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CCP 216 Cardiovascular Emergencies ❤️ Flashcards

1
Q

preload equation (Laplace’s law)

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

Preload = (Ventricular pressure x Ventricular chamber radius) / 2x ventricular wall thickness (i.e. P⋅R/2h)

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2
Q

afterload definition

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. “load” that the heart must eject blood against
  2. a result of stress (or “tension”) that the cardiac wall (LV) experiences during systolic ejection
  3. the amount of pressure that the heart needs to exert to eject the blood out if it during the contraction
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3
Q

preload definition

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Myocardial sarcomere length just prior to contraction, for which the best approximation is end-diastolic volume
  2. Tension on the myocardial sarcomeres just prior to contraction, for which the best approximation is end-diastolic pressure

cardiac preload is about the length-tension relationship. this is the core principle of the frank-starling mechanism

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4
Q

factors leading to increased cardiac afterload

A
  1. Afterload is increased when aortic pressure and systemic vascular resistance are increased.
  2. aortic valve stenosis and ventricular dilation will both increase afterload
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5
Q

cardiac afterload equation

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. [(LV Pressure x LV Radius) / LV wall thickness] or [(P x r)/h]
  2. LV Wall Tension = [(SVR - Pleural Pressure) x LV Radius] / LV wall thickness

Afterload reduction can be achieved through:

  1. Decreasing SVR (arterial dilation)
  2. Increasing pleural pressure (PPV/PEEP)
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6
Q

hydralazine MOA

A

direct acting arterial vasodilator

  1. stimulates the formation of nitric oxide by the vascular endothelium
  2. inhibits release of calcium from the smooth muscle sarcoplasmic reticulum
  3. causes smooth muscle hyper-polarization through the opening of K+ channels
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7
Q

mechanisms to reduce cardiac afterload

A
  1. Decreasing SVR (arterial dilation)

2. Increasing pleural pressure (PPV/PEEP)

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8
Q

primary determinants of cardiac preload

A
  1. Pressure filling the ventricle

2. Compliance of the ventricle

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9
Q

primary determinants of “pressure filling the ventricle” (cardiac preload)

A
  1. Intrathoracic pressure (pleural pressure aka esophageal pressure)
  2. Left atrial pressure
  3. Right atrial pressure
  4. Mean systemic filling pressure
  5. Cardiac output
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10
Q

primary determinants of “Compliance of the ventricle” (cardiac preload)

A
  1. Pericardial compliance

2. Ventricular wall compliance

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11
Q

primary determinants of “myocardial wall stress” (cardiac afterload)

A
  1. [(LV Pressure x LV Radius) / LV wall thickness] or [(P x r)/h]
  2. LV Wall Tension = [(SVR - Pleural Pressure) x LV Radius] / LV wall thickness

P: ventricular transmural pressure (difference between intrathoracic pressure and ventricular pressure)

r: radius of the ventricle (Increased LV diameter increases wall stress at any LV pressure)
h: thickness of ventricular wall (thicker wall decreases wall stress by distributing it among larger number of sarcomeres)

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12
Q

primary determinants of “input impedance” (cardiac afterload)

A
  1. Arterial compliance (Aortic compliance, Peripheral compliance)
  2. Inertia of the blood column
  3. Ventricular outflow tract resistance (HOCM, AS)
  4. Arterial resistance (Length of arterial tree, Blood viscosity, Vessel radius)
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13
Q

input impedance definition (cardiac afterload)

A

describes ventricular cavity pressure during systole

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14
Q

contractility definition

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

“Contractility describes the factors other than heart rate, preload, and afterload that are responsible for changes in myocardial performance.”

  1. change in peak isometric force (isovolumic pressure) at a given initial fibre length (end diastolic volume)
  2. length-independent activation
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15
Q

Type 1 MI

A
  1. caused by acute atherothrombotic CAD
  2. usually precipitated by atherosclerotic plaque disruption (rupture or erosion)

“Vaso-occlusive”

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16
Q

Type 2 MI

A

MI caused by oxygen supply/demand mismatch

“Demand”

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17
Q

Type 3 MI

A

Patients with a typical presentation of myocardial ischemia/infarction with unexpected death before blood samples for biomarkers could be drawn

“Sudden cardiac death”

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18
Q

Type 4 MI

A

MI as a complication of PCI

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19
Q

Type 5 MI

A

MI as a complication of CABG

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20
Q

typical value for right atrial pressure (RAP) in an adult

A

RA 5 mmHg

“nickel”

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21
Q

typical value for right ventricular pressure (RVP) in an adult

A

RV 25/5 mmHg (systolic/diastolic)

“quarter”

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22
Q

typical value for left atrial pressure (LAP) in an adult

A

LA 10 mmHg

“dime”

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23
Q

typical value for left ventricular pressure (LVP) in an adult

A

LV 100/10 mmHg (systolic/diastolic)

“dollar”

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24
Q

tachyphylaxis definition

A
  1. very rapid development of tolerance or immunity to the effects of a drug
  2. sudden decrease in response to a drug after its administration
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25
Q

Virchow’s triangle (venous thrombosis)

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Hyper coagulability
  2. Stasis
  3. Endothelial injury
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26
Q

Five causes of hypoxemia

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Low partial pressure of inspired oxygen
  2. VQ mismatch
  3. Diffusion impairment
  4. Hypoventilation
  5. Shunt (venous admixture)
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27
Q

differentials for sinus bradycardia

A

“EPI-ID” (a reichertism)

  1. Electrolytes
  2. Parasympathetic response
  3. Infarction
  4. ICP elevation
  5. Drugs/Pharmacologic
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28
Q

Stanford type “A” aortic dissection

A
  1. Affects ascending aorta
  2. Accounts for 60% of aortic dissections
  3. Initially managed surgically
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29
Q

Stanford type “B” aortic dissection

A
  1. Affects descending aorta
  2. “B begins beyond brachiocephalic vessels”
  3. Accounts for 40% of aortic dissections
  4. Initially managed medically
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30
Q

primary risk factors for aortic dissection

A
  1. advancing age
  2. male sex
  3. systemic hypertension
  4. preexisting aortic aneurysm
  5. atherosclerosis
  6. connective tissue disorders
  7. sympathomimetic drug abuse
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31
Q

cardiac steal syndrome

A
  1. The heart’s vessels naturally auto regulate to facilitate even flow to all areas
  2. In the presence of a coronary lesion, the vessel will dilate to accommodate improved flow distal to the plaque
  3. If you have two vessels branching off a main vessel, and one branch vessel contains a plaque, the flow to each vessel will still be 50/50 via auto regulation
  4. If the person becomes vasodilated, the vessel containing the plaque is already maximally dilated d/t auto regulation. Now, the second branch vessel will dilate, causing what was previously 50/50 flow distribution to shift to a disproportional distribution, such as 80/20, which means the tissue distal to the site of the plaque will get reduced flow.
  5. The good vessel is “stealing” flow from the occluded vessel d/t vasodilation beyond what the shitty vessel is capable of
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32
Q

primary determinants of cardiac contractility

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Preload
  2. Afterload (the Anrep effect)
  3. Heart rate (the Bowditch effect)
  4. Myocyte intracellular calcium concentration
  5. Temperature
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33
Q

Biochemical and cellular factors which affect cardiac contractility

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Catecholamines and the autonomic nervous system (Calcium concentration)
  2. ATP availability (eg. ischaemia)
  3. Extracellular calcium (Calcium concentration)
  4. Temperature

this shit is super important and you gotta know how it impacts the heart in a range of disease. everything from your bread and butter HFrEF all the way to your septic-induced cardiomyopathy and your post-cardiac-arrest myocardial stunning

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34
Q

Key clinical findings for diagnosing cardiac tamponade

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Beck’s Triad (JVD, muffled heart sounds, hypotension)
  2. Compressed RA (ultrasound)
  3. Non-collapsible IVC (ultrasound)
  4. pulsus paradoxus (arterial waveform)

remember kids, tamponade is a clinical diagnosis. just because the guy has a big old pericardial effusion on ultrasound it does NOT mean he is in tamponade.

tamponade is a clinical SYNDROME characterized by shock which can be interpreted through your clinical exam as seen in the above points

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35
Q

define pulsus paradoxus

A
  1. During normal spontaneous breathing, negative pleural pressure against the heart during inspiration produces a slight increase in transmural pressure and cardiac afterload
  2. During normal spontaneous breathing, inspiration causes blood to fill the RA from the vena cava, and causes increased RV filling with a slight bulge of ventricular septum into the LV
  3. This causes a small decrease in LV ejection with systole (increased afterload, decreased LVEDV). In normal breathing, SBP can normally fall on inspiration by 10 mmHg
  4. Pulsus paradoxus is an exaggeration of this normal blood pressure variation with breathing. It is defined as a fall in systolic pressure by more than 15 mmHg during spontaneous inspiration
  5. In a mechanically ventilated patient, a reversal of this pressure variation occurs. PPV displaces the LV wall inward during systole to assist in LV emptying. This causes a slight rise in the systolic pressure during mechanical inspiration.
  6. Reversed Pulsus Paradoxus (PPV) is defined as an exaggeration of the rise in systolic BP during mechanical inspiration. A rise in peak systolic pressure on mechanical inspiration by more than 15 mmHg is considered significant.

you can measure this with Korotkoff sounds but really the best/easiest way to see it is in A-line Δ pulse pressure variation

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36
Q

delta (Δ) pulse pressure variation definition

A

the difference between the maximal and minimal pulse pressure during one breathing cycle, divided by their mean

you can measure this with korotkoff sounds but really the easiest way is to watch the ΔPP variation on A line. there will be a drop in BP during negative pressure spontaneous breathing, and a rise in BP during positive pressure MV

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37
Q

systolic blood pressure definition

A

the maximum pressure experienced in the aorta when the heart contracts and ejects blood into the aorta from the left ventricle

this can be seen on the cardiac cycle PV loop at the point where the AV closes

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38
Q

diastolic blood pressure definition

A

the minimum pressure experienced in the aorta when the heart is relaxing before ejecting blood into the aorta from the left ventricle

this can be seen on the cardiac PV loop as the point where the AV opens at the end of systolic iso-volumetric contraction

this is because the valve is just opening but the aorta hasn’t actually “seen” any of the pressure yet, so it is actually at the lowest pressure state it will be in in the pressure-volume cycle

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39
Q

mechanism behind naturally occurring hypertension as people age

this slide is legit don’t just write it off cause you think old people are boring

A
  1. With aging, there is a decrease in the compliance of the large elastic arteries.
  2. This change is due to structural molecular changes in the arterial wall, including decreased elastin content, increased collagen I deposition, and calcification, which increases the stiffness of the wall
  3. This process is often described as “hardening of the arteries.”
  4. As the LV contracts against stiffer, less compliant arteries, SBP and DBP increase
  5. In response, the LV tends to hypertrophy

this is legit to know cause it factors into our cardiac afterload equation nicely. factors that increase cardiac afterload include intra cardiac factors or extra cardiac factors. extra cardiac factors are things the impede LV outflow of blood. part of this is the “compliance” of the arterial system. meaning, as people age and get shitty calcified vessels they will have significantly elevated cardiac afterload d/t worsening arterial compliance

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40
Q

Differentials for a narrowed pulse pressure in shock

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. heart failure (decreased pumping)
  2. hypovolemia (decreased blood volume)
  3. aortic stenosis (reduced stroke volume)
  4. cardiac tamponade (decreased filling time)
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41
Q

Normal amount of pericardial fluid

A

10–50 mL

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42
Q

TnK vs alteplase in the fibrinolysis of AMI

A

TnK is associated with a lower rate of non-cerebral bleeding complications (ASSENT-2 trial)

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43
Q

summarize the benefits of beta blockers in AMI

A

1) Decreased MvO2
2) Decreased risk of VF/dysrhythmias
3) Decreased automaticity
4) Prolonged diastole & increased coronary perfusion
5) Reduction in cardiac remodelling
6) Slows progression of atherosclerosis
7) Inhibits platelet aggregation and thromboxane synthesis
8) Reduction in reperfusion injury

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44
Q

At what phase in the cardiac cycle does the majority of ventricular filling occur?

A
  1. early diastole

2. a large initial pressure gradient leads to rapid ventricular filling

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45
Q

How can a paralytic drug affect hemodynamics?

A

Loss of skeletal muscle tone leads to a relative vasodilation, reducing venous return to RA

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46
Q

A 0.6mg/hr (600mcg per hr) transdermal NTG patch has the equi-pharmaceutical potency of what IV NTG infusion rate?

A

10mcg/min

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47
Q

Describe the approach to staged dosing for labetalol

A

Labetalol is designed to be given in bolus-dose pushes q10min

  1. 5mg (wait 10)
  2. 10mg (wait 10)
  3. 20mg (wait 10)
  4. 40mg (wait 10)
  5. 80mg (wait 10)

Stop at total of 300mg and consider another vasodilator like hydralazine, phentalomine, nitroprusside or nifedipine

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48
Q

cardiac index definition

A
  1. a measure of cardiac function that can be normalized for the patient’s body habitus
  2. a haemodynamic parameter that relates the cardiac output (CO) from left ventricle in one minute to body surface area (BSA)
  3. Calculated as CI (L/min/m2) = CO (L/min) / TBSA (m2)
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49
Q

Clinical findings associated with pericarditis

A
  1. Positional “pleuritic” chest pain (improved with sitting up and leaning forward)
  2. Pericardial “Friction rub” on auscultation of left lower sternal border
  3. Diffuse, concave ST-E on ECG with P-R depression
  4. low-grade fever
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50
Q

What patient cohort requires “emergent rescue PCI” in the setting of STEMI (post thrombolysis)

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

1) Persistent ST-E that hasn’t decreased by at least 50% following thrombolysis
2) Persistent ischemic C/P post thrombolysis

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51
Q

What is the target time-frame for achieving rescue PCI in the setting of STEMI failed thrombolysis

A
  1. Ideal time frame is within 2 hours

2. Necessary within 24 hours

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52
Q

What is the preferred P2Y-12 inhibitor agent for patients who will be receiving primary PCI?

A
  1. Ticagrelor (Brilinta) 180mg is the preferred P2Y-12 inhibitor agent for patients who will be receiving primary PCI
  2. If using clopidogrel (Plavix) for PCI, double the usual age-based dose that would be administered in the setting of fibrinolysis
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53
Q

What is the preferred P2Y12 inhibitor agent for patients who will be receiving primary fibrinolysis?

A
  1. Clopidogrel (Plavix) is the preferred P2Y12 inhibitor agent for patients who will be receiving primary fibrinolysis
  2. Age ≤75 Clopidogrel 300 mg
  3. > 75 Clopidogrel 75 mg
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54
Q

P2Y12 inhibitors MOA (platelet activation)

A
  1. Inhibition of platelet aggregation impairs formation and progression of thrombotic processes
  2. A core part in the platelet activation process is the interaction of adenosine diphosphate (ADP) with the platelet P2Y12 receptor
  3. P2Y12 inhibitors provide irreversible blockade of the P2Y12 component of the ADP receptor on platelet surface
  4. Results in reduced platelet adhesion, activation and aggregation
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55
Q

aspirin MOA (platelet aggregation)

A
  1. Inhibition of platelet aggregation impairs formation and progression of thrombotic processes
  2. A core part in the platelet activation process is the activation of thromboxane A2 (an important lipid responsible for platelet aggregation)
  3. aspirin use irreversibly blocks the formation of thromboxane A2 in platelets, producing an inhibitory effect on platelet aggregation
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56
Q

Transfer to PCI-capable centre is preferable compared to primary fibrinolysis if PCI can be achieved within ___ minutes of first medical contact

A

120 minutes

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57
Q

The gold standard timeline for PCI in STEMI is within ___ minutes of first medical contact

A

90 minutes

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58
Q

indications for emergent PCI in NSTEMI

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Hemodynamic instability
  2. Electrical instability
  3. Persistent C/P
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59
Q

Time-target for fibrinolysis (TnK) administration once a diagnosis of STEMI has been made, and the decision has been made to thrombolyze

A

30 minutes

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60
Q

Contraindications for PCI

A

1) Risk of bleeding during procedure.
2) Inability to take dual anti-platelet therapy (DAPT) for 1yr
3) Severe renal failure
4) Triple vessel disease (ie. needs CABG)
5) Palliative status

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61
Q

Anticoagulant of choice for an NSTEMI patient who is to be catheterized within 24 hours

A

unfractionated heparin (UFH)

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62
Q

Anticoagulant of choice for an NSTEMI patient who is to be catheterized in a timeframe beyond 24 hours

A

LMWH or Fondaparinux

  1. Single dose LMWH or fondaparinux provides 24 hours of coverage
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63
Q

Amiodarone dosing for ventricular irritability/acute tachyarrhythmias (bolus and infusion)

A
  1. Initial bolus: 150mg over 10 minutes
  2. First 6 hours: 1mg/min
  3. Next 18 hours: 0.5mg/min
  4. total dose over 24 hours should not exceed 2.4 grams
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64
Q

What is the percentage of cardiac output used up during heavy diaphragmatic breathing/tachypnea

A
  1. Up to 30% of CO can be used up during periods of tachypnea/heavy breathing
  2. This is why sometimes it is necessary to intubate a patient in shock, as a mechanism for reducing their total oxygen demand, reducing myocardial workload, improving systemic oxygen delivery
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65
Q

What patients with AMI are candidates for beta blocker therapy?

A

trick question sonn

  1. all patients with acute myocardial infarction (MI) should be treated with beta blocker therapy, unless there are gross contraindications
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66
Q

common clinical findings for aortic dissection

A
  1. Thorax Pain (95.5% of individuals with AD report pain, with 84.8% of all individuals with AD describing an abrupt onset of pain; 90.6% of the individuals studied reported their pain as “severe or worst ever.”)
  2. Abnormal CXR (Widening of the mediastinum 61.6% of cases, Widening of the aortic knob or abnormal contour 49.6% of cases
  3. New aortic murmur (Approximately 40% of patients with a dissection demonstrate an aortic insufficiency/regurgitant murmur, reflecting unseating of the aortic valve by an ascending AD)
  4. New onset peripheral pulse deficit (30% of patients with a Stanford Type A dissection and 15% with a Type B dissection demonstrate a pulse deficit.)
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67
Q

What patients with AMI are candidates for statin therapy?

A

trick question buddy

  1. Intensive statin therapy should be initiated as early as possible in ALL patients with STEMI
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68
Q

Characteristic ECG finding for HOCM

A
  1. large dagger-like “septal Q waves” in the lateral — and sometimes inferior — leads
  2. due to the abnormally hypertrophied interventricular septum
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69
Q

Clinical approach to “sympathetic crashing acute pulmonary edema”

A

1) Nitrates (hydralazine is also an option, but it is less titratable and less predictable)
2) PEEP/NIPPV
3) Diuretics (IV Lasix)
4) Beta blocker (if HR > 150)
5) Transition to long-term antihypertensive (ie. labetalol and hydralazine)

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70
Q

Two common alpha 2 agonists used in the critical care/ICU environment

A
  1. Clonidine

2. dexmedetomidine

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71
Q

Clinical approach to “symptomatic bradycardia”

A

1) Atropine
2) Pacing (Transcutaneous or TVP)
3) Chronotropy (epinephrine, dopamine, isoproterenol)
4) Calcium (if secondary to hyper-kalemia)
5) Insulin (for beta blocker/CCB overdose)

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72
Q

differential diagnosis for narrow complex PEA arrest (Littman PEA algorithm)

A

Mechanical RV problem

  1. Tamponade
  2. tension PTX
  3. dynamic hyperinflation
  4. PE
  5. Acute MI with rupture
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73
Q

differential diagnosis for wide complex PEA arrest (Littman PEA algorithm)

A

Metabolic LV problem

  1. Hyperkalemia
  2. Sodium channel blockade
  3. Agonal (terminal) rhythm
  4. Acute MI with pump failure (severe myocardial dyskinesis)
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74
Q

ECG findings characteristic for hypercalcemia

A

QTc shortening

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75
Q

ECG findings characteristic for hypocalcemia

A

QTc lengthening

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76
Q

most common cause of right heart failure

A

Left-sided heart failure

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77
Q

Causes of Right Heart Failure due to RV Pressure overload

A
  1. Left-sided HF (most common cause)
  2. Pulmonary embolism (common)
  3. Other causes of PH
  4. RV outflow tract obstruction
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78
Q

Causes of Right Heart Failure due to RV volume overload

A
  1. Tricuspid regurgitation
  2. Pulmonary regurgitation
  3. Atrial septal defect
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79
Q

Causes of Right Heart Failure due to RV ischemia

A
  1. RV myocardial infarction

2. Ischemia may contribute to RV dysfunction in RV overload states (especially pressure overload)

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80
Q

Causes of Right Heart Failure due to Intrinsic myocardial disease

A
  1. Cardiomyopathy and heart failure
  2. Arrhythmogenic RV dysplasia
  3. Sepsis
81
Q

Common ICU problems which lead to increased pulmonary vascular resistance (aka, shit that will increase your PVR)

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Positive pressure ventilation
  2. Acidosis
  3. Hypercapnia
  4. Hypoxia
  5. High dose vasopressors
82
Q

ventricular preload requirements in left vs right HF

A
  1. with LV failure the LV preload needs to be on the lower side, because high LV preload tends to lead to pulmonary oedema (all the extra preload just backs up into the lungs…)
  2. with RV failure the preload needs to be highish, aka, RV failure is “preload dependent” (the RV requires a higher filling pressure) because the RV is essentially a passive conduit into the pulmonary circulation (RV lacks the same sort of intrinsic structural contractile force that the LV has so it’s more dependent on length-tension starling relationship provided by preload.

In RV failure you gotta force that shit into the lungs, cause if there’s no forward flow, the LV isn’t gonna receive any volume, which means there won’t be any forward flow and you’ll just go into shock and die..

83
Q

dangers of beta-blockade in the context of critical illness

A
  1. fixed cardiac output
  2. With beta blockade, the ICU patient is unable to reflexively increase their contractility or heart rate in response to stress

for example if you have a patient who is in severe sepsis and has a rapid AF with a ventricular rate of 130 and you knock them down with some metoprolol you could kill them by taking away their compensatory tachycardia and tanking their pressure

84
Q

lusitropy definition

A

the relaxation of the myocardium

85
Q

how to manipulate pulmonary vascular resistance to “unload the right ventricle”

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Maintain SpO2 >92% (Hypoxic pulmonary vasoconstriction is to be avoided)
  2. Avoid excessive PEEP. PPV/PEEP is transmitted to the pulmonary circulation, adds to afterload. Unless patient is refractory hypoxemia d/t ARDS and needs to be oxygenated
  3. Avoidance of hypercapnea. CO2 increases pulmonary arterial pressure and RV afterload
  4. Pulmonary vasodilators (nitric oxide, prostacycline, bosentan, sildenafil, milrinone, levosimendan)
86
Q

indications for cardiac resynchronisation therapy (CRT) in heart failure patients

A
  1. patients who have an LVEF less than 35% and a LBBB with a QRS duration of greater than 150 msec
87
Q

Conditions in which one would get a “right to left shunt”

A

ASD or VSD in the presence of high right sided pressures (pulmonary HTN)

88
Q

Metabolic and electrolyte variables contributing to negative cardiac inotropy (aka, metabolic shit one must correct to improve cardiac inotropy…)

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

all of these things will fuck up the contractility component of your CO equation

  1. Acidosis (pH <7.20)
  2. Hypoxia (PaO2 < 60mmHg)
  3. Hyperkalemia (K+ > 5.5)
  4. Hypomagnesaemia (Mg++ <0.9)
  5. Hypocalcaemia (iCa++ <1.0)
  6. Hypophosphataemia (PO4- <0.8)
  7. Thiamine deficiency
  8. Cortisol deficiency
  9. Thyroxine deficiency
  10. Alkalosis
89
Q

What are the four phases of the cardiac cycle (different “phases” on your cardiac PV loop)

A
  1. Isovolumic relaxation
  2. Ventricular filling
  3. Isovolumetric contraction
  4. Ventricular ejection
90
Q

describe the concept of ventricular “elastance”

A
  1. change in pressure per change in unit volume
  2. relates best to the stiffness of a mechanical system
  3. tendency to recoil back into its original dimensions in response to a distending force
91
Q

describe the concept of ventricular “compliance”

A

change in ventricular volume per change in ventricular unit pressure

represents the compliance (distensibility) of the ventricular wall

92
Q

define the end-systolic pressure-volume relationship (ESPVR)

A
  1. the maximal pressure that can be developed by the ventricle at any given LV volume
  2. one of the ways of measuring and describing cardiac contractility
93
Q

Target electrolyte levels in the setting on an AMI

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. iCa+ > 1.0 mmol/L (Low serum calcium is independently correlated with LV systolic dysfunction in CAD patients with and without AMI)
  2. K+ 3.5-4.5 mmol/L (in setting of ACS, hypokalemia defined as potassium levels <3.5 is associated with ventricular arrhythmias)
  3. Mg+ >1.0 mmol/L (low serum Mg levels may be associated with cardiac arrhythmias and sudden death. Magnesium has antiarrhythmic effects)
94
Q

NSTEMI treatment pathway

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. “Dual anti platelet therapy” (ASA + P2Y12 inhibitors)
  2. Statin therapy (atorvastatin)
  3. Beta blockade (metoprolol)
  4. Nitrates (NTG)
  5. Systemic anticoagulation (heparin/LMWH)
  6. Maintain normoxia (SpO2 >90%)
  7. Optimize electrolytes (target normal range)
95
Q

CVS labs

A
  1. Troponins
  2. BNP
  3. Lactate
  4. SvO2
  5. Extended lytes
  6. BUN:Cr
  7. CBC
96
Q

What is the harm in paralyzing/intubating an RV failure patient?

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. The intubation procedure will most likely lead to some degree of Hypoxia/hypercapnia
  2. Hypoxia/hypercapnia lead to pulmonary vasoconstriction, which causes increased right sided afterload
  3. BMV/PPV will lead to high pulmonary pressures, again causing increased RV afterload, drop their CO
  4. All this elevated RV afterload will put more stress/strain on the RV, eventually causing the person to arrest
  5. induction will lead to decreased RV preload d/t vasodilation
  6. Just try not to intubate or BMV RV failure patients.
97
Q

treatment pathway for tamponade

A
  1. Optimize preload with a fluid bolus (remember that tamponade is OBSTRUCTIVE and not cardiogenic shock. obstructive shock patients are preload dependent d/t elevated RV afterload
  2. Augment rate: Allow tachycardia (in your CO equation your preload/afterload/contractility are all fucked so if you want to maintain MAP you’ll have to keep the HR a little bit higher)
  3. Improve Forward flow: Levophed (if they are in shock you’ll have to support their hemodynamics with vasopressors. levy is 1st line)
  4. Remove effusion: pericardiocentesis
98
Q

explain the relationship between CVP and RAP

A
  1. CVP is measured at the SVC
  2. The RA is more compliant than the SVC/IVC
  3. The RA is also dynamic (ie. respiration variability)
  4. there is rarely a point in time where RAP is able to truly equalize with CVP (as represented in the SVC)
  5. there is a very poor relationship between CVP and blood volume and CVP/DeltaCVP is a poor predictor of the hemodynamic response to a fluid challenge
  6. interpretation of CVP should be in association with information relating to other haemodynamic variables
99
Q

correctable negatively inotropic metabolic variables

(this list is 🔥 af)

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Acidosis (pH <7.20)
  2. Hypoxia (PaO2 < 60mmHg)
  3. Hyperkalemia (K+ > 5.5)
  4. Hypomagnesaemia (Mg++ <0.9)
  5. Hypocalcaemia (iCa++ <1.0)
  6. Hypophosphataemia (PO4- <0.8)
  7. Thiamine deficiency
  8. Cortisol deficiency
  9. Thyroxine deficiency
  10. Alkalosis
100
Q

Biomarkers of cardiac disease

A

BNP (brain natriuretic peptide)
CK-MB (creatine kinase)
Cardiac Troponin
ANP (Arial Natriuretic Peptide)

101
Q

Key features to include when describing a cardiac murmur heard on auscultation

A
  1. Location (A, P, T, M)
  2. Intensity (scale 1-6)
  3. Pitch (eg harsh vs rumbling)
  4. “Shape” (eg crescendo vs decrescendo)
  5. Timing (eg early systole vs late systole)
  6. Radiation (carotids, subclavians)
102
Q

the four different ways of conceptualizing heart failure

A
  1. Acute vs chronic
  2. Right vs Left
  3. Systolic vs diastolic
  4. High output vs low output
103
Q

typical values for pulmonary arterial (PA) pressures in an adult

A
  1. Systolic 25mmHg
  2. Diastolic 10mmHg

25/10

104
Q

typical values for aortic pressures in an adult

A
  1. Systolic 125mmHg
  2. Diastolic 75mmHg

125/75

105
Q

CO goals in aortic stenosis

aka how to augment your CO equation to optimize forward flow (DO2) in aortic stenosis.

everything in critical care is DO2. DO2 is life

A
  1. preload high (force blood through the tiny little hole)
  2. afterload normal
  3. HR low (prevent pulmonary edema/back flow)
  4. contractility high (force blood out)
106
Q

treatment pathway for acute aortic regurgitation

💵💵💵💵 MONEY SLIDE 💵💵💵💵

aka how to augment your CO equation to optimize forward flow (DO2) in aortic regurgitation

these guys are fucked and the AR is usually due to either a dissection or a savage endocarditis

A
  1. HR high (P1 → P2 relationship. Keep flow moving forward. Don’t allow time for backflow). these patients will be in a compensatory tachycardia in an attempt to maintain forward flow. if you slow their HR down you could put them into worsening AR, profound cardiogenic shock, and kill them.
  2. afterload low (Improve your P1 → P2 relationship). you have to target afterload reduction in these patients. the afterload reduction is going to keep volume moving forward via P1 → P2. oftentimes these patients are d/t aortic dissection. typically we would want to use labetalol in dissection but if you use labetalol in these cats you’re gonna knock out their HR and fucking kill them. going to hydralazine or NTG would probably be a better option
  3. contractility high (force blood out. Don’t allow time for backflow). you might have to start a concurrent dobutamine infusion in these guys to keep their contractility high to keep volume moving forward otherwise they’re just gonna keep backing up and fucking die.
  4. put them on BiPAP or tube them and put them on PPV. It will decrease their MvO2 and improve their pulmonary edema and help with preload and afterload reduction
107
Q

treatment pathway in acute mitral stenosis

aka how to augment your CO equation to optimize forward flow (DO2) in mitral stenosis.

A
  1. preload normal (Phenylephrine or vasopressin)
  2. afterload normal
  3. HR low (prevent pulmonary edema/back flow) [Esmolol or amiodarone]
  4. contractility normal
108
Q

treatment pathway in acute mitral regurgitation

💵💵💵💵 MONEY SLIDE 💵💵💵💵

(rupture of chordae tendinae or papillary muscles from ischemia)

aka how to augment your CO equation to optimize forward flow (DO2) in mitral regurgitation

A
  1. HR high (P1 → P2 relationship. Keep flow moving forward. Don’t allow time for backflow). these patients will be in a compensatory tachycardia in an attempt to maintain forward flow. if you slow their HR down you could put them into worsening AR, profound cardiogenic shock, and kill them.
  2. afterload low (Improve your P1 → P2 relationship). you have to target afterload reduction in these patients. the afterload reduction is going to keep volume moving forward via P1 → P2. oftentimes these patients are d/t aortic dissection. typically we would want to use labetalol in dissection but if you use labetalol in these cats you’re gonna knock out their HR and fucking kill them. going to hydralazine or NTG would probably be a better option
  3. contractility high (force blood out. Don’t allow time for backflow). you might have to start a concurrent dobutamine infusion in these guys to keep their contractility high to keep volume moving forward otherwise they’re just gonna keep backing up and fucking die.
  4. put them on BiPAP or tube them and put them on PPV. It will decrease their MvO2 and improve their pulmonary edema and help with preload and afterload reduction
109
Q

primary manifestations of acute left sided valvular regulation (AR/MR)

A
  1. pulmonary edema

2. cariogenic shock

110
Q

primary cause of acute mitral regurgitation

A
  1. Acute or subacute myocardial ischemia
111
Q

primary causes of acute aortic regurgitation

A
  1. Aortic dissection (widening of the valvular lumen d/t the dissection)
  2. Endocarditis (vegetation causing leaflet destruction or periaortic valvular abscess rupture)
112
Q

what is the preferred modality to diagnose acute mitral regurgitation at the bedside?

A
  1. POCUS with colour doppler

2. Stethoscope is pretty useless tbh (only 50% of patients will have a new murmur on auscultation)

113
Q

classic case auscultation findings in aortic stenosis

A
  1. crescendo-decrescendo systolic ejection murmur

2. best heard at the right upper sternal border and radiates to the neck

114
Q

treatment pathway for aortic stenosis

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

PRELOAD DEPENDENT

  1. give fluids/Avoid preload-decreasing drugs
  2. Vasopressors for cardiogenic shock (Phenylephrine or vasopressin)
  3. sensitive to both bradyarrhythmia and tachydysrhythmias (Treat both aggressively)
115
Q

pathophysiology of aortic regurgitation

A
  1. regurgitation volume fills the LV → increased LV diastolic pressure → decrease in forward flow + increased LA + pulmonary venous pressure
  2. Decreased forward flow → hypotension and cardiogenic shock
  3. Increased LA + pulmonary venous pressure → pulmonary edema
116
Q

classic murmur found in aortic regurgitation

A
  1. “to-and-fro” murmur
  2. The combination of a soft systolic and low-pitched diastolic murmur produces a “to-and-fro” murmur at the cardiac apex
117
Q

two primary causes of acute mitral regurgitation

A
  1. Ischemic MR (Papillary muscle rupture due to AMI)
  2. Nonischemic MR (Ruptured chordae tendineae due to other cause [myxomatous disease, infective endocarditis, trauma, rheumatic heart disease])
118
Q

pathophysiology of mitral regurgitation

A
  1. regurgitation volume fills the LA → increased LA pressure → increased pulmonary venous pressure and pulmonary edema
  2. LV volume is decreased due to the regurgitant volume → a decrease in forward flow → hypotension and cardiogenic shock
119
Q

gold standard for “door to needle time” in STEMI (thrombolysis)

A
  1. 30 minutes door-to-needle for thrombolysis (if PCI unavailable)
120
Q

12-lead ECG progression in ACS/STEMI

A
  1. Normal
  2. Hyperacute t-waves (minutes to hours)
  3. ST-elevation (minutes to hours)
  4. Q-wave develops (hours)
  5. ST-elevation resolves, residual t-wave inversion (hours to days)
  6. T-wave recovery (days)
121
Q

current formal STEMI ECG criteria

A
  1. new ST elevation measured at the J-point relative to the PQ junction, in two contiguous leads
  2. V2-V3: ≥2 mm in men ≥40 y old
  3. V2-V3: ≥2.5 mm in men <40 y old
  4. V2-V3: ≥1.5 mm in women regardless of age
  5. Other leads: ≥1 mm
122
Q

transfer guidelines for STEMI at a non-PCI facility

A
  1. STEMI diagnosis-to-balloon time (at another facility) should not exceed 90 min (urban transfers)
  2. The first medical contact-to-balloon time in transfer patients should not exceed 90-120 min (urban transfers)
  3. If the total time from the first medical contact to PCI is estimated to exceed 90-120 min, fibrinolytics are recommended for symptom duration <12 h or 12-24 h if “a large area of the myocardium is at risk or hemodynamic instability is present.”
  4. After thrombolytics, the patient should be transferred immediately to a PCI facility, if available and feasible.
123
Q

Concerning features and findings with significant positive likelihood ratios for the diagnosis of ACS

A
  1. Prior known coronary artery disease (CAD) (2.0)
  2. A change in the pattern of symptoms over the previous 24 h (2.0)
  3. Pain similar to prior ischemia (2.2)
  4. Pain radiating to both arms (2.6)
  5. History of peripheral arterial disease (PAD) (2.7)
  6. Abnormal previous recent stress test (3.1)
  7. High risk overall of clinical gestalt (4.0)
  8. High-risk HEART score 7-10 (13.0)
124
Q

Define unstable angina

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

ACS that does not have:

  1. at least one troponin greater than the 99th percentile
  2. an increase and/or decrease in troponin (defined for each assay)

and:
3. Is characterized clinically by angina that is new in onset, occurs at rest, occurs with minimal exertion, or is otherwise worsening from a previously stable pattern

125
Q

Acute myocardial infarction (AMI) definition (includes STEMI and NSTEMI)

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

requires both:

  1. The detection of an increase and/or decrease of cardiac troponin values with at least 1 value greater than the 99th percentile upper reference limit
  2. Clinical evidence of acute myocardial ischemia
126
Q

NSTEMI PCI guidelines per AHA

which people with NSTEMI get a PCI

A
  1. Immediate PCI recommended for ischemic symptoms <12 h after onset, or 12-24 h if there is “ongoing ischemia”
  2. NSTEMI with electrical/hemodynamic instability (acute pulmonary edema, shock, recurrent/refractory ventricular dysrhythmias, etc.)
  3. NSTEMI with refractory ischemia (symptoms of angina or ECG findings of ischemia) despite maximum medical management

consider reperfusion therapy in:

  1. “STEMI equivalents” (aka STEMI(-) occlusion MI patterns) - this is like your wellens, avR STEMI and shit like that
127
Q

emergency reperfusion therapy (thrombolysis) is recommended by American College of Cardiology/AHA guidelines for…

A
  1. It will be >90-120 min total time from the first medical contact to PCI, or >90 min from STEMI diagnosis to PCI

and

  1. Symptoms <12 h, or between 12-24 h if “a large area of the myocardium is at risk or hemodynamic instability is present”, or ECG shows high “acuteness” (large upright T waves, persistent R waves, persistent ST elevation)
128
Q

STEMI Post-thrombolytic guidelines for non-PCI capable hospitals

A
  1. Transfer to a PCI-capable facility should be carried out after the administration of thrombolytics
  2. Immediate PCI is indicated if there is no ECG evidence of reperfusion after thrombolytics (“rescue PCI”)
  3. ECG evidence of reperfusion is at least a >50% reduction in ST segments
129
Q

ACS treatment pathway

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Dual antiplatelet therapy (Aspirin + P2Y12 inhibitor)
  2. Anticoagulant (UFH/enoxaparin/fondaparinux)
  3. Oxygen (sats >94%)
  4. Rate control (Metoprolol)
  5. Analgesia (NTG, opioids)
  6. Statin therapy
  7. Reperfusion (TnK or PCI)
  8. Angiotensin-converting enzyme inhibitors
  9. Optimize electrolytes (target normal range)
130
Q

which ACS patients should receive Opioid analgesics

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. opioids should be reserved for patients who are committed to immediate reperfusion therapy (PCI or thrombolysis)
  2. Goal is to reduce ischemic pain during the time between the decision to perform definitive reperfusion and actual reperfusion
131
Q

define “acute coronary syndrome”

A
  1. ACS refers to a spectrum of coronary diseases involving atherosclerotic plaque rupture and platelet-rich thrombus formation, causing stenosis or occlusion of the coronary artery with acutely diminished blood flow and resulting in hypoperfusion and ischemia, with or without infarction of the myocardium
132
Q

describe the factors that contribute to Myocardial infarct size

A
  1. the myocardial territory at risk
  2. collateral circulation present
  3. degree of coronary obstruction
  4. showering of downstream platelet-fibrin aggregates into smaller vessels
  5. myocardial oxygen demand (which is dependent on the heart rate and wall stress)
133
Q

Clinical Spectrum and Definitions of ACS

A

The spectrum of ACS currently includes:

  1. unstable angina
  2. NSTEMI
  3. STEMI
  4. sudden cardiac death (type 3 MI)
134
Q

frequently cited “STEMI equivalents” in the setting of ACS

A
  1. posterior STEMI (V1-V2 depression)
  2. hyperacute T waves
  3. de Winter’s T waves
  4. modified Sgarbossa criteria
  5. ST elevation in aVR associated with widespread ST depression
135
Q

right coronary artery territory supplied

A
  1. right ventricle
  2. inferior wall of the LV
  3. the AV and SA nodes
  4. some or most of the posterior
136
Q

branches of the left main coronary artery

A
  1. LAD

2. Left circumflex

137
Q

MOA for P2Y12 inhibitors

A
  1. blocks adenosine diphosphate (ADP) production in platelets
  2. ADP is one of the principal platelet activators
138
Q

what does “Dual antiplatelet therapy” refer to?

A
  1. aspirin plus a P2Y12 inhibitor

2. could also refer to aspirin + a glycoprotein IIb-IIIa inhibitor, if no P2Y12 inhibitor is given

139
Q

why is it important to give a higher dose of P2Y12 inhibitor in patients going for PCI?

A
  1. It is essential to achieve maximum platelet inhibition at the time of PCI, since this is a highly thrombogenic procedure.
  2. the rapid onset of platelet inhibition with a P2Y12 inhibitor is especially important for immediate PCI
  3. Higher doses act more rapidly than lower dose; this is especially useful for clopidogrel: 600 mg achieves earlier platelet inhibition than 300 mg
140
Q

role of anticoagulation in ACS

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. anticoagulation is a short-acting, temporizing therapy
  2. anticoagulation treatment should be given to all patients with confirmed, active ACS without contraindications
  3. anticoagulant administration is supported by the transient protection from MI granted by anticoagulation as a bridge to PCI for patients with unstable plaques
141
Q

contraindications for Beta blockers in ACS

A
  1. signs of CHF (Killip class III or IV)
  2. low cardiac output (SBP <120, sinus rhythm heart rate <60 or >110 bpm)
  3. high risk of cardiogenic shock
  4. elderly (>70 y old)
  5. heart block
  6. any signs of acute SA or AV node dysfunction (most commonly seen in RCA occlusions).
142
Q

role of beta blockers in ACS

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. If there are no contraindications (no heart failure, SBP at least 120, no tachycardia, no AV block) metoprolol IV offers benefit prior to PCI in anterior MI
  2. Anterior MI patients treated with PCI (not fibrinolytics) without contraindications to beta blockers, who are anticipated to undergo PCI within 6 h of symptom onset and who have an SBP >120, have benefit from IV metoprolol given prior to PCI
  3. All patients without contraindications benefit from oral metoprolol after PCI
  4. Oral beta blockers are recommended for all ACS within the first 24 h without contraindications
  5. it is reasonable to administer IV beta blockers at the time of presentation to patients with STEMI and no contraindications to their use who are hypertensive or have ongoing ischemia
143
Q

role of calcium channel blockers in ACS

A
  1. CCB’s given with the intent of decreasing MvO2 have very little role in the early treatment of ACS in normal sinus rhythm
  2. CCB’s role in ACS occurs in downstream scenarios as a substitute for beta blockers that have proven ineffective or are contraindicated, or in the chronic management of coronary artery spasm
  3. there is no effect on the risk of death or initial/recurrent infarction when given routinely for AMI or unstable angina
  4. CCB’s may be used to lower HR, and thus MvO2, in patients who are experiencing AF/Af w/ RvR or SVT in the setting of ACS
  5. CCB’s are relatively contraindicated in patients with reduced systolic LV function for fear of acutely worsened CO and hypotension (put the echo probe on)
144
Q

role of Angiotensin-converting enzyme inhibitors in ACS

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. The early initiation of angiotensin-converting enzyme (ACE) inhibitors has been shown to reduce short- and long-term mortality in patients with AMI
  2. ACE inhibitors should be used with caution within the first 24 h, since they may result in hypotension and/or renal dysfunction
145
Q

role of statin drugs in ACS

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. statins convey long-term preventive mechanisms in ACS
  2. statins offer benefits in the acute setting of ACS attributed to the “pleiotropic” effects of statins, including the inhibition of inflammatory and coagulation cascades and thrombus formation
  3. reduced rates of periprocedural MI and other short-term clinical outcomes for ACS patients who received statins prior to PCI
  4. it is reasonable to give the first dose of statin ASAP in any patient with ongoing ACS
146
Q

cardiogenic shock in the setting of ACS

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. pump failure (LV and/or right ventricle)
  2. mechanical complications (papillary rupture, free wall rupture, etc.)
  3. class I, level B recommendation for emergency PCI of STEMI in cardiogenic shock, regardless of the time since onset
  4. class I, level B recommendation for emergency fibrinolysis for STEMI patients with cardiogenic shock who are unsuitable candidates for either PCI or CABG
  5. Optimize the preload with fluids/blood as necessary based on fluid responsiveness and tolerance
  6. Consider intubation, MV, and paralysis to reduce the demand for CO during the delay to definitive management
  7. Norepinephrine is first-line pressor, then consider adding dobutamine for persistent low CO after norepinephrine
147
Q

PULMONARY EDEMA + SHOCK (“wet and cold” Cardiogenic Shock) treatment algorithm

A
  1. IV/O2/Monitor
  2. Differentiating the shock (pump failure vs mechanical complications)
  3. optimize the MAP (Norepinephrine +/-
    Inotropic agent)
  4. “fix the lungs” (CPAP/NIPPV/Intubation)
  5. differentiate + optimize volume status (fluid bolus vs lasix)
  6. consider inotrope for HFrEF/shitty contractility (dobutamine/epi)
  7. treat underlying etiology
  8. mechanical circulatory support
148
Q

Heart failure definition

A
  1. broad term that encompasses the pathophysiological end result of a multitude of disease processes
  2. HF develops when any structural or functional cardiac disorder causes impaired ventricular filling or ejection of blood at a rate commensurate with the requirements of the metabolizing tissues while maintaining normal filling pressures
149
Q

HF with reduced EF (HFrEF) definition

A
  1. Impaired ejection, left ventricular ejection fraction (LVEF) ≤40%
150
Q

HF with preserved EF (HFpEF) definition

A
  1. Abnormal filling, LVEF ≥50%
151
Q

define Acute heart failure

A
  1. Acute HF occurs when an acute event causes the heart to suddenly become unable to generate an adequate stroke volume
  2. may be caused by, AMI, acute valve rupture, dysrhythmia, myocarditis, tamponade, or infection
  3. May present as sudden “flash” pulmonary edema and/or shock.
  4. Heart size may be normal as it has not had time to change in size
152
Q

define Chronic HF

A
  1. develops over time, often months to years.
  2. Usually caused by ischemia, chronic HTN, or chronic valvular disease.
  3. In ischemic heart disease, chronic valvular disease, and chronic uncontrolled HTN, the heart’s growth and remodelling process is an attempt to compensate for its decreasing function
  4. An acute exacerbation of chronic HF can be triggered by infection, anemia, dietary or medication non-compliance, or coronary artery disease (CAD)
153
Q

define left-sided HF

A
  1. failure of the LV to pump blood forward → hypotension and hypoperfusion and the resulting backup of blood into the lungs (pulmonary edema)
154
Q

define Right-sided HF

A
  1. failure of the RV to pump blood forward → failure of the RV to “feed” the LV its preload and a right sided backup of blood (causing JVD, hepatomegaly, and peripheral edema)
  2. most common cause of right-sided failure is left-sided failure, and patients often present with manifestations of both
  3. Isolated right-sided failure can occur acutely (eg, in PE, hypoxia, or acidemia) or chronically (eg, in COPD)
155
Q

define “diastolic” HF

A
  1. Abnormal filling, preserved ejection

2. LVEF ≥50%

156
Q

define “systolic” HF

A
  1. Impaired ejection

2. LVEF ≤40%

157
Q

explain and define HF with reduced EF (HFrEF)

A
  1. Impaired ejection; LVEF ≤40%.
  2. characterized by abnormalities in systolic function, usually with progressive chamber dilation and eccentric remodeling
158
Q

explain and define HF with preserved EF (HFpEF)

A
  1. Abnormal filling; LVEF ≥50%.

2. characterized by a normal LVEF, normal LV end-diastolic volume, and abnormal diastolic function

159
Q

pathophysiology of Acute Decompensated HF

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. Hemodynamic abnormalities and circulatory failure from HF → neurohormonal activation and autonomic imbalance → increase in sympathetic activity and withdrawal of vagal activity
  2. compensatory mechanisms exists to counteract circulatory failure from HF (eg, increase blood volume and filling pressures, increase HR and muscle mass)
  3. Chronic wall stress → myocyte hypertrophy, death, and regeneration → eccentric remodeling that progressively impairs contractility, increases O2 demand/ischemia, and promotes arrhythmogenesis
  4. Altered relaxation and increased stiffness of the ventricle (delayed Ca2+ uptake and efflux from myocytes) occur in response to an increased afterload (pressure overload)
  5. Impaired relaxation → impaired diastolic filling of the LV
  6. These processes occur slowly over time
  7. when a trigger (eg, illness, dietary changes, medication non-compliance) temporarily worsens the cardiac output or increases the body’s demand, it overwhelms the compensatory mechanisms → acute decompensated HF
160
Q

pathophysiology of Sympathetic Crashing Acute Pulmonary Edema (SCAPE)

A
  1. Severe subset of acute HF presentations characterized by rapidly progressing pulmonary edema (minutes to hours) and sympathetic overdrive
  2. Decreased systemic perfusion and worsening oxygenation → sympathetic surge
  3. sympathetic surge → further increases the afterload, resulting in worsening pulmonary edema, further sympathetic activity, and a rapidly decompensating patient
  4. These patients are often overall fluid-depleted, even though they have significant pulmonary edema
  5. SCAPE patients may not have signs or symptoms associated with chronic HF, such as cardiomegaly or lower extremity edema, because the condition develops over a very short period
161
Q

common triggers for acute cardiogenic shock

A
  1. AMI (12-lead + trops)
  2. Acute valvular rupture (auscultation/bedside echo)
  3. Pericardial tamponade (bedside echo)
  4. Alcohol withdrawal (History and physical)
  5. Arrhythmia (ECG)
  6. Missed dialysis
  7. Physiologic stress (eg septic cardiomyopathy or CO)
  8. Thyrotoxicosis (history and physical, labs)
  9. Medication non-compliance
162
Q

treatment goals for Hypertensive acute decompensated HF

A
  1. treatment should be targeted to afterload and preload reduction
  2. Afterload can be reduced with a number of medicines, including nitrates and ACE inhibitors
  3. Nitrates are first line, with NTG being the most common
  4. loop Diuretics can be used in intravascularly volume-overloaded patients for preload reduction (Lasix)
  5. Check and replenish electrolytes, particularly magnesium and potassium (arrhythmias)
163
Q

treatment goals for acute cardiogenic shock

A
  1. Address the underlying cause of shock
  2. If shock is from pump failure, patients are frequently extravascularly fluid-overloaded but intravascularly volume-depleted
  3. Fluid challenges in 250-mL isotonic crystalloid boluses with frequent re-assessment of intravascular volume status
  4. if patient is still hypotensive post fluids, start an adrenergic agonist (norepinephrine)
  5. Dobutamine is a good option for inotropy when the primary mechanism of shock is poor cardiac contractility. Patients may still require levo for hemodynamic support
164
Q

non-invasive evidence on bedside assessment of systemic perfusion

AKA

🔥 PERFUSION vs 💩 PERFUSION

A

🔥 PERFUSION: warm extremities, normal capillary refill, preserved renal function, good urine output, and adequate mentation.

💩 PERFUSION: cool extremities, poor capillary refill, acute kidney injury, oliguria, poor mentation, and elevated transaminases (“shock liver”)

165
Q

non-invasive evidence on bedside assessment of Pulmonary capillary wedge pressure (pulmonary congestion)

A
  1. High wedge pressure is suggested by pulmonary edema (dyspnea, rales on lung auscultation, edema on chest X-ray, and B-lines on lung ultrasound).
  2. Low wedge pressure is suggested by dry lungs (no dyspnea, clear lungs on auscultation and chest X-ray, A-lines on lung ultrasound)
  3. The best test to determine wedge pressure is lung ultrasonography.
  4. Bilateral diffuse B-lines imply elevated wedge pressure, whereas bilateral A-lines suggest a low or normal wedge pressure.
  5. Ultrasonography is more sensitive than chest X-ray or exam to detect mild cardiogenic pulmonary edema.
166
Q

non-invasive evidence on bedside assessment of Total body volume status (systemic congestion)

A
  1. it’s possible for patients to have an elevated PCWP without total body volume overload (e.g. euvolemia plus an acutely deteriorating left ventricle).
  2. Clinical history can be very useful here: is there a history of volume loss (e.g. gastroenteritis, over-diuresis) or volume gain (e.g. diuretic nonadherence, iatrogenic fluid administration)? Weight gain or loss?
  3. Echocardiographic assessment of the IVC and jugular veins may allow estimation of the CVP
  4. Peripheral pitting edema suggests systemic congestion
167
Q

Forrester Class I

A

warm and dry

168
Q

Forrester Class II

A

warm and wet

169
Q

Forrester Class Ill

A

cold and dry

170
Q

Forrester Class IV

A

cold and wet

171
Q

treatment for cardiogenic shock patients who are “warm and wet”

aka

Vasodilatory warm and wet or mixed cardiogenic and vasodilatory shock

A
  1. Fix lungs (CPAP/BIPAP)
  2. Fix perfusion (Norepinephrine +/- inotrope)
  3. Determine volume status and address
172
Q

discuss vasodilated cardiogenic shock and septic-induced cardiomyopathy

aka how can cardiogenic shock mimic septic shock and how can septic shock mimic cardiogenic shock?

fukkk

A
  1. cardiogenic shock may trigger a SIRS response with elevated cytokine levels and ↓ SVR. This may occur later in the course of cardiogenic shock, possibly d/t ischemic tissue damage. This condition will mimic septic shock 🤯
  2. some patients w/ septic shock will develop a sepsis-induced cardiomyopathy. So, advanced-stage septic shock and advanced-stage cardiogenic shock can look clinically quite similar (e.g., shock, vasodilation, reduced systolic heart failure, systemic inflammation)
173
Q

key labs for working up/differentiating acute HF

A
  1. CBC, Electrolytes including Ca/Mg/Phos (if hypocalcemia suspected check iCa)
  2. Troponin (HF 2nd to MI?)
  3. Lactate level (how sick is this dude)
  4. LFT’s (marked transaminase elevation suggests shock liver with poor cardiac output)
  5. TSH if thyroid disease suspected. (cardiac manifestations of myxoedema or thyrotoxicosis)
  6. Digoxin level for patients on digoxin
  7. BNP levels are unhelpful (cardiopulmonary ultrasonography is a superior test).
174
Q

Acute HF treatment goals

A
  1. fix the lungs (O2 vs NIPPV vs Tube them)
  2. optimize perfusion (Levo support?)
  3. optimize volume status (fill the tank vs diurese)
  4. optimize contractility (inotrope? electrolytes?)
  5. treat underlying etiology (cath lab?)
  6. consider mechanical circulatory support (does this dude need IABP/ECMO/LVAD)
175
Q

discuss inotropes for HFrEF

ie, which HF patients do you throw on dob>?

A
  1. Inotropes will cause a short-term improvement in hemodynamics
  2. avoid catecholamine inotropes when possible
  3. In hypotensive cardiogenic shock patients in whom nitroglycerine or diuresis is contraindicated inotropes may be used with a goal of reducing the PCWP and decongesting the lungs (cold and wet, hypotensive). Resuscitate with norepi FIRST!! Or else they could crash when you start the dob from the afterload reduction

Inotropes should be used only if necessary, for the following indications:

  1. Hypoperfusion with low-normal blood pressure
  2. Refractory cardiogenic pulmonary edema eg failed BiPAP, nitroglycerine (if blood pressure is adequate), and diuresis (if there is evidence of volume overload)
176
Q

when to consider an inotrope (dobutamine or milrinone) for the patient with HFrEF?

A
  1. Normotensive patient with evidence of end organ hypo perfusion (shitty pump)
  2. Refractory cardiogenic pulmonary edema in the hypotensive patient (mega shitty pump. resuscitate with NOREPI first)
177
Q

how does one optimize MAP (optimize your starling curve) in a patient with acute heart failure?

A
  1. HTN or normotension you’re gonna target preload/afterload reduction (NTG)
  2. hypotension you’re gonna resuscitate with norepi (or epi if they’re mega fucked) then maybe consider adding in some dobutamine
178
Q

discuss “thrombolytic facilitated PCI”

A
  1. thrombolytic facilitated PCI is using thrombolysis as a mechanism to facilitate a “better” PCI. (Ie giving a dose of lytics’ before PCI even when the person would be within the window timeframe for primary PCI)
  2. Don’t do it
  3. Facilitated PCI is bullshit
179
Q

mechanisms of volume status assessment

A
  1. Passive leg raise
  2. Decrease in HR when you give a fluid bolus
  3. Use ultrasound to assess IVC collapsibility (patient must be sedated/paralyzed/on VCV
  4. CVP assessment
  5. JVP height measurement
  6. Arterial waveform pulse pressure variation (SBP delta P variation of 16%)
180
Q

physical exam signs of PERFUSION

A

Extremities colour, temperature, cap refill, mottling

181
Q

DeBakey Classification

A

The DeBakey classification, is used to separate aortic dissections into those that need surgical repair, and those that usually require only medical management

  1. type I: involves ascending and descending aorta (Stanford A)
  2. type II: involves ascending aorta only (Stanford A)
  3. type III: involves descending aorta only, commencing after the origin of the left subclavian artery (Stanford B)
182
Q

typical value for pulmonary artery pressure (PAP) in an adult

A

PA 25/10 (systolic/diastolic)

183
Q

typical value for aortic pressure in an adult

A

125/75 (systolic/diastolic)

184
Q

Heparin vs LMWHs vs Fondaparinux What’s the Difference?

A
  1. Heparin – Binds to and potentiates the actions of antithrombin (AT) to inactivate factor Xa and prevent the conversion of prothrombin to thrombin, as well as prevent the conversion of fibrinogen to fibrin.
  2. LMWHs – Also bind and accelerate the activity of AT, but with a preferential, and longer lasting effect on factor Xa. When compared to heparin, LMWHs are less able to inhibit the production of thrombin and bind to plasma proteins and endothelial cells less due to their decreased sized. This accounts for an 85-99% bioavailability when administered SC, more predictable anticoagulant response, less inter-patient variability, and longer duration of action than heparin
  3. Fondaparinux - Binds and enhances the anti-Xa activity of AT by 300-fold. AT specificity does not allow binding to other plasma proteins. It has no direct effect on thrombin, has excellent bioavailability after SC administration and a long half-life
185
Q

hemodynamic strategies and targets in aortic dissection

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. HR <60
  2. SPB <120 mm Hg
  3. art line for accurate titration of antihypertensives
  4. If BP differs between arms on NIBP use the extremity/value with the higher BP
  5. Labetalol IV 10-20 mg bolus over 2 min, then 20-80 mg bolus q10-15 min to a max of 300 mg, or initiate labetalol infusion at 0.5-2 mg/min, titrate up by 0.5 mg/min every 10 min to a max of 10 mg/min.

might have to stack hydralazine on top of your labetalol to hit the alpha reduction

186
Q

% change in mortality per hour following onset of symptoms in aortic dissection

A

1-2% increase in mortality per hour for each hour delay to definitive care (SURGERY)

187
Q

pathophysiology of aortic dissection

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. aortic wall is composed of tunica intima, media, adventitia (inside → out)
  2. AD is a failure of the aortic intima → propagation of dissection between intima/media d/t the patient’s pulse pressure
  3. The passage of blood into this space can extend the tear and create a false lumen, → impaired perfusion at branch vessels or causing rupture
  4. occurs when the integrity of the tunica intima is disrupted, allowing pulsatile blood to dissect through the tunica media
  5. The pulsatile aortic flow propagates the dissection, typically in an antegrade fashion, from the intimal tear
  6. Fenestrations between the true lumen and false lumen can occur downstream from the initial intimal defect, typically near the ostia of vessels branching off the aorta, maintaining false lumen patency
  7. Areas of repeated mechanical stress associated with the cardiac cycle as well as higher hydrodynamic forces, such as the ascending aorta and first portion of the descending thoracic aorta, are at increased risk of AD
188
Q

CCP principals of blood pressure management in acute aortic dissection

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A

CCP treatment consists of reducing the pulse pressure-related shear force (Δp/Δt) through pharmacologic rate control followed by blood pressure control

  1. Treat the pain. The most common presenting symptom of AD is pain. Pain is classically described as sudden in onset and severe. Ongoing pain leads to sympathetic stimulation causing tachycardia and worsening shear stress. Use IV opioids to treat the pain
  2. Following adequate analgesia, a Class I recommendation based on expert consensus is to initiate intravenous β-blockade and titrate to an HR of 60 beats per minute or less. Use labetalol or esmolol if available. Start an a-line
  3. If the SBP remains >120 mm Hg following the initiation of β-blockade, an intravenous vasodilatory agent should be initiated to reduce the SBP to <120 mm Hg while maintaining adequate end-organ perfusion. Use hydralazine

don’t forget ongoing analgesia. start an a-line and watch your BP closely

189
Q

three basic physiologic mechanisms that may cause or contribute to circulatory failure

A
  1. pump dysfunction
  2. insufficient vascular tone
  3. hypovolemia

PUMP, PIPES, FLUID

190
Q

“pump factors” which contribute to pump dysfunction

💵💵💵💵 MONEY SLIDE 💵💵💵💵

A
  1. heart rate
  2. cardiac loading conditions (ADCHF)
  3. contractility
191
Q

“circuit factors” which contribute to circulatory dysfunction

A
  1. intravascular volume

2. vessel tone

192
Q

ECG signs of right heart strain

A
  1. Tachycardia
  2. Right axis deviation
  3. RBBB
  4. S1Q3T3 (insensitive and non-specific)
  5. T-wave inversion anterior leads
193
Q

define right heart STRAIN (or more precisely right ventricular strain)

A
  1. ventricular dysfunction where the RV is deformed
  2. used to denote the presence of RV dysfunction usually in the absence of an underlying cardiomyopathy
  3. can be caused by PHTN, PE, RV infarction, chronic lung disease (pulmonary fibrosis or COPD), pulmonic stenosis, bronchospasm, and pneumothorax
194
Q

clinic features of right heart STRAIN on echo

A
  1. dilatation of the RV (ideally measured in the RV focused apical 4 chamber view)
  2. interventricular septal flattening (commonly referred to as “D sign”. look for the presence of septal flattening in LV via parasternal short axis)
  3. paradoxical septal motion
  4. right atrial enlargement
  5. right ventricular hypertrophy
  6. right ventricular systolic dysfunction (RV free wall hypokinesis with apical sparing “McConnell’s sign”)
  7. RV hypokinesia
  8. fat IVC (diameter >2.1cm with loss of phasic variation throughout the respiratory cycle)
  9. tricuspid regurgitation
195
Q

Massive (High Risk) Pulmonary Embolism definition

A

Persistent hypotension (systolic blood pressure <90 mm Hg) lasting >15 min or a baseline systolic pressure decrease of >40 mm Hg

196
Q

High Intermediate Risk Pulmonary Embolism definition

A

Normotensive or intermittent hypotension with both radiographic and biomarker findings of heart strain

197
Q

Low Intermediate Risk Pulmonary Embolism definition

A

Hemodynamically stable with either right ventricular strain on CT pulmonary angiography/echo OR abnormal biomarkers, but not both abnormalities.

198
Q

Low Risk Pulmonary Embolism definition

A

Hemodynamically stable with NO right ventricular strain on CT pulmonary angiography or echo with normal biomarkers

199
Q

Killip Classification for Heart Failure

A

Quantifies severity of heart failure in ACS and predicts 30-day mortality.

Class I: No signs of congestion/CHF
Class II: S3 and basal rales on auscultation and/or JVD
Class III: Acute pulmonary edema
Class IV: Cardiogenic shock

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