Cardiac CPGs Flashcards
ACS definition
A spectrum of conditions
ranging from unstable angina to NSTEACS to STEMI, which all share common pathophysiology of a disrupted atherosclerotic lesion, followed by superimposed thrombus formation.
ACS signs and symptoms
L) sided chest pressure nausea and vomiting SOB pale and diaphoretic pain radiating to jaw, neck, back anxiety hT (R infarct) HT (L infarct) ST segment elevation or depression t wave inversion in NSTEACS pathological q waves
Pathophysiology of Atherosclerosis in relation to ACS
- irritant/injury - toxins, hyperlipidaemia, HT
- endothelial dysfunction causing breakdown of cells
- LDL infiltrates tunica intima
- macrophages follow, ingesting LDLs creating foam cells (dead macrophages) - accumulation of LDL and foam cells called a fatty streak
- smooth muscle cells from tunica media migrate into tunica intima
- SMCs make fibrous cap over fatty streak (Fat Cap) which further disrupts endothelium. Contains collagen and elastin proteins
- SMCs put Ca2+ into endothelium causing hardened arteries
- inflammatory substances breakdown collagen and weaken the cap
- rupture of plaque exposes contents to blood
- initiates clotting cascade
- thrombus formation - reduces arterial size and blood flow
- ischaemia/infarct to distal point of occlusion.
Clotting cascade - intrinsic pathway
in blood, occurs when Hageman Factor XII (12) comes into contact with damaged vasculature
Clotting cascade - extrinsic pathway
owing to release of tissue protein Tissue Factor III from damaged tissue into circulating blood
Clotting cascade
Prothrombinase (with ca)
prothrombin converts to thrombin, converting
Fibrinogen to fibrin (soluble)
with help of fibrin stabilising factor (Factor XIII)
becomes a
Stablisied Fibrin clot (insoluble)
What causes pain in ACS?
buildup of waste products (lactic acid) generated as the o2 starved cells switch from aerobic to anaerobic metabolism
Why do we not give GTN to a right ventricular/inferior infarct with BP <160?
Right ventricle is preload dependent because the muscle is small. It needs good preload to stretch ventricle to activate Starling’s Law. Take away pre-load and reduce contractility results in reduced CO
Whe no Aspirin in psychostim OD?
increased risk of CVA results from vasospasm not thrombosis as SBP greater than 160
Why no GTN in HR over 150
decreased fill time causes disproportionate drop in BP if preload reduced
Why no GTN in bradycardia
HR already low, GTN will take away SV therefore CO will be poor
Tachycardia (narrow complex) definition
A group of tachyarrhythmias greater than 100bpm that originate from above the ventricles or bundle of his
Causes of SVT
drugs hyperthyroidism conduction abnormality caffeine emotional stress cocaine abuse heart failure WPW
SVT signs and symptoms
regular rapid greater than 100 narrow qrs palpitations dizzy SOB, crackles chest pain hT
SVT patho - AVRT
Involves AV node conduction and an accessory pathway outside the AV node. It is triggered by a PAC that activates the ventricles via the AV node before reactivating the AV node via an accessory pathway, forming a re-entry circuit.
Valsalva patho
- bearing down increases intra-thoracic pressure
- Venous return is decreased, decreasing BP
- baroreceptors detect drop in BP
- sympathetic compensation increases HR and causes peripheral vasoconstriction
- Pressure is released
- sudden increase in venous return and cardiac output as ITP returns to normal
- barorececeptors detect increase
- parasympathetic innervation occurs via vagus nerve causing interruption of re-entry circuit
Pulmonary oedema definition
Leakage of fluid from pulmonary circuit and interstitium into alveoli of lungs due to imbalance between: capillary hydrostatic and oncotic pressure, lymphatic drainage and alveolar permeabillity
Causes of APO
cardiogenic - CCF/LVF, AMI
non-cardiogenic - drowning, toxic inhalation, high altitude, fluid overload, anaphylaxis, renal disease, sepsis
Signs and symptoms of APO vs infective
hx of APO, CCF, cardiac meds, bilateral, fine crackles, tachy, SOB, poor perfusion
Infective: course crackles, febrile, sepsis, cough, hx of infection, antibiotics, unilateral, chest pain, sputum
Patho of APO
- LVF/CCF
- decreased ejection fraction/stroke volume
- increased left ventricular end diastolic volume
- increased left ventricular pressure
- increased left atrial pressure
- increased pressure in pulmonary circulation
- increased pulmonary capillary hydrostatic pressure
- hydrostatic pressure exceeds oncotic pressure
- fluid shift into lung tissue and alveoli
- loss of surfactant
- alveoli collapse
- reduced surface area for gas exchange
- increase WOB
- hypoxia
- inadequate perfusion
Pharma of APO
GTN- venous dilation causes decreased VR and preload which increases contractility
-arterial dilation which decreases PVR which decreases afterload, decrease work of left ventricle
-coronary artery dilation which increases perfusion to left ventricle
Morphine: causes vasodilation which will reduce preload and therefore improve LV function - reduces anxiety, reducing HR and BP
CPAP use patho
Splints open alveoli at the end of expiration following a loss of surfactant. It increases surface area for gas exchange.
Why do we not use Salbutamol in APO?
bronchodilation decreases alveoli pressure which increases fluid into alveoli
Increases HR causing increased demand on heart resulting in further decline in contractility
Indications for CPAP
APO with mod-severe distress and full field crackles or fulminating
Precautions for CPAP
COPD, hT
Contras for CPAP
pneumothorax active vomiting hyperventilation facial trauma life threatening arrhythmias airway secure GCS less than 13
signs and symptoms of right ventricular infarct
peripheral oedema
hT
ST elevation in LII, LIII, aVF
elevation greater in LII: inferior infarct
elevation greater in LIII: R vent infarct
Bc/heart blocks may indicate RCA blockage
Patho of right ventricular infarct
ACS - RCA occlusion - myocardial iscahemia - infarct
RVF - congestion behind right ventricle - peripheral oedema
right ventricule stops feeding left ventricle - deceased CO - decreased BP
Atrial fibrillation characteristics
rate: controlled less than 100, uncontrolled over 100
rhythm: irregular
p wave: fibrillation
qrs: less than 0.12
no p waves, wandering baseline
Atrial fibrillation patho
- fibrillation of atria causing multi-diretional excitation caused by multiple foci in atria
- loss of atrial kick, turbulent blood flow and stastis in atria
- risk of blood clot formation
- causes f-waves (wiggly) baseline on ECG
Atrial flutter characteristics
rate: atrial-100, ventricular 300/150/100/75
rhythm: regular
p wave: saw tooth
qrs: less than 0.12
ratio of saw tooth to qrs
Atrial flutter patho
- type of atrial tachycardia
- ectopic pacemaker causing inappropriate depolarisation of muscle cells in atria
- depolarisation caught in re-entrant circuit of atria causing rapid firing (up to 300)
- AV node only excited an appropriate amount of times (e.g. every 3rd atrial circuit, causing a 3:1 ratio of p waves to QRS complexes)
1st degree block characteristics
conduction delayed at AV node rhythm: regular pr: over 0.2 qrs: less than 0.12 every p wave followed by qrs
2nd degree block (wenkebach) characteristics
atrial impulse becomes increasingly longer until qrs dropped
rhythm: regularly irregular
pr: increasing
qrs: less than 0.12
2nd degree block (mobitz) characteristics
fixed inability to conduct impulses through AV node rhythm: regularly irregular pr: constant qrs: less than 0.12 regular dropped beat
3rd degree block characteristics
no communication between atria and ventricles
rhythm: regular p, regular qrs
pr: disassociated
qrs: depends on origin of escape beat
Causes of bradycardia
R) coronary artery occlusion
normal variant - elite athletes
drugs/meds
hypothermia
changes in leads 1 and avl indicates
lateral
changes in leads 2, 3 and avf indicates
inferior
changes in leads v1 and v2 indicates
septal
changes in leads v3 and v4 indicates
anterior
changes in leads v5 and v6 indicates
lateral
Management of ACS
Aspirin 300mg
GTN 300mcg if no previous admin, borderline Bp or small, elderly or frail, 600mcg if none of the above
Repeat every 5 mins titrated to pain or side effects
GTN patch 50mg (.4mg/hr) upper torso - remove if BP falls below 90
STEMI: if onset over 12 hours, transmit 12 lead and notify. If onset less than 12 hours, treat as per stemi guideline
Management of SVT
SBP over 90:
- record 12 lead
- modified valsalva or standard valsalva - repeat x2 every 2 mins (max 3 attemps)
Managment of APO
Short of breath and fine crackles: -GTN as per ACS No improvement or full field crackles: -CPAP -Suction and assisted ventilation if required
STEMI management
- transmit ECG
- request MICA
- treat as ACS
- Inclusion and exclusion criteria determines thrombolyis vs transport
SVT patho - AVNRT
Involves an abnormal loop of electricity directly involving the AV node. A premature beat enters the slow pathway within the AV node which depolarises the bundle of His and also finds the distal end of the fast pathway that has now repolarised, allowing the impulse to be transmitted backwards along the fast pathway into the atria. The impulse will then re-enter the slow pathway creating a re-entry circuit which sustains the tachycardia
Types of SVTs
AVRT AVNRT Sinus Tach Atrial Flutter Atrial Fibrillation
Definition of Angina
A symptom of an underlying heart problem. It occurs as a result of an imbalance between myocardial oxygen demand and supply; characterised by chest pain.
Definition of Unstable angina
pattern of chest pain that has changed in it’s onset, frequency, intensity, duration or quality. Includes new onset chest pain. Indicative of changes in the degree of occlusion in the coronary arteries.
Definition of Stable angina
Chest pain caused by physical exertion or stress. Relieved at rest, GTN. Attacks are usually similar in nature and relieved the same way each time.
AMI definition
Death of myocardial tissue due to persistently inadequate perfusion, as a result of a blockage in a coronary artery.
