6. CVS Flashcards
1
Q
What is cardiac tamponade?
A
When the pericardium fills with fluid so the heart can’t fill and contract and eventually stops.
2
Q
What causes cardiac tamponade?
A
Pericardial effusion (infection), or haemorrhagic effusion.
3
Q
How is cardiac tamponade treated?
A
Pericardiocentesis -aspiration of fluid within pericardium..
4
Q
What is pericarditis?
A
Infection of the pericardium leading to pericardial effusion.
5
Q
What can pericarditis cause?
A
Cardiac tamponade.
6
Q
What is an atrial septal defect?
A
Hole in the atrial septum that allows communication between atria.
7
Q
What is the blood shunting direction in an atrial septal defect?
A
Left to right due to pressure.
8
Q
What can a complication of atrial septal defect be?
A
Huge left to right flow overloads the right ventricle and leads to right heart failure.
9
Q
What is a ventricular septal defect?
A
A hole in the ventricular septum, usually in the membranous portion, that allows communication between the ventricles.
10
Q
What is the direction of blood shunting in a ventricular septal defect?
A
Left to right shunt due to pressure.
11
Q
What is Eisenmenger syndrome?
A
Left to right shunting from a ventricular septal defect causes pulmonary hypertension, if this increases enough, the pressure gradient reverses and there is a paradoxical shunt.
12
Q
What is a patent ductus arteriosus?
A
The ductus arteriosus stays open after birth so there is communication between the aorta and pulmonary trunk/arteries so blood does the pulmonary circuit twice and there is pulmonary hypertension.
13
Q
What is a patent foramen ovale?
A
The foramen ovale doesn’t close at birth, mostly asymptomatic as only small.
14
Q
What is a possible complication of patent foramen ovale?
A
A venous embolism can join the systemic circulation via the ovale.
15
Q
What is coarctation of the aorta?
A
Constricting of the aorta in the region near the ductus arteriosus causing hypoperfusion in the distal vessels and hypertension in proximal vessels.
16
Q
What is tetralogy of Fallot?
A
4 key defects giving rise to a cyanotic patient due to circulation of deoxgenated blood.
17
Q
What are the 4 defects of tetralogy of Fallot?
A
Ventricular septum misalignment, pulmonary stenosis, VSD, over-riding aorta.
18
Q
What are the consequences of the defects in tetralogy of Fallot?
A
Ventricular septum misalignment leads to right ventricular hypertrophy, pulmonary stenosis causes right ventricle hypertension. These lead to shunting of blood right to left through VSD. More deoxygenated blood circulates through misaligned aorta taking blood from RV.
19
Q
What is tricuspid atresia?
A
Missing or close tricuspid valve so there is no pulmonary circuit.
20
Q
How is tricuspid atresia managed?
A
Need a right to left ASD and a VSD or PDA to allow access to lungs.
21
Q
What is transposition of great arteries?
A
The spiral septum doesn’t form correctly so the aorta is connected to RV and pulmonary trunk to LV so there are two separate circuits in parallel.
22
Q
How is transposition of great arteries managed?
A
A PDA needs to be opened and maintained.
23
Q
What is hypoplastic left heart?
A
The LV and ascending aorta are undeveloped or absent, LA is small and PDA is maintained so right ventricle takes over systemic and pulmonary circulation.
24
Q
What is needed for hypoplastic left heart to be viable?
A
PDA to allow blood into aorta past ascending section, and communication between LA and RA via ASD.
25
What is pulmonary atresia?
No pulmonary valve so no access to pulmonary circuit.
26
What is needed for pulmonary atresia to be viable?
A PDA.
27
What is aortic atresia?
No aortic valve so no access to systemic circulation.
28
What is needed for aortic atresia to be viable?
PDA, ASD/VSD to stop accumulation in left side of the heart.
29
What is hyperkalaemia?
Too much K+ in the blood so too much K+ in the ECF, so less steep concentration gradient and permanently depolarised membrane.
30
What is the consequence of hyperkalaemia on the heart?
Na+ channels are inactivated due to the permanent depolarisation from less steep K+ concentration gradient. This causes bradycardia, bundle blocks, and eventually heart failure.
31
What are the ECG features of hyperkalaemia?
Prolonged QRS complex, prolonged PR interval, tented T waves.
32
What is hypokalaemia?
Too little K+ in the blood so too little K+ in ECF, so concentration is steeper and membrane is permanently hyperpolarised.
33
What is the consequence of hypokalaemia on the heart?
Permanently hyperpolarised membrane causes hyperexcitability of Na+ channels so tachycardia, atrial or ventricular fibrillation and eventually cardiac arrest.
34
What are the ECG features of hypokalaemia?
Enlarged P waves, shortened PR interval, T wave flattening/ inversion.
35
What is atrial fibrillation?
Lack of a discernable P wave.
36
Why is atrial fibrillation not fatal?
Most filling of the ventricles occurs in diastole.
37
What are ventricular ectopics?
Ventricles occasionally contract without an impulse from the SAN, so initiated by AVN instead.
38
What is the result of ventricular ectopics?
Different shaped QRS complex - wider and taller.
39
What is long QT syndrome?
Genetic or acquired syndrome that leads to abnormal repolarisation of the heart and therefore prolonged QT interval.
40
What is the risk of long QT syndrome?
Longer QT interval allows a greater chance for re-entry arrhythmias. More likely to develop torsades de pointes, or ventricular tachycardia that progresses to VF.
41
What is torsades de pointed?
Associated with prolonged QT interval, it is a type of ventricular tachycardia that gives the appearance of winding round the baseline in 3d on the ECG, normally self-resolves in a few seconds but can develop into VF.
42
What is ventricular tachycardia?
Increased rate of contraction of the ventricles, more QRS complexes on ECG with some P waves visible.
43
Wat does ventricular tachycardia lead to?
Ventricular fibrillation.
44
What is ventricular fibrillation?
The ventricles no longer contract in a coordinated manner.
45
What does ventricular fibrillation lead to?
Immediate loss of cardiac output and rapid death unless treated.
46
What is the ECG appearance of ventricular fibrillation?
Rounded, shallow peaks and then troughs, no discernible PQRS or T waves.
47
What is needed in ventricular fibrillation?
Defibrillation.
48
What is 1st degree heart block?
Delay between contraction of atria and ventricles due to issue at AVN.
49
What is the ECG appearance of 1st degree heart block?
Prolonged PR interval.
50
What is 2nd degree heart block?
Irregularity of contraction between the atria and ventricles. PR interval gets more and more prolonged until AVN generates its own depolarisation and there is an abnormally shaped QRS, then it resets and repeats.
51
What is 3rd degree heart block?
Complete dissociation between the P and QRS complexes from complete block between SAN and AVN.
52
What is left bundle branch block?
An abnormality slows the electrical conduction down the left bundle of Purkyne fibres.
53
What is the ECG appearance of bundle branch block?
Abnormally shaped 'rabbit ears' QRS complex as the two ventricles depolarise at different rates.
54
What is right bundle branch block?
An abnormality occurs that slows the electrical conduction down the right bundle of Purkyne fibres.
55
How can right and left bundle branch block be differentiated on an ECG?
WiLLiaM MoRRoW:
If QRS is shaped like a W on septal leads and M on lateral leads, then it's left BBB.
If QRS is shaped like an M on septal leads, and W on lateral leads, then it's right BBB.
56
What is ischaemic heart disease?
Inability of the blood supply of the heart to match the demand placed on it by the body.
57
Which factors influence on supply in ischaemic heart disease?
Coronary flow, and O2 carrying capacity of the blood.
58
What factors influence on demand in ischaemic heart disease?
Heart rate, contractility, wall tension.
59
What is the most likely pathogenesis of ischaemic heart disease?
Coronary atheroma causes lumen of coronary artery to narrow and increases coronary resistance and decreases flow.
60
What is stable angina?
A plaque occludes >70% of the artery lumen and leads to ischaemia of the myocardium when demand is increased.
61
What is the pain like in stable angine?
Ischaemic (central to left, crushing or tightening) and disappears within 5 minutes of rest or with GTN spray.
62
What is unstable angina?
Like stable angina but crescendo pain, that doesn't go away with rest.
63
What is an NSTEMI?
MI without ST elevation on ECG. From partial/brief occlusion of coronary artery.
64
What are the clinical features of NSTEMI?
Pain that isn't relieved by rest/GTN spray. Autonomic features - sweating, pallor, vomiting. Sense of impending doom.
65
Are there any biomarkers present with NSTEMIs?
Troponin and creatine kinase.
66
What is a STEMI?
MI with ST elevation on the ECG on leads facing the infarct. It's from total occlusion of a coronary artery.
67
What are the clinical features of STEMI?
Crushing pain not relieved by rest/ GTN spray. Autonomic features and sense of impending doom.
68
What are the biomarkers for STEMI?
Troponin and creatine kinase.
69
How is necrosis prevented/ minimised with STEMIs?
Re-open blood supply within two hours.
70
What is acute coronary syndrome?
A cluster of symptoms from occlusion of coronary arteries as a result of unstable angina, NSTEMI, or STEMI.
71
What is heart failure?
Syndrome of symptoms and signs that are a result of the heart being unable to pump enough blood to meet the physiological demands of the body.
72
What is heart failure primarily caused by?
Ischaemic heart disease.
73
What is a key sign of heart failure?
A breakdown of the relationship in Starling's law - pumping less efficieny so force of contraction no longer corresponds to stretch.
74
What are the four key systems/hormones involved in heart failure?
Autonomic nervous sytem, renin-angiotensin-aldosterone system, natriuretic hormones, ADH.
75
How is the autonomic nervous system involved in heart failure?
Baroreceptors sense decreased cardiac output so increase ANS to heart to increase cardiac output. This increases the demand on myocardium so damage is more extensive. Noradrenaline stimulates cardiac hypertrophy and myocytes apoptose and necrose.
76
How is the renin-angiotensin-aldosterone system involved in heart failure?
Drop in blood pressure/ renal perfusion releases renin which leads to angiotensin II being made. ATII causes vasoconstriction and increases aldosterone release which causes Na+ retention and therefore increased circulating volume and preload.
77
How are natriuretic hormones involved in heart failure?
Released by increased arterial stretch, it opposes the effects of the RAAS by promoting vasodilation, Na+ loss, and inhibiting renin/aldosterone release.
78
How is ADH involved in heart failure?
Stops water loss when dehydration, so its absence causes the opposite in heart failure. No ADH release means no water loss and increased circulating volume and increased preload.
79
What are the systemic changes seen in heart failure?
Vascular - vasoconstriction from several different factors.
Skeletal muscle - decreased blood low from vasoconstriction so decreased muscle mass/ strength. Includes diaphragm, so respiratory problems.
Renal system - GFR is initially preserved, but then deteriorates so there is too much urea and creatinine in the blood. This is only corrected by ATII, which further worsens heart failure.
80
What are the causes of left sided heart failure?
Hypertension, ischaemic heart disease, aortic stenosis.
81
What are the symptoms of left sided heart failure?
Exertional dyspnoea, orthopnoea, paroxysmal noctural dyspnoea. Tachycardia, cardiomegaly, mitral regurgitation, pulmonary and peripheral oedema.
82
What are the causes of right sided heart failure?
Usually secondary to left heart failure, or ASD/VSD, pulmonary stenosis, chronic lung disease.
83
What are the symptoms of right sided heart failure?
Raised JVP, pulmonary oedema, pitting oedema, ascites - all related to build up in venous/pulmonary systems.
84
What is congestive heart failure?
Both sides failing.
85
What are the preventative treatments of heart failure?
Stop smoking, reduce salt in diet, reduce alcohol, exercise more, reduce cholesterol.
86
What are the treatments of heart failure?
Treat underlying cause.
Drug treatment - ACE inhibitor and dieuretic, then beta blockers, then spironolactone, then digoxin.
Surgery - valve replacement, pacemaker implantation, revascularisation, mechanical assist devices, heart transplant.
87
What is peripheral valve disease?
Usually from atheromatous plaques in arteries and thrombus in veins, commonly in the lower limbs.
88
What are the consequence of peripheral valve disease?
Reduced blood flow to or from limbs, causing intermittent claudication classically. Thrombus in deep veins can break off and cause pulmonary embolism. Valve failure in superficial veins leads to varicose veins.
89
What is shock?
Inadequate perfusion of all tissues throughout the body, leading to widespread ischaemia and death.
90
How is mean arterial BP calculated?
BP = CO x TPR = HR x SV X TPR
91
What is Poiseuille's law?
Resistance decreases with radius to the power of four.
92
What causes shock?
A large fall in cardiac output: cardiogenic; mechanical; hypovolaemic, or a huge fall in TPR: toxic; anaphylactic.
93
What is cardiogenic shock?
Shock arising from within the heart itself, like from a STEMI or serious arrhythmia. This leads to poor perfusion of the coronary arteries and kidneys.
94
What are the signs of cardiogenic shock?
Raised JVP from blood backing up through pulmonary system and right side of heart, cold hands from poor perfusion, clammy from ANS activation.
95
What is mechanical shock?
Shock from failure of the heart to pump due to a factor outside the heart, like cardiac tamponade or huge pulmonary embolism.
96
How does cardiac tamponade cause mechanical shock?
The pericardium fills so the heart has no space to expand so the pressure in all chambers reduced. Blood can't enter through venae cavae so CVP raises but arterial pressure is low as cardiac output is so low. There is reduced stroke volume.
97
How does pulmonary embolism cause mechanical shock?
Embolus occludes a large pulmonary artery leading to pulmonary hypertension. Right ventricle can't overcome resistance, this inability to pump means there is decreased return to the left so the stroke volume reduces. CVP rises as blood backs up in in venous system.
98
What are the signs of mechanical shock?
Raised CVP but low arterial pressure.
99
What is hypovolaemic shock?
Reduced blood volume - by 30% when symptoms appear, usually from a haemorrhage but can be from diarrhoea or fluid loss from burns. There is decreased venous return and decreased CO.
100
Why are symptoms of hypovolaemic shock only felt at 30% decrease?
Less than 20% loss can be dealt with by baroreceptor reflex.
101
How does the baroreceptor reflex try to deal with hypovolaemic shock?
By increasing TPR and CO, however the CO increase causes blood loss to be more rapid.
102
How is hypovolaemic shock treated?
Leak is stopped, IV fluids are given, central line for fluids until CVP is in healthy range, venoconstriction to support CVP.
103
How does the body use internal transfusion in hypovolaemic shock?
Increasing TPR means the capillary hydrostatic is reduced and plasma draws fluid from the interstitium.
104
What are the signs of hypovolaemic shock?
Tachycardia, weak and thready pulse, cold and clammy hands. Reduced CO and TPR.
105
What is the long term result of increased TPR in hypovolaemic shock?
Tissue ischaemia so local vasodilators are released and TPR drops so BP drops further and there is multiorgan failure.
106
What is toxic/septic shock?
From septicaemia, endotoxins from circulating bacteria increase permeability of blood vessels and cause systemic vasodilation so TPR plummets and vital organs aren't perfused, leading to death.
107
How does the body fail to compensate for toxic shock?
It tries to increase CO and TPR, CO is increase but endotoxins overwhelm the body's attempt to vasoconstrict so TPR remains low.
108
What are the signs of toxic shock?
Tachycardic pulse, extremities are red and warm, hyperperfusion of peripheral vessels means less blood to major organs.
109
How is toxic shock treated?
Adrenaline to counteract immediate effects and IV antibiotics.
110
What is anaphylactic shock?
Severe allergic reaction that results in massive histamine release, causing a huge drop in TPR. The inflammatory mediators override baroreceptor reflex so TPR stays very low.
111
What are the signs of anaphylactic shock?
Bronchospasm and laryngeal oedema leading to difficulty breathing, tachycardic pulse, extremities are red and warm, hyperperfusion of peripheral vessels so not enough blood to major organs.
112
What is the treatment for anaphylactic shock?
Epi-pen - addresses drop in TPR. Chlorphenamine - disables histamine.
