Clinical Conditions

Question 1

Cardiac tamponade

Answer 1

Pericardial effusion or haemorrhagic effusion -> pericardium fill with fluid -> heart harder to contract -> eventually will stop
Treatment - pericardiocentesis

Question 2

Pericarditis

Answer 2

Infection of pericardium leading to pericardial effusion

Question 3

Atrial septal defect

Answer 3

Hole in atrial septum
Left to right shunt due to pressure (non-cyanosed)
Flow can overload RV and cause right heart failure

Question 4

Ventricular septal defect

Answer 4

Hole in ventricular septum (usually membranous portion)
Left to right shunt due to pressure (non-cyanosed)
Pulmonary hypertension due to increased blood passing through
Can get so high the pressure gradient reverses and you get a paradoxical shunt (Eisenmengers syndrome) which causes cyanosis

Question 5

Patent ductus arteriosus

Answer 5

DA stays open after birth
Aorta and pulmonary trunk/arteries communicate
Blood does pulmonary circuit twice (non-cyanosed)
Pulmonary hypertension

Question 6

Patent foramen ovale

Answer 6

FO fails to close at birth
Largely asymptomatic as it’s so small
Can be route for venous embolism to join systemic circulation

Question 7

Coarctation of aorta

Answer 7

Constriction of aorta near DA
Hypoperfusion in distal vessels (lower limbs, femoral pulse weak)
Hypertension in vessels before this (aortic arch) to increase perfusion to lower limbs

Question 8

Tetralogy of Fallot

Answer 8

4 defects give rise to cyanosed patient..

1. Ventricular septum misalignment - right ventricular hypertrophy (+hypertension) due to increased difficulty of pumping to pulmonary trunk
2. Pulmonary stenosis - narrowing of pulmonary valve causes RV hypertension
3. VSD - pressure in RV exceeds LV causing right to left shunt
4. Overriding aorta - misaligned aorta connected to both LV and RV and so takes some blood from RV as well as LV, leading to more deoxygenated blood circulating

Question 9

Tricuspid atresia

Answer 9

Missing/closed tricuspid valve -> no pulmonary circuit formed
Only viable if there’s a right to left ASD and either a VSD or PDA

Question 10

Transposition of the great arteries

Answer 10

Spiral septum doesn’t form correctly; aorta connected to RV; pulmonary trunk connected to LV
Two separate circuits run in parallel instead of one big one
Only viable if there is a PDA to mix the blood

Question 11

Hypoplastic left heart

Answer 11

LV and ascending aorta undeveloped/absent
LA small; PDA maintained; RV takes over systemic and pulmonary circulation; PDA allows blood into aorta past the ascending section, maintaining viability
ASD also needed

Question 12

Pulmonary atresia

Answer 12

No pulmonary valve -> no access to pulmonary circuit except through PDA

Question 13

Aortic atresia

Answer 13

No aortic valve -> no access to systemic circulation except through PDA, ASD/VSD
Often artificially created to stop accumulation in left side of heart

Question 14

Hyperkalaemia

Answer 14

Too much K+ in blood -> extracellular fluid -> conc. grad. less steep -> permanently depolarised membrane -> some Na+ channels inactivated in pacemaker -> bradycardia occurs through accommodation

ECG features..

• Prolonged QRS complex
• Prolonged PR interval
• Tented T waves (similar to healthy QRS)

Question 15

Hypokalaemia

Answer 15

Too little K+ in blood -> extracellular fluid -> conc. grad. more steep -> permanently hyperpolarised membrane -> hyperexcitability of Na+ channels -> less inactivation -> tachycardia -> eventual atrial or ventricular fibrillation and cardiac arrest

ECG features…

• Enlarged P waves
• Prolonged PR interval
• T wave flattening/inversion

Question 16

Atrial fibrillation

Answer 16

Lack of discernible P waves
Sometimes with isoelectric line disrupted into wavey baseline
Not fatal as most filling of ventricles occurs in diastole, atrial systole isn’t that important

Question 17

Ventricular ectopics

Answer 17

Can be idiopathic
Ventricles occasionally contract without impulse from SAN but from AVN
Different shaped QRS complex; wider and sometimes taller in amongst normal complexes

Question 18

Long QT syndrome

Answer 18

Genetic or acquired, leads to abnormal repolarisation of the heart
Prolongs QT interval -> greater chance for re-entry arrhythmias
More likely to develop Torsades de Pointes or ventricular tachycardia which can progress into ventricular fibrillation

Question 19

Torsades de Pointes

Answer 19

Associated with prolonged QT
Type of ventricular tachycardia, gives widening round baseline in 3D on ECG
Mostly self-resolving within a few seconds but can cause ventricular fibrillation

Question 20

Ventricular tachycardia

Answer 20

Increased rate of contraction of the ventricles
More QRS complexes on ECG
Some P waves may be visible
Can be pulseless (defibrillate), provide sufficient CO or be asymptomatic
All cases eventually lead to VF

Question 21

Ventricular fibrillation

Answer 21

Ventricles no longer contract in coordinated manner
Loss of CO and rapid death unless treated
ECG - rounded, shallow peaks and the troughs, no discernible PQRS or T waves
Defibrillation required

Question 22

1st degree heart block

Answer 22

Delay between contraction of atria and ventricles
Issue at AVN
ECG - prolonged PR interval
(Marriage - getting fed up of one another, keeping their distance)

Question 23

2nd degree heart block

Answer 23

Irregular contraction between atria and ventricles
PR interval more and more prolonged until AVN generates its own depolarisation
ECG - shows as irregularly shaped QRS
Resets and same thing is seen again
(Marriage - get further apart, break up, get back together, repeat)

Question 24

3rd degree heart block

Answer 24

Complete dissociation between P and QRS complex
Complete block between SAN and AVN
Measure the RR interval and PP interval, two different heart rates will be calculated
(Marriage - filed for divorce, no relationship between P and QRS)

Question 25

Left bundle branch block

Answer 25

Slow/stopped electrical conduction down the left bundle of Purkyne fibres Abnormally shaped 'rabbits ears' QRS complex as ventricles depolarise at different rates WiLLiaM (shaped like W on V1 and M on V6 = LBBB)

Question 26

Right bundle branch block

Answer 26

Slow/stopped electrical conduction down right bundle of Purkyne fibres Abnormally shaped 'rabbits ears' QRS complex as ventricles depolarise at different rates MoRRoW (shaped like M on V1 and W on V6 = RBBB)

Question 27

Ischaemic heart disease

Answer 27

Inability of blood supply to meet demand Likely cause - coronary atheroma, lumen of coronary artery narrowed, increases coronary resistance, decreases coronary flow Supply Demand - Coronary flow (diastolic - Heart rate BP and coronary resistance) - Contractility - O2 capacity of blood - Wall tension

Question 28

Stable angina

Answer 28

Plaque occludes >70% artery lumen Ischaemia of myocardium when demand increased Pain typically ischaemic (central/retrosternal, left sided more than right, crushing or tightening) Disappears within 5 mins of ceasing exertion/GTN spray use

Question 29

Unstable angina

Answer 29

Similar to stable angina Pain crescendos, doesn't always go away within 5 mins Can appear with no obvious exertion/trigger

Question 30

NSTEMI myocardial infarction

Answer 30

Less severe MI Lacking ST elevation on ECG Partial/brief total occlusion of coronary artery Leads to crushing chest pain not relieved at rest/with GTN Sweating, pallor, vomiting etc. May have sense of impending doom Biomarker positive troponin and creatine kinase

Question 31

STEMI myocardial infarction

Answer 31

More severe MI ST elevation on ECG leads facing infarct Total occlusion of coronary artery Crushing pain not relieved with rest/GTN spray Autonomic features (sweating etc.) with sense of impending doom Extensive necrosis of area of myocardium supplied by artery Biomarkers positive troponin and creatine kinase Reopening blood supply within 2 hours only way to prevent/minimise necrosis

Question 32

Left sided heart failure

Answer 32

Causes - hypertension, IHD, aortic stenosis Symptoms - Exertional dyspnoea (shortness of breath when exercising) - Orthopnoea (shortness of breath when lying flat) - Paroxysmal nocturnal dyspnoea (attacks of severe shortness of breath at night) - Tachycardia - Cardiomegaly - Mitral regurgitation - Pulmonary and peripheral oedema

Question 33

Right sided heart failure

Answer 33

Causes - usually secondary to left sided heart failure (pressure backs up all the way), ASD/VSD, pulmonary stenosis, chronic lung disease Symptoms - Raised JVP - Pulmonary oedema - Pitting oedema - Ascites due to venous congestion at liver

Question 34

Congestive heart failure

Answer 34

Cause - left and right sided heart failure together | Symptoms - symptoms of left and right combined, more severe than either in isolation

Question 35

Peripheral vascular disease

Answer 35

Usually caused by atheromatous plaque in arteries and thrombus in veins More common in lower limbs Reduced blood flow to and from limbs Can manifest as intermittent claudication Thrombus breaking off in deep vein and causing pulmonary embolism - big concern Valve failure in superficial veins leading to varicose veins

Question 36

Cariogenic shock

Answer 36

From within the heart itself Causes incluse STEMI or serious arrhythmia (VF/VT) Poor perfusion of coronary arteries and kidneys Raised JVP (blood backs up in venous system) Hands will be cold and clammy

Question 37

Mechanical shock

Answer 37

Heart fails to pump due to outside factor - Cardiac tamponade - heart has no space to expand, blood can't enter through venae cavae, central venous pressure raises, arterial pressure stays low, reduced stroke volume - Pulmonary embolism - pulmonary hypertension, mechanical failure of RV as it cannot overcome resistance, inability of right side to pump leads to decreased left return, low LV and low arterial pressure, CVP rises as blood backs up in venous system, reduced stroke volume

Question 38

Hypovolaemic shock

Answer 38

Reduced blood volume, usually result of haemorrhage but can be due to diarrhoea or fluid loss from burns Less than 20% loss can be dealt with by baroreceptor reflex, > 30% shows symptoms of hypovolaemic shock Decreased venous return, decreased CO, baroreceptors detect this, increase TPR and CO to compensate, BUT increased CO just causes blood to hose out quicker Solution - stop leak, give IV fluids to re-address blood vol and undergo venoconstriction

Question 39

Toxic/septic shock

Answer 39

From septicaemia Endotoxins released by circulating bacteria that increase permeability of blood vessels and cause systemic vasodilation TPR plummets, vital organs no longer perfused -> death Baroreceptors sense decreased BP, attempt to increase CO and TPR (can increase CO but toxins prevent vasoconstriction) Signs - tachycardic pulse, extremities and skin red and warm Treatment - give adrenaline and IV antibiotics

Question 40

Anaphylactic shock

Answer 40

Severe allergic reaction resulting in massive histamine release, causes huge drop in TPR Inflammatory mediators override baroreceptor reflex and keep TPR low Mediators may also cause bronchospasm and laryngeal oedema Signs - tachycardic pulse, extremities and skin red and warm Treatment - epic-pen, chlorphenamine (to disable histamine)