Cardiovascular Flashcards
What CHADS2 score requires anticoagulation?
Greater than 2
Apixaban drug class
Non vitamin k antagonist oral anticoagulant (NOAC)
Enlarged cardiothoracic ratio could be due to (4)
Enlarged heart, pericardial effusion , elevated diaphragm, narrow chest width
Left atrial enlargement signs on CXR
Straight left heart border, double bubble right border
Heart perfusion stress testing
Exercise, persantine (dipyridamole), dobutamine
S1 sound is caused by
Mitral and tricuspid valve closure
S2 heart sound is caused by
Aortic and pulmonary valve closure
S1 qualities
High frequency, best heart in left lower sternal border or mitral area at apex
S2 best heard at
Upper left and right sternal border
S3 heart sound: 1. Pitch. 2. Due to?
- Low pitched at the apex. 2. Due to increased flow from volume overload
S4 heart sound
Atrial kick, at apex and low pitched
Caused by LVH or ischemia, atrium contracts against stiff ventricle
Diastolic murmurs include
Mitral stenosis, severe mitral regurgitation, aortic regurgitation
Steth side for each pitch?
With high frequency use diaphragm, low frequency use bell
Inspiration increases what murmur
A right sided (pulmonary) murmur due to increased venous return during inspiration
Standing increases what murmurs
MVP and HOCM
Squatting decreases which murmurs
MVP and HOCM
Valsalva changes murmurs
By decreasing cardiac filling, accentuating HOCM and MVP
Reguritant murmurs
LS - mitral regurg, ventricular septal defect
RS - tricuspid regurg
Triad of symptoms associated with aortic stenosis
Angina, syncope, dyspnea
Sustained apex beat can occur due to
LVH
Peripheral findings of tricuspid regurg
Ascites, pulsatile liver, peripheral edema
Causes of JVP distention PQRST
Pericardial effusion, quantity of volume, RS heart failure, SVC obstruction, tricuspid stenosis or regurg
Normal JVP height
<4cm
Aortic valve location for auscultation
2nd ICS, R sternal border
Tricuspid valve location for auscultation
5th ICS, L sternal border
Apex beat, Mitral valve, PMI location for auscultation/palpation
5th ICS, mid clavicular line
Things to note on palpation of apex beat (LSAD)
Location (5 ICS, MCL), size coin, amplitude, duration
Normal grade of pulse
2
JVP demonstrates
Fluid status, central venous pressure, right atrial pressure
Eliciting the JVP
Patient looks to the left, tangential light between two heads of SCM muscle, look for double waveform
Apixaban, Dabigatran, Rivoroxaban, Edoxaban are all what type of drug?
NOAC
Normal JVP distance
Less than 4cm
Hepatojugular reflex
Apply pressure to liver for 10s, sustained JVP rise after 2 breaths is pathological
S1
MT closures
S2
AP closures, higher pitched
Type A aortic dessection
Ascending aorta and possibly the aortic valve
Type B aortic dissection
Descending thoracic distal to the left subclavian
Mainstay of treatment for a type B aortic dissection
Medical management with blood pressure and pulse pressure control
Patient with confirmed STEMI should be started on
ASA, platelet inhibitor, anticoagulant, and a high dose statin
Give o2 to a patient with a STEMI when stats drop to
Below 90
Treating chest pain in a patient with a STEMI
Nitroglycerin
When should you measure troponin?
6+ hours after onset of chest pain, and 2 samples 2 hrs apart
What meds should be started in a patient recovering from STEMI? (No longer in danger)
Beta blocker (metropolol), ACE inhibitor
Structural defects in tetralogy of fallot
VSD, pulmonary stenosis, overriding aorta, and RVH
Natural history for tetralogy of fallot
Progression of pulmonary stenosis and cyanosis
Congenital heart diseases in patients with Down syndrome
AVSD (45%), VSD(20%), TOF, PDA
Beta blockade and orthostatic hypotension
Beta blockade inhibits the baroreceptors response and so there isnt the usual rise in HR you might expect with standing
Sotalol is used to control
Rhythm
Stage three pressure ulcer
Through dermis, no bone exposed
Orthostatic hypotension testing indicated for
Syncope, heart problems in the past
To test for orthostatic hypotension, measure BP
Laying down, sitting, standing
Shock is defines as
Cellular and tissue hypoxia due to recused oxygen delivery/consumption/utilization
Types of distributive shock
Septic, SIRS, neurogenic, anaphylactic, toxic
Cardiogenic shock may be due to
MI, arrhythmia, valve or septal rupture, outflow obstruction
Hypovolemic shock can be due to
Hemorrhage or other fluid losses
Obstructive shock can be due to
PE, pulmonary hypertension, tension pneumothorax, constrictive pericarditis, restrictive cardiomyopathy
Features highly suspicious of shock
Hypotension, tachycardia, oliguria, abnormal mentation, tachypnea, cool/clammy/cyanotic skin, metabolic acidosis, high lactate
Absolute hypotension
Systolic <90 mmHg, MAP <65 mmHg
Relative hypotension
A drop in systolic BP >40 mmHg
Orthostatic hypotension definition
> 20 mmHg fall in systolic or >10 mmHg fall in diastolic pressures with standing
Approach to the hypotensive patient very first steps
Airway, IV access, breathing and circulation
Hypotensive emergency IV access should be
Peripheral venous access with 14 to 18 gauge catheters or intraosseous access
Typical adult dose of epinephrine
0.3mg injected every 5-15 minutes as needed
Workup of strongly suspected tension pneumothorax
Skip the chest radiograph and go straight for an emergent tube thoracostomy
Cardiac preload
The stretch in ventricles just before contraction, estimated by end diastolic volume (immediately after filling)
What is the cardiac afterload? How can we estimate it?
Cardiac afterload is the resistance that must be overcome for the ventricle to contract.
It is approximated by the systolic ventricular pressure.
Ejection fraction
Fraction of the end-diastolic volume ejected with systole
Normal range for ejection fraction
55-75%
Cardiac output calculated by
SV x HR
Cardiac output is
The volume of blood ejected from the ventricle per minute
Resting cardiac output in men and women
Men is about 5.6L/min, women 4.9L/min
The intrinsic ability of the heart to adapt to increasing volumes of inflowing blood is called
The frank starling mechanism of the heart
How does increase peripheral resistance affect cardiac output?
It decreases the cardiac output
How does decreased peripheral resistance affect cardiac output?
It increases cardiac output
What kind of nervous stimulation increases cardiac output
Sympathetic stimulation and parasympathetic inhibition
Beriberi disease is caused by
Thiamine (B1) deficiency
How does hyperthyroid affect cardiac output
It increased venous return and cardiac output
Low cardiac output is caused by abnormalities that
Decrease pumping effectiveness of the heart, or decrease venous return
Low cardiac output can be due to low preload as a result of
Hemorrhage, dehydration
Low cardiac output due to obstruction can occur cause of
External cardiac compression (pneumothorax, pericardial tamponade)
4 classes of shock
Distributive, obstructive, cardiogenic, hypovolemic
Distributive shock differs clinically because
Extremities are warm to the touch cx
Initial treatment of narrow-QRS-complex tachycardia
IV adenosine
Signs of hemolytic anemia
Increased bilirubin, LDH and reticulocytes. Decreased hemoglobin and haptoglobin
Management of delayed hemolytic transfusion reaction
Supportive (e.g. fluids)
Onset of delayed hemolytic transfusion reactions occur
More than 24 hrs, and up to a month post transfusion
What is a typical iron level for someone with sickle cell disease
Iron overload due to frequent transfusions
Why is a patient with sickle cell disease at high risk of delayed hemolytic transfusion reactions?
Alloimmunization from frequent transfusions
How can the diagnosis of delayed hemolytic transfusion reaction be confirmed?
A newly positive Coombs test
Ascending aortic dissection is type
A
Descending aortic dissection is type
B
Pulmonary edema in patients with acute decompensated heart failure should be treated with
Preload reduction by IV diuretic like furosemide
What percent of people are right coronary artery dominant? (RCA supplies the PDA)
> 65% RCA dominant
SA node sets pace at
60 BPM
AV node sets pace at
40 BPM
AV bundle sets pasce at
20 BPM
Sympathetic cardiac nerves increase
HR and force of contraction
Tricuspid valve between which two chamber
RA to RV
Mitral valve between which two chambers
LA to LV
Anisotropy is
The preferential conduction of electricity along certain directions
Circle of Willis is an anastomoses
Between vertebral artery and internal carotid artery at the base of the brain
Fetal circulation bypasses
The lungs and liver
ECG p wave represents
Atrial depolarization
QRS complex represents
Ventricular depolarization (mostly the left)
T waves represent
Ventricular repolarization
RRIAHI stands for (in ECG)
Rate rhythm interval axis hypertrophy and ischemia/infarction
NSR ranges from
60-100BPM for an adult
Rate on ECG can be calc by
Number of beats x 6
Prolonged PR interval on ECG indicates
First degree heart block
RBBB looks like
Bunny ears
Leads I and II positive, what axis
Normal
Leads I and II negative, what axis
RAD or NW
Lead 1 negative, what axis?
RAD
Lead 2 negative, what axis?
LAD
Tall p waves aka
P pulmonale (RAE)
M shaped p waves aka
P mitrale (LAE)
The mitral valve is open during
Diastole
What heart rate is bad for mitral stenosis
Fast ones
Aortic valve is open during
Systole
Aortic regurg is the
Leak of blood from aorta back to LV during diastole, we want enough time for the atria to fill before valve opens
For someone that has aortic regurg, which speed of heart rates are bad?
Slow ones, need to pump before it all flows back
Kerley B lines on CXR
Pulmonary edema
Septal leads
V1 V2
No discernible p waves
A fib
`
What can hyperkalemia do to the PR interval?
Prolong the PR interval
T waves in hyperkalemia
Peaked
Bunny ears V1-V3
RBBB
The most common ECG abnormality for pulmonary embolism is
Sinus tachycardia
Atrial tachyarrhythmias include
Atrial fibrillation, atrial flutter, atrial tachycardia
Losing the atrial kick is extra detrimental in
Heart failure
Sudden shortness of breath during sleep
Paroxysmal nocturnal dyspnea
Sensation of breathlessness in recumbent position
Orthopnea
Hyperkalemia ECG
PR prolongation, M shaped p waves, peaked T waves
Peaked T waves occur in
Hyperkalemia, hyperacute STEMI
Negative axis in leads I and II
NW or RAD
Compensated heart failure occurs when
The heart works well enough to compensate without showing systemic symptoms
Kerley B lines are indicative of what diagnosis
congestive heart failure, pulmonary edema
Blunting of costophrenic angles on CXR may indicate
Pleural effusion
Vascular redistribution to the upper lung zones occurs in
Congestive heart failure
MONA BASH for ACS treatment
Morphine O2 Nitrates ASA
BBlockers, Ace Is, Statins, Heparin (Clopidogrel)
Investigating a suspected MI
EKG, Troponins stat
2 characteristics of sub sternal pain associated with ACS
Worse with exertion, relieved by nitroglycerin
Treating mitral stenosis
Balloon valvuloplasty, replacement
Aortic insufficiency treatment
Replacement, CABG
Mitral insufficiency treatment
Replacement
Aortic stenosis treatment
Replacement, CABG
Wide QRS complex indicates what rhythm?
Ventricular
Narrow QRS complex indicates what kind of rhythm
Atrial
An arrhythmia with no symptoms should be treated with
Nothing - just supportive care (IV, O2, Monitor)
Characteristics of an unstable heart rhythm
Chest pain, SOB, altered mental status, hypotension
How to treat an unstable arrhythmia
Electricity
A patient with stable arrhythmia can be treated with
Pharmacotherapy
If an arrhythmia is fast and unstable treat with
Shock
If an arrhythmia is slow and unstable treat with
Pacemaker
Stable arrhythmia that is fast and narrow (atrial arrhythmia), medication
Adenosine
Stable arrhythmia thats fast and wide (ventricular) treat by
Amiodarone
Stable arrhythmia that is slow is treated with
Atropine
Afib/flutter is treated with
Rate control via beta blocker, CCB
SVT is narrow and fast with a loss of p waves, its treated by
Adenosine
Ventricular tachycardia is wide and regular, it can be treated by
Amiodarone
Cardioverting an AFIB that’s lasted >48 hrs runs the risk of
Embolism and stroke
Sinus bradycardia responds to drug
Atropine
2nd degree heart block type II, and 3rd degree heart block are treated by
Pacing
Total AV node dissociation is called
3rd degree AV block
Shocking the heart is indicated only in
VTac/Vfib arrest
VT/Vfib treatment
Epi + 2 min CPR, shock, REPEAT
Symptoms of hypertrophic cardiomyopathy are
Shortness of breath, angina, sudden death in athletes
Medical treatment for restrictive cardiomyopathy includes
Gentle diuresis and heart rate control
Bad cholesterol
LDL
Good cholesterol
HDL
Vascular disease (stroke, CAD, PVD, carotid stenosis) or LDL >190 should be treated with
High intensity statins (atorvastatin or rosy a statin)
High intensity statin examples
Atorvastatin or rosuvastatin
If a patient has LDL 70-190, 40-75YO, and diabetic or high risk they get
Statins
Myositis presents with
Soreness, weakness, muscle pain
Hepatitis presents with
RUQ pain, jaundice
Risk factors for coronary artery disease
Diabetes, smoking, hypertension, dyslipidemia, >55YO woman, >45 YO men
A1C should be monitored
Every 3m in diabetics
Statin myositis treatment
Stop it and start a lower dose
Statin hepatitis treatment
Stop statin and start a lower dose
Statins decrease
LDL and triglycerides
Side effects of statins
Myositis, increased LFTs
Second line meds to statins are
Fibrates
Statin alternative that causes flushing
Niacin
Treat niacin flushing with
Aspirin prophylaxis
Stable vs unstable angina
Stable has pain with exercise and relief with rest and nitrates
Unstable has pain at rest, no relief with meds
Risk factors for all vascular diseases are
Diabetes, smoking, hypertension, dyslipidemia, obesity, age, FHx
Identification of STEMI goes to
Emergent cath
Identification of NSTEMI goes to
Urgent cath
Prinzmetals angina is
Clean coronary arteries producing ischemia as a product of vasospasm
Prinzmetals angina is treated with
Calcium channel blockers
3 types of reflex syncope
Vasovagal, situational, carotid hypersensitivity
Syncope with a trigger, and prodrome
Vasovagal
Syncope with micturition, defecation, swallow, cough
Situational reflex syncope
Tactile stimulation of the carotid sinus plus syncope is called
Carotid hypersensitivity reflex syncope
Medications that can cause orthostatic syncope
Vasodilators (alpha1 blockers, antihypertensives), ionotropic/chronotropic blockade (beta blockers)
3 main causes of orthostatic syncope
Medications, hypovolemia, autonomic dysfunction
3 main causes of cardiac syncope
LV outflow obstruction, ventricular tachycardia, conduction impairment
Increased afterload worsens which murmur?
Mitral regurg
Grading scale for diastolic murmurs
1-4
Grading scale for systolic murmurs
1-6
Mitral stenosis murmur is
Diastolic
Aortic stenosis murmur is
Systolic
Chronic, severe tricuspid regurg presents with
Right sided heart failure
Which rhythms are shockable?
Ventricular fibrillation and pulseless ventricular tachycardia
In a tachycardic emergency if the rhythm is regular with narrow complexes consider
Adenosine
What is the dosage of adenosine for tachyarrhytmia
6mg IV rapid push
If a patient is in ventricular tachycardia with wide complexes on the heart monitor, what steps should the provider take?
Establish IV access, obtain ECG, consider using adenosine
In vtac, if the complexes are narrow
Try vagal maneuvers, adenosine 6mg IV rapid push if rhythm is regular
Synchronized cardioversion dose for regular and irregular rhythms are
50-100J, 100-200J
Adenosine first and second dose
First dose 6mg IV followed by saline flush, second dose 12mg IV rapid push
Greatest BP decrease by lifestyle change is seen with
DASH diet
Preferred anti hypertensive for patients with gout
Losartan (mild uricosuric effect)
Best antihypertensive for LVH
ARBs
Target diastolic BP for a diabetic
Less than 80
Two drug types important in chronic heart failure
ACE inhibitors and beta blockers
Diagnosing hypertension
At least 3 readings 140/90 or higher
Treating hypertension with DMT1
ACE inhibitor preferred
Treating HTN in heart failure
ACE inhibitors and diuretics
Treating hypertension in MI
Beta blockers and ACE inhibitors
Treating hypertension in someone with kidney disease
ACE inhibitors and ARBs
Which antihypertensives are not okay in pregnancy
ACE inhibitors because they are teratogenic
Treating hypertension in migraine patients
Beta blockers can be helpful
1st line medical treatment for hypertension in someone with osteoporosis
Thiazide diuretics - can help increase calcium reabsorption
Labetalol drug class is
Combination alpha beta blocker
Most common side effect of ace inhibitors is
Cough bradykinin induced
Some patients who are allergic to sulfonamides are also allergic to
Hydrochlorothiazide
Thiazide diuretics can have 6 metabolic side effects
High glucose, uric acid, lipids
Low magnesium, sodium, potassium
What antihypertensive should be avoided in asthmatics
Beta blockers - bronchoconstriction and wheezing
Why is HCTZ contraindicated in gout
May raise uric acid levels
Treatment of atrial premature beats
No treatment - just investigate the cause
Treatment for PSVT when the patient is stable
Vagal maneuvers and adenosine
Pulmonary embolism is suggested by the triad of
Cough, hemoptysis, and pleuritic chest pain
Patients with VTE and contraindication to anticoagulation should get
IVC filter
Crescendo decrescendo systolic murmur, left upper sternal border
Pulmonary stenosis
What CHADS2 score requires anticoagulation?
Greater than 2
What CHADS2 score requires anticoagulation?
Greater than 2
What CHADS2 score requires anticoagulation?
Greater than 2
Apixaban drug class
Non vitamin k antagonist oral anticoagulant (NOAC)
Apixaban, Dabigatran, Rivoroxaban, Edoxaban are all what type of drug?
NOAC
Stable patients should recieve packed red blood cell transfusion for Hgb less than
7g/dL
Managing variceal bleeding
Somatostatin analogs like octreotide
Treatment of AF in patients with WPW who are hemodynamically unstable require
Electrical cardioversion
Treatment of AF in patients with WPW who are stable require
Anti-arrhythmic drugs like IV ibutilide or procrainamide
Adenosine, beta blockers, calcium channel blockers all block which electrical pacemaker in the heart?
AV node
