Note

Catheter
 1Fr = 0.33mm diameter (i.e 6 Fr = 1.98mm)
 Pushability: ability to transmit force from proximal end of catheter to distal end
Trackability: ability to navigate tortuous vasculature
Crossability: ability to navigate balloon catheter across narrow restriction in vessel
 after putting in catheter and GW, aspirate and flush the manifold and catheter
 best catheter cross stenotic aortic valve : AL1 or AL 2
 Berman (Arrow) catheter primarily used for Rt heart catheterization
 Amplatz catheter for high take-off RCA / LCA
 IMA catheter resembles JR4
 when performing LV gram, increase rate of rise is to make a smoother injection, less
catheter whip, and limit ectopy , but no change in amount of contrast needed
 LV gram on stenotic AO valve
1. Advance straight wire and end hole catheter like AL catheter to LV
2. Exchange wire for long 260 j wire
3. Remove AL catheter
4. Replace with PIG
5. Aspirate, flush and attach to injector tubing
 Injector for LV gram, 3 numbers: flow rate , total volume, PSI
 Distance btw Primary and secondary curve in JR4 is 4cm
 Distance btw Primary and secondary curve in JR5 is 5cm
* Primary curve engages the coronary ostium while the secondary curve stabilizes the
catheter along the opposite wall of the aorta
 Head hunter catheter is used to visualize the Lt and Rt ICA and ECA
 Dilated aortic root for LAD use JL 5

Sheath
 Color of sheath
- 4F red, 5F grey, 6F green, 7F orange, 8F blue, 9F black

GW
 compatible GW size for most catheter: diameter: 0.035’’
 coronary wire : 0.014’’
 0.035’’ x 260cm wire for intervening lower extremities from radial appoach
 GW features: Trackability, Steerability (tip can be shaped by pushing or pulling),
torqueability (amount of torque transmitted thru GW)
 Position the GW 2-4mm range distal to lesion but not as far as possible
 2-3mins for GW and catheter to be placed before removing it to wipe and flush it

FFR (fractional flow reserve)

 Pd(P after lesion) / Pa (P before lesion) < 0.8 (threshold for stenosis) = need PCI
 FFR 0.8 means stenosis cause 20% drop in blood pressure distal to lesion
 Adenosine IVI : contraindication: Asthma & beware of heart block
 Adenosine dose based on Pt BW. not IC but IV route
 Equalizing should be done before the lesion (radiopaque tip just pass out GC )
 mean arterial pressure after lesion / mean arterial pressure before lesion
 Exercising won’t dilate coronary artery but only arterioles and arterioles bring extraO2 to
cardiac muscle when exercising, pressure goes down when arterioles dilate
 * if MI, arteriles would not need to oxygenate dead muscle so the impacted arteriles shut
down and collapse
 FFR dilate the arterioles, but if the arterioles not dilating (muscle fibers dead), do not fix
the lesion
 IFR = similar to FFR without adenosine. IFR wire is more sensitive than FFR wire, can
get more information without adenosine
 Place IFR wire as distal as possible to lesion
 IFR >0.9, no need to fix ; <= 0.86 need to fix
 Exceptional case: >70% stenosis may yield FFR > 0.8 if there is significant collateral
flow to the vessel with the lesion in it

IVUS
 sound wave
 IVUS confirm proper stent apposition
 1: Adventitia; 2: Media; 3: Intima; 4: Lumen

 A: Catheter; B: Intima or true lumen; C: Thrombus/ blood behind the flap; D: Flap or
dissection

 Best way to told by IVUS that a stent is properly apposed: struts will be equidistant
 0.5mm per sec pullback speed recommended. not using sled will cause artifact

OCT
 light wave + contrast medium clearing blood which block light
 A: Stent Strut ; B: GW; C: OCT catheter; D: Vessel wall; E: Lumen
  B: concentric fibrous plaque; C: Calcified plaque

Echo imaging
 A:RV ; B: LV ; C:AO ;D: LA
 *

Balloon
 Scoring balloon -> treat fibrotic plaque and neo-intimal hyperplasia (post-intervention,
vascular remodeling due to the proliferation and migration of vascular smooth muscle
cells into the tunica intima layer)
 * NC, scoring, cutting -> calcified lesion
*S+C -> calcified nodules, fibrotic lesion, ISR
* NC -> for stent underexpansion
 cutting balloon showed inflate 60-90sec at nominal pressure; 1 atm per sec up and down
 Best practice for inflating and deflating scoring balloon: 1 atm per sec up and down. not
too fast and not too slow
 compliance describe balloon ability to yield change in pressure
 Adv of using filter over occlusion balloon for distal protection is allowing distal perfusion
 Purpose of Embolization filter: catch and minimize distal vessel thrombi from debris
 3 cm far should be maintained btw lesion and distal filter
 Balloon and (cover) stent used to treat flow-limiting dissection
 SVG angioplasty and carotid angioplasty will also use filter wire
*SVG more likely to release debris during angioplasty due to thinner wall, smaller
diameter, worse blood flow then LIMA (artery)
 over-tightening tuohy borst (head of Y piece) will prevent balloon inflation and deflation
 Balloon inflation into artery on healthy parts, will cause muscle fiber and capillaries
demage

Stent
 Wallstent is self expanding stent , for carotid artery
 Balloon expandable stent use in coronary; self expandable stent use in carotid
 Stent invented to prevent coronary artery muscle fiber from returning to their old fiber
size btw 31-180days
*expanding balloon is resetting the muscle fiber memory so that it believes that the over
expansion is normal
 *31-180days generally taken for coronary artery to recall old memory and try to back to
its regular size
 best stent: thinnest struts.
 Crushing stent technique
- Created for lesions in a side brance
- Created for lesions in a bifurcation
- First stent is positioned in the side branch with about 1/3 of its length protruding
into the main branch
- Side branch stent is deployed first
- Main branch stent is deployed second crushing the portion of the side branch
stent in the main branch

Embolization
 Fogarty balloon used to remove clot from vessel
*fogarty balloon catheter pass through blood clot then inflate balloon, push back balloon
with clot back to GC
 Type of devices to macerate blood clot: Angiojet, embolization device, thrombolytic
infusion
*angiojet = once catheter positioned, delivering saline solution under high pressure and
break blood clot pieces out thru same catheter
*Angiojet: mechanical thrombectomy device
 Angiojet = best device for management of an acute thrombus in vessel
 thrombolysis with thrombectomy includes: medication blood thinner + mechanical
maceration of clot
 Absolute contraindication for peripheral thrombolysis are recent surgery, pregnancy, Hx
of GI disorder, bleeding disorder
 DVT, PE with contraindication of blood thinner use vena cava filter
 Drug used for peripheral thrombectomy
1. thrombolytic (streptokinase, tPA, urokinase)
2. Antiplatelet
3. Anticoagulant
 Fibrinogen converted to Fibrin under the action of thrombin


Atherectomy
 Atherectomy of RCA, 1: vasodilator, 2. GC with SH, 3: temp pacing
 rotational atherectomy effectively treat calcified lesion
 rotablator involve use of burr to pulverize plaque into minute particles
 rotablator bur is diamond burr
 recommended rate of burr rotation when using rotablator 160000 - 210000
 Flush recipe for rotablator: 10ml rotaglide lubricant, NS, heparin, TNG, Verapamil
 Contraindication of rotaglide : Eggs and olive oil allergy
 burr rotate just proximal to lesion
 common complication of rotablator: distal embolization, perforation and dissection
 contraindication for rotational atherectomy: existing dissection, unprotected LMCA, ostial
lesion
 orbital and directional atherectomy catheter shave and debulk plaque
  Rapid saline injection is used to reduce the cavitation effect and expanding gas bubbles
inside the artery during laser atherectomy
*cavitation effect: Static pressure reduce to below liquid vapor pressure, lead to
formation of small vapor-filled cavities in liquid
 Laser atherectomy to vaporize the plaque (lesion)
 Excimer lasers treat thrombotic SVG, CTO
 Everyone needed to wear glasses in laser case

IABP (Intra Aortic balloon pump)

 increase blood flow to coronary arteries + whole body
 balloon position: descending aorta (btw subclavian artery and renal arteries)
 balloon inflate with helium
 heart diastolic, aortic valve close, balloon inflate to push blood to coronary arteries
= increase coronary perfusion
= increase blood flow to whole body
= reduce afterload
= increase SV and CO
 contraindication: aortic regurgitation, aortic dissecting aneurysm, abdominal aneurysm,
AV shunt
 desired physiologic effect of IABP: increase coronary blood flow
 Adjustment needed to IABP to Pt with reduced UO : advance balloon not to occlude
renal artery/ use subclavian access to place the balloon
 IABP balloon inflate when diastole ; deflate when systole
 IABP balloon deflate with ECG A wave (heart start to contract)
 IABP timed ratio: 1:1 (= full support) ; 1:2 typically
 this waveform shows IABP balloon inflation

LVAD (left ventricular assist device)

 provide perfusion regardless of intrinsic HR
*use in Pt who reached RSHF, help LV to pump blood to rest of the body
*implant surgically, blood from LV to aorta
 New device to LVAD for early severe cardiogenic shock : impella / IABP (older)

Impella
  When use impella:
- Cardiogenic shock
- High risk procedures
- Poor surgical risk that needs angioplasty
 impella catheter closely resembles pigtail
 Impella 2.5 = pump up to 2.5L/min RPM = 51000rpm
Impella 5.0 = pump up to 5.0L/min ; Revolution per min (RPM) = 33000rpm (= frequency
of rotation)
Impella CP = pump up to 4.3L/min
Impella RP = Rt side heart pump with 4.0L/min
 7Fr catheter for impella
 proximal end of aorta located in aorta ; distal end in LV
 4 reasons to impella
1. systolic heart failure
2. Big MI
3. cardiogenic shock
4. high risk PCI
 impella use archimedes screw mechanism instead of suction to draw blood. so it doesn’t
traumatize the RBC
 the impella can’t be turned off , but the patient has to wean off impella
 contraindication: AO valve disease, mechanical valve, moderate to severe aortic
regurgitation, and if the patient has significant Peripheral artery disease (as sheath and
catheter are large)

Pharmacology
1. Nitroglycerin: dilate c. arteries, reduce BP, relieve chest pain
2. metoprolol (beta-blocker): reduce BP, reduce HR
3. Adrenaline: cardiac arrest, increase BP
4. Atropine: increase HR
5. Heparin: blood thinner drug during PCI * ACT: determine effect of heparin
6. Aspirin (NSAID) inhibit arachidonic acid action
7. Plavix: antiplatelet for pre and post PCI
8. Protamine: reversal for heparin
9. Integrilin: use IV instead of Plavix
 Digoxin = cardiac glycoside
 primary indication for NAHCO3 : metabolic acidosis
 CCB : Nifedipine (Adalat) -> reduce BP + treat angina by relaxing blood vessel ,
increase blood to heart
*block Ca2+ channel in conduction process, slow the movement of Ca2+ across K+/Ca
channel and keep cardiac and arterial muscle dilated, reduce BP
* CCB (med with -pine at the end)
- verapamil/ isoptin; Cardizem/Diltiazem; amlopidine/Norvasc; nifedipine/ procardia;
felodipine
 TNG IC -> reduce BP + vasodilation
 TNG is a preload reducer (vein dilate, less venous return, reduce preload, less hard to
pump, relieve chest pain)
 TNG is also a afterload reducer
 Glycoprotein IIb/IIIa inhibitor = Epitifibatide (Integrelin)
 ReoPro (Abciximab) work on IIb/IIIa receptor. it is antiplatelet
 Antiplatelet: Plavix, ReoPro, ASA (acetylsalicylic acid)
 Commonly used + best short acting med for sedation in CCIC : Midazolam (Dormicum)
 Initial dose of midazolam: 0.5-1mg
 medication commonly use in hx of contrast allergy
1. Famatidine (reduce stomach acid)
2. diphenhydramine = Benadryl (antihistamine)
3. solu-medrol (synthetic corticosteriod)
 pretreat pt with contrast allergy: prednisone, the night before; Benadryl before procedure
 Common allergic response to contrast
- Cardiac and major anaphylactic response
- Smooth muscles and major anaphylactic responses
- Cutaneous and muscosal manifestations
 Inotropic agent: dobutamine predominantly stimulate beta-1 receptor
*act as inotrope to increase SV by increasing contractility
 Lasix inhibit Na+ reabsorption causing increasing UO
 Patient on Lasix, should monitor K level
 NPH insulin can’t be given with protamine together because of causing formation of
insoluble complexe with NPH insulin, impairing insulin absorption and thus the blood
sugar level & may cause anaphylactic reaction
 amiodarone treat atrial and ventricular arrhythmia; slow the HR
*K+ blocker
 Angiotensin receptor blockers (ARBS) : Losatan, Valsartan
 another name of warfarin = coumadin
 Patient with elevated creatinine and reduced GFR don’t take lasix (coz lead to
accumulate of lasix which pose increasing side effect like electrolyte imbalance, reduced
kidney function)
 ACEI (med with -pril at the end)reduce BP via kidney
*patient with renal artery stenosis will cause relaxation of renal artery leading to more
issue
 ACEI side effect : dry cough
 Benzodiazapines used in cath – midazolam/versed ; valium/diazepam
 flumazenil (Romazicon) is benzodiazepine receptor antagonist , antidote for valium
(diazepam)
 Heparin potentiate antithrombin
 Adenosine commonly given to patient with SVT
*slow electrical impulses, affect K+ and CA channel in conduction system, slow the HR
effectively
*slow e- impulses in SA node and perkinje fiber
 Dopamine
- low dose dopamine 1-5mcg/kg/min: go to kidney and only dilate those vessel.
Slow blood flow in kidney and improve renal function and UO
- 5-10mcg/kg/min: no benefit to kidney, UO goes down. Goes to heart and raise
HR
- >10mcg/kg/min: raise BP, raise HR, almost no UO

 BP med change one the CO SVR HR

 Adrenaline stimulate beta sites on heart and it bring heart rate up
 Atropine and Isoprel is a chronotrope and it bring heart rate up
*beta blockers are negative chronotrope
*beta blockers block the beta site that adrenaline is looking to sit on, thereby lowering
heart rate
*beta 1-selective antagonist only choose to block the site in the heart
 eg: metoprolol/Lopressor and atenolol/Tenormin
*beta 2-selective antagonist blocks beta site in lung and heart
eg: propranolol/ Inderal – narrow airway ; contraindication: COPD, Asthma, emphysema
 Atropine act on SA node. Atropine work directly on vagal nerve, which control the SA
node
 Bearing down stimulate vagal nerve, reduce HR
* Bearing down means that you try to breathe out with your stomach muscles but you
don't let air out of your nose or mouth
*Atropine and vagal maneuvers both stimulate vagal nerve, but they have opposing
effect on heart rate as they stimulate different receptor in heart
 Opiates in cath – Fentanyl/Sublimaze ; morphine
 Reversal agent for opiates : Narcan/Naloxone
 TNG treat coronary spasm

Drug name
 Novocain = Procaine (local)
 Lidocaine = Xylocaine (local)
 Buplvacaine = Marcaine (local)
 Diazepam = Valium (Benzodiazepines)
 Lorazepam = Ativan (Benzodiazepines)
 Versed = Midazolam (Benzodiazepines)
 Propofol = Diprivan (Benzodiazepines)
 Fantanyl = Sublimaze (Opiates)
 Morphine = MS Contin/ Astromorph (Opiates)
 Dilaudid = Hydromorphone / Hydrocodone (Opiates)
*Dilaudid 7 times stronger than Morphine
 Demerol = Meperidine (Opiates)
 Flumazenil = Romazicon (Reversal Benzo)
 Narcan = Naloxone (Reversal Opiates)
 Protamine Sulfate = Heparin reversal
 Verapamil = Calan / Isoptin (CCB) (Vasodilator)
 Dilitiazem = Cardizem (CCB) (Vasodilator)
 Nifidepine = Procardia (CCB)
 Nicardipine = Cardene (CCB)
 Norvasc = Amiodipine (CCB)
*inhibit entry of Ca2+ into heart muscle cells which slows the heart rate, lessens the
demand for O2 and nutrients and relaxes smooth muscle cells of blood vessels to cause
dilation
*treat angina pectoris, some arrhymias and hypertension
 Propranolol = Inderal (beta bocker)
 Metoprolol = Lopressor (beta bocker)
 Atenolol = Tenormin (beta bocker)
 Esmolol = Brevibloc (beta bocker)
 Labetalol = Normodyne / Trandate (beta bocker)
* beta bocker reduce HR, force of contraction, and conduction velocity of heart. Use in
tachycardia and angina
 Amiodarone = Cordarone (Antiarrhythmic)
 Adenosine = Adenocard (Antiarrhythmic)
 Atropine = Anticholinergic (Antiarrhythmic)
 Dobutamine = Dobutrex (Inotropic)
 Epinephrine = Adrenaline (Inotropic)
  Norepinephrine = Levophed/ Noradrenaline (Inotropic)
*Inotropic treat hypotension and poor organ perfusion
 Dopamine = Intropin (Inotropic) (Vasoconstrictor)
 Digoxin = Lanoxin (Inotropic)
 Heparin = unfractionated heparin (Antithrombin)
 Warfarin = Coumadin (Antithrombin)
 Dabigatran = Pradaxa (Antithrombin)
 Angiomax = Bivalirudin (Antithrombin)
 Eliquis = Apixaban (Antithrombin)
*Thrombolytic are acting quicker with combination of antithrombin
 Effient = Presugrel (Antiplatelet)
 Aspirin = ASA acetylsalicylic acid (Antiplatelet)
 Anagrelide = Agrylin (Antiplatelet)
 Clopidogrel = Plavix (Antiplatelet)
 Ticlopidine = Ticlid (Antiplatelet)
 Losartan = Cozaar (Angiotensin II Receptor Blocker)
 Valsartan = Diovan (Angiotensin II Receptor Blocker)
 Phenylephrine = Neo – Synephrine (Vasoconstrictor)
 Metaraminol = Aramine (Vasoconstrictor)
 Midodrine = ProAmatine (Vasoconstrictor)
 Ergonovine = provoke coronary spasm (provocation test)
 Nitroglycerin = Tridil (Vasodilator)
 Nitropresside = Nipride (ACEI)
 Captopril = Capoten
 Lisinopril = Prinivil, Zestril (ACEI)
*Treat high BP, heart failure and heart attacks, relaxes blood vessels
 Lasix = Furosemide (Diuretic)
 Prednisone = Solumedrol (steroid)
 Benadryl = Diphenhydramine (Antihistamine)
 Pepcid = Famotidine (Antacid)

Radiation
 Source to image distance (SID)
= distance btw tube (X-ray source) and image receptor (image intensifier , II)
 increase SID = better image and reduce exposure
= raise Pt table , increase SID indirectly (= larger space btw tube and II)

 Object to image distance (OID)

= distance btw object being imaged and II
 reduce OID = increase quality of image and reduce exposure
 Attenuation (衰減) reduces beam energy as passes through tissue
 major source of radiation scatter : Patient
 Radiation safety measures:
reduce exposure time
distance: increase SID , reduce OID
shielding : Apron 0.5mm(Pb) thick
Dosimeter
 reduce frame per sec
select magnification and exposure detail as needed only
 annual occupational radiation whole body dose limit: 50mSv = 50mGy = 5rem
 when generating ionizing radiation, photon emitted from focal spot
*focal spot = anode surface (+ve)
*source of x ray (xray tube)= cathode (-ve)
*photon no charge follow light wave path
 LAO lateral and LAO cranial -> highest dose operator receive
 Lateral , LAO lateral 60 cranial 30, RAO 40
 requirement measurement of image intensifier: 23cm field size for cardiology; 40cm field
size for general vascular
 image intensifier converts light rays into image
 kilovoltage determine no. of electrons generated by Xray tube
 exposure factors made up of 3 components : KV, mA, time
 minimum safe distance oneself to Xray source = 6 feet
 low osmolality contrast best for patient as less osmotic pressure and thus less tissue
damage
*osmolality refer to contrast’s ability to pull fluid into intravascular space
 Ideal contrast vol = 3ml/kg
 hypertonic contrast will pull particles from cell causing fold up on themselves
 Visipaque is the most like the human body and has similar number of particles
 Using collimator lowers the radiation dose to patient ; reduced size of xray beam
 Zooming increase the patient radiation dose
 Safer to collimate than to zoom an image : zoom use more radiation
 Tissue burn are more likely with collagen vascular diseases: as cell wall is thicker
 Patient with higher BMI will generate greater scatter and will have less radiation being
absorbed and less able to interact with film
 safest view for the patient is AP, low radiation dose
*LAO 60 cranial 30 (1) ; LAO 30 (2)
* 1 results in more xray absorption to patient
* 1 will give more scatter as more tissue engaged , more scatter, less radiation to make
picture
* 2 will have clearer detail, closest to AP less tissue interact with, less scatter
 Best view for visualization of stent: LAO 60, Cranial 30 or LAO 30, Cranial 0 (2)
- 2 is better (always ans the view that is closest to AP)
 Isocenter: the height we put the table at to minimize panning. This reduce the amount of
radiation
 Cine delivers higher amount of energy to patient ; Fluoro result in image with more noise
RAD stand for radiation absorbed dose (=equal to the radiation exposure)

Xay angle

AP: Straight angle entering anterior side and exit posterior side
PA: Straight angle entering posterior side and exit anterior side
Lateral: Straight angle from Lt to Rt or Rt to Lt
Caudal: Longitudinal angulation that is angle away from head
Cranial: Longitudinal angulation that is angle towards the head
RAO(Rt anterior oblique): angle towards Pt right side
LAO(Lt anterior oblique): angle towards Pt left side
Spider view: LAO caudal

LCA
 AP cranial
for most lesions in the p-m LAD. shows the diagonal and septal branches in opposite
directions, well separated from the LAD.

 RAO cranial
reducing the overlap of proximal LAD

 LAO cranial
straightens out the proximal and mid LAD
bifurcation of Diag
 RAO caudal
p-mLCX and bifurcation of OM branches are seen

 LAO caudal (spider view)

bifurcation of LM, LAD, LCx
dLAD
RCA
 RAO
p-mRCA seen, extend of PDA
no ostium RCA seen

 LAO
ostium RCA, full RCA seen
bifurcation PLB and PDA seen
 AP cranial

 RAO view for LV best visualization: anterior and inferior

LAO view for LV best visualization: lateral
AP view for LV best visualization: anterior
 LA is the most posterior in AP projection ; RV is the most anterior in AP projection
 If the spine is on the right, it is a LAO view; spine is on the left side, it is a RAO view
 LAO view; A: aortic valve; B: posterolateral; C: inferior; D: Apex; E: Septum
1. anterobasal; 2: anterolateral; 3: apical; 4. Diaphragmatic; 5. Posterobasal; 6: septal; 7:
Posterolateral

*
 Anything LAO to check aortic dissection
ECG
 1st degree HB = AV nodal conduction delay
 Normal PR interval = 0.12 - 0.2sec
  STEMI in V5 V6 I aVL = LCx infract
STEMI in V1 - V4 = LAD infract
STEMI in II III aVF = RCA infract (inferior wall LV MI)
 Sharply pointed T wave could indicate hyperkalemia
*Hypo K predisposes the patient to ventricular arrhymias
 QRS complex represent duration of ventricular contraction
 Q wave represent initial phrase of depolarization
 Posterior infract: V7-V9 , V1 and V2

Formula
1. Fick Cardiac output -> Normal 5-6L/min
Golden standard to measure CO
CO = O2 consumption / Arteriovenous O2 difference
 O2 consumption = BSA x 125
 VO2 mean O2 consumption
 Arteriovenous O2 difference = (AO sat - PA sat) x (Hb x 1.34) x 10 or (AO sat x
Hb x 1.34) – (PA sat x Hb x 1.34)
 Arterial O2 content = AO sat x Hb x 1.34
 Venous O2 content = PA sat x Hb x 1.34
 FICK is the most accurate in pt with tricuspid regurgitation
2. normal cardiac index -> Normal 2.5 - 3.5
 BSA greatly affect CO, CI eliminate this factor
 CI (L/min/m2) = CO / BSA

3. Gorlin (Aortic valve area) -> Normal 3.0cm2 ; Severe AS 1.0cm2; Critical AS < 0.7cm2
  Valve area (cm2) = [(CO x1000) / systolic ejection period (s) x HR] / 44.5 x
√mean gradient

 Gorlin is gold standard of valve calculation

 4 steps to determining gorlin aortic valve area
- convert CO from L/min to ml/min
- cal the systolic ejection period in sec/min (i.e SEP x HR)
- cal the aortic valve flow = CO/SEP(sec/min)
- cal the aortic valve area: Aortic valve flow/ 44.5x square root of the mean
gradient

4. Gorlin (Mital valve area)

 Valve area (cm2) =[(CO x1000) / Diastolic filling period (s) x HR] / 37.7 x √mean
gradient
 4 steps to determining gorlin mitral valve area
- convert CO from L/min to ml/min
- cal the diastolic ejection period in sec/min (i.e DEP x HR)
- cal the mitral valve flow = CO/DEP(sec/min)
- cal the mitral valve area: mitral valve flow/ 37.7x square root of the mean
gradient

5. Hakki (for aortic valve area)

 Valve area (cm2) = CO / √peak to peak gradient
*peak to peak gradient = LV systolic - AO systolic
6. Systemic vascular resistance (SVR) -> Normal 700-1600
 SVR (dyn.s.cm-5) = 80x(AO mean P - RA mean P) / CO

 Amount of work the LV has to do to push blood out of aorta

7. total systemic vascular resistance

 SVR (dyn.s.cm-5) (absolute resistance unit) = 80x AO mean P / CO

8. SVR in wood units -> Normal 9-12

 wood unit (hybrid resistance unit)= SVR(dyn.s.cm-5) / 80

9. pulmonary vascular resistance (PVR) -> Normal 20-130

 PVR (dyn.s.cm-5) = 80x(PA mean P - PCW mean P) / CO
 Amount of work the RV has to do to push blood into pulmonary artery

10. Total pulmonary vascular resistance

 PVR (dyn.s.cm-5) (absolute resistance unit) = 80x PA mean P / CO

11. PVR in wood units

 wood unit (hybrid resistance unit) = PVR(dyn.s.cm-5) / 80

12. Qp (pul circuit) / Qs (systemic circuit)

 >1 = Lt to Rt shunt
 <1 = Rt to Lt shunt
 Qp/Qs = (Ao sat - mixed venous sat)/ (PV sat - PA sat)
 * mixed venous sat = (3xSVC sat ) + (1 x IVC sat) / 4 -> flamm’s equation

13. Mean arterial pressure (MAP)

  MAP = (systolic P x1 + Diastolic P x2) / 3

14. Regurgitant fraction (% of blood that regurgitate back thru aortic valve)
 = (Angiographic CO - Thermal CO) / Angiographic CO

 Angiographic SV - Thermal SV) / Angiographic SV

15. Angiographic CO (Lt ventricular minute flow)

 = SV x HR / 1000

16. Stroke vol

 End diastolic vol (EDV) - End systolic vol (ESV)

 or CO/HR

17. BP
 CO x SVR / HR x SV x SVR

18. Ejection fraction

 SV/ EDV or (EDV-ESV)/EDV

Normal value
 normal O2 consumption: Adult- 250ml/min ; child - 150ml/min

unit

 1g = 1000mg
1mg = 1000mcg
 0.5kg = 0.5L = 500ml
 CO unit : L/min
  Cardiac index: L/min/m2
 1 inch = 2.54cm

Physiology
 Pt hyperventilate, blood gas: reduce CO2, increase pH
 Repiratory acidosis treated by increasing ventilation
 LDH reaches peak conc. 3-4 days post MI
*LDH increase 24-72hrs following MI
* were widely used in the past for dx MI , but now TnI
* release when tissue damage
* CKMB also cardiac marker when MI
 O2 (blinding) capacity at 1atm = 1.36mlO2 x 1g Hb
 normal mean blood pressure for systemic circulation = 70-105mmHg
 renal function indicator in blood chemistry : creatinine
 Aortic regurgitation will increase pulse pressure
*pulse pressure = systolic - diastolic pressure , normal = 40mmHg
 LV dp/dt is a barometric measure of LV contractility , normal >200mmHg
(i.e. pressure difference /time difference)
 RV dp/dt is a barometric measure of RV contractility and measure of tricuspid
regurgitation
 Normal pH acidosis < 7.35 - 7.45 < alkalosis
PaCO2 acidosis < 35 - 45 < alkalosis
HCO3 acidosis < 22 - 26 < alkalosis
 preload affected by blood filling vol.
 Stroke vol mostly affected by or relate to preload
 chronic untreated hypertension increase afterload
*afterload = pressure of heart needed to exert to eject blood during each ventricular
contraction
 S1 heart sound = Lubb (AV valve close) ; S2 heart sound = Dubb (semilunar valve
close)
 Dicrotic relates 2nd part of arterial pulse occurring during diastolic = closing of aortic
valve + closure of pulmonic valve
Anacrotic notch = small notch on ascending limb of arterial pulse waveform, before peak
of waveform, caused by momentary halting of blood flow when aortic valve half closed
 Pulsus Alternans is an arterial pulse with alternating strong and weak beats found in Pt
with Lt heart ventricular failure

 Pulsus paradoxus is a phenomenon when your blood pressure decreases with inhalation
, cause:
1. sign of temponade
2. domontrate abnormal variation in filling pressure during inhalation
3. can be seen in PCW tracing
 ABI (ankle - brachial index) measures ratio btw ankle / brachial BP
*simple way to check for peripheral artery disease
*low ankle-brachial index number can indicate narrowing or blockage of the arteries in
the legs.
*<0.9 = Dx of PAD

 end expiration is optimal measurement point for measuring pulmonary arterial wedge
pressure (PAWP)
 LV apical akinesis: Lack of apical wall movement in LV
 akinesis = no movement ; dyskinesis = disorganized movement; hypokinetic = reduced
movement
 Cardiac power output is the single hemodynamic indicator of in-hospital mortality in
cardiogenic shock
*cardiac power output: amount of work the heart can do in a given amount of time
 coronary arteries perfuse heart at diastole ; when the aortic valve closed, ostium opens
for blood
 Person with no respiratory disease need elevated CO2 to trigger drive of breathing
 kidney is responsible for metabolic change in pH
 tests to evaluate kidney function: creatinine, GFR, creatinine clearance, urine output
 A Fib and A flutter increase risk of stroke
 Paitent with COPD maintain O2 sat at 88-92%, and have increased CO2 and decreased
O2 sat , increasing respiratory rate
*high O2 will suppress respiratory drive
* COPD cause higher PCWP, Hb goes faster , take less O2
* higher PA pressure too as high PCWP causing back flow of blood to PA
 Deep skeletal muscle pump system act on the blood to maintain RA pressure at 5mmHg
 O2 conc. in Hb leaving the lung 98% ; entering RA 70%
 30% of Hb O2 will give to organ
 Higher PCWP, Hb goes faster in lung , less O2 acquired by Hb
 Electrical conduction order : SA node -> AV node -> Bundle of His -> L/R bundle
branches -> Purkinje fibers
 Mean arterial pressure needed to maintain cerebral profusion is 75-85mmHg
  Kidney and liver regulate BP
*1st , SV drop, brain tells kidney to circulate renin in storage;
*2nd angiotensinogen in liver
*work tgt to make angiotensin I
 Angiotensin II is potent vasoconstrictor. Tell kidney not to eliminate salt and increase the
amount of fluid in blood, causing SV to go up and increasing CO
 Angiotensin I and ACE equal to angiotensin II
 ACEI to lower BP:
- Stop angiotensin I from converting to angiotensin II. Stop Kidney from store up
fluid. Reduce SV
 ARB – look for angiotensin II and inactivate it to prevent it from returning to kidney to
hold fluid
 Properly timed atrial contraction can increase SV and CO

Clotting cascade
 there are 2 pathways to imitate clotting cascade (intrinsic and extrinsic)
 when endothelial cell in coronary artery knocked off and muscle fiber exposed, clotting
cascade starts
 Clotting cascade: series of chemical reactions involving 12 plasma clotting factors that
lead to final conversion of fibrinogen into a stabilized fibrin mesh to control bleeding
 Platelets are not activated until they stick to the collagen on the muscle fiber of the
coronary artery. This sends a msg to the liver to release the first clotting factor
* first clotting factor = Von Willebrand clotting factor(VWF) : released by liver, and it
make sure platelets stick to the muscle fiber
*Factor VIII released right after the VWF . It make sure platelet stick even better than
VWF, but it cannot be released by liver until after the VWF
*Body will release calcium and liver will release arachidonic acid after the release of
VWF and Factor VIII
*Arachidonic acid: goes to the platelet allowing it to stick even more tightly. it can’t be
released until after VIII
 Pt with heart attack take aspirin as it blocks the action of arachidonic acid. Person is
under MI continues to make clot and aspirin help prevent the formation of more clot
 After arachidonic acid back to liver, Adenosine diphosphate (ADP) release ; ADP
prepare IIb/IIIa sites of platelet for fibrin and help to stick to the corner of another platelet
 Plavix(Clopidogrel), Brillenta(Ticagrelor), effient(Prasugrel), Kengreal (Cangrelor): block
the action of ADP and hence prevent it’s action of preparing the IIb/IIIa site for fibrin.
They are P2Y12 ADP receptors inhibitor
 ReoPro (abciximab) is a IIb/IIIa inhibitor, sit on IIb/IIIa site so that fibrin can’t sit there , and
platelet can’t stick together
 All med working in phrase I of the clotting cascade are called antiplatelet agents
 antiplatelet agents: aspirin, plavix, brillenta, effient, ReoPro, eptifibatide (Integrelin)
 Phrase I clotting factors: : VWF, VIII, body release calcium, arachidonic acid, ADP, IIb/IIIa
 first step in phrase II of clotting cascade: Liver releases tissue factor
 all clotting factors created by liver
 all clotting factor required vit K
 most effective agent for thinning blood : Coumadin (warfarin)
*Coumadin inactivate vit k
*reversal agent of coumadin : Vit K
 Lovenox (enoxaparin) (Clexane): prevent conversion of X to Xa and hence the formation of
thrombin (i.e. no thrombin, no fibrin)
 Heparin (heparin sodium) prevent prothrombin to thrombin
  angiomax prevent prothrombin to thrombin + prevent thrombin from acting on fibrinogen to
become fibrin
 Angiomax(Bivalirudin) is more effective than heparin as 2 clotting process inhibited involved
in angiomax
 Antithrombin agent: Heparin, Angiomax, Lovanox
 antithrombin also called anticoagulants
 Pradaxa (Dabigatran) is antithrombin
 normal range of K+ = 3.5-5.0
 CVP (central venous pressure) reflect ability of the heart to pump blood into the arterial
system and the amount of blood returning to the heart
 CVP measure at SVC

Cardiogenic shock
 Cardiogenic shock marker: BNP, Tnl, Lactate (by product of anaerobic metabolism,
marker of tissue hypoxia)
 Cause of cardiogenic shock: LV failure > severe MR > ventricular septal rupture > RV
failure > tamponade
 Leading cause of STEMI : cardiogenic shock
 DM patient have greater incidence of developing renal failure after contrast
administration
 LA protective mechanism in case of increasing blood vol. due to MS / MG : have protein
to sense vol. and allow muscle fiber to get longer so as to hold rising vol and prevent
blood from flowing back to lung

Pathology
 Hypertrophic cardiomyopathy reduce LV compliance, normal systolic function
 LMCA disease is the highest risk of mortality during PCI
 ASD / VSD will invalidate Fick CO result
 Proximal renal artery stenosis is the most commonly found
 commonly cause of renal artery stenosis : atherosclerosis
 arteriosclerosis is the thickening/ hardening and loss of elasticity of the walls of the
arteries; build up of plaque on the arterial wall
 Water hammer pulse is caused by Aortic regurgitation
*abrupt, rapid upstroke of peripheral pulse followed by rapid collapse

 Imaging used to Dx aortic insufficiency: CT, MRI, TEE

 Pericarditis = infection can scar and fuse both walls of pericardium together, limit the
heart to expand (coz of stiffness) and keep AV valve open during diastole -> not enough
blood fill in ventricle btw heart beat -> produce high pitched sound due to early diastole =
pericardial knock -> indicate diastolic dysfunction
 Kussmaul sign: inspiration -> -ve intrathoracic pressure -> increase venous return to Rt
heart -> Anything condition reduce heart compliance (eg contrictive pericarditis, cardiac
temponade, restrictive cardiomyopathy, tension pnemothroax) -> Rt heart can’t
accommodate increased venous return -> JVP rise during inspiration + RA pressure
increase
 restrictive cardiomyopathy/ contrictive pericarditis cause equalization of RVEDP and
LVEDP
*normally, LVEDP > RVEDP
*RC cause stiffness of ventricular wall, making both RVEDP and LVEDP rise
*Make them similar
+RC decrease SV and CO
 Tetralogy of Fallot (TOF) -> mainly congenital
1. pulmonary valve stenosis
2. VSD
3. Aorta lies directly above VSD (overriding aorta)
4. Rt ventricular hypertrophy

 Truncas arteriosus -> congenital

*VSD + one large blood vessel leads out of heart (Aorta fuses with PA)

 Abdominal aortic pulsation > 3cm -> may have aortic aneurysm
 Type of ASD : 1. ostium secundum (located in the middle 1/3 of atrial septum)
2. ostium primum (located in the lower portion of atrial septum)
 Tricuspid stenosis raise RA pressure
 RV MI, no change in systolic pressure (P to get the blood pass thru pul. valve), increase
in RVEDP, no change in diameter of pul. valve and tricuspid valve ; LV MI the same
 RV systolic pressure will rise (>25mmHg) in case of pulmonic stenosis, higher pressure
needed to push blood across stenotic valve
*so PA pressure can’t higher than RV systolic pressure all the time
 lesion in coronary artery exerts pressure to the cell wall causing arterioles not to be able
to deliver O2, causing muscle fibers start to die + making artery less able to expand and
contract


 anterior wall MI associate with LV MI (coz’ LAD supply anterior wall )
*S/S: Lung congestion, reduced O2 sat, BP drop
*anterior wall MI is the most serious MI and associated with worst prognosis
*anterior wall MI can use TNG (but not inferior wall MI)
 Transmural MI = involve 3 layers (full thickness) of heart
 Inferior wall MI associate with RV MI
*S/S: JVD, potential AV block. bradycardia
* don’t use TNG
 Transposition of the great vessel. Patient can live as VSD present. Cyonotic

 Mitral stenosis, LVEDP at first remains unchanged (LA try best to get ventricular filling),
later, LA can’t fill it enough, LVEDP drops
 Pulmonic stenosis (narrowing of pulmonic valve) is mostly caused by congenital
 Bleeding abnormalities: Bleeding > 10mins after cath , Platelet < 80000mm^3,
Prothrombine time (PT) > 1.2sec, Partial thromboplastin time (PTT) > 1.2sec
 Coarctation of aorta = congenital narrowing of descending aorta
Haemodynamic waveform
 Transducer zeroed and fall on floor, pressure being read is higher, and transducer need
to re-zero
 ECG can’t read A wave = AF ; elevated V wave in RA pressure = TR (coz blood back
flow)
 RA pressure reduced = poor preload -> hypovolemia
 V wave of PCWP indicate mitral insufficiency
 PCWP best reflect LV preload
 increased RVEDP = RV infract
 increased LVEDP = increased LV preload (can be caused by LV failure)
 RVEDP normal: 0-8mmHg
*high RVEDP = pulmonary hypertension / pulmonic stenosis or chronic COPD, RV MI

 Normal value of diff. pressure

RA pressure = 2-6mmHg (5)
RV systolic pressure = 20-30mmHg (25)
*high RV systolic pressure: PE, COPD, Pul. Stenosis, pul. hypertension
RVEDP = 0-8mmHg (5)
PA systolic pressure = 20-30mmHg
*high PA pressure: PE, COPD, Pul. hypertension
PA diastolic pressure = 7 -12mmHg
mean PCWP = 7-12mmHg
LA pressure = 7-12mmHg
EDP systolic pressure = 90 - 140mmHg (120)
LVEDP = 7-12mmHg
AO systolic pressure = 90 -140mmHg (120)
AO diastolic pressure = 60-90mmHg
 RA waveform
*normally A wave (A contraction) > V wave (venous filling)
*regurgitation, V wave > A wave
 increase RA waveform / RA pressure caused by 1. TR, 2. RVMI, 3. ASD
 PCWP = LA pressure = LVEDP (normally PCW A-V wave similar) , coz no valve btw
*right heart pressure (PCWP) best reflect LV preload
*MR, V wave > A wave
*Chronic MR, MS, LA protective, PCWP elevated than normal
 RA mean = RVEDP
RV systolic = PA systolic
 PA diastolic = PCW mean
LV systolic = AO systolic
 RV pressure shows us : systolic, diastolic and RVEDP
 RVEDP not zero because some blood are not ejected out, making RVEDP
 normal RV ejection fraction = 55-60% , making RVEDP
 RVEDP can be measured at the peak of R wave on ECG where it crosses the waveform
is RVEDP
 EF rise, EDP reduce
 Mitral valve close immediately following the peak of A wave
 A: RA ; B: RV; C: PA; D: PCW

 Dampened pressure: occur in the RCA ; Ventricularized pressure: occur in the LCA
*dampened pressure = catheter tip fully occluded ; ventricularized pressure not
completely occluded, still have small steam of blood coming in vessel
* both waveform don’t inject contrast, otherwise trigger VF, or dissection
*normal engaged catheter can detect AO pressure (blood freely come in coronary vessel)
 PA pressure components: systolic, diastolic, mean pressure
 PA wedge show reading of LA
 PA and AO pressure wave forms look alike, but scale can tell the difference
 Mitral stenosis, will see gradient btw LV and PCWP ; AS, will see gradient btw AP and
LVP
 MR, LA pressure increase and show elevated V wave
 LV/AO pullback to shows AS

Anatomy
 Conus is usually 1st branch of RCA
 anterior triangle of neck = anatomical landmark for internal Jugular vein (IJV), and hence
for RV biopsy
 arterioles has the most impact on vascular resistance
 vascular resistance/ pressure mostly affected by radius / diameter of vessel


LAD anterior, lateral wall of LV + ⅔ interventricular septum

Diag anterior, lateral wall of LV

LCx lateral, posterior wall of LV + LA

OM lateral wall of LV

Septa anterior septum

l

RCA RA, RV, inferior wall of LV , AV node , SA node

PDA RV, LV posterior wall, posterior inferior interventricular septum

 LAD supply greatest portion of myocardium
 LAD run down interventricular septum
 RCA and LCx run in the AV groove (=AV sulcus) of heart
 RCA is dominant in over 85% of the population
 LMCA diameter is 4-5mm
 LCx diameter is 3-4mm
 Epicardial layer of heart arise in coronary arteries
 Coronary sinus: collects blood from the coronary veins and returns the blood to the RA
 muscle fiber in coronary artery run longitudinal not in circular
 Intima of artery covered with cell called endothelium
 Innermost layer of artery is intima
 Main jobs of endothelium
1. create a slippery environment for blood flow
2. reproduce quickly to replace any lost endothelial cells
3. make nitric oxide to dilate the arteries and make easier flow
4. act as a magnet for bad cholesterol
 medial part of artery is muscle layer
 Adventia layer of artery: outside layer of coronary artery, allow O2 come in and give to
muscle fibers (pressure of arterioles delivering O2 to adventia is 7-12mmHg, i.e. PCWP)
 Cephalic vein located at antecubital fossa (=anterior side of elbow) of the lateral side of
arm
 subclavian vein is continuation of axillary vein
 Position of kidney relative to spine: L1 & L2
 IJV landmark: head of sternocleidomastoid muscle and clavicular head
 Myxoma (cardiac tumor) mostly in LA
*benign gelatinous growths found most often in the LA of females that cause flow
obstruction and embolic phenomena
 Eustachian valve lies at the junction of IVC and RA
 A: popliteal artery; B: anterior tibial artery; C: peroneal artery; D: posterior tibial artery
  A: Lt subclavian artery; B: Lt vertebral artery; C: Lt carotid artery; D: Rt vertebral artery;
E: Rt carotid artery; F: Rt subclavian artery; G: innominate artery (=brachiocephalic
artery)

 largest valve in heart is tricuspid valve

 pulmonic valve is 5x smaller than tricuspid valve. - 5mmHg (RA pressure) to cross T
valve, and 25mmHg (RV pressure) to cross p valve
 RV chamber is larger than LV , as LV is more muscular
 Baroreceptors located at arch of the aorta and carotid arteries
 Aortic valve have smallest area

Symptom related
 chest pain occurs at rest = unstable angina
 chest pain when acting but subside at rest = stable angina
 physical sign of (Rt) heart failure: distention of jugular vein, edema in leg feet , abdomen,
SOB
  RA pressure rised , JV distention in phy. exam
 initial signs of retroperitoneal bleeding : reduce BP, lower back pain/ flank pain (below rib
and above ilium), reduced hematocrit(proportion of RBC in blood), tachycardia
 Vasovagal reaction s/s: reduce BP, reduce HR, nausea


Acute tamponade hypotension

venous distension

diminished heart sound

Chronic tamponade increase venous pressure

Ascites

diminished heart sound

 symptoms of cardiogenic stock: reduced BP, increase HR, weak pulse, pallor skin
 Aortic dissection symptom: back pain , not associated with ECG change and not relieve
MONA

Puncture related
 high common femoral puncture associate risk of retroperitoneal bleeding
*the back wall of artery is stuck. Manual pressure or closure device do not close the
back hole and blood leaks into the retroperioneal space
 5 vascular access sites for Lt common femoral artery intervention:
1. Lt radial 2. Rt raidal 3. Rt femoral 4. Lt or 5. Rt popliteal artery
 posterior tibial pulse located near medial malleolus
 Dorsalis pedis pulse located at anterior foot
 Cannulation of femoral artery should be one finger breath below inguinal fold (can
prevent retroperitoneal bleed)
 2-3cm or more below the inguinal fold puncture increases incidence of vascular
complications
 Radial artery access: 1-2cm cranial to the boney prominence of the distal radius
 Sheath placement should be below inguinal ligament, above the bifurcation of the
superficial femoral and the profunda, medial to the femoral head
 common femoral arterial puncture not commonly cause PSA
 If femoral puncture site is too lateral, patient will feel pain down the leg because of the
irrigation of femoral nerve
 puncture SFA or profunda or external iliac artery, or puncture low side of femoral artery,
pseudoaneurysm can occur as complication
 should always cannulate above the bifurcation
 contraindication of using radial access : occluded ulnar artery
 Heparin, verapamil, TNG are potentially use with radial access

Pre procedural checking and preparation

 informed consent for catheterization valid for 24hrs
 Door to balloon time : 90mins
  Pt with diabetes and renal failure -> give fluid to hydrate
 at least 500ml IV NS before cath coz of toxic effect of contrast on kidney, which secrete
antidiuretic hormone to hold contrast in kidney
 8 hrs fasting prior to catheterization
 INR and PT/PTT need to be in normal range prior to cath, as it can affect hemostasis
and affect cannulation
*normal PT/PTT: 11-16sec
*normal INR: 0.8-1.2
 WBC count can evaluate patient for infection
 vaso vagal reaction are more likely when Pt is dehydrated
 procedure for picking up patient:
 check for informed consent
 use 2 pt identifiers
 check IV
 NPO status
 Confirm with patient procedure being performed
 Emergency room equipment checked in the procedure room
 Xray and crash cart (e trolley), check first when coming into lab
 Locate the pulse prior to draping

Procedure related complication

 Greatest risk of Lt ventriculography = Arrhythmia
 Top 3 cath complication: MI, dissection, stroke
 Longer procedure increase risk of stroke
 frequent equipment change increase risk of stroke
 ACT to be kept during PCI: >250 ; 250-300
 Heparin needed to give during PCI: 50-70unit per kg
 Minimum amount of following giving heparin that you can check ACT : 5 mins
 After 5 mins, ACT reading is 150, give 2000-5000unit heparin, repeat ACT and heparin
until ACT 250 -300 sec
 PT/PTT used to monitor heparin therapy if ACT is not avaliable
 If LV aneurysm, don’t perform LV angiogram as it can dislodge clot causing stroke
 Vaso vagal reaction tend to occur when placing the sheath. Mx: give IV fluid to increase
vol. , Atropine, protect airway if needed
 Foley should keep at the level of the bladder or lower at all times
 Snare can be used to retrieve a foreign body
 Washer that is visualized on fluoroscopy is placed to mark the proximal vein graft
*opaque

Aseptic technique and sharps disposal

 Open packages away from you first
 Drape the side closest to you first
 ethylene oxide used to sterilize equipment
 first thing to do when cleaning the room: remove sharps

Post procedure related issue and complication

 depigmented scar in post radial procedure, caused by overly tighten closure device for
long period
 radial artery hemostasis -> every 15mins for 1st hr monitoring
  hold manual pressure 2-3cm above sheath insertion point when removing an arterial
sheath
 for each French size plan on 3 mins of manual pressure of holding
 post cath vital sign: Q15min x4 then every 30mins until discharge (at least twice)
 Always measure hematoma in cm and mark with pan. Never compare it to a fruit / other
objects
 arterial spasm is common complication of transradial approach
 critical limb ischemia lead to Cellulitis , wound infection and amputation of limb
 Procoagulant used to obtain hemostasis when using vascular closure device -> collagen
*procoagulant = sub. promoting blood clotting process
 Vascular closure device mechanism

Perclose suture-mediated Active: mechanical/ Chemical process to actively close

femoral artery puncture site
Angioseal collagen and
suture-mediated

Starclose Nitinol Clip

Mynx PEG hydrogel plug Passive: provide mechanical seal to hold pressure on
puncture site until body’s natural clotting process can take
over
 Loss of pulses in the foot needed to evaluated after the use of a closure device
 Hemostasis device must be monitored frequently for possible misalignment over femoral
artery : C clamp
 Complication mostly associated with closure device: infection, thrombosis, device failure
 diabetic and high WBC count are at an increased risk of infection when using closure
device
 multiple sheath exchanges within 72hrs increase risk of infection
 brachia and radial approaches reduce infection rate
 Aortic regurgitation makes hemostasis of femoral artery a challenge as
-> reduce BP will increase vascular resistance (vasocontriction)
-> constricted vessel not able to effectively clamp down on damaged vessel
-> blood clot form more quickly (coz reduced blood flow) -> challenging to achieve
hemostasis
 Analgesia, sedation and 200mg TNG IA considered for radial artery spasm during
sheath removal
 educating Pt abt hemostasis site:
1. keep bandage on site for 24hrs
2. do not submerge the site in water for 48hrs
3. do not bend the affected site
4. no strenuous movement or heavy lifting for 24hrs
 post procedural care:
- bed up 30 degree
- fluids are allowed
- coughing or laughing hold pressure on groin dressing
- call RN if you feel anything warm or wet at procedure site
 Treatment of peripheral extravasation: close IV and aspirate (never flush)
 Post PCI procedure commonly given med: Aspirin, Plavix, effient (prasugrel)
  Pulsatile mass below sheath site + bruit sound present + significant site pain-> suspect
pseudoaneurysm
 pseudoaneurysm caused by
1. arterial puncture does not seal
2. pulsatile blood tracks into perivascular space
3. result of puncture needle penetrating anterior and posterior vessel wall
4. blood is containing in perivascular structure
5. lack of compression time
 Pseudoaneuryam treated with USG guided injection of thrombin, USG guided
compression and surgical management
 Post procedure renal dysfunction is more likely to occur in patient with
- Diabetes
- Pre procedure dehydration
- Frequent use of NSAID
- ACEI

TAVI
 minimally invasive procedure to replace a narrowed aortic valve that fails to open
properly
 before deployment of TAVI: 1. hold respiration 2. aortic root angiography, 3. Rapid
pacing
 Rapid ventricular pacing for TAVI, because stablize aortic valve during deployment

Thermodilution

 2 lumen catheter
 through RA, RV and into PA
 5-10ml NS injected to port A (injection port)
  thermistor in PA detect temp. change
 repeat 3-5 time, take avg
 computer cal CO

 increase CO make thermodilution more accurate

 we measure RV , but we assume RV = LV in calculating CO
 Swan ganz catheter : distance btw proximal port to distal port - 30 cm
 proximal port can inject saline
 Room temp NS for thermodilution; 10°c difference btw injectate and body temp
 swan ganz catheter: A:thermistor ; B: proximal injectate ; C:RV pacing or infusion; D:
Distal PA port; E: balloon port

 0.025’’ GW used in swan ganz catheter

Pacing
 pacing threshold: minimum amount of mA require to elicit response
 reduce sensitivity will change temp pacing device from demand to asynchronous
* high sensitivity = any small electrical signal will be regarded as cardiac signal (may
oversensing)
*low sensitivity = will pace even intrinsic signal generating (may undersensing,
dangerous causing R on T )
 Pacing wire for LV in CRT therapy placed in coronary sinus
 Conductivity: ability to transmit an impulse
Sensitivity: minimum cardiac activity required to consistently trigger a pulse generator
Automaticity: ability to initiate an impulse
 synchronous pacemaker = demand pacemaker that gives stimulus only when needed
 asynchronous pacemaker = Fixed pacemaker that gives stimulus regardless of the heart
activity3 reasons need pacemaker:
1. sick sinus syndrome
2. AV conduction issue
3. needed surgery
 generator of pacemaker trigger the beat, til end of life (no battery)
 PPM venous access: Rt subclavian
 electricity of heart measure in millivolts / milliamps
 time measured when speaking electricity in heart: milliseconds
 common complication of pacing wire: perforation, pericardial effusion, temponade
 Capture: The amount of energy needed to cause contraction
 Failure of capture: electricity is sent but does not cause systole
 * reason: lead fracture / lead not in contact with RV wall
 5-10mins should be waited btw capture/ threshold before doing another capture/
threshold. 2nd capture is usually lower as heart adapts to the lead
 2nd capture should be recorded and kept
 VVI, one lead, lead in RV

 Failure to sense

 Bi-ventricular pacemaker: to reestablish btw the synchrony btw the RV and LV

*3 leads : RA RV CS
 one lead in RA, Pt have SA node problem
 one lead in RV, Pt have AV conduction delay
 Lead placed in the subclavian vein
 Paced beat looks like PVC: signal moves in negative direction. The signal comes from
the purkinje fibers up to SA node
 Transvenous pacing best location is subclavian area allows patient to move around
easier. Jugular can be used as well. Patient remain on bedrest while the pacemaker is in
place
 When Temp pacing? : rotablator, angiojet, mitral valvuloplasty, Mitral clip, TAVI
 Pacemaker syndrome symptoms include: Fatigue, CHF, Dizziness, Hypotension

AHA
 Rescue breathing in cardiac arrest: 6s per breath
 Defibrillator used for reperfusion arrhythmia (= injury to heart muscle arised when blood
flow to heart resumed)
 immediate treatment for MI : MONA
 Rigid oral catheter should only place above oropharynx to mouth
 soft catheter should place nasopharynx and transesophageal
 Fluid challenge = administer 500-1000ml IV saline within 20mins to increase Pt’s preload
 Deliver shock on T wave , causing R on T cause V fib
  Can defribrillate Pt with pacemaker, but don’t put the paddle on pacemaker
 Carotid message slow the flow of electricity thru the AV node and can be a therapy to
SVT
 Beside numbing the skin, lidocaine can treat ventricular arrhythmia. It works on the
perkinje fibers by reducing the flow of electricity to the perkinje fibers. This decreased
sensitivity lowers the no. of extra beats that are able to get through
 ACLS monophasic defibrillator energy delivery : 200 – 300 – 360J ; Biphasic: max 200J
 Test defibrillator: discharge into dummy load

Grading or category

TIMI Normal flow + fill distal coronary bed completely

3

TIMI delay entry and exit of dye (dye persistent after 3 cardiac cycles)
2

TIMI Dye slowly entered and exit

1

TIMI Failure dye entering (= lack of tissue perfusion)

0
 TIMI 3 are aiming for in cath lab
 Stroke acronym: Fast (F: face drooping, A: Arm weakness, S: speech difficulty, T: time
to call 911)
NYHA (New York Heart Association) classification = stages of heart failure

Class I no symptom and no limitation in phy. activities

Class II mild symptom (SOB and angine, slight limitation during phy. act.)

Class III marked limitation

Class IV severe limitation, exp symptoms even at rest, need LVAD

 Aldrete score (for PACU recovery assessment) : at least 8/10 to leave cath lab

Braunwald classification (classify chest pain)

Class 1 New onset of severe/ accelerated angina

Class 2 Angina at rest, subacute

Class 3 Angina at rest, acute

Structural procedure related
 During echocardiography guided transseptal procedure, tenting describe when
transseptal catheter makes contact with fossa ovalis
 Procedure required transseptal access: ASD repairs, mitral clips, mitral valve repair,
mitrovalvuloplasty, a fib ablation, tendam heart
* tendam heart: For LV support, the pump aspirates oxygenated blood from the left
atrium and pumps it into the femoral artery thereby bypassing the left ventricle
 Heparin should be given immediately after crossing septum in transseptal access as it
make sure no clot to form and keep clot off of wire and device.
 Complication of transseptal access: clots, air embolus, tamponade, aortic wall puncture
 complication associated with mechanical valves: thrombus formation
 Watchman procedure: implant to reduced risk of stroke by blocking off LAA
 Amplatzer septal ocluder: ASD
 ILR - subcutaneously implanted in Lt side of chest about 4th ICS
 Alcohol septal ablation for hypertrophic obstructive cardiomyopathy
*reduce the obstruction to blood being ejected from heart killing them (become less
thick)
 Inoue balloon for valvuloplasty
 Before mitral valvuloplasty, TEE needed to rule out LA thrombus
 intracardiac echocardiogram (ICE) most commonly used in PFO closure
 Before ASD closure, use ICE catheter, sizing balloon, identify shunt location
 Good time to use ICE, septal closure
 ICE catheter

 MitraClip can clip the two leaflets of the mitral valve together reducing regurgitation

Allen’s test/ Barbeau test

 The Allen test is used to assess collateral blood flow to the hands, generally in
preparation for a procedure that has the potential to disrupt blood flow in either
the radial or the ulnar artery.
 Barbeau test: pulse oximeter on thumb or index finger. Look at pulse oximeter
waveform. Occlude both arteries and observe that the waveform diminishes and falttens
out. Then let go of the ulnar artery and look for the return of the proper waveform, and
the O2 sats return to normal
 modified allen’s test and Barbean test evaluate radial artery patency
 Reverse Barbean test is used to evaluate radial artery patency following radial sheath
removal and placement of compression device
 How to do: occlude both radial and ulnar arteries and make them move their hand.
Release ulnar artery and be sure that the hand pinks up
  Barbeau test scale:
A Upon releasing pressure on the ulnar artery, (no change) in pulse wave
B Upon releasing pressure on the ulnar artery, temporarily reduces the amplitude
and returns to normal amplitude within 2 minutes.
C Upon releasing pressure on the ulnar artery, Immediately shows a flat line and
slowly waveform returns at 2 minutes. But the amplitude is dampened.
D Upon releasing pressure on the ulnar artery , Shows a flat line on
plethysmography tracing throughout 2 minutes. Which indicates inadequate
ulnar artery circulation

Pericardiocentesis
 puncture angle 30-45° angle
 Function of pericardial fluid: lubricant allowing heart to beat without rubbeng the
pericardium and keep friction to a minimum
 normal amount of pericardial fluid : 5-50ml
 Pericardium: protect heart from being bruised in normal movements.
 Pericardium is the outer protective layer; inner layer is endocardium (thin layer of
epithelial tissue act as inner layer of myocardium) ; thick middle layer is myocardium
(can conduct electrical impulses enabling cardiac contraction)
 pericardial sac: 2layers with 5-30ml of fluid in btw
 Cardiac tamponade: compression of heart by an accumulation of fluid in the pericardial
sac ; caused by percaridal effusion or chest trauma
 S/S: hypotension + tachycardia
 first sign of tamponade: O2 sat drop, pH of blood in pericardial sac is acidic, irritate
nerves causing chest pain, Pt slightly unresponsive as perfusion pressure is lost to brain
 Process of pericardiocentesis: put needle to subxiphoid area / Apical , elevate Pt to 30-
45°; if patient on warfarin, must use USG to guide the needle to ensure do not puncture
the heart
 Pulsus paradoxus reduce 10mmHg in systole during inspiration; 20-30 pressure diff.
noted in tamponade , also sign of tamponade

Cardiac biopsy
 Myocardial biopsy taken from RV
 commonly RV biopsy access site: Rt subclavian vein , Rt IJV, Left femoral vein
 complication commonly arised from endomyocardial bx: perforation
 myocardial biopsy after cardiac transplant is to evaluate potential for rejection of the
transplanted heart
 Main complication : perforation of RV (reduce BP, increase HR, conduction abnormality,
death)
 cardiac biopsy sample placed in formalin solution