Cardiovascular Flashcards
haemodynamics equations
Pulse pressure (PP) = systolic blood pressure (SBP) - diastolic blood pressure (DBP)
Mean arterial pressure (MAP) = DBP + (SBP-DBP)/3) = DBP + 1/3 PP
Cardiac output (CO) = Heart rate (HR) x Stroke volume (SV)
BP = CO x Total peripheral resistance (TPR)
ECG leads- which view is seen from each lead+ placement of chest leads
insert picture of table from session 6, lecture 2
acute limb ischaemia presentation
6 P’s Pain Pallor Perishing with cold Pulseless Paraesthesia Paralysis/ reduced power
pacemaker potential
If (funny current, HCN channels) cause slow depolarisation of pacemaker cells.
triggers upstroke by VG Ca2+ channels.
downstroke caused by repolarisation through voltage gated K+ channels.
ventricular myocyte AP
K+ permeability sets the resting membrane potential close to Ek.
Depolarisation from adjacent myocytes triggers rapid Na+ influx from fast Na+ channels.
Initial repolarisation due to outward VG K+ channels.
plateau due to opening of L-type Ca2+ channels.
Ca2+ channels close and VG K+ channels open returning to resting MP
Secondary prevention of MI
BADS
B- beta blockers
A- ACEi or ARBs
D- dual antiplatelet therapy
S- statin
types of shock
distributive shock- profound peripheral vasodilation and increased TPR e.g anaphylactic shock/ toxic shock (sepsis)
hypovolaemic shock- reduced blood volume e.g from haemorrhage
cardiogenic (pump failure) shock- acute failure of heart to maintain cardiac output e.g MI
mechanical shock- restriction of filling of heart e.g cardiac tamponade
Locations to auscultate different valves
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Aortic= right 2nd IC space Pulmonary= left 2nd IC space Tricuspid= left lower sternal border (4th IC space) Mitral= 5th left IC space @ mid clavicular line
beta adrenoceptor blockers/ beta blocker action
e.g propranolol/atenolol, blocks sympathetic action acting @ beta 1 adrenoceptors
Slows If, therefore prolongs pacemaker potential and slows conduction @ avn
Used following MI, can prevent supraventricular tachycardia and ventricular arrhythmia, also decreases O2 demand
Ca2+ channel blocker action+ examples
e.g verapamil, diltiazem
Decreases slope of action potential @ SAN, decreases AVN conduction
Also -ve inotropic effect + some coronary/peripheral vasodilation
adenosine mechanism of action
Acts on alpha 1 receptors but v short half life
Enhances K+ conductance therefore hyperpolarises conducting cells
Anti-arrhythmic + used to terminate re-entrant SVT, produced endogenously but also can be administered intravenously
action, uses + examples of cardiac inotropes
e.g Cardiac glycosides (digoxin), beta-adrenergic agonists (dobutamine)
improve symptoms of HF but not outcome, blocks Na+/K+ ATPase
increases i[Na+], which decreases Na+/Ca2+ exchanger activity, increased Ca2+ stores in SR leads to +ve inotropy
Cardiac glycosides also increase vagal activity, slows AV conduction and therefore HR, used w/ arrhythmia such as AF
Organic nitrates- action+usage
Primary action is VENODILATION-lowers preload thus less workload
Secondary action is on coronary collateral arteries, improving O2 delivery to the ischaemic myocardium
Antithrombotic drugs and uses
prevention of venous thromboembolism (from Afib/ DVT)- heparin (given intravenously), warfarin (given orally)
Following MI/ high risk of MI- antiplatelet drugs prevent arterial thrombus formation e.g Aspirin
Hypokalaemia signs, symptoms and ECG changes
K+ level <3.5mmol/L, moderate <3mmol/L, severe <2.5mmol/L
decreased extracellular potassium leads to myocardial excitability- palpitations, arrhythmia, cardiac arrest
increased amplitude + width of P wave, prolonged PR, T wave flattening + inversion, ST depression, prominent U waves
