1
Q
What events cause the PQRST waves?
A
- P - atrial depolarization
- QRS - ventricular depolarization
- T - ventricular repolorization
2
Q
What is S4 heart sound?
A
It is normally inaudible but represent atrial systole. Can be heard if forceful ejection of the atrium into an already distended or non-compliant ventricle occurs.
3
Q
What is S1 heart sound?
https://www.youtube.com/watch?v=IS9TD9fHFv0
A
Onset of ventricular systole associated with AV closure (blood column hitting the closed valve). And to a lesser extent opening of semilunar valves after isovolumetric contraction, louder than S2.
4
Q
What is the S2 heart sound?
A
Opening of the AV valves and closure of the semilunar valves (Columbia of blood rushing back).
5
Q
What is the S3 heart sound?
A
Usually inaudible. Is causes by rapid ventricular filling.
6
Q
In terms of heart sound when is systole vs. diastole?
A
Systole - S1-S2
Dyastole - S2-S1
7
Q
Where are the S1 and S2 sounds in relation on the ECG?
A
- S1 is near the end of the S wave
- S2 is towards the end of T wave
8
Q
What is a split S1 and split S2?
A
- Split S1 - asynchronous closure of the AV valve
- Split S2 - asynchronous closure of the aortic then pulmonary valve in a healthy big dog but can be pathologic due to pulmonary hypertension. Psuedosplit can occur secondary to aortic stenosis.
9
Q
Describe preload and afterload?
A
- Both are related to the L ventricle.
- Preload = volume of blood present in the pulmonary capillaries and veins
- Afterload = resistant of flow in the systemic circulation (arteries, capillaries, and veins)
10
Q
What would reduce or increase preload?
A
- Reduce - ventilators
- Increase - venoconstrictors
11
Q
What would reduce or increase afterload?
A
- Reduce - vasodilators
- Increase - vasoconstrictors
12
Q
What are the basic sympathetic and parasympathetic controls of the heart rate?
A
Heart rate is controlled by medullary via afferent glossopharyngeal n. (CN 9) and vagus nerve (CN 10). Efferent vagus nerve (CN 10).
- Sympathetic: atropine is a parasympatolytic which can blow the vagal stimulus.
- Parasympathetic: Vagal stimulus (CN 10) causes acetylcholine to bind to the SA node and decrease HR
13
Q
Define CO (formula)
A
SV x HR
14
Q
What is the Frank Starling Law of the heart?
A
It states that if all forces remain constant, the force of the contraction of the left ventricle will be dependent upon the preload (direct relationship). In heart failure there is is very weak response compared to a normal heart.
15
Q
When does the coronary blood flow and why?
A
Coronary blood flows during diastole because during systole the ventricular contraction collapses the coronary arteries.
16
Q
What do alpha and beta receptors due?
A
- Alpha - vasoconstrictor
- Beta - vasodilator
17
Q
What should be the reflex is the myocardium needs more oxygen?
A
Slow the heart rate to increase time in dyastole
18
Q
In 2000 JVIM article, what 2 substances may play a role in the pathogenesis of cardiomyopathy and/or arterial thromboembolisms in cats?
A
- Vit B-12
- Arginine
19
Q
For a successful PDA coil embolization, a 200 JVIM article suggested not to do this technique if ___. They also reported that even with a very small PDA (< 2mm) it may still be possible to use the __ coil.
A
- If the smaller diameter of the PDA > 5 mm
- Use the 8mm coil rather than the 5 mm.
20
Q
What are 2 different shapes of ductus that is important in coil selection?
A
Tubular or conical shape
21
Q
What are two ways that increased venous return increased CO?
A
- Starling’s law = increased contractility with increased stretch
- And also increases HR
22
Q
Which side of the heart is volume overloaded with VSD and ASD?
A
- VSD = left atrium and left ventricle. Blood passes directly into the pulmonary artery without affecting the right side.
- ASD = right atrium and right ventricle. Blood returning to the left atrium goes right back to the right atrium.
23
Q
Describe the pulmonary and vascular changes in HW dz?
A
The main abnormalities are caused by inflammatory reaction to chemicals and antigens (not physical presence of the worms). These include:
- Intimal proliferation
- Arteritis which expose the endothelium and promotes thrombosis, perivascular inflammation, interstitial edema (can lead to alveolar flooding), alveolar wall thickening and fibrosis and bronchial constriction.
24
Q
What causes the inflammatory response in HW dz?
A
Both worms (L5 larvae, adults, microfilaria in the vasculature) and the chemical they produce.
25
Pressure-Volume curve
26
Define compliance
Compliance= **change in volume/change in transmural pressure**.
* Arteries have low compliance- are not very distensible, so they can maintain a high pressure throughout the cardiac cycle and provide continuous flow of blood
* Veins have high compliance- they can act as blood reservoirs because they can expand or contract to accommodate changes in blood volume
27
Define **Poisuille's Law**
**Poiseuille’s law** says that the resistance of a tube varies inversely with the radius to the fourth power so doubling the radius decreases resistance by a factor of 16. Also varies with length and viscosity of the liquid that’s flowing.
* Still true that small capillaries have less resistance than arterioles but only overall- the net resistance of capillaries is way less than the arteriole because there are so many of them. If it were only one tiny capillary there would be very high resistance
* In the body **arterioles** have the **highest resistance** of any of the vessels. Plus arterioles can change their radius to increase or decrease resistance as needed.
* Control can be instrinsic (the result of local responses, eg metabolic control is due to the metabolic rate of the tissue or paracrine regulators such as thromboxane, endothelin, histamine has local effects) or extrinsic (nerves and hormones can alter resistance).
**Total peripheral resistance**= (mean aortic pressure – caval pressure) / cardiac output
* Can ignore the **caval pressure** since it is **close to zero** and just call it aortic pressure/CO
* This says that the only **things affecting aortic pressure are cardiac output and peripheral resistance!**
* Pulmonary resistance is the same idea…pulm artery pressure-pulm vein pressure/CO
* Pulmonary resistance is ~1/12 what peripheral resistance is.
* Pulmonary vessels are very compliant so if you increase CO (eg exercise) the resistance decreases to get more blood through.
* Resistance of pulmonary vessels occurs with hypoxic vasoconstriction- low PO2 results in vasoconstriction to divert blood to areas with higher O2 and maintain low VQ mismatch. Problem comes when there’s low PO
28
Describe the systemic vs. pulmonary pressure system.
**Systolic pressure:** Mean systemic **arterial pressure is ~100**. Peak **aortic pressure (~120 mmHg)**, **Diastolic pressure**= minimum aortic pressure (**~80 mmHg)**. Mean aortic pressure is the potential energy to drive the blood through the system.
* As blood goes through the system pressure is lost via friction.
* At vena cava, pressure is ~3mmHg
* Perfusion pressure is mean aortic minus cava so 98-3 mmHg or ~95 mmHg.
**Pulmonary artery system**-**~20 mmHG systolic** and **~8mmHg diastolic**. Pulmonary **venous pressure is \<5 mmHg** so perfusion pressure is ~9 mmHg, much less1
* This is because systemic vessels have much more friction and therefore greater resistance.
* Pulmonary circulation called low pressure-low resistance side, systemic circulation called high pressure-high resistance side.
29
What are the normal intracardiac pressures by chamber
* RA = 5
* LA = 10
* RV = 25
* PA = 25/10
* LV = 125
* Ao = 120/80
30
What are the normal blood gasses in mmHG?
When is cyanosis visible?
Visible **cyanosis** occurs when **paO2 \<45mmHg**
31
Describe the **coronary blood supply**
Coronary arteries get **~3% of cardiac output** and **15% of the output of the left ventricle**
The coronary arteries arise from 2-3 sinuses that sit just above the semilunar cusps at the beginning of the aorta.
* **Left coronary artery** is the largest…it passes between the **left auricle and pulmonary trunk** and to reach the **coronary groove** and **divides immediately**.
* **Left paraconal interventricular branch** follows the groove of the same name to the apex. Aka cranial descending coronary artery
* Seven left ventricular branches come off this and supply the left ventricular wall.
* Five right ventricular branches also arise from here and supply a bit of the right ventricular wall.
* Usually septal branches come from here but not always
* One goes down the subsinusoidal interventricular groove and is named the same. Aka caudal descending coronary artery
* The left coronary trunk continues as the **circumflex branch** around the coronary groove terminating close to the right interventricular groove (IN HORSES AND PIGS) or continues into this groove (DOGS, CATS, RUMINANTS)
* There is large variation in the number of branches leaving the **circumflex branch- 5** is maybe most common. The largest is usually the left marginal branch
* The **right coronary artery** passes between the **right auricle and pulmonary trunk**. It continues to the r**ight subsinusoidal interventricular groove** where it fades (DOGS, CATS, RUMINANTS) or goes down the groove (IN HORSES AND PIGS)16.
* There are 4-9 branches of the right coronary artery- The **right marginal branch** is biggest and supplies the middle of the **right ventricular free wall**.
* The right coronary artery supplies most of the right ventricular free wall- it never goes beyond the margins of the right ventricle. It also sends twigs to the right atrium and aortic and pulmonary roots.
* Both coronary arteries send off a ton of small vessels to reach all parts of the heart, including into the core of the valve cusps.
* **No anastamoses** between the main coronary artery branches but there are lots between the little branches. Regardless, **occlusion of one of the small branches** results in **infarction** of muscle.
Coronary blood flow- return to the heart. Many small veins called the **besian veins empty directly into all the heart chambers**. Main blood return via great cardiac vein- enters the right atrium via the coronary sinus.
32
What is **Laplace's Law**
**Laplace’s Law-** says that the work performed by the heart (related to oxygen demand) is determined by wall stress, heart rate and contractility.
* Wall stress = (pressure)(radius) / (2)(wall thickness)
* Says that if chamber size increases, wall thickness must also be increased to maintain normal wall stress but work also increases
33
What does the pressure of the **LV** have to be before **L-CHF** occurs?
LV \> 25 mmHg
Has to be higher than pulmonary pressure
34
What is **SAM** - Systolic Anetrio Motion
of the Mitral Valve?
SAM- Systolic Anterior Motion of the Mitral Valve is a pathognomonic feature of HCM in cats9.
* The **anterior mitral leaflet** creates a **dynamic outflow** obstruction during **systole**, worse with harder contraction.
* Think it’s from **hypertrophied papillary muscles** that pull the chordate and anterior mitral leaflet into the outflow tract or contact the septum during systole.
* Makes the ventricular hypertrophy worse.
* Ddx mitral valve dysplasia
35
How does HCM result in PTE?
Arterial Thromboembolism- HCM most common cause
* Requires left atrial dilation to occur
* Thrombi form w/ an abnormality in one of the components of Virchows Triad- hypercoagulability, endothelial disruption, blood stasis.
* Atrial enlargement results in **reduced blood flow velocity** so **RBC aggregate and thrombi form**. Often cats are also hypercoagulable
36
How does heart failure relate to **RAAS**?
Renin-Angiotensin-Aldosterone System (RAAS)- Stimulated by heart failure
* **Renin** is released from the **juxtaglomeular apparatus** in the kidneys due to decreased perfusion, B1 adrenergic stimulation or reduced Na reabsorption
* Purpose of renin is to **activate angiotensin I** (made in the **liver** and hangs out in the plasma) which is **converted to angiotensin II** by **Angiotensin converting enzyme**.
* Angiotensin II inhibits release of Renin via a feedback loop
* Angiotensin II is a potent **vasoconstrictor**, and it promotes **sodium and water retenti**on by acting on the renal tubules.
* **Aldosterone release** from the adrenals is stimulated by angiotensin. It helps to regulate water and sodium balance and therefore maintains blood pressure. It also enhances sympathetic response of the heart and peripheral vasculature.
* Reactive oxygen species released by RAAS are central to cardiac hypertrophy and the detrimental vascular and ventricular remodeling in chronic heart failure.
37
How does **HW dz** lead to **proteinuria**?
**Antigen-antibody complexes** formed in response to heartworm cause **glomerulonephriti**s and subsequent proteinuria (rarely renal failure)
38
How is portal velociy altered with portosystemic shunts?
(intra- vs. extrahepatic)
* **Intraheptic shunts** = portal velocity at the porta hepatis is **increased** (decreased resistance as it enters CVC instead of capillary bed). Portal vein size is isually large with intrahepatic shunts.
* **Extrahepatic shunts** = **decreased portal velocity** b/c portal so small, and decreased with portal hypertension when can even have hepatofugal flow (vs normal hepatopedal). Portal vein size is usually small with extrahepatic shunt and microvascular dysplasia.
Poirtal vein size = Always measure in systole. Pv/Ao ratio is 0.7-1.25
39
What are some predisposing factors to **thrombosis/thromboembolism**?
40
What is the difference between **thrombi vs. thrombosis**?
* Thrombus is clot in the artery.
* **Thromboembolism**= infarction of an arterial bed by embolic material derived from a distant thrombus. Here the **vessel is normal** until an emboli settles there
* Not the same as **thrombosis**, where there is **abnormal endothelium** and a clot forms in the vessel (rare in animals).
Veterinary Physiology
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