Ses 6 Cvs Arrythmia And Circulation (bice) Flashcards
Veins how do they drain notion
Superficial veins within the subcutaneous tissue
perforating veins running from superficial to deep veins.
Deep veins below deep fascia and between muscles.
Varicose veins cause, complications, symptoms, risk factors
Varicose veins – valves ineffective and blood movement is slow or even reversed.
Walls of veins weaken → varicosities develop and valve cusps separate, becoming incompetent.
Veins tend to be tortuous and twisted.
Saphenous veins are common site of pathology.
Complications:
Development of chronic venous insufficiency - reflux or obstruction → venous hypertension
Superficial vein thrombophlebitis (inflammatory processes resulting from a clot in vein). Painful erythematous follows varicose veins increased risk of DVT.
Lipodermatosclerosis (inflammation and thickening of fat layer under the skin)
Haemosiderin staining – brawny oedema
Venous ulceration
Symptoms - Heaviness and aching, muscle cramps and throbbing, ankle swelling, varicose eczema, haemorrhage from damaged veins.
Risk factors - Age, family history, female sex, number of births, occupation-standing allot
Explain the role and functioning of the calf muscle pump
Soleus and gastrocnemius muscles contribute to pushing blood against gravity
back towards the heart.
Valves open → blood pushed through to deep veins → valves close. Superficial to deep to heart.
Venous pressure in the foot reduced during exercise (compared to standing still).
Venous eczema and ulceration cause and presentation
Eczema - chronic, itchy red and swollen
tight and can lead to lipodermatosclerosis –
hard to the touch compared to other fatty
tissues above or below
Ulcer - chronic, painful, often develop around
hard nodular areas like medial malleolus
Treat ulcer and cause!
- Result of venous hypertension
calf muscle pump failure
Need to be using calf muscles properly – plantar flexion of the
ankle joint during walking
Who is at risk? • Deep vein incompetence – retrograde flow – system overwhelmed • Superficial vein incompetence – superficial → deep becomes deep
→ superficial
calf muscle pump “overflows”
Gait
Treatment- Ligation and vein stripping to treat – improves ulceration
Arterial + venous Thrombosis characteristics + Virchow’s triad
Arterial thrombosis
- atheroma
platelet rich – activated platelets – aggregate – plaque formation
Venous thrombosis
- stasis and usually another factor eg trauma, medication, dehydration, pregnancy.
Low flow and little platelet component, fibrin rich.
Triad:
Stasis
Hypercoagubility
Vessel wall damage
DVT what is it, consequences and signs
Clotting of blood in a deep vein – commonly calf
Consequences:
Impaired venous return
Inflammatory response produced following thrombosis
- pain, swelling, redness
Fatal - pulmonary embolism
Signs:
Calf tenderness + warmth
distended and visible superficial veins - oedema
Pyrexia with no other obvious cause
Asymmetry
Differential diagnoses – soft tissue trauma,
cellulitis, lymphoedema
Wells score – pre test probability forms part of diagnosis
-all suspected DVT patients
Why does surgery inc risk of DVT and how to prevent
during surgery - Stasis – no calf muscle pump
after surgery - trauma – cutting means blood in prothrombotic state
Prevent by:
Promote mobility soon after surgery
Prophylaxis (anticoagulants) ↓DVT associated with surgery
Gradient stockings
Collateral circulation
Physiological design to limit incidence of acute ischaemia when you flex a joint eg knee(genicular branches of popliteal artery), shoulder, hip
Or
Adaptive response to stenosis of a major vessel over a period of months or years.
Angiogenesis
Sprouting- FGF(fibroblast GF) produced by mesenchymal cells • Pericytes convert into smooth muscle cells • Slow, takes hours to days
Intussusception - Twinned vessels from primary vessel - multiple GFs - quick, mins to hrs
Acute limb ischaemia
Occlusion occurs acutely – minutes to days – no collateral circulation can develop in this time
Trauma and embolism - atrial fibrillation, popliteal artery aneurysm,
sudden rupture of atherosclerotic plaque
6 Ps
Pain - initially
Pallor*
Perishing with cold*
Pulseless
Paraesthesia*
Paralysis or reduced power*
* may be subtle –compare both limbs
imaging → angioplasty/thrombectomy/intra-arterial thrombolysis or amputation.
Compartment syndrome can be a complication if revascularisation possible.
Chronic peripheral arterial disease notion
Can be considered in similar terms to coronary artery disease
intermittent claudication of the lower limb (or upper limb) • Claudication – cramping pain in the leg induced by exercise
caused by atherosclerosis
exercise induced – like stable angina (oxygen demand/supply ratio disupted) • Pain goes away upon rest “only painful when I am walking”
• Management - exercise, smoking cessation,
antiplatelet drugs, angioplasty, bypass graft
Ankle-brachial pressure index (ABPI)
• ABPI part of early diagnostics for peripheral artery disease
• Divide ankle systolic by brachial systolic
• ABPI <0.8 suggests presence of peripheral artery disease
Pathology of claudication
atheroma → atherosclerosis of
superficial femoral artery • Present with calf claudication • Untreated becomes critical ischaemia - dry gangrene
Where the stenosis is identified will dictate where the claudication
presents and which pulses can be palpated
Critical limb ischaemia
Progression of chronic peripheral vascular disease
rest pain - blood supply so poor pain at rest– like unstable angina
“hanging foot out of bed relieves pain” - gravity to perfuse leg
untreated leads to ulceration and gangrene – viability of limb severely compromised – like AMI • Strong pain relief likely needed at this stage
• Referral to vascular surgical unit immediately
– extent of threat to limb survival dictates action
– imaging → angioplasty/thrombectomy/intra-arterial
thrombolysis or possibly even amputation
Palpation of lower limb pulses - watch videos
Femoral pulse – felt at the mid inguinal point
Popliteal pulse – deep in the popliteal fossa - inferior to vein
Dorsalis pedis pulse – just lateral to extensor hallucis longus tendon
Posterior tibial pulse – just behind the medial malleolus
Doppler ultrasonography
Sonogram using ultrasound and the Doppler effect to measure real-time flow and velocity
Useful for estimating flow and velocity of blood:
- in the heart as part of echocardiogram – heart failure, valve disease etc.
- in distal vessels – legs when diagnosing peripheral arterial disease
atheroma → stenosis → turbulence
• Echoes produced from moving blood that are detected and computed into flow direction and velocity.
echoes from stationary tissues are the same from pulse to pulse so able to differentiate echoes from moving objects – blood!
Velocity increases through stenosis which can be measured using Doppler
Think about squeezing a hosepipe when water is flowing
the velocity increasing – water reaches further
4 basic classes of anti-arrhythmic drugs and explain and 1 example
I. Drugs that block VG Na+ - lidocaine- Only blocks VG Na+ channels in open or inactive state.
PREFERENTIALLY BLOCKS DAMAGED MYOCARDIUM to prevent inappropriate spread of electrical activity (as they can which can spontaneously depolarise causing arrhythmias).
Will dissociate in time for the next AP.
Prevents ectopic pacemaker activity.
II. Antagonists of β-adrenoreceptors eg bisoprolol:
Block sympathetic action.
Decrease slope of pacemaker potential in SA so more time taken to initiate action potential.
SLOWS CONDUCTION TO AV NODE which means more time taken between depolarisation of atria and ventricles SO PREVENTS SVT.
Used following MI (inc SNS) and reduces O2 demand which reduces myocardial ischaemia.
Reduces force of contraction (β1) but also acts on bronchial smooth muscle (β2) - bronchoconstriction.
III. Drugs that block potassium channels
Prolong the action potential which should lengthen ARP but can be pro-arrhythmic and prolong QT interval.
amiodarone (special as it blocks everything) used to treat tachycardia associated with Wolff-Parkinson-White syndrome and for supressing ventricular arrhythmias post MI.
IV. Drugs that block calcium channels - verapamil
Decreases slope of action potential at SA node
• Decreases AV nodal conduction • Decreases force of contraction
So useful for other conditions eg hypertension, angina
Explain how arrhythmias can arise
Tachycardia:
1. SA node firing too fast (this causes sinus tachycardia - supraventricular)
2. Ectopic pacemaker activity – damaged area of myocardium becomes depolarised and spontaneously active due to ischaemia - takes over SA node
3. Afterdepolarisations
4. Re-entry loop ( atrial flutter, multiple = atrial fibrillation)
– AV nodal re-entry
– re-entry by accessory pathway (allows depolarisation to bypass AV node and spread from atria to ventricles) - Wolfe Parkinson white
Bradycardia:
Sinus bradycardia
1. Sick sinus syndrome - Intrinsic SA node dysfunction where it fires too slowly – other area in atria can take over and cause SVT to compensate.
- Conduction block at AV node or bundle of His
Heart blocks - 1, 2 (Mobitz 1 and 2), 3
Afterdepolarisations - tachycardia notion
Early after-depolarisations
• become depolarised again during repolarisation phase as cells are irritated.
leads to oscillations - see graph on notion
• More likely to happen if AP duration is prolonged - Longer AP means longer QT interval on ECG
Happen due to low electrolytes eg low K+
Also certain drugs eg anti-arrhythmics(Ca2+, Na2+, K+ channel blockers), anti-psychotics
Delayed after-depolarisation
Longer upstroke as some Na+ channels deactivated so more time to reach threshold but faster repolarisation. Cell irritated, can happen due to ectopic activity.
• Be self-perpetuating causing oscillations
• More likely to happen if intracellular [Ca2+] is high
• May involve Na+-Ca2+ exchanger
Re-entry notion has better explained
Myocardium is damaged so there is unidirectional block - electrical impulse can take an alternative route that travels backwards - spreads the wrong way through the damaged area - loop of excitation.
In atrial flutter electrical impulse travels in a loop in the RA.
AV nodal re-entry
AV re-entry - there is an accessory pathway between atria and ventricles leads which can have a re-entry loop. E.g. Wolff-Parkinson-White syndrome.
atrial fibrillation
Multiple small re-entrant circuits in the atria
Adenosine -what is it used for and mechanism
USED FOR TERMINATING RE-ENTRANT SVTs
Adenosine - Produced endogenously but can be administered
Acts on adenosine coupled G proteins and inc K+ conductance so hyperpolarises so transient AV node block so terminates SVTs.
Reduces funny current by reducing cAMP so dec SA node pacemaker potential
has a very short half-life
General - other drugs acting on CVS and conditions
ACE inhibitors and AngII receptor blockers -heart failure + hypertension + angina
Diuretics - hypertension+ heart failure + angina+ coronary artery spasm
Dihropiridine Calcium channel antagonists - hypertension
Positive inotropes - cardiac glycosides (arrhythmias as well as they enhance vagal input) and beta agonists - cardiogenic shock + acute but reversible heart failure
Alpha adrenoceptor blocker and Beta blockers - chronic/stable heart failure + hypertension
Antithrombotic drugs
Organic Nitrates - angina
Diuretics
Decrease preload and afterload by decreasing blood volume. Eg furosemide
Used in heart failure and hypertension
Loop diuretics useful in congestive heart failure - Reduces pulmonary and peripheral oedema
Dihydropyridine Ca2+ channel blockers
Amlopidine
Dihydropyridine Ca2+ channel blockers act on vascular smooth muscle
Decrease peripheral resistance – Decrease arterial BP – Reduce workload of the heart by reducing afterload
Used in hypertension, angina, coronary artery spasm, SVTs
ACE inhibitors- remember from hypertension lecture
AngII receptor blockers
dry cough (excess bradykinin)
Important in heart failure by dec after and preload by dec vasoconstriction ( so dec CVP) and blood vol (by dec angiotensin 2 and aldosterone so lower arterial BP)
AngII receptor blockers- (when patients can’t tolerate ACE)
Positive inotropes
Cardiac glycosides – Example: digoxin
β-adrenoreceptor agonists – Example: dobutamine
Positive inotropes increase contractility and thus cardiac output
CG:
Primary mode of action is to block Na+/K+ ATPase which leads to inc in intracellular Na+
decrease in activity of Na+-Ca2+ exchanger so intracellular Ca2+ inc - Increased force of contraction
Used in arrhythmia as they slow AV conduction by inc vagal activity.
Don’t use for heart failure as no long term benefit.
Selective β1 – adrenoceptor agonist
– Stimulates β1 receptors present at SA node AV node and on ventricular myocytes
• cardiogenic shock • acute but reversible heart failure (eg following cardiac surgery)
Adrenoreceptor antagonists
Beta blockers - Bisoprolol and adrenaline - CHD eg angina
slows heart rate and reduces force of contraction (β1) but also acts on bronchial smooth muscle (β2) - bronchoconstriction
Alpha 1 - prazosin
vasodilation - inhibits NA action on vascular smooth muscle
anti-hypertensive agent
How to treat angina - 2 main ways and drugs for each
What is it - O2 supply does not meet needs - ischaemia of heart tissue
Reduce the work load of the heart
1. Organic nitrates - venodilation
NO activates guanylate cyclase —> Increases cGMP —> Lowers intracellular [Ca2+] —> Causes relaxation
Dec preload - dec force of contraction- lower O2 demand of heart
2. β-adrenoreceptor blockers - dec HR - more time in diastole
3. Ca2+ channel antagonists
Or
Improve the blood supply to the heart
1.Ca2+ channel antagonists
2. Minor effect of organic nitrates - dilation of coronary collateral arteries
What could Antithrombotic drugs be used for, name and how do they work
Atrial fibrillation
Acute myocardial infarction
Prosthetic heart valves
Anticoagulants - prevent venous thromboembolism:
– Heparin - inhibits thrombin, used acutely
– Warfarin (given orally) - antagonises action of vitamin K
Antiplatelet drugs
– Aspirin - following acute MI or high risk of MI - blocks thromboxane A2 and ADP secretion from platelets.
How does automacity affect heart
slow conduction at AV/SA node due to inc vagal tone:
Sleeping
Athletes
Inferior MI
Slowing at AV node:
extrinsic factors - beta blockers, Ca2+ channel blockers, digoxin
Dec metabolic activity - Hypothyroidism, hypothermia
Hyperkalemia
Inc in intracranial pressure - Cushing’s triad - inc HR, hypertension, irregular resp rate
Inc SNS tone due to:
Hypovalaemia
Hypoxia - PE, anaemia, lung diseases
Inc metabolic activity - fever, hyperthyroidism
Pain + anxiety
Sympathomimetics
