Blood Vessels Of The Heart Flashcards

1
Q

What does the RCA supply?

A

Right atrium, SA and AV nodes and posterior part of IVS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does the LCA (left coronary artery) supply?

A

Left atrium and ventricle
IVS
AV bundle
May supply AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the difference between chronotrophy and inotrophy?

A

Increased chronotrophy = increased heart rate

Increased inotropy = increased force of contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Metabolites are more important for insuring adequate perfusion of skeletal and coronary muscle than activation of B2 receptors.
True or false?

A

True

Metabolite production e.g. Adenosine, potassium, H+ ion conce increases, pCO2 increases which all act on vascular smooth muscle cells to cause relaxation

A lot of relaxation takes place in response to metabolite production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where are the CVS baroreceptors located?

A

Aortic arch and carotid sinus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which type of receptor does noradrenaline bind to more favourably in vasculature under normal conditions?

A

B2 receptors

At higher concentrations will also bind to alpha-1 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Is B2 in the vessels vasodilatory or vasoconstrictory?

Remember tho: B2 receptors only present in skeletal muscle, myocardium and liver

A

Vasodilatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does the baroreceptor reflex work?

A

Increased mABP is detected by baroreceptors in the carotid sinus and aortic arch.

THese send signals to the medulla the co-ordinating centre

These then causes reduced sympathetic outflow to heart and vessels to cause vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Is the baroreceptor reflex short term or long term?

A

Short term - moment to moment changes in BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What factors stimulate renin release?

A

Reduced NaCl to distal tubule
Reduced perfusion pressure in the kidney causes release of renin - detected by baroreceptors in afferent arteriole
Sympathetic stimulation to JGA increases release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What cells in the afferent arteriole is renin released from?

A

Granular cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Bradykinin is a vasodilator. True or false?

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What other action does ACE have that increases vasoconstriction?

A

Breaks down bradykinin which is a vasodilator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is ADH stimulated by?

A

Increased plasma osmolarity

Or severe hypovolaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does ANP do and how does it work?

A

Promotes Na+ excretion

Synthesised and stored in atrial myocytes

Released from atrial cells in response to stretch

Low pressure volume sensors in the atria

Reduce effective circulating volume INHIBITS the release of ANP to support BP

Reduced filling of the heart –> less stretch –> less ANP released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is hypertension called when the cause is unknown?

A

Primary or ‘essential’ HTN

-95% of cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are some causes of secondary HTN?

A

Hyperaldosteronism
Cushing’s syndrome
Renovascular disease
Chronic renal disease

Think rx primary cause !

18
Q

What effect does dopamine have on BP?

A

Causes vasodilation and increased renal blood flow

Dopamine causes reduced reabsorption of NaCl
Inhibits Na H+ exchanger and Na+/K+ ATPase in principal cells of PCT and TAL

19
Q

What is Conn’s syndrome?

A

Aldosterone secreting adenoma
- hypertension and hypokalaemia

(Quite a fatty rich tumour)

20
Q

What is Cushing’s syndrome?

A

Excess secretion of glucocorticoid cortisol

At high concentration acts on aldosterone receptors - Na+ and water retention

21
Q

What is the name of a tumour of the adrenal medulla?

A

Phaeochromocytoma - secretes catecholamines (noradrenaline and adrenaline)

22
Q

Hypertension causes increased afterload (along with arterial damage)

What are the consequences of increased afterload?

A

Left ventricular hypertrophy - leads t heart failure

Increased myocardial oxygen demand - myocardial ischaemia and MI

23
Q

Hypertension causes arterial damage.

What are the different types of arterial damage it can cause?

A

Atherosclerosis –> leads to myocardial ischaemia and MI

Atherosclerosis + weakened vessels can cause: 
CVA
Aneurysm
Nephrosclerosis and renal failure
Retinopathy
24
Q

What are the non-pharmacological approaches for treating HTN?

A

Exercise
Diet
Reduce Na+ intake
Reduce alcohol intake

25
Q

What 2 main things can cause shock?

A

Fall in cardiac output

Fall in total peripheral resistance

26
Q

What can cause a fall in cardiac output?

A

Mechanical- pump cannot fill
Pump failure
Loss of blood volume - haemorrhage and decreased to a point where cardiac output cannot be maintained enough

27
Q

What can cause a fall in peripheral resistance?

A

Excessive vasodilation

28
Q

What does cardiogenic shock mean?

A

Ventricles cannot empty properly - pump failure

29
Q

What does mechanical shock mean?

A

Ventricles cannot fill properly - obstructive

30
Q

What does hypovolaemic shock mean?

A

Reduced blood volume leads to poor venous return

31
Q

What is an example of mechanical shock?

A

Cardiac tamponade

32
Q

What type of shock is a pulmonary embolism? What is the mechanism behind this?

A
Embolus concludes a large pulmonary artery
Pulmonary artery pressure high
Right ventricle cannot empty
CVP high
Reduced return of blood to the left side 
Limits filling of left heart
Left atrial pressure low
Arterial pressure low
SHOCK

Also chest pain, dyspnoea

33
Q

What is the management of stable angina?

A

Sub lingual nitrate spray/tablet

Prevent episodes: beta blockers, Ca2+ channel blockers, statins, oral nitrates

Prevent cardiac events: aspirin, statins, ACE-i

Long term: consider re-vascularisation

34
Q

What is the difference between NSTEMI and STEMI?

A

NSTEMI - non-ST elevation
Infarct is not full thickness

STEMI- ST elevation
Full thickness myocardium damage

35
Q
Case one 
86 female
Shortness of breath
Minor ankle oedema
AF 130 on ECG
T inversion V4 5 6 
Scoliosis and calcified costal cartilage on CXR 
Troponin 160

Diagnosis?

A

The reason her troponin has gone up
She has heart failure
Troponin has gone up

Myocardial damage due to other primary cause

Had this patient came in with a focal episode of symptoms eg. Sweatiness then yes could say plaque rupture mI but doesn’t really fit if slow onset

36
Q
71 year Ltd man 
ETOH many years
Poor mobility
Difficult history 
Tachycardia 110 
Raised WCC
Troponin 400 - significantly raised 
CXR - difficult to interpret poor inspiration

Diagnosis ?

A

Troponin spills out with pneumonia

Diagnosis pneumonia

37
Q
47 year old Man, ex smoker 
6 episodes of chest pain intermittently 5 or so minutes at a time over last 2 days 
One 10 min episode with clamminess, one episode stopped him while walking the dog, others at rest. 
Pain free now, normal examination.
Normal ECG
Normal CXR
Troponin 80 
Diagnosis?
A

Unstable angina

38
Q
67 year old man COPD
Peripheral vascular disease
SOB, cough, 4 days 
Mild left sided chest ache for several hours, worse in certain positions
Wheezy chest, scattered crackles
CRP 30, WCC 15
CXR- chronic changes of COPD
Trop 100
ECG sinus tachy, atrial ectopics. 
Possible short runs of AF
Diagnosis?
A

Could be an MI however no speicific plaque rupture

Probably treat as COPD exacerbation

39
Q
Severe aortic stenosis, declined TAVI, recent balloon aortic valvuloplasty
Severe coronary artery disease
CXR -pulmonary venous congestion
ECG- LBBB new or old? 
Troponin 800
Diagnosis?
A

Could be ACS
Or could be entirely due to severe aortic stenosis
Could be both

40
Q
83  y/o 
"Collapsed" at church
Abdomnal pain and distension 
BP 110/60
ECG LBBB
WCC normal, Hb normal, urea 12, creatinine 130
Trop. 60
Diagnosis?
A

Could be MI but unlikely
However later examined on CCU- bladder distended
Treated with a urinary catheter

41
Q

What is the main cause of systolic heart failure?

A

Ischaemic heart disease

Other causes include:

HTN 
Dilated cardiomyopathy: bugs, alcohol/drugs/poisoning, pregnancy
Valvular heart disease/congenital
Restrictive cardiomyopathy e.g. Amyloidosis 
Hypertrophic cardiomyopathy 
Pericardial disease 
High-output heart failure
Arrhythmia
42
Q

What is diastolic heart failure caused by?

A

When the muscles in the heart enlarge e.g. To overcome aortic stenosis then the lumen of the ventricle decreases in size (as the muscle mass takes up more room) therefore cannot fill as well and less blood is able to be pumped out as less blood is coming in