.
Myocarditis can occur alone or often seen along with pericarditis.
Typically patient presents with raised CRP and ESR and has ECG changes similar to pericarditis (saddled (bend in ST elevation). Elevated troponin levels.
Describe Costrocondritits (Tietze’s Syndrome).
Inflammation and swelling of the cartilage between the rib & breastbone(costochondra l or chondrosternal joint) is known as Tietze’s syndrome.
Such chest pain tends to be superficial rather than deep, is aggravated by breathing, and is very tender if the area is pressed.
• In female patients it can be missed diagnosed as mastitis pain.
• In Tietze’s syndrome pain is localised but can radiate to arms and shoulder.
• Often results from repeated coughing, sneezing or vomiting or sometimes from impacts to the chest.
What is the name of fluid in the capillaries and the interstitial space?
Capillary - plasma
Interstitial space- interstitial fluid
Fluid moves from the arterial end of the capillary into the interstitial space
Fluid moves from the interstitial space back into the capillary at the venous end
Describe capillary exchange.
Capillary blood pressure (CPB) pushes fluid out of the capillary into the interstitial fluid (taking nutrients, gases etc) - filtration
Blood colloid osmotic pressure (BCOP) pulls fluid back into capillary (bringing wastes, gases etc) – reabsorption - BCOP is mainly due to plasma proteins - re absorption
CBP decreases with progression along capillary where as BCOP remains relatively constant
CBP is greater than BCOP at the arterial end → filtration BCOP is greater than CBP at the venous end → reabsorption
Approximately 85% of fluid is reabsorbed
The remainder must be removed from the interstitial space otherwise oedema will result
The remaining 15% is picked up by the lymphatic capillaries
Describe the removal of excess interstitial fluid:
Lymph capillaries are blind ended tubes that are located adjacent to capillary beds
The excess interstitial fluid enters the lymphatic capillary and is called lymph Lymph passes through the lymphatic circulation and returns to the blood system
Describe the order of lymphatic drainage.
lymph capillaries
lymph vessels
lymph nodes
lymph trunks
thoracic duct (near bottom rib) drains lymph from remainder of the body - left subclavian vein
or
right lymphatic duct (near first rib) drains lymph from the right side of the head and thorax and right upper limb - right subclavian vein
Therefore lymph re enters the blood vascular circulation
How would a patient describe their palpitations?
Fluttering
Flip Flop
Pounding
Actual definition - unpleasant awareness of forceful, rapid or irregular beating of the heart
Benign vs life threatening?
Remember its a symptom and not a diagnosis
Name some general causes of palpitations.
Cardiac 43%
Psychiatric 31%
Miscellaneous (drugs, caffeine, thyroid etc) 10%
Unknown 16%
Name some cardiac causes of palpitations.
Cardiac arrhythmias due to:
• Underlying structural heart disease (e.g, cardiomyopathy, prev. MI)
• Identifiable conduction abnormality (e.g, long QT syndrome, WPW, complete heart block) • Idiopathic
• Tachyarrhythmias, bradyarrhythmias, ectopic beats
• Valvular heart disease (e.g mitral valve prolapse)
• Pacemaker syndrome (AV dysynchrony due to single chamber pacing)
• Atrial myxoma (tumour)
• High output cardiac states
Cardiac etiology of palpitations:
More common if:
Male
Described as irregular
Personal history of heart disease
Lasting longer than 5 mins
Non cardiac causes of palpitations
Psychiatric disorders
• Panic attacks
• Anxiety and Stress
• Generalised anxiety disorder
• Somatization
Other causes
• Medications
• Substance abuse
• Endocrine disorders
• Metabolic abnormalities
• Caffeine, nicotine
• Exercise
• Phaeochromocytoma
• Pregnancy
• Fever
Which narrow complex tachycardia has an abnormal p wave before the regular QRS complex?
Atrial tachycardia
Which narrow complex tachycardia has regular QRS complexes however has flutter waves
Atrial flutter
Which narrow complex tachycardia has no PO waves or atrial activity just after regular QRS complexes?
AVNRT or AVRT
Which narrow complex tachycardia has multiple p waves morphologies before irregular QRS complexes?
Multi focal atrial tachycardia
Which narrow complex tachycardia has flutter waves and irregular QRS complexes?
Atrial flutter with variable conduction
