Cardio-CS Flashcards
What is High output HF
HF as a result of high cardiac output to meet the needed oxygen demands.
CF of high output HF ?
Non-specific:
Tachypnea, tachycardia, edema
Specific:
Mid-systolic murmur, pulsatile tinnitus, Distended JVP,
wide pulse pressure due to increased Stroke volume.
What is Apixaban ?
NOAC, Inhibits factor X
thus prevents cleavage of prothrombin to thrombin
Causes of high Output HF ?
Hyperthyroidism
Pregnancy
How to asses a patients risk of thromboembolic events ?
CHA2DS2VASC SCORE
CHF
HTN
Age > 75: 2 points
DM
Stroke, TIA
Vascular event
Age 65-74 +1 point
Sc: Sex: Female
What are the Cardiovascular effects Hyperthryrpidism
- direct effect on Cardiac myocytes: increase contractility
- Direct effect on BV: vasodilation
- Direct effect on body tissue: increased metabolic demand –> which also increases Cradiac contractility, leading to hypertrophy
- Due to low SVR –>Blood retruns easily and fast to RV
Anterolateral MI is due to occlusion of
L. anterior desconding Cor. A
Why do patients who suffer from OSA have HTN ?
in view of elevated chatecholamines ( patient is aroused when the carotid sinus detects hypoxemia, hypercapnia).
Pathophysiology of Congenital Long QT-syndrome
Defect in k+ rectifier channels, responsible for repolarization.
Management of long-QT
Stop the offending agent ( Hypomagnesemia, hypokalemia)
Non-selective beta blockers (propranolol, nadolol), decrease QT at fast HR.
Implantable cardioverter defibrillator
Long QT increases the risk of ?
Torsades de points
Persistent Pulmonary HTN in neonates ?
high PVR, leads to right to left shunt across the PDA and thus difference in o2 saturation between arm and feet.
Physical findings with severe AS ?
- Late peaking crescendo-decrescendo murmur ( in view of needing high LVF p. to open the valves, which takes more time).
- Soft and single S2 sound during inspiration, to the point where AV and PV almost close at the same time
- Palsus parvus et tardus ( diminished and delayed pulses)
Complications of Mitral Stenosis ?
Left atrial p. Increase -> Pulmonary edema.
L. atrial streching –> AF –> Increased risk of thromboembolism.
Mechanical Complications post-MI
MV leaflet rupture (3-5 days)
Interventiricular septal rupture (3-5 days)
Ventricular free wall rupture ( up to 2 weeks)
LV wall aneurysm ( up to months after MI)
LV wall eneurysm
Is a delayed trasnmural wall MI.
Happens up to several months after
Persistent ST-elevation and deep q-waves in same leads as MI ECG
Acute MR vs Chronic MR
No atrial enlargemnet
Pulmonary edema
No LV hypertrophy
Increased LV end-diastolic pressure
Types of Ventricular Hypertrophy
- Pressure Overload: Concentric
- Volume Overload: eccentric Hypertrophic
What are the indication for AV replacement ?
AS with severe symptoms
EF < 50%
Undergoing any other cardiac surgery
Characteristics of MR murmur
Holosystolic
Heard at the apex
Radiates to the axilla
MVP murmur ?
Midsystolic click followed by late systolic Murmur
Mitral Stenosis
early diastolic heart sound followed by rumble
Aortic Regurgitation murmur ?
Early diastolic murmur. Increased with full expiration.
Pulses paradoxus.
Wide Pulse pressure known as Bounding water hammer pulse.
Heard best at:
L. sternal border if caused by valve dysft.
R. upper sternal border”if caused by aortic root dilation.
How does Severe Aortic Regurgitation affect the Heart ?
regurgitation, causes eccentric Hypertrophy to increase compliance (increased volume) and increase conractility to maintain CO. ( in the short run).
Ventricular Septal defect murmur ?
Holosystolic at L. sternal border
What medication are used in NSTEMI/ UA ?
- Antiplatlet/ Anti-coagulant
- Statin
- beta-blocker
- Nitrate
Heart abnormalities in Turner Syndrome ?
Bicuspid aortic valve
Coartaction of aorta
CF of coarctation of Aorta ?
brachio-femoral pulse delay
Continuous systolic murmur cause of collateral vessels
Classic 3 sign on CXR
Asymptomatic HTN of upper extrimities, headaches and epistaxis.
What is the pretest probability for CAD ?
dependent on age, gender (women), low risk cardiac RF and features of chest pain
Classical Angina Features ?
- starts with exertion relieved with rest or nitroglycerine
- substernal
What is the first line management of Sustained monomorphic VT ?
Amiodarone
What type of toxicity does nitroprusside cause ?
Cyanide
esp. in pts with renal failure
What is the MC cause of MR ?
MVP
Pacemaker insertion causes what defect ?
TR
What are the hemodynamic changes in AV fistula
Bypassing the arrterioles ( decreased SVR) afterload
More volume in veins ( Increase Preload)
Increased CO, to compensate for SVR
CF of Tetralogy of fallot ?
- Pulmonary stenosis
- Oveririding of Aorta
- VSD
- R. sided hypertrophy
R. to L. shunt, Blue babies
Holosystolic murmur, and mid-left of sternum
How does squatting affect the murmur and cyanosis
Squatting increases both preload and afterload
Increase the intensity of murmur.
What is becks triad ?
Hypotension
JVD
Muffled heart sounds
Common in Cardiac Tamponade.
ECG changes in cardiac Tamponade ?
- low voltage QRSs ( electrical alternans) and
- drop in SBD >10 ( pulses paradoxus) during inspiration.
CF of aortic dissection ?
HTN
Lightheadedness
sharp, severe, tearing chest pain
hemopericardium
Mediastinal widening on CXR.
Diagnostics of Aortic dissection ?
CT angiography
Transesophageal echo in unstable patients
Effect of Nitrate in MI
Systemic venodilation
and systemic vasodilation –> preload, dec. end Diastolic volume and systolic volume –> and thus decrease LV wall stress and oxygen demand .
What is the diagnostic test in preganants with high BP
24-hour urine collection for total protein
to exclude pre-eclampsia
Chronic HTN
HTN before pregnancy or < 20 w
What is Gestational HTN
Newonset HTN SBP > 140 and DBP > 9 after 20 w
What is Pre-eclampsia
New onset HTN > 20W + Proteinuria or end organ damage ( Cr, LFTs,..)
What is Eclampsia ?
Pre-eclampsia and tonic-clonic seizures
Pathophysiology of HOCM ?
Assymetrical thickening of interventricular septum, Obstruction of LVOT
Concentric Hypertrophy of LV
IV septum pulls on MV and widens the MV ring –> MR
CF of HOCM
LVOT obstruction –> syncope, presyncope
Murmur –> Crescendo-decrescendo at the left sternal border
no blood to aorta –> no blood to CA –> Angina
What type of S2 spilitting do we see in HOCM ?
Paradoxical splitting.
The valve is waiting for the blood to get to the aorta so it can close. But because of the obstruction its taking longer time.
Thus Aortic valve closes after Pulmonic valve.
What shall we avoid in HOCM ?
Anything that decreases blood flow, because it increases obstruction and murmur.
Dehydration
Alcohol
Beta agonists
CCB ( nifedipine)
Digoxin
Diff. between AS and HOCM murmur
right second intercostal space: AS
HOCM: left strenal border
Rx of HOCM ?
Iv saline
Non-dihydropyridine CBB
Beta blockers
Alpha 1 agonist- vaspconstricters like phenylnephrine.
Rule of thumb of murmurs
If you increase the Blood flow, murmur intensity increases except in HOCM.
Mech. of action of beta blockers on HOCM
neg chronotrope: decrease HR allow heart to fill, inc. EDV
neg Ionotrop: decrease contractility and inc. in EDV of LV
thus increase blood flow and dec. obstruction
Squatting –> Increase preload
Hand griping –> increase after load
leg raise –> increase preload
increase murmur intensity except in HOCM.
works the opposit
MVP murmur with sqautting ?
Squatting increases preload, inc. LV size and Volume, delays MVP click and makes the murmur softer.
Difference between BAV and MVP
BAV: ejection click mid systolic murmur (systolic), heard at second R. intercostal
MVP: Non-ejection click , midsystolic murmur, heard at Apex.
Why doesnt HCOM murmur increase iwith increased blood flow?
because when we increase the blood flow to the heart, we decrease the obstruction caused by IVS –> thus decreasing murmur intensity.
What Indicates Digoxin toxicity ?
Atrial Tachycardia and AV block.
1. Atrial Tachy due to increased automaticity
2. AV block due to Increased vagal tone ( usually Mobitz Type I)
Mech. of action of Digoxin ?
Competes with K+ to Na-k+ Atpase
What exacerbates dig toxicity ?
Hypokalemia
Cardiac Manifestation in Kawasaki ?
Coronary artery aneurysm.
Always proceed with echo
Rx of Kawasaki ?
IV immunoglobulins
Causes of Aortic stenosis
- Bicuspid Aortic valve < 70 years
- senile calcified AV in > 70 years old patients
Why is the S4 sound in hocm/ AS ?
S4 is the atrial kick against the stiff LV.
Because of the concentric Hypertrophy to overcome High P.
What is restrictive cardiomyopathy ?
inability of the heart to expand. Defective diastole
Decreased input and output ( decreased EDV and CO)
Causes:
Sarcoidosis
Amyloid
Hemochromatosis
Cancer and fibrosis
CF of restrictive Cardiomyopathy ?
Signs of R. and L. HF
plus signs of decreased CO: angina, syncope, fatigue, lightheadedness
Indications of Amiodarone
Cardiac arrythmias esp. ventricular to decrease HR
SE of amiodarone:
Cardiac: Bardycardia
Chest: Interstial pneumonitis, organizing penumonia, alveolar hemorrhage, soliatry nodules
Thyroid: Hypo/ hyper thryroidism
Optic: microdeposition
Derm: blue-grey skin discoloration
Neuro: peripheral neuropathy
What is the MC cause of SVT
ANRT (AV nodal re-entry tachycardia) mainly affects young individuals.
Pathophysiology of ANRT ?
it starts when a premature complex, cannot slide down the fast pathway ( because it is still in refractory phase), so it slides down the slow pathway.
By the time it reaches the AV node, it slides back up through the fast pathway that is not in refractory phase anymore.
It goes all the way up and causes a retrograde atrial contraction, happening at the same time as ventricular depolarization.. leads to burried Pwave in the narrow complex QRS on ECG.
Continuous activation of this pathway leads to sustained Tachycardia.
Management of AVNRT ?
maneuvers that increase parasymapthetic sys, to slow AV conduction.
1. Carotid sinus massage
2. Cold water Immersion
3. eyeball massage
4. valsalva maneuvere
Lipid lowering therapy is recommended for all patients
> age 40 and has DM or <40 with ASCVD
Management of Claudication in PVD ?
- low dose aspirin
- Lipid loweing agent
- Rx of DM
- smoking cessation
- Excercise program
if all fail, percutaenous or Surgical revascularization.
CF Atheroembolic event
Occurs post catheterization of CAD.
Leads to blue toe syndrome
levido reticularis
Abdominal ischemia, perforation
pancreatitis
yellow plaues in retinal artery (Hollenhorst)
and Kidney disease
What should be avoided in Gout ?
Diuretics
because they can increase Uric acid levels
HTN Rx in osteoporosis ?
Thiazide.
Because they increase calcium reabsoprtion in DCT and decrease calcium wasting.
Which Antihypertensive has the greatest effect on LVH ?
ARBS > CCB > ACEI > Diuretics.
Difference between HCOM and atheletes heart
HCOM: ECG CHANGES ( T-wave inversion in V5 and V6) + LV dysft. + LV hypertrophy (thickness >15mm), L. atrial enlargment, LV cavity decreased
Athletes heart: only ECG changes and slightly enlarged LV cavity.
Dialted Cardiomyopathy
V. good at Diastole
sucks at systole.
ECG changes in Pericarditis ?
Diffuse ST elevation or PR depression.
Kidney causes of pericarditis ?
Uremia.
RVMI involves ?
ST elevation in II, III and avF
Also affects ischemia to sinoatrial node –> Bradycardia.
High Rv preload, dec. pcwp, DEC. CO and Compensatory inc. in SVR.
Management of AF
Hemodynamically unstable: synchronixed cardioversion
Hemodynamically stable: rate control –> AV block
Beta blocker (metoprolol), CCB (diltizem).
Digoxin or amiodarone.
Where do we see Tet spells ?
In tetralogy of fallot
Why does knee to chest improve cyanosis in Tetralogy of fallot ?
Knee to chest, kinks the femoral vessels, increasing SVR.
then SVR in aorta is > SVR in PA. this leads a L. to R. shunt and allows blood to flow easier into the PA.
Mangement of Tet Spell ?
- Knee to chest position
- Oxygen causes vasodilation of Pulmonary vessels
- V fluids improves preload.
Characteristics of Mobitz Type 1, second degree AV block
PR prolongation until a QRS is dropped.
Cardiovascular manifestation of Turner syndrome ?
Bicuspid aortic valve
coarctation of aorta
aortic dissection
HTN
Major Manifestation of Chagas ?
- Megacolon/ megaesophagus
- Cardiac disease
Caused by Protozoa Infection
MC in South America
What is the Cause of Isolated Sytolic HTN ?
increased stiffness and decreased compliance of the arterial wall.
What type of cardioversion should be used in SVTR ?
Synchronized Cardioversion. (low voltage shock).
What medications improve mortality in HFrEF
- Angiotensin system blocker ( saccubitril-valsartan) or ACEI or ARBs
- Beta blocker
- Mineralocorticoid ( spir, epleronone)
- Sodium-glucose Cotransport ( empagliflozin).
Cause of Sick Sinus Syndrome
degeneration of the cardiac conduction pathway
CF of Sick Sinus Syndrome
Sinus pause: lightheadedness, pre-syncope, syncope, dizziness
Bradycardia-tachycardia syndrome: Tachyarrythmias leading to palpitations
ECG findings of sick sinus syndrome
Sinus Bradycardia
Sinus pause (delayed p-wave)
SA node exit block ( dropped P wave).
3 letters, 3 ECG findings
ECG findings of WPW syndrome ?
- Short PR
- Wide QRS interval
- slurred upstroke (delta wave)
Difference between Mobits Type 1 and 2, second degree AV block
First Degree AV block
Mobitz I: PR prolongation until and QRS is dropped (Block is within AV node), constant P-P interval
Mobitz II: PR is constant and QRS is randomly dropped. ( Block is within His purkinji fibers).
First Degree: Constantly prolonged PR ( but doesnt change)
Ruptured AAA
Can presenet with severe abdominal pain, Flank or Umbilical Hematoma/ echymosis
Hemodynamic instability.
Difference between AAA and Renal infarct
both have flank pain
AAA: hypotension.
Renal Infarct: HTN
Thoracic Aortic Aneurysm with intimal flap causing obstruction
Proximal HTN
Distal hypotension ( faint femoral pulses).
Difference in BP between RVMI and LVMI
RVMI: Hypotension, high CVP, LOW PCWP.
LVMI: Hypertension, High PCWP and CVP/
Indication for MV repair
EF between 35-60% regardless of symptoms.
EF<30% with symptoms
EF>60% w/o symptoms
Newborns should undergo
screening for congenital heart disease ( pre- and post ductal),
Pos. screening, indicated a echo.
Direct Renin inhibitor ?
Aliskirin.
Induce Nateruresis
Dec. Angiotensin II Con.
Dec. Aldosterone production.
What are the lifestyle intervention recommended to dec. HTN ?
- Dash diet
- weight loss
- aerobic exc
- Decrease sodium intake
- Decrease alcohol intake
features of Femoral Artery Aneurysm
Pulsatile mass
Lab findings of Primary Adrenal insufficiency
- Hyponatremia (Hypovolemia induced ADH-secretion).
- Hypoglycemia
- Eosinophillia ( cannot be inhibited cause steroids are low).
Management of Adrenal Crisis
- Fluids
- Steroids (dexamethasone)
- Fludrocortisone (replaces aldosterone).
Causes of TR dysft.
2
- flial Leaflets: like in cases of MR, because of MI, chordea tendinea rupture
- Enlarged annulus : due to HF and fluid over load.
Truncus Arteriousus
common opening for Aorta and PA + VSD
Presents with cyanosis and common in Digeorge Syndrome
Management of Stable Angina
Beta blockers or CCB.
CF of Ehlers Danlos Syndrome
Hyperlaxity of joints, skin ( poor wound healing cigarette paper like ), tissue fragility
Pectus excavatum
Beta blockers overdose ?
Use Glucagon
Antihypertensives in Pregnancy
Beta blockers
CCB like nifedipine
Methyldopa
Hydralazine
Complications of Large VSD (Acute vS. Chronic):
Acute: L to R. shunt, increase flow across Pulmonary vessels, increase LA and lV enlargement
Chronic: changed to R. to L. shunt eisenmenger syndrome.
LV aneurysm
Late complication of MI usually after months.
ECG: persistent ST elevations from previous MI and deep Q waves.
Physiologic murmurs
intensity 1-2
Systolic
Decrease with vagal maneuvers.
What is Leriche Syndrome ?
The disease of the rich :) who have alot of atherosclerosis.
Obstruction of Aortoiliac artery.
Triad of:
1. decreased femoral pulses bilaterally, with distal muscle limb atrophy
2. Impotency
3. Hip, buttocks and thigh pain.
