Cardiovascular Flashcards
1
Q
What % of CO do the atrial contractions contribute?
A
25-30%
Atrial “kick”:
Atrial kick is the phenomenon of increased force generated by the atria during contraction. This event occurs late in atrial systole when blood flows from the left atrium into the left ventricle. The purpose of the atrial kick is to increase flow across the mitral valve by increasing the pressure gradient. In a healthy patient, the atrial kick can be responsible for 20 to 30% of the blood transferred to the left ventricle and may be heard as the fourth heart sound.
2
Q
Name the AV valves:
When are they open?
Name the Semilunar valves:
A
Tricuspid and Mitral.
Open during DIASTOLE
Pulmonic and Aortic.
Open during SYSTOLE
3
Q
How many main coronary arteries are there?
A
- The left and the right.
RCA: Right Coronary Artery
4
Q
What does the RCA perfuse?
A
Right atrium
Right ventricle
SA node
VA node (nodes = heart rhythm)
Posterior wall in 90% of population.
5
Q
When you hear “RCA occlusion” what main wall should you be thinking of?
A
Inferior wall. (distally=of the LEFT ventricle)
Inferior wall includes:
Rt atrium
Rt ventricle
SA
VA
Back of the septum
90% of population will have posterior wall affects as well.
6
Q
Why is an occlusion of the Left Main (LM) called the widow-maker?
A
The LM supplies the LCA (left coronary artery), LAD (left anterior descending), and Circumflex artery.
7
Q
What wall should you think of with a left anterior descending LAD occlusion?
What are the affects of this injury?
A
Anterior and Septal Wall.
Affects:
Front and bottom of left ventricle.
Front of septum.
8
Q
What wall should you think of with a circumflex artery occlusion?
A
Lateral wall.
Affects:
Left atrium.
Back of left ventricle.
10% of population = posterior wall
9
Q
Regarding perfusion, why is tachycardia an issue?
A
The coronary arteries are filled during DIASTOLE. If the heart is beating too fast, this decreased coronary filling and perfusion.
10
Q
What do we call the concept/event of when the myocardium is stretched prior to contraction?
A
Preload.
Therefore, it’s r/t the sarcomere length at the end of diastole.
So, high preload would be associated with volume overload. (not always clinically true)
11
Q
How to measure preload on RT side of heart?
Left?
A
Right sided measurement is done with CVP, central venous pressure. (have fallen away w/a lot of CVPs r/t not being able to tell if they’ll be fluid responsive or not)
Left sided by PAOP, pulmonary artery occlusive pressure, aka the “wedge” pressure.
12
Q
What is the RESISTANCE your heart has to overcome in order to eject/contract called?
A
Afterload.
Vasoconstriction, chronic HTN has chronic high resistance (what leads to LV hypertrophy).
13
Q
How to measure afterload on RT side of heart?
On Left?
A
PVR
Pulmonary vascular resistance
Left side of heart is measured by SVR, Systemic vascular resistance.
14
Q
Where would you listen for the aortic valve?
A
Right sternal, 2nd intercostal space
15
Q
Where would you auscultate the pulmonic valve?
A
Left sternal, 2nd intercostal space
16
Q
Where would you auscultate the tricuspid valve?
A
Left sternal, 4th intercostal space
17
Q
Where would you auscultate the mitral valve?
A
Left mid-clavicular, 5th intercostal
18
Q
What is the “lub” of S1?
A
Closure of mitral and tricuspid valves.
Systole.
Loudest over the mitral auscultation point 5th ICS.
19
Q
What is the “dub” of S2?
A
Closure of the pulmonic and aortic valves.
Diastole.
Loudest over the aortic auscultation point, 2nd ICS.
20
Q
What is an S3 heart sound indicative of?
A
Fluid overload. Abnormal finding in adults.
Best heard over apex/ mitral valve site.
AKA ventricular “gallop.” (pre-systolic)
Ken-tuck-y or I Be-lieve
Normal finding in some kids.
Possibly during 3rd trimester.
21
Q
What does a S4 indicate?
A
Sound of vibration from Atria ejecting blood against non-compliant ventricles…
AKA atrial gallop.
Best heard at apex. May have pt lie on left side.
* Cannot have S4 in Afib; would be a S3.
Typical pt = Left ventricular hypertrophy, Ischemia, HTN, pulmonary stenosis, CAD, aortic stenosis,
You hear the S4 right before the S1.
Ten-ne-ssee or Be-lieve me
22
Q
When are splits best heard?
A
During INSPIRATION.
Split S1 - mitral closes before tricuspid
Ex: RBBB, V-paced rhythms, PVCs
Split S2 - aortic closes before pulmonary
Ex: Overfilled R ventricle, atrial septal defect (ASD)
23
Q
What are our “heart strings?”
A
Chordae Tendinae (Kor-day Tendi-nay)
Thin strands of connective tissue that anchor the leaflets of each AV valve (to papillary muscles) so that they cannot open into the atrium (thus allowing backflow of blood into the atrium).
24
Q
Sten-OH-sis mumur is heard when the valve is open or closed?
A
OH-pen.
Forward flow of blood through NARROW stenotic OH-pen valves.
Most common valve dysfunction.
25
Sten-OH-sis mumur is heard when the valve is open or closed?
OH-pen.
Forward flow of blood through NARROW stenotic OH-pen valves.
Stenotic murmurs are LOW pitch sounds.
Most common valve dysfunction.
26
What are the valves doing when you hear a murmur from insufficiency?
The valves are CLOSED.
You're hearing the backflow of blood through incompetent valves.
27
After S1 (mitral and tricuspid valves are closed) and before S2, you hear a murmur. What type of murmur is this?
Systolic.
Could be aortic or pulmonic stenosis OR mitral/tricuspid regurgitation or mitral valve prolapse.
28
If you hear a murmur after S2 (aortic/pulmonic valves are closed), what type of murmur is this?
Diastolic.
Could be aortic/pulmonic regurgitation or mitral/tricuspid stenosis.
Left-sided valve problems are much more common than right-sided.
29
What two skills are needed to help determine what type of murmur... what 2 questions do you need to ask?
1. Where is the murmur heard the loudest?
2. What is the shape of the murmur?
Ex: ascendo-decrescendo (a-shen-doe, de-cresh-en-doe): Increasing intensity then decreasing as in aortic stenosis; "diamond" shaped murmur. This type can be best heard at 2nd ICS R sternal and often radiates sound to the neck/carotids. Pulmonic is the same type but doesn't radiate to carotids and is best heard left sternal.
30
What type of murmur is called holysystolic or pansystolic?
Mitral valve. Best heard at apex, mid-clav 5th ICS.
Begins right at S1. With chronic MR, the L atrium gets larger and is able to hold more blood so the murmur shape is rectangular. It doesn't really change in intensity.
Same goes for tricuspid murmur but heard at L sternal 4th ICS. (also difficult to hear and no radiation of sound)
Holo/pansystolic means that it lasts throughout systole. AKA "Flat murmur" bc the intensity doesn't change.
Sound will radiate to axilla!
31
Are most murmurs high pitched or low?
Most are high-pitched.
Stenotic valves give low-pitched sounds.
32
A pt with mitral insufficiency is prone to which dysrhythmia?
Atrial Fibrillation.
Due to the over stretch of the left atrium, leading to internodal pathways (from SA node to atrium, back to the AV node) becoming dysfunctional.
33
Causes of regurgitation (9 of them):
How are stenotic valves EARNED?!
Regurgitation:
1. MI
2. Ruptured chordae tendinae
3. Severe left HF; dilated CM
4. Hypertrophic cardiomyopathy
5. Left ventricular hypertrophy
6. Mitral Valve prolapse
7. Myxomatous degeneration
8. Rheumatic fever
9. Endocarditis
Stenotic valves are EARNED! Earned with AGE!!!
34
Symptoms of mitral regurgitation (8 of them):
1. SYSTOLIC MURMUR
2. Orthopnea/dyspnea
3. Fatigue
4. Angina
5. Increased left atrial pressure
6. R sided HF
7. Prone to Afib d/t L atrial enlargement
8. L heart failure
Treatment :
- BP Rx and anticoagulants
- Diuretics
- Lifestyle changes
- Valve clip/ replacement
35
What type (systolic/diastolic) of murmur would mitral stenosis be?
Side effects of?
Treatment?
Sten-OH-sis is when the valves are OH-pen, the mitral valve is open during diastole, so this is a DIASTOLIC murmur.
- pinkish cheeks
- pulmonary edema
- prone to Afib (d/t L atrial enlargement)
can lead to...
- pulmonary HTN
- R HF
TREATMENT:
- Medical mngmt (pre/afterload reduction)
- Surgical replacement
- Balloon valvuloplasty (commissurotomy)
36
What findings reflect RIGHT atrial enlargement on ECG?
P wave amplitude > 2.5 mm in II (2.5 boxes)
and/or
> 1.5 mm in V1
Right atrial enlargement, so, from mitral stenosis leading to pulmonary HTN, tricuspid regurg, or Afib.
37
Which lead is best to evaluate the P wave?
II
38
What findings reflect LEFT atrial enlargement on ECG?
P wave DURATION >or= 0.12 (usu in II)
Notched P wave in limb leads with the inter-peak duration >or= 0.04
39
What findings reflect BiAtrial enlargement on ECG?
Features of both RAE and LAE in same ECG:
* P wave amplitude >2.5 mm in lead II plus duration >= 0.12
40
What 2 inotropes may be given to post op valve repairs?
What else should you be monitoring for and prepare for possible interventions?
DOBUTAMINE
MILRINONE
Monitor for Afib and heart blocks d/t Mitral and aortic valves being right next to Bundle of His, which could be damaged during procedure.
Be prepared to pace!
41
Downside to:
1. Mechanical valve
2. Biologic valve
1. Mechanical valves require lifelong anticoagulation but last longer than biologic (>20 years), click.
2. Biological valves only last about 8-10 years.
42
?? Random ??
AMIODARONE
Used for... mechanism of action... Avoid?
ANTIARRHYTHMIC aka Pacerone, Nexterone
1. Treats heart rhythm problems: Afib, Aflutter, SVT, cardiac arrest, cardiomyopathy
2. Mech of action: Amiodarone has multiple effects on myocardial depolarization and repolarization that make it an extremely effective antiarrhythmic drug. Its primary effect is to block the potassium channels, but it can also block sodium and calcium channels and the beta and alpha adrenergic receptors.
3. Can cause QT prolongation, thyroid issues
4. Avoid:
*Grapefruit. This can increase the amt of Rx in your body.
*AV block or sick sinus w/out a pacemaker, cardiogenic shock, CHF, or bradycardia.
43
?? Random ??
DOPAMINE
Used for... mechanism of action... Avoid?
NEUROTRANSMITTER - Catecholamine
Dopamine is a chemical released in the brain that makes you feel good. Having the right amount of dopamine is important both for your body and your brain. Dopamine helps nerve cells to send messages to each other.
Increases HR, BP and system vascular resistance
1. Used for BP support: Dopamine is a peripheral vasostimulant used to treat low blood pressure, low heart rate, and cardiac arrest. Low infusion rates (0.5 to 2 micrograms/kg per minute) act on the alpha receptors -visceral vasculature to produce vasodilation, including the kidneys, resulting in increased urinary flow.
At moderate rates (5-10 mcg/kg/min) has a greater effect on beta1 receptors = vasopressor.
At rates >10 mcg/kg/min has only alpha effects.
2. Dopamine is an important regulator of systemic blood pressure via multiple mechanisms. It affects fluid and electrolyte balance by its actions on renal hemodynamics and epithelial ion and water transport and by regulation of hormones and humoral agents.
3. Dopamine may interact with droperidol, epinephrine, haloperidol, midodrine, phenytoin, vasopressin, diuretics, antidepressants, beta blockers, cough or cold medicine that contains antihistamines or decongestants, ergot medicines, phenothiazines.
* WATCH for extravasation; tachy arrhythmias and ventricular ectopy.
44
?? Random ??
DOBUTAMINE
Used for... mechanism of action... Avoid... Dosing?
Beta1-adrenergic agonist
Inotrope
aka Dobutrex
Increases CO and heart rate (increases). Used in cardiac surgery, cardiogenic shock, HF, septic shock
1. It can treat heart failure and help the heart pump blood. Dobutamine is USED SHORT-TERM to treat cardiac decompensation due to weakened heart muscle (HEART FAILURE). Dobutamine is usually given after other heart medicines have been tried without success.
2.Dobutamine's ionotropic effect increases contractility, leading to decreased end-systolic volume and, therefore, increased stroke volume.
3. The medication is contraindicated in patients with an allergy to sulfites, w/an acute myocardial infarction, unstable angina, left main stem disease, severe hypertension, arrhythmias, acute myocarditis or pericarditis, hypokalemia and idiopathic hypertrophic sub-aortic stenosis.
4. Dosing:
2.5 - 20 mcg/kg/min (infusion up to 40 mcg/kg/min)
Onset 1-2 min, up to 10
Plasma half-life 2 min
--Monitor for tachycardia, hypo/hypertension, ectopy, hypokalemia.
45
Beta 1 receptor locations and effects:
Alpha?
Beta-1 receptors are located in the heart. When beta-1 receptors are stimulated they increase the heart rate and increase the heart's strength of contraction or contractility.
Remember: 1 heart, 2 lungs
Alpha-1: peripheral vasoconstriction
46
Beta 2 receptor locations and effects:
Beta-2 receptors are located in the bronchioles of the lungs and the arteries of the skeletal muscles.
Remember: 1 heart, 2 lungs
beta(1)- and beta(2)-adrenergic receptors are G protein-coupled receptors expressed throughout the body and serve as receptors for the catecholamines epinephrine and norepinephrine. They are targets for therapeutive agonists and/or antagonists in treatment of heart failure and asthma.
47
?? Random ??
MILRINONE
Used for... mechanism of action... Avoid?
Phosphodiesterase (PDE) inhibitor
aka Primacor
often called an "inodilator" It's an inotrope but also vasodilator.
Increases CO, decreases Pulmonary artery occlusion pressure and SVR; doesn't affect HR.
Milrinone is a medication indicated for cardiac support in patients with:
ACUTE or CHRONIC HEART FAILURE
PULMONARY HYPERTENSION
It is often used during cardiac surgeries, including coronary artery bypass graft surgery, cardiac transplantation, and other cardiac surgeries requiring cardiac support.
*Watch BP (vasodilation); LONG half-life 2.5 hrs!!!
DOSING Bolus 50 mcg/kg over 10 min
Maintenance 0.375-0.75 mcg/kg/min
48
AORTIC INSUFFICIENCY/REGURGITATION
1. Causes?
2. Signs?
3. Associated with?
1. Caused by:
- HTN
- Rheumatic fever (strep)
- Endocarditis
- Syphilis
- Idiopathic
2. Signs:
* De Musset - heading bobbing w/heartbeat
* Brisk carotid upstroke
* Wide pulse pressure > 40 mm Hg
* "Water-hammer" pulse - rapid upstroke and downstroke with a shortened peak.
3. Associated with:
- Marfan's syndrome
- Ventricular Septal Defect (VSD)
49
AORTIC STENOSIS
1. Concerns if not treated?
2. Symptoms?
3. Gold standard diagnostic tool?
4. Treatments?
1. Heart failure. Patho: Narrowing of valve = higher pressure in left ventricle = leads to hypertrophy = which can lead to HF. If HF, then has a 50%, 2-year mortality rate.
2. Symptoms:
- SOB
- Activity intolerance
- Chronic ^ afterload (SVR) d/t narrow, stenotic valve
- HF
3. *** Echocardiogram is Gold Standard.
Also Xray: =Left Atrial & Ventricular enlargement; pulmonary venous congestion.
& 12 lead: Left Atrial and Ventricular hypertrophy Atrial=P wave elongation; >120 ms in lead II
Ventricular=amplitude changes in mult leads
4. Treatments:
Surgical Valve replacement
Transcatheter Aortic Valve Replacement (TAVR)
50
AORTIC STENOSIS
POST-OP Considerations?
AORTIC REGURG
POST-OP Considerations?
AORTIC STENOSIS:
Can't tolerate swings in BP, keep it steady.
Avoid HTN.
Avoid or take care with inotropes.
Ensure adequate preload.
Monitor for heart block (r/t valves proxim to Bundle of His)
AORTIC REGURGITATION:
Might be hypertensive
Might need inotrope Dobutamine/Milrinone to improve forward flow & left vent emptying/ IABP.
Monitor their afterload... ^SVR = vasodilator (nitro), decreased SVR = Vasopressor
Monitor for Afib - likely wont tolerate
51
What does TAVR stand for?
Who undergoes this procedure?
What to monitor for post-procedure?
Transcatheter Aortic Valve Replacement.
Procedure done while the heart is still beating.
Done in moderate to high risk patients.
Monitor:
* Bleeding/hematoma at insertion site (femoral most common, also trans-carotid, trans-axillary)
* Signs of stroke 2/2 plaque rupture
* Bradycardia/ Heart Block (may need perm. pace maker)
52
Acute Coronary Syndrome is an umbrella term for what conditions?
Pathophys: Progressive atherosclerosis with plaque rupture causing blood clot formation leading to an imbalance of O2 supply & demand.
1. STEMI: ST Elevation Myocardial Infarction
* Infarction w/complete obstruction of blood flow
* Q wave MI
* Non Q wave MI
2. NSTE-ACS (old aka NSTEMI): Non ST Elevation Acute Coronary Syndrome.
*Ischemia w/partial obstruction of blood flow (usu multiple vessels)
* Unstable angina
* Non-ST Elevation MI
- Non Q wave MI
- Q wave MI
- Hallmark sign ***
53
What is the Levine sign?
Levine's sign is a universal sign of ischemic chest pain, defined as an individual holding a clenched fist over the chest that has a low sensitivity but is relatively specific for ischemia.
54
What does the acronym:
OLD CART
help you asses in regards to chest "symptoms"? (many times - esp women - present w/discomfort; not pain)
O - Onset
L - Location
D - Duration
C - Characteristics
A - Associated s/s? nausea, restless, sweating...
R - Relieving factors
T - Treatment
55
What is the #1 sign that a diabetic patient is having an ACS event?
SOB
Because they're in pulmonary edema.
56
What ACS does this describe?
May have fixed vessel stenosis w/demand ischemia; Exertional symptoms ease when exertion stops
Stable Angina
May require sublingual nitroglycerin.
57
What ACS does this describe?
Sudden pain that occurs at rest or when sleeping; will see ECG changes w/pain + symptoms
Variant - PRINZMETAL'S Angina
* Sudden pain caused from coronary artery vasospasm
* Important to get an ECG WITH and WITHOUT symptoms - so you can see the changes.
* Treat w/nitro and Calcium Channel Blockers (Dilt) to relieve spasm
- Seen in the younger population
- 60% have mild underlying atherosclerosis
- ECG ST elevation often looks like a sail
58
What ACS does this describe?
Chest pain/symptoms that increase in frequency, time and duration
Unstable Angina
* Sign and precursor to a MI
- 10-20 % have a MI
* May consider anti-platelet therapy
59
What ACS does this describe?
Pain occurs at rest and may last >20 min; hallmark is increased frequency of pain/symptoms; ST depression or T wave inversion (ischemia).
NSTE-ACS (NSTEMI)
* PARTIAL occlusion of coronary artery
* 8+ leads w/ST depression or T wave inversion & ST elevation in aVR - high suspicion for proximal LAD occlusion (most severe NSTEMI)
* Cardiac biomarkers elevated
* TREATMENT: PCI; early PCI if high risk (thru stratification tools)... anticoags, nitrates
60
Which cardiac biomarkers are the most specific to tissue injury?
Where do they originate?
How many hrs until detected?
*TROPONIN I & Troponin T
TROPONIN I
- Originates in myocardium.
- Detected 3-6 hours from injury
- Peaks in 14-20 hrs
- Returns to normal w/in 1-2 weeks
TROPONIN T
- Originates in myocardium & skeletal muscle
- Detected w/in 3-4 hrs of injury
- Peaks in 12-24 hrs
- Returns to normal w/in 2-3 weeks
61
What does ST elevation indicate?
What does ST depression indicate?
ST elevation = injury
ST depression = ischemia
62
What can cocaine use, a vessel dissection, fixed atherosclerotic lesion, inflammation, or coronary artery vasospasm lead to?
These can all cause a MYOCARDIAL INFARCTION.
Plaque rupture with clot formation is the most common cause.
63
DURING A STEMI...
1. When will you see the T wave elevation on the ECG?
2. When will you see the ST elevation?
3. Several hours after revascularization, what will happen on the ECG?
4. When might you see Q waves develop?
1. T wave elevation is seen immediately
2. ST elevation follows suit after the T wave elevates.
3. ST will normalize and the T wave inverts.
4. Several hours to days. Q waves may develop, reduced R waves, low voltage R wave (sometimes for life)
64
What are the limb leads?
What are the precordial leads?
II, III, aVF (RT lower limb lead is neutral & only closes the circuit)
Precordial leads are the chest leads (V leads)
65
What is a Q wave on an ECG?
Pathologic Q waves are a sign of previous myocardial infarction. They are the result of absence of electrical activity. A myocardial infarction can be thought of as an electrical 'hole' as scar tissue is electrically dead and therefore results in pathologic Q waves.
Pathologic Q waves are not an early sign of myocardial infarction, but generally take several hours to days to develop. Once pathologic Q waves have developed they rarely go away. However, if the myocardial infarction is reperfused early (e.g. as a result of percutaneous coronary intervention) stunned myocardial tissue can recover and pathologic Q waves disappear. In all other situations they usually persist indefinitely.
66
What door-to-balloon-time for STEMI?
If you can't get them to the cath lab in time, what is alternative treatment?
90 minutes or less.
Fibrinolytic (rarely done).
67
What is the first medication to give STEMI pt?
Followed by...
-- 325 mg chewable ASPIRIN. If unable to chew then give rectal.
-- Then give 0.4 mg SL NITROGLYCERIN Q 5min x 3. Venous dilation, reduces preload & ventricular wall tension, decreases myocardial O2 consumption.
**AVOID in R ventricular MI (bc nitro reduces preload from the vasodilation. RV MI's can become VERY preload dependent and then if it's taken away, no bueno). AVOID giving w/ phosphodiesterase (PDE) inhibitors such as Viagra or Cialis.
* Caution in Inferior wall MI
Monitor for hypotension
May use IV if continued chest discomfort
- MORPHINE should only be used in incremental doses and only if absolutely needed (drops BP); 1-2 mg IV Q 5-15min.
- OXYGEN should only be used if needed: <94%
(Hyperoxemia leads to oxidative stress and perpetuates oxidative injury after MI); in Europe their guidelines are <90%). Oxygen is not benign.
-- *Consider loading w/ P2Y12 INHIBITOR
- Clopidogrel (Plavix); Ticagrelor (Brilinta)
68
What does ASA inhibit to prevent clot formation?
Inhibits CYCLOOXEGENASE-1 w/in the platelets which prevents formation of THROMBOXANE A2 (TXA2's main role is in amplification of platelet activation and recruitment of additional platelets to the site of injury); thus disabling platelet aggregation.
69
What is plasma?
What is in FFP?
What are platelets?
What does whole blood contain?
PLASMA is the straw-colored liquid that blood components are suspended in. PLASMA accounts for about 55% of the whole blood.
FFP contains all of the clotting factors, fibrinogen (400 to 900 mg/unit), plasma proteins (particularly albumin), electrolytes, physiological anticoagulants (protein C, protein S, antithrombin, tissue factor pathway inhibitor) and added anticoagulants.
PLATELETS are small, colorless, disk-shaped cell fragments found in large numbers in the blood. PLATELETS and leukocytes account for less than 1% of whole blood. PLATELETS are involved in blood clotting.
WHOLE BLOOD is simply the blood that flows through your veins. It contains red cells, white cells, and platelets, suspended in plasma.
70
What is the onset of action for Aspirin?
1 - 7.5 min when chewed.
71
MORPHINE
1. Reduction of preload or afterload?
2. Analgesic or anxiolytic?
3. Population to avoid use in?
1. PRELOAD and some afterload.
2. MORPHINE is a potent analgesic AND anxiolytic.
3. Do not use in Right Ventricular MI.
Use cautiously in inferior wall MI (who can have an extension to their right ventricle).
72
What is the Gold Standard for acute STEMI treatment?
REVASCULARIZATION PCI
Cardiac cath lab.
Radial approach becoming more common than femoral.
Femoral Sheaths and venous/arterial locations:
"Venous is next to the penis" or mnemonic NAVL:
Starting from lateral going toward midline...
Nerve
Artery
Vein
Ligament
73
Signs of retroperitoneal bleeding:
Treatment:
Possible complication of femoral approach. D/T accidental backside puncture of fem artery while cannulating.
S/S
1. Tachycardia. Are they on BB? If so, this may not be present d/t the medication.
2. Hypotension (that is very fluid responsive).
3. Pain. Back pain or groin.
--- labs will reflect decrease in H&H
4. Flank ecchymosis (Grey Turner's Sign). Very late sign.
TREATMENT
- Medically manage. Surgical repair <10% needed.
Fluids, transfusion
- Possible PCI w/balloon tamponade
74
What is the treatment for a STEMI if unable to get to the cath lab?
FIBRINOLYTIC therapy:
1. Tenecteplase (TNKase) has better data behind it than tPA - esp in regards to an MI.
- Rapid IV bolus
or
- 5-second bolus: no infusion or 2nd bolus needed; weight-based dosing, no more than 50mg.
2. Activase (recombinant tPA)
- Bolus followed by infusion (d/t its short half life of a couple of minutes)
**Will still need Cath lab once bleeding risk is diminished for visualization of atherosclerotic plaques.
75
ABSOLUTE contraindications for fibrinolytic therapy (8 of them):
ABSOLUTE contraindications for fibrinolytic therapy:
1. Active bleeding
2. Intracranial hemorrhage
3. Known cerebral vascular lesion
4. Ischemic stroke in the last SIX months
5. Malignant intracranial neoplasm
6. Suspected aortic dissection
7. Closed head or facial trauma w/in THREE months
8. A-V malformation
76
RELATIVE contraindications for fibrinolytic therapy (there are of them):
RELATIVE fibrinolytic contraindications:
1. Chronic, severe, poorly tolerated HTN
2. SBP > 180 mm Hg or
DBP > 110 mm Hg
Need to lower the BP before administering
3. Ischemic CVA > 3 months
4. Dementia
5. Traumatic or prolonged CPR
6. Major surgery < 3 weeks
7. Internal bleeding < 2-4 weeks
8. Pregnancy
9. Active peptic ulcer disease
10. Current use of anticoagulants
77
What is the reversal agent for heparin?
Protamine sulfate
78
Treatment for bleeding complication after fibrinolytic therapy?
- Discontinue all anticoagulants
- Monitor labs PT/INR/aPTT/ fibrinogen for up to 24 hrs
- Cryoprecipitate and platelet transfusion. Think of cryo as liquid fibrinogen.
- Frequent neuro exams
- Avoid punctures/ invasive devices/ compression devices for 6-12 hrs
- Monitor urine output/ BUN/ Cr
79
Post PCI:
What do you need to keep a close eye on when a patient is on one of the following medications?
Abciximab (Reopro)
Eptifabatide (Integrillin)
Tirofiban (Aggrastat)
Monitor PLATELETS
These meds are Glycoprotein IIb/ IIIa inhibitors and are used at the time of PCI.
Platelet monitoring goes for ANY of the anti-platelet therapy meds (bleeding risk):
* P2Y12 Inhibitors:
1. Plavix (Clopidogrel)
2. Effient (Prasugrel)
3. Ticagreolor (Brillinta)
* Unfractionated heparin
* Bivalirudin (Angiomax) (done in cath lab)
80
What are the "Big 5"?
r/t meds pt will be discharged home w/after MI
1. Aspirin (indefinitely)
2. Thienopyridines (P2Y12 inhibitor) for at least 1 year
3. Beta Blocker (indefinitely)
4. Statin (high dose indefinitely)
5. ACE inhibitor or ARB (If EF < 40%, indefinitely)
*** Dual anti-platelet therapy for one year is critical - patient education ***
81
What type of medication ends in "-olol"?
What are the two most common, post MI?
Beta Blockers: treats high BP and HF
BB = "Block" the heart (slow HR)
"Breaks" on the heart (decrease contractility)
Metoprolol tartrate (Lopressor)
or
Carvedilol (Coreg)
These are both cardioprotective...
* They block the sympathetic nervous response.
* Negative inotrope - to reduce workload and oxygen consumption of the heart.
* Decrease AV node conduction
* Decrease automaticity, less risk for arrhythmias
Warn pts they may feel exhausted for a few months after starting this medication.
82
What is the difference between metoprolol TARTRATE and metoprolol SUCCINATE?
TARTRATE
1. Metoprolol tartrate is the only form of metoprolol that's cardioprotective.
2. **Used post MI
3. Immediate release tablet, liquid or IV
PO dosing: 100-400mg/day
IV dosing: full dose 15 mg
SUCCINATE
1. Used in HF
2. Extended release tablet daily
PO dosing: 25-100 mg/day
If tolerating, max PO dose 200mg
Either one can be used for angina or HTN
83
What are some LUNG affects from Beta Blockers?
On the VESSELS
KIDNEYS
LUNG
- Prevents bronchodilation and may induce bronchospasm.
- If a patient has asthma or COPD use w/caution
VESSELS
- Blocks receptor sites for catecholamines, blocks fight or flight response.
- Prevents vasodilation in arterioles and veins
KIDNEYS
- Decreases renin production.
Renin is a hormone made by the kidneys. It controls the production of another hormone, aldosterone, which is made in the adrenal glands. Aldosterone helps manage blood pressure and maintain healthy levels of potassium and sodium in the body.
84
Which drug (hint: HMG CoA Reductase Inhibitors) is the most prescribed class in the US?
Over 17 million take this class of Rx
STATINS
* Decrease cholesterol by interfering w/the body's ability to produce it
* Decreases the inflammatory response that theoretically may be responsible for atherosclerotic process
* Cardio-protective
* Decreases the risk of recurrent MI/stroke
* High-dose recommended for all post MI's
* Target LDL < 70
* Decrease MI recurrence by up to 40%!
* Decrease cardiac death 25-35%
85
What should you monitor for and what side affects are possible in patients taking statins?
Most statins are taken at night. Which 2 can be taken in the morning?
MONITOR
* For muscle myopathies and myositis:
Myositis is the name for a group of rare conditions. The main symptoms are weak, painful or aching muscles (muscle inflammation). This usually gets worse, slowly over time. ** Statin plus fibrate increases this risk.
* Monitor LFTs (rarely becomes a problem)
SIDE AFFECTS
- May exacerbate DM2 (theory is they'd develop DM2 anyway... benefit far outweighs the risk)
- Rhabdomyolysis - extremely rare
- Fog brain
- Digestive issues
You can take
1. Atorvastatin (Lipitor)
2. Rosuvastatin (Crestor)
in the morning.
86
What does a patient look like/ present with with an INFERIOR wall MI?
1. Bradycardia
2. Hypotensive
3. N/V
4. Diaphoretic
Always be on the hunt for high grade AV blocks... if they develop Winkebach, they may be able to tolerate but be prepared to pace (rare). Atropine for bradycardia available.
87
3 classic signs of a RV MI?
Treatment?
1. HYPOTENSION
2. Compensates with TACHYCARDIA
3. JUGULAR VENOUS DISTENTION (w/clear lungs)
TREATMENT:
Fluids (preload important)
**The only type of MI that gets fluid**
Then inotrope like dobutamine (fast on fast off)
AVOID anything that'd drop their preload:
Nitro
Morphine
Diuretics
Beta Blockers
88
Equation for CO?
CO = HR x SV
So, if a muscle wall is infarcted, not performing as well = stroke volume will go down. This leads to decreased CO, so the body will compensate by increasing the HR.
89
Which two coronary arteries perfuse to the septal wall?
LAD = anterior septal wall; 2/3rd's of the septum
RCA = Posterior Descending Artery (PDA) branches off of the RCA to perfuse the posterior septal wall; 1/3 of the septum.
90
What type of heart block would you look out for if anterior mI?
2nd degree type II or 3rd degree/complete heart block
If some R's don't get through, prepare to pace that Mobitz II!
These conduction blocks occur below the atria, so possible in ventricle injuries.
91
What is the most common complication in a CABG/sternotomy related surgery?
Atelectasis.
Encourage IS, deep breathing, coughing
92
CABG post op considerations:
1. BP. Higher increases risk for bleeding.
2. Pain. Non-opioid around the clock like Ofirmev.
3. Electrolytes
4. Bleeding
5. Post op ischemia. Get a 12 lead.
6. Dysrhthmias/Blocks *esp w/aortic valve replacement
7. ***Atelectasis***
93
What does a wide mediastinum, narrowed pulse pressure, and hypotension indicate?
CARDIAC TAMPONADE
Wide mediastinum on xray. Bleeding into pericardial sac. Usu holds 20-50 mLs of pericardial fluid. Anything more than that=compression.
94
What is Beck's Triad?
1. Elevated CVP w/JVD
2. Hypotension (from poor forward flow)
3. Muffled heart sounds
95
What are the following signs of?
Sudden drop in chest tube output.
Narrowed pulse pressure.
Tachycardia.
Pulsus paradoxus
Pulseless Electrical Activity (PEA)
CARDIAC TAMPONADE
Pulsus paradoxus is a > 10 mm Hg drop during INSPIRATION
96
TREATMENT for cardiac tamponade:
Medical tamponade:
Post surgery:
Coagulopathy:
MEDICAL
Pericardiocentesis - risk: lac of coronary artery
POST SURGICAL
Thoracotomy
Re-sternotomy
Locate and control source of bleed
COAGULOPATHY
Correct the coags
97
Stable SVT not reactive to vagal maneuvers. What's the next step in treatment?
Treatment if UNstable?
Administer Adenosine (Adenocard) 6 mg IVP FAST
-- Repeat 12 mg x 2, Q 1-2 min
--- If that does work: DILTIAZEM (CCB)
Unstable: cardioversion
Adenosine slows down the conduction through the AV and SA node.
Warn the pt that they're going to feel "breathless" or "not well" before giving adenosine.
98
Which heart condition causes the heart to beat abnormally fast for periods of time?
WOLFF-PARKINSON -WHITE SYNDROME (WPW)
A "pre-excitation" tachyarrythmia. R/T abnormal conduction pathway between atria and ventricles (an extra electrical connection in the heart).
99
What are the classic symptoms seen on an ECG who has WPW syndrome?
How is WPW treated?
1. Short PR < 0.12
2. Delta wave
A delta wave is slurring of the upstroke of the QRS complex. This occurs because the action potential from the sinoatrial node is able to conduct to the ventricles very quickly through the accessory pathway, and thus the QRS occurs immediately after the P wave, making the delta wave.
TREATMENT:
1. Beta blocker.
2. Cardiovert if unstable.
2. Long term: EP referral for ablation. (Electrophysiologist)
100
What medications to AVOID in pts with WPW syndrome (3 of them):
1. DIGOXIN - may accelerate the ventricular response
2. CALCIUM CHANNEL BLOCKER - can speed up the ventricular response
3. ADENOSINE - may induce VFIB!!!
101
Polymorphic ventricular tachycardia is aka?
What can this dysrhythmia deteriorate into?
- Torsades de Pointes "twisting of the point".
** Associated with prolonged QT interval.
Ventricular rates 150 - 250 bpm
Usually terminates spontaneously, can be recurrent.
- Can deteriorate into VFib!
102
What dysrhythmia can be caused by:
Brugada syndrome
Prolonged QT
Takotsubo CM
Electrolyte imbalance
Methadone toxicity
Tricyclic antidepressants
Bradycardia (more prone)
Some fluroquinolone abx
Torsades de Pointes.
TREATMENT
#1 Magnesium
-- may cause hypotension & bradycardia if given too fast
-- 1-2 grams over 1 hour
-- Emergency/loading dose 1-2 gm given over 5-20 min, diluted 10 mL D5W
#2 Assess electrolytes
** Calcium is the reversal **
3. Can try:
- Amiodarone
- Beta blockers
- Lidocaine (if ischemic cause)
- assess the preceding QT interval
4. Overdrive pacing. Hooking ventricle pacing wires to pacemaker going at a higher rate (100 bpm) to decrease QT interval and reducing risk.
5. If pulseless = treat as cardiac arrest
103
What should you have at the bedside when you're going to cardiovert?
O "Oh"
S "Say"
I "It"
I "Isn't"
S "So"
O - Oxygen
S - Sedation, Suction
I - Intubation /airway supplies
I - IV's
S - SYNCH button!!
Tell the pt what is going on... use a sedative w/amnesic affect (Midazolam/Versed)
104
Of the following conditions, which arrhythmia are they at risk for developing?
CABG
Valvular dz
MI
Atherosclerosis
Rheumatic Heart Dz
Lung dz
ATRIAL FIBRILLATION - "the stroke rhythm"
Treatments vary depending on symptoms (how fast it is; how long they've been in it...)
-- Do we rate control or rhythm convert? --
RVR = Rapid Ventricular Response = > 100 bpm
A heart failure pt may not tolerate Afib... r/t the loss of "atrial kick" that's lost = decrease in CO up to 20-25%
Left atrial appendage in left atria is where the clot formation develops.
105
This arrythmia has the following symptoms:
Atrial rates 240-400 bpm
Possible syncope
Palpitations
Fatigue
Exercise intolerance
SOB
ATRIAL FLUTTER
Luckily the AV node slows the conduction down by blocking those impulses before they get to the ventricles.
60% of pts have underlying CAD.
Not uncommon to see this post open heart surgery.
TREATMENT
** Ablation is superior long term treatment.
TTE - preferred method for evaluating flutter
TEE - best for viewing left atrium for thrombus (trans esophageal echo)
106
Medication/Treatment options for atrial arrhythmias?
4 meds
2 other
1. Amiodarone - safe regardless of EF%
2. Beta Blockers - Metoprolol; Esmolol (IV infusion)
* Use cautiously in those w/reduced EF
3. Calcium Channel Blockers - Verapamil; Diltiazem (IV infusion: Cardizem)
* Use cautiously in those w/reduced EF
4. Digoxin
5. Anticoagulation
6. Synchronized Cardioversion if new (vs chronic) & unstable.
107
1. What class of medication is digoxin?
2. What is it primarily used for?
3. Signs of toxicity?
1. Digitalis Glycoside
2. Afib, Aflutter, HF
3. N/V/ Irregular heartbeat
Therapeutic levels of digoxin are 0.8-2.0 ng/mL. The toxic level is >2.4 ng/mL
Digoxin toxicity causes hyperkalemia. The sodium/potassium ATPase pump normally causes sodium to leave cells and potassium to enter cells. Blocking this mechanism results in higher serum potassium levels.
108
This medication is used to treat atrial OR ventricle arrhythmias but is only FDA approved for ventricle arrhythmias. Can give metallic taste.
Medication class: Antiarrhythmic
AMIODARONE
- Does not suppress cardiac contractility; so good for HF pts... unlike BBs or CCBs which have negative inotropic affects.
- Slow load via oral route or IV then bridge to oral.
*Afib: give 150 mg over 10 minutes.
*Vfib: give 300 mg push during a code (pulseless)
- Short term side affects: Brady, prolonged QTc, metallic taste.
- Long term side affects:
-- Pulmonary toxicity (usu at higher doses)
-- Prolonged QT
-- Loooooong half life (25-50 days!)
Further dosing: Max dose - 2.2 g/ 24hr
- First load as above, then:
-- slow infusion - 360 mg over 6 hr @ 1 g/ min
-- maintenance infusion - 540 mg over 18 hr @ 0.5 mg/ min
109
Considerations/ Risks of Amiodarone/ Antiarrhythmics?
Every antiarrhythmic can become arrhythmogenic...
º Note baseline K+ and Mg++ levels
º Hold for bradycardia & prolonged QTc
º Check for medication interactions:
-- BB can decrease HR
-- Coumadin & amio can increase PT
-- Digoxin & amio can increase dig serum levels = toxicity
º When giving bolus of amio, watch for hypotension.
** Consider the need for central venous access **
-- not all the time needed. Irritable to venous system.
110
What medication class is most commonly given for arrhythmias?
What two main reasons are they used/prescribed for?
CALCIUM CHANNEL BLOCKERS
Mechanism of action:
They work by preventing calcium from entering the cells of the heart and arteries. Calcium causes the heart and arteries to squeeze (contract) more strongly. By blocking calcium, calcium channel blockers allow blood vessels to relax and open.
This decreases BP and afterload.
2 main reasons to use CCBs:
1. HR control
2. Lower BP
111
a) Which CCB are used to treat HTN?
Hint: Dihydropyridines (DHP) aka "D-pines"
b) Which CCBs are used to treat arrhythmias?
(Non-dihydropyridines are used to treat tachyarrhythmias and vasospasms)
a) Vaso-selective. BP.
1. Amlodipine (Norvasc)
2. Felodipine (Plendil)
3. Nifedipine (Procardia)
4. Nicardipine (Cardene) - IV. Works on arterial side to vasodilate = decrease in BP
5. Clevidipine (Cleviprex). - IV. Works on arterial side to vasodilate = decrease in BP
b) Cardio and vaso-selective. Used to slow the HR.
1. Verapamil (Calan, Isoptin)
2. Diltiazem (Cardizem)
112
1. Which minimally invasive procedure (could also be open chest) makes scar tissue within both atriums to block conduction of the erratic impulses?
2. What arrhythmia is this procedure used on?
1. MAZE procedure: 75-90% success rate.
2. ATRIAL FIBRILLATION
Post op:
Monitor surgical site
Monitor rhythym
113
Which medication is used on symptomatic bradycardia?
Dosage?
ATROPINE
Works by inhibiting parasympathetic NS.
Works on AV node so, pointless in complete heart block.
Dosage:
0.5 mg IV push - see how pt responds
-- May repeat 3-5 min for a total of 0.04 mg/kg (~3mg)
If you give more than 0.5 mg it can cause ischemia 2/2 tachycardia.
Side affects:
Tachycardia
Dry mouth (also used to decrease secretions)
Urinary retention
Blurred vision
114
What does HFpEF mean?
Heart Failure with preserved Ejection Fraction. DIASTOLIC Heart Failure.
EF >/= 50%
115
What does HFrEF stand for?
Heart Failure with reduced Ejection Fraction. SYSTOLIC Heart Failure. aka CHF.
EF
116
Top 4 causes of HF:
1. MI 8-10 x increased risk
2. HTN 2-3 x increased risk
3. DM 2-5 x increased risk; metabolic syndrome
4. Valve disease
117
What do the following symptoms suggest?
Tachycardia, tachypnea
Increased BNP level
S3 ventricular gallop
Mitral regurgitation
Displaced PMI (point of maximal impulse)
Crackles
Cough, frothy sputum
Increased PA pressures
Decreased CO/CI
** Wet lungs **
Left sided HF
PMI palpated supine, mid-clav 5th ICS
118
What do the following symptoms suggest?
JVD
Hepatojugular reflux
Peripheral edema
Hepatomegaly
Anorexia, N/V
Ascites
Tricuspid regurg
Increased CVP
Increased liver enzymes
** Clear lungs **
Right sided HF - clear lungs only in isolated RHF (d/t COPD; PHTN, OSA)
Hepatojugular reflux: Commonly done to detect heart failure. With right-sided heart failure, abdominal compression increases venous return to the heart and may markedly increase jugular vein distension (JVD) and pressure.
- Pt supine, elevate the head of his bed to 45 degrees. Stand at right. Ask pt to turn head to the left and to breathe normally through open mouth. Assess for distension of the internal and external jugular veins. Obvious bilateral distension when the head is elevated above 30 degrees indicates an abnormal increase in venous volume.
- With your right hand, apply firm pressure on your patient's midabdomen (at the periumbilical area) while assessing the highest point of oscillation in his right internal jugular vein.
- Continue applying firm pressure to his abdomen for 30 to 60 seconds. This moves venous blood from the liver sinusoids to the venous system. If the heart can pump this additional volume, the jugular veins will rise for a few seconds, then return to the previous level.
- If the patient has volume overload 2/2 to HF, jugular venous pressure rises and stays elevated for as long as you apply firm pressure. If the height of neck veins increases by at least 3 cm throughout compression, they have positive hepatojugular reflux.
119
Normal BNP level?
Under 100.
Anything over 100 suggests HF.
120
What 3 meds will a HF patient need to be on?
1) BB (3 most common: metoprolol succinate, carvedilol, bisoprolol)
2) ACE inhibitor - end in "-pril" (blunting angiotensin I from changing to angiotensin II - angio II is a potent vasoconstrictor)
-- If pt develops the ACE cough, they can switch to an ARB instead those end in "-sartan". ARBs directly block angiotensin II.
3) Aldosterone antagonist. You want to blunt the aldosterone bc they tell the kidneys to hold onto Na and H2O. The most common is spironolactone.
These block 2 systems: Sympathetic and the RAAS
121
Can a pt be on an ACE inhibitor AND and ARB?
No.
Only one or the other.
122
What class of medication blocks catecholamines?
Beta Blocker
Decrease HR and myocardial oxygen consumption
long term. May feel tired a month or 2 after starting.
123
Which enzyme activates hormones causing an increase in BP?
Hint: It is also a POTENT vasoconstrictor.
Angiotensin II
Causes the body to hold onto Na and H2O.
Acts on the efferent arterioles in the kidneys causing a back pressure in the glomerulus.
The goal in HF is to blunt angiotensin 2!!! This decreases the workload of the heart by decreasing afterload by more vasodilation (since angio 2 constricts) and excretion of Na/H20 = less volume to work against).
124
How do ACE inhibitors decrease preload & afterload?
Preload: Na & H2O excretion; veno-dilation
Afterload: arterial dilation. Causes increase of bradykinin = vasodilation. *Can develop angioedema from bradykinin (rare but higher in African American and females).
Increase in prostaglandins/ nitric oxide = vaso-dilation & endothelial protection.
Decreases remodeling by decreasing preload.
Watch potassium levels and creatinine.
125
What is the new class of medication, called ARNI, used for?
Its an ARB/Neprilysin inhibitor. aka Entresto.
Indicated for use in chronic HF and reduced EF. 20% mortality reduction compared to Enalopril.
126
If a pt has a true allergy to sulfa, which diurectic is contraindicated?
Loop diuretics
Furosemide/Lasix
Torsemide/Demedex
Bumetamide/Bumex
Ethacrynic acid
127
Ototoxicity or tinnitus can occur when which medication is given in high doses or frequently?
Loop diuretics
More common in higher doses given over prolonged period of time.
128
What is an aldosterone antagonist?
Spironolactone (Aldactone) - blocks aldosterone to prevent Na & H2O retention.
Also lesser known Eplerenone (Inspra)
Aldosterone antagonists are used congruently with loop diuretics in those who have class III & IV heart failure.
And those w/ EF
129
When is hydralazine/isosorbide dinitrate used in heart failure pts?
aka H-ISDN
When they're not able to tolerate beta blockers.
Since hydralazine is a vasodilator, it decreases afterload/SVR. Prescribed ~ QID PO/IV
The Isosorbide dinitrate is mostly a venodilator, so this decreases preload.
This combination helps decrease the pathologic cardiac remodeling (r/t overworking on heart).
Population that benefits most from this is African American.
130
Which medication is given as the following?
Loading dose 1.0 - 1.5 mg over 24 hours.
Average dose is 0.125 to 0.25 mg daily.
With a therapeutic range from 0.5 - 2.5.
DIGOXIN: Inotrope. Also slows conduction through AV node.
Cardiac glycoside: a class of organic compounds that increase the output force of the heart and decrease its rate of contractions by inhibiting the cellular sodium-potassium ATPase pump.
Check dig levels 6 - 8 hours after dose
This Rx can cause almost any arrhythmia with toxicity... prolonged QT.
Used to control ventricle rate in Afib/flutter (by slowing AV conduction)
*Best used in pts w/HF w/afib
131
Which medication toxicity my result in the following s/s?
Vision changes (yellow; halos)
N/V
Dizziness
Digoxin toxicity **
Cardiac symptoms:
-- Bradycardia
-- Long PR interval
-- QT elongation
-- Possibly ST depression
132
Safety considerations before administering digoxin:
Know apical HR
Know K+ (hypokalemia can increase risk of dig toxicity)
Renal function. If higher Cr, may need to lower dose.
Also:
-- Amiodarone can increase dig levels (SO, decrease dose by 1/2 when amio started)
-- PPI's can increase dig levels
-- Antacids can decrease dig levels (decreasing bio-availability of it)
133
Other more invasive treatment options for HF?
1. Biventricular pacing - esp if BBB
2. Transplant
3. Cardiac assist devices
4. Palliative: Inotrope infusions
134
Most HF diagnostics are with an ECHO. When would a TEE be beneficial?
When assess for a possible clot in setting of Afib.
Heart cath if ischemia suspected
CXR for congestion assessment or cardiomegaly
Myocardial biopsy for restrictive CM
135
"MAWDS" pneumonic for discharge education for HF & cardiomyopathy management:
M: Medication adherence
A: Activity; get up and moving
W: Weight; same scale, same clothes, same time
D: Diet; sodium restricted
S: Smoking cessation; limit alcohol
Prevent Infections - get vaccinated; flu & pneumococcal
136
Many can have a wide BBB with no issues; why is it a concern in the setting of HF?
What is usually done for long term therapy?
Can get valvular regurgitation from it.
Biventricular pacemaker placed/ Cardiac resynchronization therapy.
137
For Ventricular Assist Devices, they are usually used (short term) for bridging therapy while awaiting a heart transplant. When they are placed for destination therapy, what does this refer to?
Sending them home on the device to "buy" them more time - that they will not likely survive.
138
What's severed for a heart transplant that will affect your judgement on what medications to give or not to give?
The vagus (cranial nerve X) nerve is severed. So Atropine will not work in bradycardia. Will need to pace the pt.
139
What cardiac condition is described as having a thickened myocardium that decreases its ability to pump enough blood?
Hypertrophic cardiomyopathy
aka HOCM - Hypertrophic Obstructive CM; big fat septum 6-11 mm width normal; 25 mm (nicole's story size) can occlude output flow to aorta.
aka IHSS - Idiopathic hypertrophic Subaortic Stenosis
Thickening of the ventricle decrease its volume capacity leading to poor CO. Decreased compliance.
Many present with sudden cardiac death.
V4, 5, & 6 may show big tall R waves
140
Which medical regimen would be beneficial for a pt with Hypertrophic cardiomyopathy?
a) Cardiac glycoside & beta blockers
b) Calcium channel blockers & beta blockers
B. Calcium channel blockers & beta blockers
Goal is to slow the HR down.
May hear S4 sound or murmur; may have displaced point of maximal impulse d/t hypertrophy
AVOID:
Inotropes!!! Digoxin, Dobutamine Don't need to squeeze the little space... need slower HR.
Could also receive long term care of:
1. Percutaneous transluminal septal myocardial ablation (PTSMA): an alternative procedure for reducing the left ventricular outflow tract gradient;
2. Myomectomy: The open-heart surgery entails removing a portion of the septum that is obstructing the flow of blood from the left ventricle to the aorta.
141
What is Takotsubo cardiomyopathy? 90% are women.
aka "Broken heart syndrome" - stress induced cardiomyopathy. usu > 50 yrs old
Result of severe emotional or physical distress; can usually get better ~ 3 months.
Possibly the result of surge of stress hormone (epinephrine)
Apex of heart takes on a bulbous/ballooned appearance - looks like a japanese octopus trap = "takotsubo"
142
S/S & treatment of Takotsubo?
S/S
Chest pain, SOB
ST elevation/depression
Coronary cath clean
TREATMENT: HF management...
Beta blocker to blunt sympathetic NS - since theory of catecholamines causing cardiomyopathy
ACE inhibitors or ARBs
Spiranolactone
use for a couple of months.
143
What do we call the disease that results in ventricular myocardial rigidity? It is a very rare condition.
Restrictive cardiomyopathy (RCM)
Causes restrictive filling of ventricles which leads to HF overtime...
S/S are same as HF:
Exercise intolerance
Fatigue
Dyspnea
Arrythmias (pretty common in RCM)
Lower extremity edema
Elevated intracardiac pressures (filling pressures; CVP, PAP, wedge)
144
What can cause / etiology of Restrictive Cardiomyopathy (RCM)?
1. Endomyocardial fibrosis
2. Idiopathic
3. Amyloidosis
4. Sarcoidosis
5. Carcinoid heart dz
6. Radiation induced (women who've had breast CA tx)
7. Iron overload
145
Common treatment for Restrictive Cardiomyopathy?
Remember: like HF...
Diurese
Na+ and H2O restriction
Possible permanent AV pacemaker
Rhythm control and antiarrhythmic medication
Long-term: heart transplant is an option.
146
What do we call the dz that is defined as focal or diffuse inflammation of the myocardium?
2 causes?
S/S and treatment?
MYOCARDITIS
Viral or Bacterial causes.
S/S:
Fever
Chest pain
HF
Dysrhythmias
Sudden cardiac death
- May be accompanied by pericarditis
Tx:
Abx/Antiviral
NSAIDs
Diuretics
Inotropes
ACE inhibitor
147
This inflammation is of the sac covering the heart.
Can be restrictive or constrictive...
Causes?
What is Dressler's syndrome?
PERICARDITIS
Can be constrictive w/fibrous deposits on the pericardium or restrictive w/effusions into pericardial sac.
Post MI
Autoimmune disorders
Post CABG
Connective tissue dz
Infection (could be viral or inflammatory disorder such as lupus/ rheumatoid arthritis)
Dressler's syndrome: pericarditis 2-12 weeks post MI, caused by autoimmune response or viral infection
148
S/S of pericarditis?
ECG findings?
Treatment?
S/S:
- Retrosternal PLEURITIC chest pain (sharp w/breathing, lessens when leaving forward)
- Pain worsens *On inspiration * Supine * w/activity
- Pericardial friction rub
- Tachycardia
- Tachypnea
ECG: (similar to MI)
- Concave diffuse ST segment elevation (if you put sideways eyes over it, it looks like a happy face)
- Tall peaked T waves in numerous leads (except aVR)
- Down-sloping TP segment (Spodick's sign) on V lead
-- Depressed PR interval
Lead I and II should not be elevated together, if they are = possibly pericarditis
May see pulsus paradoxus - BP falls during inspiration by 10+ mm Hg
TREATMENT:
TIME!
Symptom management
NSAIDs - corticosteroids if NSAIDs not effective
Treat infection
149
During what cardiac dysfunctions might you see pulsus paradoxus?
Cardiac tamponade
Constrictive pericarditis
Advanced HF
Dehydration
150
The following are all possible complications of what cardiac inflammatory issue?
Pleural effusion
Constrictive pericarditis
Cardiac tamponade
Pericarditis. So, monitor for them.
May perform partial pericardiectomy in chronic setting - window is created where fluid can drain into pleural space
For constrictive: total pericardiectomy.
151
3 Pericardial rubs:
1 systolic
2 diastolic (occurs w/ ventricular stretch at early and late diastole)
Scratching, grating, squeaking leather quality... sounds like when you rub your hair between your fingers
MI
Pericarditis
Autoimmune
Trauma
S/P Cardiac surgery
152
What do we call the infection to the endocardium or tricuspid valve; often from IV drug use?
What are some other causes?
S/S?
Emboli are possible complications of this infection; r/t vegetation development on leaflets.
**Monitor for neurological changes**
ENDOCARDITIS
Could result in damaged leaflets.
Can be from trauma or bacterial sources.
Higher risk:
Cardiac surgery
Rheumatic heart dz
Dental procedures
IV drug abuse
S/S
** Sharp stabbing pains that worsen w/inspiration and may radiate to neck/ shoulders/ arms/ back
SOB
Pulsus paradoxus
Cough
JVD
Friction rub
ST elevations
Narrowed pulse pressure
Elevated WBC, ESR (erythrocyte sedimentation rate)
153
Common organisms that can cause endocarditis:
Streptococcus (Rheumatic fever if strep throat untreated; or skin Impetigo)
Staphylococcus (on skin and nose)
Gram negative bacilli (cause infections including pneumonia, bloodstream infections, wound or surgical site infections, and meningitis)
Fungi (ie candida) thrush
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