Exam 1 Flashcards

Question

5 phases of cardiac cycle?

Answer 1

1. **atrial systole** (atrial contracts small amt of additional blood into relaxed ventricles) 2. **isovolumetric ventricular contraction** (AV valves close, pressure increases but volume stays the same) 3. **ventricular ejection** (semilunar valves open, high pressure) 4. **early diastolic filling** (ventricles begin to relax, semilunar valves close) 5. **late diastolic filling** (all chambers relaxed and ventricles fill passively)

Answer 2

S1 "Lub" = start of systole (AV closure, semilunar opening) S2 "Dub" = end of systole (semilunar closure, AV opening)

Answer 3

Normal equine and bovine patients | S3 = early diastole S4 = late diastole

Answer 4

**Relaxed: parasympathetic activation** shifts systemic venous pool to peripheral vessels (away from heart) -> decreased SVR -> decreased CO and HR = decreased SV **Stressed: sympathetic activation** shifts systemic venous pool centrally (towards heart) -> vasoconstriction and increased SVR -> increased CO and HR = increased SV (more filling) parasymp influences HR and CO symp influences SV, HR and CO | SVR = systemic vascular resistance ## Footnote BP = CO x SVR CO = SV x HR SV = EDV - ESV

Answer 5

Right parasternal, long axis

Answer 6

LV (mushroom) and RV | LV @ level of papillary muscles

Answer 7

Aortic valve (mercedes benz 3 cusps), and left atrium and its appendage (whale)

Answer 8

all 4 chambers

Answer 9

**2-D** = 2d place of u/s waves cross-sectioning the heart, either by long axis or short axis - can visualize cardiac morphology and chamber dimensions **M-Mode** = motion mode. single beam through the heart - can visualize time-dependent measurements of the chambers (for dimensions, function)

Answer 10

Both used to measure **blood velocities** **Spectral**: blood velocities displayed on Y-axis (signal above x-axis = RBC towards probe, signal below x-axis = RBC away from probe) **Color**: blood velocities displayed as colored pixels (BART)

Answer 11

**Pulse Wave (PW)** - Higher spatial resolution - Poorer measure of high velocities **Continuous Wave (CW)** - Lower spatial resoultion - Better measure of high velocities

Answer 12

mix of red/blue = ~orange-tinge color

Answer 13

- ID of turbulent blood flow (stenotic valves, valvular insufficiency) - determination of direction of blood flow through a shunt - assessment of severity of stenosis, shunt or valve regurg

Answer 14

Subjective = 2D Objective = M-motion; 2D using Simpson's disc summation method for obtaining left ventricular ejection fraction ## Footnote LVEF = [(EDV - ESV) / (EDV)] x 100% normal = ~70%

Answer 15

better for visualzing RA and RV

Answer 16

change in pressure = 4V^2 Blood always flows from high pressure -> low pressure; detects pressure difference that generated the flow b/w chambers (e.g., in valve regurg) | Bernoulli equation

Answer 17

increased pressure in lungs = greater pressure RV needs to overcome to force blood out into pulmonary trunk (increased after-load) -> pressure increases in RV to point where RV pressure is > RA pressure -> blood backflows into RA

Answer 18

"Clinical syndrome in which impaired systolic or diastolic events causes clinical signs of exercise intolerance and/or congestion." CHF = most common type

Answer 19

**Left-sided CHF** = backflow into lungs --> pulmonary edema (cardiogenic PE) **Right-sided CHF** = backflow into systemic circulation --> ascites, +/- peripheral edema

Answer 20

Mitral Valve Insufficiency/regurge Dilated Cardiomyopathy ## Footnote mitral valve regurg = volume overload DCM = systolic myocardial dysfunction

Answer 21

**A: predisposed breeds** **B: have heart disease, but not in failure yet** **C: in CHF** (current or past; even if CHF has been treated, you will almost never treat the disease that caused it) **D: refractory CHF** (end-stage)

Answer 22

**Volume overload = eccentric hypertrophy**: in-series replication of sarcomeres --> hypertroophy + dilation. Preserved wall thickness:lumen **Pressure overload = concentric hypertrophy**: parallel replication of sarcomeres --> hypertrophy without dilation. *Increased* wall thickness:lumen

Answer 23

Volume overload: Eccentric hypertrophy -- e.g., mitral valve regurgitation ## Footnote (note hypertrophy + dilation and the preserved wall thickness:lumen ratio)

Answer 24

Pressure overload: Concentric hypertrophy -- e.g., severe pulmonic stenosis ## Footnote (note hypertrophy but NO dilation, and the INCREASED wall thickness compared to lumen)

Answer 25

Diastolic dysfunction - hypertrophic myopathy | causes impaired ventricular filling. ## Footnote MUSHROOM = LEFT VENTRICLE very difficult to assess non-invasively!

Answer 26

Systolic myocardial dysfunction: dilated cardiomyopathy (DCM) | dilation is secondary to systolic dysfunction!!

Answer 27

Arrhythmias Top: 3rd degree AV block Bottom: ventricular tachycardia ## Footnote 3rd degree AV block: all impusles are blocked at AV node --> bradycardia b/c HR generated entirely by slow-firing ventricles. Ventricular tachycardia: significantly decreases CO and can worsen CHF

Answer 28

Ventilation: the movement of air in (inhalation) and out (exhalation) of alveoli. Determinants: - respiration rate - tidal volume | also known as alveolar ventilation ## Footnote inhalation: alveoli pressure less than atmosphereic exhalation: alveoli presure greater than atmospheric similar to CO = SV x HR

Answer 29

Gas exchange = of O2/CO2 at the alveolar-pulmonary capillary interface Gas transport = of O2/CO2 to/from systemic tissue capillary beds through the circulatory system

Answer 30

Repsiration: the transportation of O2 in the air to systemic cells and the transportation of CO2 in systemic cells back out into the atmosphere - ventilation, gas exchange and gas transport

Answer 31

by responding to the systemic blood levels of O2, CO2, and pH (acids) ## Footnote decrease in pH (more acidic) -> brain stimulates deeper and faster breaths

Answer 32

Vt = Volume of air inhaled or exhaled into lungs *during a normal breath* Vdeadspace = Volume of air in conducting airways (physiologic dead space) + volume of air in pathologic dead space Valveolus = Volume of air in the alveoli

Answer 33

Volume of air entering (or leaving) the alveoli per minute | AMV = (Vt - Vdeadspace)xRR

Answer 34

reduced RR reduced Vt increased dead space | all decrease chances of air moving in/out of alveoli

Answer 35

**Conducting Airway** = transport air - upper airway = nares to pharynx - lower airway = trachea to bronchus - physiologic dead space; warm/humidfy air and remove particulate matter **Transitional Airway** = bronchioles **Exchange Airway** = gas exchange - alveolar duct to alveoli - occurs b/w alveolus and pulmonary capillary beds

Answer 36

1. single-cell thickness (0.5 um) 2. surfactant (lowers surface tension / keeps alveoli open)

Answer 37

1. **Brachycephalic Syndrome** (stenotic nares, elongated soft palate, hypoplastic trachea) 2. **Laryngeal Paralysis** (dogs; failure of cricoarytenoid muscle to contract during inhalation -> air cannot enter trachea) 3. **Dorsal Displacement of the Soft Palate** (horses' soft palate extends to epoglottis -> obligate *nasal* breathers)

Answer 38

**Glottis**: laryngeal orifice **Epiglottis**: cartilaginous structure that prevents aspiration during swallowing

Answer 39

radius is inversely proportional to airflow resistance. more nasal dilation = less airflow resistance = better ventilation

Answer 40

During inspiration, the dorsal cricoarytenoid muscle contracts, -> abduction of vocal folds and arytenoid -> air can enter trachea | allows for decreased airway resistance so air can flow in

Answer 41

The lungs’ elastic recoil tends to collapse them, while chest wall’s elastic recoil allows for it to expand -> PLERUAL PRESSURE IS NEGATIVE B/C OF THESE OPPOSING FORCES

Answer 42

Negative: inspiration Positive: expiration Equal: in between inspiration and expiration

Answer 43

1. Subatmospheric pleural space pressure 2. High surface tension of pleural fluid (helps maintain position of lungs against thoracic wall) 3. Alveolar surfactant (decreases surface tension, allowing lungs to inflate more easily)

Answer 44

Diaphragmatic contraction occurs during INSPIRATION and moves downward, while the external intercostal muscles pull the ribs upwards -> **increases size of thoracic cavity and decreases the pressure within it**

Answer 45

necessary to help move the diaphragm back upwards to give more power to/enhance expiration

Answer 46

**inspiratory RV** = additional air volume resulting from deepst possibe breath **expiratory RV** = additional air volume exhaled during maximally forceful exhalation **residual volume** = volume remaining in lungs after maximally forceful exhalation

Answer 47

Alveolar ventilation needs to be adequate (determined by Vt and RR) and blood circulation through pulmonary capillary beds must be adequate (i.e., no blood clots, etc.) for this interface and gas exchange to occur

Answer 48

1. Oxygen content of inspired air is 21% 2. Effective alveolar ventilation 3. Matching of ventilation and perfusion 4. Diffusion of gas at this interface

Answer 49

1. pressure gradient of the gases in the alveolus vs capillary 2. diffusion coefficient (the solubility and MW of the gases) 3. diffusion distance (b/w alveolus and capillary) 4. membrane area (SA of alveolar epithelium and capillaries) ## Footnote alveolar membrane thickness and fluid in interstitial space would increase diffusion distance

Answer 50

**Hypoxemia: *reduced partial pressure of O2 in arterial blood, specifically reflecting oxyHb*** Causes: - reduced inspired oxygen (fire, failure of O2 turned on during anesthesia) - alveolar hypoventilation - ventilation/perfusion mismatch - diffusion barrier

Answer 51

**DIFFUSION ISSUE AND NOT VENTILATION ISSUE** PaO2 = decreased (O2 from alveoli cannot diffuse across the fluid into capillary bed) PaCO2 = normal (CO2 has higher solubility and can still diffuse across the fluid and thus be breathed out) | pulmonary edema = diffusion issue, NOT ventilation

Answer 52

hypoventilation (e.g., too deeply anesthesized)

Answer 53

Pulmonary arterioles: vasoconstriction - want to reduce/stop bloodflow to any hypoxic regions of the arterioles (decrease chances of deoxygenated blood flowing out of lungs) Systemic arterioles: vasodilation: want to increase bloodflow to any hypoxic regions of systemic tissues (increase chances of oxygen reaching these tissues)

Answer 54

**anything that alters flow thru the capillaries** - vasoconstriction - physical obstruction (thromboembolism) - shunt (blood skips lungs -> deoxygenated blood goes straight to systemic circ.) | recall: flow = pressure change / vascular resistance

Answer 55

Low: shunt perfusion High: dead space ventilation

Answer 56

In Pike's Peak / regions of higher altitude, the partial pressure of inspired O2 is lower (still 21% but of a lower atmospheric pressure), leading to a lower drive of gas exchange in the lungs. This leads to **hypoxic conditions in the alveolus** which responds by **vasoconstriction of pulmonary arterioles** -> pulmonic hypertension --> RV pressure increases due to increased afterload --> right-sided CHF | Bottle Jaw effect (subcutaneous edema from the CHF)

Answer 57

*ventilation status* b/c PaCO2 is only changed by hypoventilation (increases

Answer 58

**SA Node = -65mV** (spontaneously depolarizes w/ no plateau phase) **Ventricular Working Myocytes = -85mV** (fixed w/ plateau phase) ***at rest, cardiomyocyte in polarized (neg. inside, pos. outside)*** **Genesis of RMP**: - the Na+/K+ ATP-dependent pump (pumps Na+ out and K+ in) - Donnan Effect (presence of large, impermeable anionic intracellular proteins) - selective permeability membrane (K+ leakage channels allow it "leak" out w/out allowing Na+ in)

Answer 59

SA Node: 4 RMP -> 0 Spontaneous Depolarization -> 3 Repolarization Ventricular Working Myocytes: 4 RMP -> 0 Non-Spontaneous Depolarization -> 1 Overshoot -> 2 Plateau -> 3 Repolarization

Answer 60

SA node's ability to become (+) whenever is due to its Funny (Na+) channels, **Transient Ca2+ and Lasting Ca2+ channels**. Funny Na+ channels = activated on hyperpolarization during diastole and by phosphorylation by cAMP. The ventricular working myocytes CANNOT depolarize spontaneously b/c they depend on a voltage-gated Na+ channel.

Answer 61

voltage-gated "slow" Ca2+ channels that allow for ventricular refill

Answer 62

Atropine (parasympatholytic)

Answer 63

Bipolar Leads: detect positive (depolar.) and negative (repolar.) vectors Augmented Limb Leads : only detect positive (depolar.) vectors ## Footnote Size of deflection on ECG tracing always corresponds to size/magnitude of dipole in direction of electrode (leads)

Answer 64

**X-axis = 5mm**

Answer 65

I = normal, healthy patient; elective procedure II = slight-to-mild systemic disease with no obvious clincial signs III = mild-to-moderate, under control systemic disease with clinical signs IV = severe systemic disease, life-threatening, patient decompensated V = morbund patient, not expected to survive >24h | Add 'E' if ER ## Footnote American Society for Anesthesiologists (ASA) physical status: to quantify the amount of physiological reserve that a patient possesses at the time at which they are assessed for a surgical procedure, and which should also not be used as a sole predictor of operative risk to the patient.

Answer 66

1. Any pre-existing diseases? (CV, resp, renal, CNS) 2. What is the procedure to be performed? (elective, minimal vs. high risk, etc.) 3. How will you choose the appropriate anesthetic drugs? (what are your desired effects, what side effects do they cause, etc.)

Answer 67

1. Atropine 2. Glycopyrrolate Use = parasympatholytic (prevent bradycardia) Contrainindications: pre-exisiting tachycardia, narrow-angle glaucoma, equine colic ## Footnote competitive antagonists of ACh @ muscarinic cholinergic receptors

Answer 68

Glycopyrrolate does NOT cross BBB or placenta, but it has a longer onset and duration than Atropine

Answer 69

- Acepromazine - Benzodiazepines (diazepam, midazolam, zolazepam) - Alpha-2 agonists (xylazine, dexmed, romifidine)

Answer 70

Benzodiazepines

Answer 71

Alpha-2 receptor agonists: **biphasic BP effect: initial hypertension -> increased SVR -> reflex decr. CO -> prolonged, mild hypotension** can then be more likely for decr. perfusion -> pale mm

Answer 72

Flumazenil | competitve antagonism

Answer 73

increase affinity for GABA binding, potentiate GABA's inhibitory effects

Answer 74

Acepromazine

Answer 75

Diazepam (sedative agent, IM) and Etomidate (induction agent, IV)

Answer 76

Acepromazine and benzodiazepines

Answer 77

Buprenorphine (partial Mu agonist) and Butorphanol (Mu antagonist)

Answer 78

to decrease anesthetic requirements (aka decrease induction and maintenance drugs' doses!)

Answer 79

increases duration of GABA receptor's opening of Cl- channel -> hyperpolarization

Answer 80

smooth induction process short-acting (rapid redistrib. to vessel-rich groups) decreases ICP and IOP safe for C-sections easy/quick recovery ## Footnote vessel-rich groups = brain, kidneys, liver

Answer 81

**Profound CV and respiratory depressant** - decr. contractility -> hypotension - potential apnea; titrate/give IV slow - always provide supplemental O2 (poss. cyanosis)

Answer 82

single-use only as it has benzyl alcohol additive (no CRI b/c concern of buildup) only use as induction agent in cats b/c they metabolize it very slowly (aka very prolonged recovery)

Answer 83

MoA = indirectly potentiates GABA, directly evokes Cl- currents in absence of GABA at high doses -fast onset, short duration - MINIMAL CV and RESP EFFECTS - CAUSES ADRENAL SUPPRESSION -> DECREASES CORTISOL SYNTHESIS just after single dose (do NOT use in Addisonian pt or as a CRI) - V+ @ induction - no analgesia - hematuria

Answer 84

MoA = non-competitive antagonist @ NMDAR (a glutamate receptor) - CNS = hallucinatory behavior (is a dissociative); **increases ICP so don't use in epileptic pts**; eyes remain open but **Palpebral and Corneal reflexes maintained!** - CVS = increases HR, CO, BP - RS = no significant depression; "breath-holding"

Answer 85

Dogs/horses = extensive hepatic metabolism Cats = active metabolite (norketamine) eliminated unchanged in the urine

Answer 86

MoA = synthetic neuroactive steroid that enhances agonist binding to GABA receptor; new version has preservative that extends shelf life and has NO histamine release - NO analgesia - smooth induction and recovery (like propofol) - minimal CV effects - decreases cerebral bloodflow and ICP - no cumulative effect - crosses placenta but STILL SAFE for C-sections

Answer 87

1. **Recumbent** = field procedures (wound debridement, dehorn, PE, BW) 2. **Recument with physical restraint** = ruminants for surgical procedures requiring regional anesthesia 3. **Recumbent with back-up physical restraint, if needed** = castration, small mass removal, hoof trim 4. **Standing (horses)** = keep floor dry, cushion head, prevent dropping w/ sling, colic watch after long procedures ## Footnote Regional anesthesia: Neuraxial Anesthesia (Spinal/Epidural/Combined), Peripheral Nerve Blocks

Answer 88

Can cause priaprism b/c it prolongs penile prolapse | priaprism = prolonged rigid ejection

Answer 89

1. opioids 2. benzodiazepines 3. guaifenesin

Answer 90

Xylazine (alpha-2 agonist)

Answer 91

MoA = central muscle relaxant with no analgesia Uses: improve sedation/smooth induction agent (can be used as sole one in ruminants) with minimal CVS and RS depression Precautions: perivascular tissue irritant (hemolysis and necrosis); severe ataxis on recovery

Answer 92

Nostril flare, auscultation of crackles/wheezes or reduced thoracic sounds, SC emphysema, pain on thoracic palpation (broken rib), dull sounds on sinus percussion (fluid or mass)

Answer 93

Purpose = to ID where abnormal sound auscultated is originating from (i.e. upper or lower RT) 1. Plastic bag method 2. Exercise 3. Doxapram (a potent respiratory stimulant) 4. Obstruct the nares

Answer 94

A: normal, air-filled lungs. The horizontal lines = reverebations caused by u/s waves traveling thru the air B: indicate defect on pleural surface. "Comet Tails" = pleuritis, fibrin tags, SF abscesses (Rhodococcus equi) C: abmormally large amt. of fluid present b/w the parietal and visceral membranes (inflammation, infection, hemorrhage)

Answer 95

Respiratory secretions/samples can be collected and/or visualized from several different locaitons along the RT ## Footnote pharyngeal lymphoid hyperplasia, tracheal lesions (collapse, GCT, exercise-induced pulmonary hemorrhage)

Answer 96

**choose collection site closest to affected area / where infectious agent is most likely to be** 1. Nasal Swab or Wash - equires SEDATION; is a **non-sterile sample -> PCR** 2. Trans-Tracheal Wash (TTW) - **sterile sample -> C&S, PCR** (can be percutaneous or trans-endoscopic) 3. Bronchoalveolar Lavage (BAL) - **non-sterile sample -> PCR**