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CVS > Clinical Conditions > Flashcards

Clinical Conditions Flashcards

1
Q

Cardiac tamponade

A

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

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2
Q

Pericarditis

A

Infection of pericardium leading to pericardial effusion

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3
Q

Atrial septal defect

A

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

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4
Q

Ventricular septal defect

A

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

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5
Q

Patent ductus arteriosus

A

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

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6
Q

Patent foramen ovale

A

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

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7
Q

Coarctation of aorta

A

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

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8
Q

Tetralogy of Fallot

A

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
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9
Q

Tricuspid atresia

A

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

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10
Q

Transposition of the great arteries

A

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

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11
Q

Hypoplastic left heart

A

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

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12
Q

Pulmonary atresia

A

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

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13
Q

Aortic atresia

A

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

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14
Q

Hyperkalaemia

A

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)
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15
Q

Hypokalaemia

A

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
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16
Q

Atrial fibrillation

A

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

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17
Q

Ventricular ectopics

A

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

18
Q

Long QT syndrome

A

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

19
Q

Torsades de Pointes

A

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

20
Q

Ventricular tachycardia

A

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

21
Q

Ventricular fibrillation

A

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

22
Q

1st degree heart block

A

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

23
Q

2nd degree heart block

A

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)

24
Q

3rd degree heart block

A

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)

25
Q

Left bundle branch block

A

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)

26
Q

Right bundle branch block

A

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)

27
Q

Ischaemic heart disease

A

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

28
Q

Stable angina

A

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

29
Q

Unstable angina

A

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

30
Q

NSTEMI myocardial infarction

A

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

31
Q

STEMI myocardial infarction

A

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

32
Q

Left sided heart failure

A

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

33
Q

Right sided heart failure

A

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

34
Q

Congestive heart failure

A

Cause - left and right sided heart failure together

Symptoms - symptoms of left and right combined, more severe than either in isolation

35
Q

Peripheral vascular disease

A

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

36
Q

Cariogenic shock

A

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

37
Q

Mechanical shock

A

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
38
Q

Hypovolaemic shock

A

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

39
Q

Toxic/septic shock

A

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

40
Q

Anaphylactic shock

A

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)

CVS (6 decks)

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