WK 3- Cardiovascular Emergencies Flashcards Preview

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Flashcards in WK 3- Cardiovascular Emergencies Deck (52):

Describe the conduction system of the heart

1. Sinoatrial (SA) node initiates action potential through automaticity→ these automated cells are adjunct to contractile muscle cells and depolarisation wave passes over atria taking 0.03sec
2. Specialised fibres pass depolarisation rapidly to left atria and atrioventricular (AV) node
3. AV node delays impulse approx 0.13 sec allowing the atria to fully contract before the ventricles contract
4. Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His)
5. AV bundle splits into two pathways in the interventricular septum (left and right bundle branches)
5. Bundle Branches split into Purkinje Fibres and spread to the endocardium, depolarising within 0.03 seconds
6. Heart contracts left to right in the septum + base to apex (contracts faster on the left)


Describe blood flow throughout the heart

1. Deoxygenated blood moves via the superior vena cava into the right atrium
2. From the right atrium, the blood moves through the tricuspid valve into the right ventricle
3. From the right ventricle the blood moves into the pulmonary artery via the pulmonary valve, where it is able to move into the lungs and become oxygenated and for carbon dioxide to be removed
4. Once oxygenated, the blood moves from the pulmonary vein, into the left atrium
5. The oxygenated blood moves from the left atrium, through the mitral valve and into the left ventricle
6. The left ventricle then pumps oxygenated blood into the aorta via the aortic valve, and oxygenated blood is able to move throughout the body


What does the right coronary artery supply

supplies the right atrium, right ventricle, bottom portion of both ventricles and back of the septum


What does the left coronary artery divide into

the circumflex artery and the left anterior descending artery


What does the circumflex artery supply

supplies blood to the left atrium, side and back of the left ventricle


What does the left anterior descending artery supply

left anterior descending artery supplies the front and bottom of the left ventricle and the front of the septum


What forms the P wave

the depolarization of the atria. The electrical impulse moves through the atria and stimulates the depolarization to move away from the negative electrode. This causes a peak.


What forms the Q wave

is formed by the depolarization of the septum, moving from base to apex and the left ventricle towards the right. The depolarization is in fact moving towards the negative electrode, meaning there is a depression instead of a peak.


What forms the R wave

by the depolarization of the ventricles, moving from the endocardium out to the epicardium (from apex to base). The depolarization is moving towards a positive electrode and therefore causes a peak (the peak is dependent on the force of contraction of the ventricle)


What forms the S wave

depolarization of the free wall, moving from apex to base along the purkinje fibres (moves from mid myocardium outwards). As the net weight is away from the positive electrode and towards the negative, the overall charge is negative and causes a depression.


What causes the T wave

repolarization of the ventricles from apex to base. As repolarization is a negative charge and the impulse is heading towards a negative electrode, the end result is a peak (neg+neg=positive)


What is the PR interval-time

time between the onset of atrial depol and the onset of ventricular depol→ 0.12-.02 sec or 3-5 small squares
-allows full atrial contraction and movement of blood into the ventricles


What is the QRS complex-time

indicates ventricular depol→ <0.12 sec or <3 small squares


What is the QT interval- time

Beginning of QRS complex to end of T wave→ 0.35 – 0.43 sec


What does lead V1-V2 look at

look at the right ventricle


What does lead V3-V4 look at

look at the interventricular septum


What does lead I, II and aVL at

look at the left lateral surface of the heart


What does lead III and aVF look at

look at the inferior


What does lead aVR look at

looks at the right atrium


What does lead I compare the electrical activity between

aVR and aVL- right and left arm


What does lead II compare the electrical activity between

aVR and aVF- right arm and left foot


What does lead III compare the electrical difference between

aVL and aVF- left arm and left foot


What lead do most electrical signals travel along and why

Lead 2- as lead to looks between the aVR and aVF- right arm and left foot- so looks from base to apex, this is the direction in which the heart contracts


If the heart is in normal axis, where will deflection be in lead 1, 2 and 3

All upwards, greatest in lead 2


What axis deviation does right ventricular hypertrophy cause

Right axis deviation-> if the right ventricle is large, more depolarisation will occur here, shifting the depolarising wave to move towards aVR (and away from aVL)- causes a negative deflection


What are the 2 abnormal complexes that occur with QRS complexes

Narrow or broad complex shift


What is a narrow QRS complex (timing, cause, origin)

Narrow complexes (QRS < 100 ms) are supraventricular in origin→ Narrow (supraventricular) complexes arise from three main places:
1. Sino-atrial node (= normal P wave)
2. Atria (= abnormal P wave / flutter wave / fibrillatory wave)
3. AV node / junction (= either no P wave or an abnormal P wave with a PR interval < 120 ms)


What is a broad complex (timing, cause, origin)

(QRS > 100 ms)- slowing of ventricular depolarisation- may be either ventricular in origin, or due to aberrant conduction of supraventricular complexes (e.g. due to bundle branch block, WPW, hyperkalaemia or sodium-channel blockade)


What are the 4 most common types of rhythm abnormalitis

Superventricular tachycardia, atrial flutter, atrial fibrillation, heart block (either first degree, second degree or complete block)


What is a STEMI

ST segment is elevated in the leads overlying the zone of infarction
-thought to represent acute ischaemia and injury to a large percentage of the ventricular wall
-immediate reperfusion is likely to help


What is an NSTEMI

ST segment is depressed or unchanged in overlying ECG leads
-T wave may be abnormal
-usually associated with less severe infarcts and better outcomes


What are some serum markers for infarction

Based on measuring the blood levels of intracellular macromolecules that leak out of fatally injured myocardial cells through damaged cell membranes
-Molecules include;
-Creatine kinase MB (CK-MB)
-Ratio of CK-MB to total CK
-Myoglobin (less specific but gets elevated very quickly)
-Lactate dehydrogenase and many others
-most important is cardiac troponin


What leads will anterior damage (ie an LAD infarct) be seen

V leads as these look at the anterior surface of the heart- specifically V5 and V6


What leads will inferior damage (ie right main artery infarct) be seen

Lead 2, 3 and AVF as these look at the posterior and inferior angles


What leads will a posterior infarct be shown in

ST depression in V1-V2


What ECG changes are noted in an NSTEMI

No full thickness damage to myocardium therefore no “electrical window” created
-T wave inversion without Q waves


What is the effect of giving GTN to a patient with a RIGHT VENTRICULAR INFARCT?

-in RVI there is reduced blood being delivered to the lungs for oxygenation→ leading to decreased return of oxygenated blood to the left ventricle and systemic circulation
-GTN is a vasodilator so will dilate the venules returning oxygenated blood to the LV→ causing lower blood volume return→ decreased oxygenated blood moving around the body


How do GTN (glyceryl trinitrates) work

- Metabollically liberated NO activates guanylate cyclase in vascular smooth muscle
→Activation of guanylate cyclase increases cGMP levels→ Elevated cGMP closes vascular smooth muscle Ca⁺² channels & causes dephosphorylation of myosin light chain
→ Causes immediate and potent vasodilation due to inhibiting the contraction of the smooth muscle cells. Causes decreased preload, slightly decreased afterload, optimised ejection→ reduce BP
- Reduction in myocardial work => ↓ myocardial O2 demand


What ECG changes are associated with left bundle branch block

QRS duration of > 120 ms (normal is 120ms)
-Dominant S wave in V1
-Broad monophasic R wave in lateral leads (I, aVL, V5-V6)
-Absence of Q waves in lateral leads (I, V5-V6; small Q waves are still allowed in aVL)
-Prolonged R wave peak time > 60ms in left precordial leads (V5-6)


What is a bundle branch block

is a condition in which there's a delay or obstruction along the pathway that electrical impulses travel to make your heart beat. The delay or blockage may occur on the bundle braches that send electrical impulses to the left or right ventricles→ causing abnormal contractility


What changes are seen in right bundle branch block

-Broad QRS > 120 ms
-RSR’ pattern in V1-3 (‘M-shaped’ QRS complex)
-Wide, slurred S wave in the lateral leads (I, aVL, V5-6)


What are some examples of severe chest emergencies

-Perf oesophagus→ onset while eating/vomiting


What are some cardiac risk factors

-Previous MI/angina/stent etc
-Family history
-Diabetes, hypertension, PVD


When analysing an ECG, what must you comment on

Patient ID
-Voltage & timing
-Rate- tachy, brady or normal
-Rhythm- sinus, irregular, regularly irregular
-Axis- deviated
-PR interval- extended- block?
-QRS morphology- broad or narrow
-Septal Q v pathological Q
-ST segment & T wave changes
-QT interval
-Other eg pacing, U or J waves


How do you calculate HR from an ECG

Count number of big squares between the two R waves and divide this number by 300


When taking chest pain history why is site important- what differentials could occur

site is important as it can differentiate between MI (crushing central chest pain), perf oesophagus (high central chest pain), dissecting aorta (tearing chest pain that begins in chest and moves to back)


When taking chest pain history why is onset important- what differentials could occur

onset is important as it an determine whether the pain is constant (MI) or transient (colicky pain) and when the pain came on (at rest= unstable angina, whilst moving= stable angina)


When taking chest pain history why is character important- what differentials could occur

character allows you to determine if it is an MI (crushing pain), reflux/gord (burning pain), sharp (pleuritic chest pain- worse when patient moves/breathes/coughs), prolonged dull pain (perf. Oesophagus)


When taking chest pain history why is radiation important- what differentials could occur

if radiates to back and then downwards (dissecting aorta), if radiates down arm and jaw (MI)


When taking chest pain history why are associated symptoms important- what differentials could occur

associated symptoms can often be less useful and reflect a patient being in sympathetic overdrive→ pallor, sweating, tachycardia, nausea, SOB: these symptoms mean a severe medical emergency


When taking chest pain history why is timing important- what differentials could occur

duration is important when considering treatment→ if began a long time ago than some tx become useless→ need to have an angiogram/reperfusion within 90 minutes to reduce mortality


When taking chest pain history why are exacerbating factors important- what differentials could occur (ie what movements aggravate certain conditions)

if worse on breathing/coughing (pleuritic), if worse with exercise (ACS), if worse on leaning forward (pericarditis), if worse after eating fatty food (Gall bladder), if worse when sitting up (indigestion)