CRS 1 Revision Flashcards
Draw the Wigger’s diagram to show the pressure changes during one cardiac cycle in the left ventricle and the right ventricle.
What events happen to generate the S1 heart sound?
The first heart sound (S1) is produced by the closure of the mitral and tricuspid valves in early systole, and is loudest near the apex of the heart. It is described as a Lubb, is more complex, is louder, and lasts longer than the second sound.
What events happen to result in the S2 heart sound?
The second heart sound (S2), described as a dupp, results from the sudden closing of the aortic and pulmonic valves, which bulge backwards towards the ventricles until their elastic stretch recoils the blood back into the arteries. This recoil produces vibrations that reverberate back and forth between the heart walls, arteries, and valves. When the vibrations contact the chest wall, they create what can be heard as the second heart sound. Since the sound is created by the aortic and pulmonic valves, it has aortic (A2) and pulmonic (P2) components. The components of S2 vary with the respiratory cycle: they are normally fused as one sound during expiration, but become audibly separated during inspiration.
What events happen to result in the S3 heart sound?
When present, a third heart sound (S3) can be heard in early diastole, during the rapid filling phase of the ventricle after the opening of the atrioventricular valve. It is a dull, low-pitched sound, best heard in the tricuspid area. Production of the S3 sound appears to be the result of the tensing of the chordae tendinae as rapid filling of the ventricles causes the chamber to expand.
What events happen toresult in the S4 heart sound?
The fourth heart sound (S4) is very quiet, and is not usually heard with a normal, unamplified stethoscope. When present, it occurs in late diastole and coincides with the contraction of the atria. It is generated by the left (or right) atrium contracting against a stiffened ventricle. Because of this, the presence of a fourth heart sound usually indicates the presence of a cardiac disease - specifically a decrease in ventricular compliance. This is usually due to ventricular hypertrophy or myocardial ischaemia.
What are gallop sounds, and in what circumstances do were hear them?
In the dog and cat normal heart sounds are S1 (closure of atrioventricular valves; heard best at left heart apex) and S2 (closure of semilunar valves; heard best at left heart base); Lub-Dup sound. Abnormal Heart Sounds: S3 & S4 occur during diastole and should not be audible in dogs and cats. If either one is present, this is called a GALLOP RHYTHM and suggests poor ventricular filling. Du-Lub-Dup sound.
Suggestive on congestive heart failure
What are the principle factors which contribute to BLOOD PRESSURE AND CARDIAC OUTPUT, what is the relationship of these factors to heart failure?
- CO: amount of blood pumped by heart in unit of time
- CO: stroke volume x HR
- Stroke volume: amount of blood ejected by ventricles each beat
- Blood Pressure: CO x total peripheral resistance
- Total peripheral resistance- arterial vascular tone, which is controlled by RAAS, SNS, and endothelial factors like Nitric Oxide
- Resistance in arterials, less resistance, better blood flow
- BP drops, less blood going to heart
- Higher resistance, higher BP, puts more effort on the heart
- Too low resistance, low BP, cardiac output drops, when you get compensatory mechanisms working which is when you see clinical signs – i.e. retention of salts, oedema
- If increase CO, increase BP
- Afterload: resistance to ventricular resistance, something external, extrinsic factor putting pressure on heart preventing ventricles from fully ejecting.
- Preload: end diastolic volume, which is intrinsically regulated, amount of blood in heart after diastole.
What are common causes of heart failure in dogs, cats and horses?
Dogs - congestive heart failure - mitral valve insufficiency and dilated cardiomyopathy,
Cats - congestive - hypertrophic cardiomyopathy is most common
Horses - systolic myocardial failure, impedance to cardiac inflow, pressure overload, volume overload - degenerative valve disease, left or right shunts
What are the ion movements responsible for the generation of the cardiac action potential? (Oh, wow, this answer is long. SOZ)
Phase 4: The resting phase
- The resting potential in a cardiomyocyte is −90 mV due to a constant outward leak of K+ through inward rectifier channels.
- Na+ and Ca2+ channels are closed at resting TMP.
Phase 0: Depolarization
- An action potential triggered in a neighbouring cardiomyocyte or pacemaker cell causes the TMP to rise above −90 mV.
- Fast Na+ channels start to open one by one and Na+ leaks into the cell, further raising the TMP.
- TMP approaches −70mV, the threshold potential in cardiomyocytes, i.e. the point at which enough fast Na+ channels have opened to generate a self-sustaining inward Na+ current.
- The large Na+ current rapidly depolarizes the TMP to 0 mV and slightly above 0 mV for a transient period of time called the overshoot; fast Na+ channels close (recall that fast Na+ channels are time-dependent).
- L-type (“long-opening”) Ca2+ channels open when the TMP is greater than −40 mV and cause a small but steady influx of Ca2+ down its concentration gradient.
Phase 1: Early repolarization
- TMP is now slightly positive.
- Some K+ channels open briefly and an outward flow of K+ returns the TMP to approximately 0 mV.
Phase 2: The plateau phase
- L-type Ca2+ channels are still open and there is a small, constant inward current of Ca2+. This becomes significant in the excitation-contraction coupling process described below.
- K+ leaks out down its concentration gradient through delayed rectifier K+ channels.
- These two countercurrents are electrically balanced, and the TMP is maintained at a plateau just below 0 mV throughout phase 2.
Phase 3: Repolarization
- Ca2+ channels are gradually inactivated.
- Persistent outflow of K+, now exceeding Ca2+ inflow, brings TMP back towards resting potential of −90 mV to prepare the cell for a new cycle of depolarization.
- Normal transmembrane ionic concentration gradients are restored by returning Na+ and Ca2+ ions to the extracellular environment, and K+ ions to the cell interior. The pumps involved include the sarcolemmal Na+-Ca2+* *exchanger*, *Ca2+-ATPase* and *Na+-K+**-ATPase.
What drugs do we have to decrease preload? (2)
This decreases venous tone and fluid volume which can help to relieve congestion & oedema. Drugs in this class include:
- Diuretics: These decrease blood volume by increasing sodium loss from the kidneys. They include loop diuretics, that act on the renal loop of Henle such as Frusemide, and thiazide diuretics that act on the renal distal convoluted tubule, such as Chlorothiazide or Hydrochlorothiazide. Potassium sparing diuretics act on the renal collecting duct and include Spironolactone and Amiloride.
- Venodilators , as their name suggests, dilate veins causing decreased venous pressures, blood redistribution, and increased capacitance. Venodilators include Glyceryl trinitrate and a group of drugs classified as balanced vasodilators, which includes ACE inhibitors (Enalapril (dogs & cats), Benazepril (cats), alpha-antagonists and Nitroprusside.
The side effects of preload reduction include: hypovolemia, dehydration, hypokalemia, hyponatremia.
What drugs do we have to decrease afterload?? (2)
Decreasing afterload increases flow by decreasing arterial tone. This reduces resistance to outflow which reduces the cardiac workload by decreasing systolic myocardial tension and increasing systemic blood flow. Arterial vasodilators include Hydralazine or any member of the balanced vasodilators mentioned above. ACE inhibitors such as Enalapril and Benazepril are commonly used - side effects include vomiting, anorexia, diarrhea, hypotension, and azotaemia.
What drugs do we have to increase myocardial systolic function?
This helps with dilated cardiomyopathy and mitral valve disease (dog & cat) but is contraindicated in animals with hypertrophic cardiomyopathy (dog & cat).
- Positive Inotropes can be used to stimulates myocardial contractility to improve cardiac output regardless of preload. This class of drug includes digitalis compounds* (e.g. Digoxin, Digitoxin), *calcium sensitisers/ phosphodiesterase III. inhibitor* (e.g. Pimobendan), *pure phosphodiesterase inhibitors* (e.g. Milrinone, Amrinone) and *catecholamines (e.g. Dobutamine, Dopamine).
The disadvantage of positive inotropes is that increased myocardial work causes increased myocardial oxygen demand.
What drugs do we have to increase myocardial diastolic function?
This helps with hypertrophic cardiomyopathy and myocardial fibrosis where ventricular filling is compromised. Drugs include the beta blockers* (e.g. Atenolol, Propranolol) and *calcium channel blockers (e.g. Diltiazem).
