CVS Flashcards
How does ANP work?
Released when the atrial myocytes are stretched, and it vasodilates afferent arteriole to kidney to increase kidney blood flow in order to decrease Na reabsorption and lower fluid level (i.e. it causes natriuresis)
Which two endocrine glands does angiotensin II act on?
Adrenal gland to release aldosterone (increases Na reabsorption) and hypothalamus to produce ADH (increase water reabsorption)
Describe murmurs for mitral stenosis and regurg
Mitral regurg is holosystolic murmur, mitral stenosis is diastolic rumble
Describe murmurs for AV stenosis and regurg
AV regurg is early decrescendo diastolic, AV stenosis is crescendo decrescendo
Where does aldosterone act?
On principle cells of collecting duct
Name three stages of hypertension?
Stage 1 - 140/90, 2 - 160/100, 3- 180 or 110
Causes of secondary HTN?
Renal artery stenosis, CKD, Conn’s syndrome (aldosterone secreting adenoma) or Cushing’s syndrome (excess cortisol stimulates aldosterone Rs)
Complications of HTN?
Retinopathy, stroke, MI, LV hypertrophy (from increased afterload), HF, kidney failure
How to calculate maBP?
actual formula is maBP = TPR x CO
but can work out with maBP = diastolic P + 1/3 pulse pressure e.g. 60 + 10 = 70
What is shock? Give types
Shock is inadequate blood flow, so either due to reduced CO or reduced TPR.
Reduced CO: mechanical shock where it can’t fill, cardiogenic shock where it can’t pump, hypovolemic shock (haemorrhage, burns, D&V, hyponatremia)
Reduced TPR: toxic shock or anaphylactic shock
Examples of mechanical shock?
Can’t fill e.g. cardiac tamponade due to fluid in pericardial space (treat with pericardiocentesis) or massive PE occluding large pulmonary artery so RV can’t empty
At what % of fluid loss will you display signs of shock?
Less than 20% no shock, 20-30% some signs, 30-40% serious shock
Signs of shock?
Tachycardic, low BP, sweaty, flushed, pale, weak pulse
What is septic shock?
Persisting hypotension despite fluids following sepsis
Describe what electrical events each part of an ECG is representing
P wave - atrial depol Q wave- IV septum depol R wave - apex of ventricle depol S wave - base of ventricle depol T wave - repol of ventricles (double negative so appears +)
Which leads show inferior heart problems?
aVF, II, III (RCA)
Which leads show lateral heart problems?
aVL, I, V5,6 (LCA)
Which leads show anterior heart problems?
v1,V2,V3,V4 (LAD)
On ECGs how much are the boxes worth?
5 large squares 1sec, one large square 200ms, one small square 40ms, 25 small squares are 1sec
How to calculate HR from ECG?
300/no. of large squares = bpm
Or if irregular count how many in six secs (30 large boxes) and times by 10
How long should a PR interval be?
3-5 small boxes (120-200ms)
How long should a QRS interval be?
<3 small boxes (<120ms)
How long should QT interval be?
11-12 small boxes (<0.45 in M, <0.47 in F)
Describe the types of heart block (= problem with conduction between A and V)
1st degree - PR interval >5 small boxes
2nd degree - Mobitz Type 1 (Wenkebach phenomenon) is where PR gets longer and longer until one QRS isn’t transmitted
2nd degree - Mobitz Type 2 where PR normal then suddenly drops. High risk of progression to 3rd degree
3rd degree - complete heart block, atrial depol normal but NOT conducted to Vs so ventricular escape rhythm, wide QRS
Describe the types of heart block (= problem with conduction between A and V)
1st degree - PR interval >5 small boxes
2nd degree - Mobitz Type 1 (Wenkebach phenomenon) is where PR gets longer and longer until one QRS isn’t transmitted
2nd degree - Mobitz Type 2 where PR normal then suddenly drops. High risk of progression to 3rd degree
3rd degree - complete heart block, atrial depol normal but NOT conducted to Vs so ventricular escape rhythm, wide QRS
What is ventricular tachycardia?
Consecutive ventricular ectopics. High risk of VF
What does VF result from?
Multiple ectopic foci in ventricles, uncoordinated coordinate, ventricles quiver, no CO, shockable
Why is endothelial muscle more vulnerable to ischaemia than epithelial?
Because coronary arteries are on epithelial surface
What are STEMIs and NSTEMIs occlusions of?
STEMI is major coronary artery, NSTEMI is minor coronary artery or partial occlusion of major
Describe ECG STEMI progression
ST elevation, T wave inversion, pathological Q waves persist
What is a pathological Q wave?
Post STEMI indicating myocardial death- more than one small square wide and more than 25% depth of QRS. Seen in leads V1-V3 and are more negative because fat LV wall no longer goes away from the electrode because its dead
Does hypokalemia or hyperkalemia result in excitability?
In hypokalemia the inside of the cell is now more positive compared to the outside of the cell so the resting membrane potential is higher so in hypokalemia there is MORE excitability
What are acute coronary syndromes?
STEMI, NSTEMI or unstable angina
What can ischaemic heart disease cause?
stable angina, unstable angina, NSTEMI, STEMI
Causes of HF?
IHD is primary cause. Also HTN or dilated cardiomyopathies
What should ejection fraction be?
> 50-55 to 75%
Differences between systolic and diastolic dysfunction as causes of HF?
Systolic dysfunction - pumping problem e.g. MI leading to reduced inotropy. Causes eccentric hypertrophy (chambers bigger and walls bit thicker)
Diastolic dysfunction - filling/relaxing problem due to decreased compliance from thick walls e.g. chronic HTN. Causes concentric hypertrophy (walls thicker but chambers same size)
Drugs used for HF?
ACEi - inhibit RAAS to decrease preload
Beta-blockers - inhibit SNS activation to slow pacemaker
Diuretics - e.g. thiazide to reduce preload
Digoxin- blocks Na/KATPase which leads to rise in intracellular Ca which increases inotropy via the Na/Ca exchanger
Name the four classes of antiarrhythmics
I- Na (Flecainide), phase 0 II- Beta blockers (Bisoprolol) prevent NA binding, phase 4 III- K (Amiodarone), phase 3 IV- Ca (Verapamil), phase 2 Flec a Biscuit Aloe Vera
What makes an early and a late after-depolarisation more likely, respectively?
Early after-depol more likely if AP prolonged
Late after-depol more likely if Ca is high
What causes atrial flutter and what does it look like on ECG?
An atrial re-entry loop, saw-tooth
What causes AF and what does it look like on ECG?
Multiple atrial re-entry loops, no P waves and variable ventricular rate
Name 4 types of re-entry loops
Atrial flutter, AF, accessory pathway in WPW between A and V, AVNRT (AVN has one slow one fast pathway)
Causes of bradycardia
Conduction block e.g. 1st/2nd/3rd degree, or sick sinus syndrome (any SAN conduction problem)
Venous thromboses are ____ rich and arterial thromboses are _____ rich
Venous are fibrin rich, arterial are platelet rich
Name 3 presentations in peripheral arterial disease?
In chronic PAD: intermittent claudication and critical limb ischaemia. In acute PAD: acute limb ischaemia
Name complications of peripheral venous disease?
Haemorrhage, varicose eczema, thrombophlebitis (inflam from venous thrombosis and haemosiderin staining), venous ulceration, lipodermatosclerosis
Which murmurs can be heard better on inspiration?
RILE - R sided inspiration L sided expiration
What is Buerger’s test?
Raise foot upwards and its pale (peripheral arterial supply can’t overcome gravity), hang over bed and become pink (reactive hyperaemia)
How long do you have to fix acute limb ischaemia?
6 hours
Is there generally oedema in HTN?
No, because it’s caused by increased TPR so AP has increased but VP has decreased
How can chronic lung disease lead to RHF?
If not well perfused pulmonary vessels will vasoconstrict which increases pressure and afterload for RV
Defects in teratology of fallot?
VSD, pulmonary stenosis, RVH, overriding aorta
What receptor does ACh act on to decrease chronotropy?
M2
RMP of cardiac myocytes?
-90mV
How does adrenaline act on heart, lungs, and blood vessels?
On B1 for increasing heart inotropy and chronotropy, a1 for vasoconstriction, b2 for bronchodilation
Name the two pericardial sinuses
Transverse- between aorta and PA anteriorly and SVC posteriorly
Oblique- on posterior of heart between RPV RPV and LPV LPV
Tell me about laminar blood flow
Has a parabolic profile, all layers of blood are the same from the wall
Name the two limbs of the MAP graph?
Anacrotic limb (systole) and dicrotic limb (diastole)
Name causes of narrow and wide pulse pressure?
Narrow- aortic stenosis, cardiac tamponade
Wide- mitral regurg
Name the functional stages in a heart beat
Atrial contraction, isovolumetric contraction, rapid ejection, reduced ejection, isovolumetric relaxation, rapid filling, reduced filling
Causes of aortic stenosis and regurg?
AS- senile calcification, congenital bicuspid, chronic rheumatic fever
AR- rheumatic fever, aortic root dilation
What are isovolumetric relaxation and contraction?
Isovol contraction - all valves closed, short time where pressure increases but no volume change in preparation to eject
Isovol relaxation - all valves closed, short time before filling where pressure reduces but no volume change
Which aortic arch becomes the actual aortic arch and which one disappears?
IV becomes aortic arch, V disappears
Name components that make fetal heart
Aortic roots, truncus arteriosis, bulbus cordis, primitive ventricle, primitive atrium, sinus venosusq
What part of the ventricle does the bulbus cordis make?
The smooth RV & LV (the trabeculated muscly bit is from the primitive ventricle)
Describe formation of the foramen ovale
Septum primum forms, leaving a hole at its inferior just above the endocardial cushion. Septum secondum forms to its right, and ostium primum closes but ostium secondum forms (a hole higher up in the septum primum).
Tell me about spiral septum formation
So the truncus arteriosus that forms the aorta and the PT must be divided by a septum to make those two vessels.. The upper part of the truncus grows towards the right and the lower grows towards the left to twist the aorta/PT by 180 between its top and bottom. The septum forms due to migration of neural crest cells. Its the truncus arteriosis and the cordus (part of bulbus cordis) that make these vessels.
What is overriding aorta?
Defect in ToF where aorta is over the VSD rather than over the LV so it straddles the ventricles and gets blood from both
What tissue type forms the heart?
Mesoderm, which becomes primary and secondary heart fields.
What do primary and secondary heart fields become?
Primary heart fields - everything but the RV and outflow tracts i.e. LA, RA, LV
Secondary heart fields- RV and outflow tracts
What do you need to survive tricuspid atresia?
Another defect e.g. ASD, VSD
What do you need to survive transposition of the great arteries?
A shunt working e.g. ductus arteriosus
What inhibits platelet activation and vasodilates?
NO
Differences between SAN and myocyte APs?
SAN is between -60 and +10, has a long slow depolarisation due to HCN funny currents. No RMP, just spontaneously depolarises.
Myocytes are -90 to +30 and have a RMP determined by K+.
Describe role of calcium in excitation-contraction coupling in the heart and in skeletal muscles.
Heart- depol opens Ca channels in T tubules, triggers Ca release from SR, Ca binds to troponin C which moves tropomyosin to reveal actin binding site.
Skeletal muscle- voltage gated Ca channels open, Ca binds to calmodulin, Ca:Calmodulin (CCM) binds to MLCK, this complex phosphorylates myosin so it can bind to actin
Which receptors for ANS act on the heart?
B1 (GPCR as) for sympathetic, M2 (GPCR ai) for parasympathetic
In terms of ANS, the heart is ____ dominated and vessels are ____ dominated
Heart parasympathetic, blood vessels sympathetic
Cause of unstable angina?
Coronary plaque rupture
