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Flashcards in L3 ACS Deck (38)
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1

risk factors for cardiovascular disease

2

Conduction system of the heart

3

Conduction system of the heart  

Sinoatrial node initiates electrical impulse and sends this impulse thru the atrium >lower section whereby an Atrial Kick occurs >AV node >Bundle of His thru ventricles via > Right Bundle & Left Bundle Branches>Purkinje fibers

4

P wave (sinus rhythm, sinus tachy or sinus brady)

T

5

P QRS T wave on an ECG

–  Three major waves of electric signals appear on the ECG. Each one shows a different part of the heartbeat.

–  The first wave is called the P wave. It records the electrical activity of the atria.

–  The second and largest wave, the QRS wave, records the electrical activity of the ventricles.

–  The third wave is the T wave. It records the heart's return to the resting state.

6

what is normal sinus rhythm

- HR 60-100bpm

- rhythm regular

- P wave before each QRS, identical

- PR interval 0.12-0.20 sec

- QRS < 0.12 sec

7

character of AF

rhythm: irregular

P wave: fibrillatory (fine to course), no P wave

PR interval: N/A

QRS: < 0.12 sec

8

VF

HR- 300-600bpm

rhythm: extremely irregular

P wave: absent

PR interval N/A

QRS: fibrilatory baseline

9

define unstable angina

10

cause of angina

11

types of angina

- stable - plague stuck in coronary artery, blood flow restriction. Stable angina
occur on exersion, diccipate when rest.
- Unstable - plague, there mey be a blood clot. plague ruptured, platelet aggregation, thrombus formation, unopposed vasoconstriction. pt is resting, waking up with chest pain, not on exersion
- variant angina - coronary spasm, not relate to plagues.

12

stable angina

– Stable angina
– is chest pain that can occur during physical activity or extreme emotion.

13

unstable angina

– Unstable angina
– is chest pain that occurs suddenly and becomes worse over time.

– It happens seemingly without cause;
– PT may be resting or even asleep.

14

prinzmetal angina = variant angina

–  Prinzmetal angina

–  is a coronary artery spasm;

–  temporary discomfort or pain caused by a spasm (constriction) in one or more of the coronary arteries;

–  can block or decrease blood supply to the myocardium.

15

diagnosis for angina

– Clinical Hx
– PQRST assessment

–  Physical examination e.g. fingers - smoker, cholesterol level

–  12 lead ECG

–  CT coronary angiography (camera inserted from femural artery, look into the coronary artery)

–  Stress echocardiography

–  MRI for stress-induced wall motion abnormalities

16

management for angina

- pain relief: morphine

- sublingual nitroglycerin (NTG) arginine (short acting)

- beta blockers or calcium channel blocker (b-blocker decrease BP and HR), dependant on pt Hx; contraindications; Or a long acting nitrate Glyceral trinitrate (GTN) patch

- lifestyle:

- diet and exercise (we need high protein and low carbs)

- support (e.g. psychosocial welling e.g. living alone)

- stent

- CABG

17

summary of angina

–  Angina
– Caused by atherosclerosis; blood clot; spasm;

–  Results in ischemia of myocardium

–  Reversible

–  Dx PT Hx CT angio

–  Tx GTN; Beta-blocker; Stent/CABG

18

ACS

19

theory practice gap in ACS - oxygen issue

- Please note the NSW Health Policy for Chest Pain Evaluation states for oxygen to be applied to a patient who presents with cardiac related chest pain. This practice of applying oxygen is outdated. Literature now states that oxygen in a patient with shortness of breath secondary to chest pain should not be applied as it increases vasospasm and can extend the myocardial infarct. Oxygen is now applied when O2Sats are less than 93%. The ACI network is trying to have the amended NSW policy reflect the Heart Foundation flow diagram as the diagram was developed in collaboration with the Cardiac Society of Australia and New Zealand and this flow diagram reflects North American and European guidelines.

give oxygen to the pt > 93% increase the risk of vasospasm, vasospasm decrease the oxygen supply to the myocardium, increase the extent of infact and mortality rate.  check ABG for PiO2.

 give O2 if pt PO2 <93%.

oxygen monitor also dependent on a few factors e.g.  nail polish, cleaniness.

20

signs and symptoms of ACS

21

NSTEMI

–  NSTEMI occurs by developing a complete occlusion of a minor coronary artery or a partial occlusion of a major coronary artery previously affected by atherosclerosis. This causes a partial thickness damage to the myocardium;

- NSTEMI: range free of symptoms at presentation to indiiduals with ongoing ichemia, electrucal or haemodynamicac instability or cardiac arrest.

 

22

STEMI

–  STEMI occurs by developing a complete occlusion of a major coronary artery previously affected by atherosclerosis. This causes a full thickness damage to the myocardium;

–  Chest pain at rest carries a worse prognosis than symptoms elicited during physical exertion;

–  Tachycardia, hypotension, heart failure and new mitral regurgitation at presentation predict poor prognosis;

- STEMI is a clinical syndrome defined by characteristic symptoms of myocardial ischemia in association with persistent electrocardiographic (ECG) ST elevation and subsequent release of biomarkers of myocardial necrosis.

- at present, STEMI compromises ~ 25% to 40% of MI presentations

- primary PCI should be performed in pt wih STEMI and ischemic symptoms of less than 12 hours duration
(Primary PCI consists of urgent balloon angioplasty (with or without stenting), without the previous administration of fibrinolytic therapy or platelet glycoprotein IIb/IIIa inhibitors, to open the infarct-related artery during an acute myocardial infarction with ST-segment elevation.)

23

prognosis of ACS

Prognosis
- chest pain at rest carries a worse prognosis than symptoms elicited during physical exertion

- tachycardia, hypotention, heart failure and new mitral regurgitation ot presentation predict poor prognosis.

24

NSTEMI - ECG

– NSTEMI:
– ST-segment depression or T-wave inversion.
– NSTEMI does not show ST segment elevation in ECG

• (due to partial thickness injury of myocardium) and so does not progress to a Q-wave on the ECG

25

STEMI - ECG

– STEMI:
– ST segment elevation in ECG

• (due to full thickness injury of myocardium) and later progress to a Q-wave on the ECG

26

management on STEMI and NSTEMI

27

airway

–  Look Listen Feel

–  Assess for trachea being midline

–  PT speaking

– Words or sentences

28

breathing

–  Look Listen Feel

–  Sit patient upright

–  Chest symmetry

–  Auscultate for air entry

–  Only give oxygen if O2Sats <93%

–  CXR

–  ABG

–  morphine (for pain as well as RR);

–  Morphine 1mg/ml/min;

–  PQRST assessment,

29

circulation

–  Look Listen Feel

–  12 lead ECG

–  5 lead cardiac monitoring

–  IV access 2 x large bore cannulas

–  Nitrates-Sublingual (anginine 300mcgs);

–  Beta Blockers (metoprolol 25mg);

–  Aspirin 300 mg (soluble);

–  Clopidogrel 300 - 600 mg

–  Enoxaparin 30 mg IV then chart at 1mg/kg bd s/c;

–  IVF 0.9% N/saline 1ml x kg;

–  FBC, UEC (urea electrolytes and creatinine) Ca Mg PO4, COAGS, troponin, LFTs, ABG;

–  TF to Cath Lab

 

30

disability

–  Look Listen Feel

–  GCS

–  Eyes=4

–  Voice = 5

– TPP

–  Motor = 6

–  Limb strength

–  PEARTL