Cardio Flashcards
Blood pressure classifications
Normal:<120/180
Elevated:120-129/80
Stage 1 HTN: 130-139/80-89
Stage 2 HTN:>140/90
What is the goal blood pressure
<130/80
<120/80 if pt has CKD
Primary HTN
Genetic
Onset between 30-50y/o
95% of cases
Secondary HTN
Can be cured
Weird
Suspect if early or abrupt onset.
HTN Physical exam findings
Left ventricular heave
Abdominial bruit
Radial femoral delay
Pulsatile abdominal mass
HTN diagnostic tests
LVH on ECG or echocardiogram
proteinuria on UA
Common diseases associated with secondary HTN
Obstructive sleep apnea
Cushings
Renal artery stenosis
Aortic coarctation
Pheochromocytoma
Hyperthyroid
Hyperaldosterone
Hypercalcemia
Hyperparathyroid
Common causes of secondary HTN
Alcohol
Amphetamines
Antidepressants
Atypical antipsychotics
Caffeine
Cocaine
Decongestants
EPO
Herbal supplements
Immunosuppressants
OCPs
NSAIDs
Systemic cortisol
Renal artery stenosis cause
Usually caused by atherosclerosis
Sometimes caused by fibromuscular dysplasia (usually in young adults).
What makes someone high risk for ASCVD
Coronary artery disease
Diabetes
CKD
Or any three of the other risk factors
What to do if BP is 120-129/80
TLCs
Follow up in 3-6 months
What to do if BP is 130-139/80
Calculate 10 yr ASCVD risk Follow give meds and follow up in one month if ASCVD risk >10%
Follow up in 3-6 months if ASCVD risk <10%
What to do if BP>140/90
TLCs and follow up in 3-6 months
Start two meds
Four meds for HTN
Ace or arb
Hydrochlorothiazide
Calcium channel blocker
Spironolactone
What med to give someone with diabetes or CKD for HTN
ACEi or ARB
Non-pharmacological therapy of HTN
Weight loss of 10% body weight
Reduced sodium diet
<2 alcoholic drinks per day
Reduced sat fats
Exercise 30 mins per day
Stop smoking
Thiazide diuretics
Inhibit sodium reabsorption in distal renal tubules.
Drug of choice for HTN if no compelling indications
Calcium channel blocker
-dipine
inhibit transmembrane influx of extracellular calcium that inhibits cardiac and vascular smooth muscle contraction
Good for HTN in blacks
Beta blockers
-olol
Do NOT use for cocaine MI or pheochromocytoma until after alpha blockage
Decrease heart oxygen consumption
Decreases BP and HR
HTN drug of choice for pregnant
Labetalol
Nifedipine
HCTZ
Methyldoapa
HTN drug of choice in pt with Advanced CKD
Calcium channel blocker
Clonidine
Hydralazine
Alpha blocker
Aliskren
Direct renin inhibitor
Do NOT use in combo with ace/arb
Alpha-1 blockers
-zosin
Used for BPH and PTSD
First dose syncope
Arteriolar vasodilators
Hydralazine, minoxidil
Centrally acting HTN drugs
Clonidine, Methyldopa, Guanfcine
Last line agents
Clonidine gets BP to drop quickly but once gets out of body can have bad rebound HTN (very dangerous) so dose three times per day
Dangerous side effect of clonidine
Rebound HTN
HTN urgency
BP>180/120
No evidence of end organ damage
Goal is reduce BP in hours
HTN emergency
BP >180-220/120
Evidence of organ damage
Goal is reduce BP by 10% in first hour
Troponin
Measured to detect eschemia
Has predictive value for prognosis in patients post ACS
Levels begin to rise 4-8 hrs after injury and peak 12-24 hrs after and can be elevated for days.
TREND
Brain natriuretic peptide (BNP)
released when ventricular myocytes are stretched
Used to evaluate for HF and valvular disease
TREND
Elevated by CKD, PE, Pulm HTN, and sepsis
When to order echocardiogram (TTE or TEE)
To evaluate murmurs or congenital disease
TTE
Transthoracic echocardiogram
TEE
Transesophageal echocardiogram
Pros of Echocardiogram
Noninvasive
Lots of info
cheap
Cons of echocardiogram
Body habitus and heart rate can limit
Cardiac CTA
Angiogram to determine the anatomy of arteries including aorta.
More of a special test for cardiac specialties
When to order cardiac CTA
Low/intermediate risk for CAD
Abnormal stress test in pt you don’t want to cath
Pros of Cardiac CTA
High specificity
Leads to diagnosis of ASCVD
Cons of Cardiac CTA
Dye
Weight restriction
HR must be <60bpm
Must hold breath for 20 sec
Hard to get covered by insurance
Blooming artifact
Coronary angiography
Heart cath
How to order Coronary angiography (heart cath)
Hold DOACtx or for 48 hrs
Do NOT hold antiplateletes (aspirin)
Hold nephrotoxic agents (ace/arb/arni/metformin/loops)
48 hours before procecdure
When to order coronary angiography
High suspicion of ASCVD
Abnormal MPS
STEMI/unstable angina
Right heart catheterization
Measures pressures in chambers of the heart
When to order right heart catheterization
Shock
HF
Valvular disease
Pulm HTN
Congenital heart disease
When to order cardiac MRI
pre-op “mapping”
Suspeced amyloidosis
Cardiac MRA
Info about arteries not tissues or organs
Alternate for pt that can’t get CTA bc HR<60 or can’t tolerate die
When to order cardiac MRA
To evaluate for stenosis or clot
Bruce protocall stress test
HR, BP, EKG changes to stress.
Run on treadmill hooked up to monitors
Stress test MPS imaging
Myocardial perfusion scan
Myocardium uptake of dye at rest vs exertion.
Should look like a good donut
Stress test echocardiogram
Looks at myocardium’s response to exercise
Good for lean pts because can get good views of heart
Cheap
Why would you do a stresss test
Evaluate possible blockage
Risk stratification for surgery
Evaluated electrical systems in response to exertion
Contraindications to stress test
Active chest pain
Active ECG changes
Aortic stenosis
Endocarditis
Unstable vital signs or rhythm
Ambulatory event monitor
Can be continuous or triggured
Worn between 24 hrs to 4 weeks to monitor heart
Electrophysiology test
Advanced and invasive.
Maps cardiac electricity
Induce arrhythmias
Requires venous access
Tilt table
Monitors B, HR, and rhythm in various position.
Use in workup of syncope
Coronary artery calcium score
Gives you a score to tell calcified plaque in arteries.
Anything greater than 0 is abnormal
Arterial brachial index
Get blood pressure at arms and legs.
Looking for peripheral arterial disease
Arterial brachial index interpretation
Normal: >0.9
Mild obstruction: 0.71-0.9
Moderate obstruction: 0.41-0.7
Severe obstruction: 0-0.4
CTA with runoffs
Looking for peripheral artery disease.
Can evaluate for clot, aneurysm, bblockage
Do ABI first because this uses lots of dye and radiation
When to do a carotid doppler
Bruit on physical exam
TIA/CVA symptoms
What is needed to rule out blockage
Heart cath
Best test to measure ejection fraction
Echocardiogram
Types of lipids
Cholesterol
Triglyceride
Lipoproteins
Cholesterol
Animal cell membrane
Backbone of steroid hormones and bile acids
Triglycerides
Transfers energy from food into cells
Lipoproteins
Transport lipids
Apoprotein is dense
Triglyceride is less dense
Types of lypoproteins
Chylomicrons
Very-low-density lipoproteins
Low-density lipoproteins
High-density lipoproteins
Chylomicrons
Least dense lipoprotein
Mostly triglyveride
Found in blood after fat containing meals
Travel from gut via portal vein
Creamy layer on top of non-fasting serum
Very-low-density lipoproteins
Large
Mostly triglycerides
Converted to LDL once TG is transferred into cells
Low-density lipoproteins
Carry most of the cholesterol
Increase of 10mg/dL increases CHD by 10%
High-density lipoprotein
Most dense and smallest lipoprotein
Made of apoprotein and cholesterol
Reverse cholesterol transport
Increase of 5mg/dL reduces risk of CHD by 10%
Apolipoprotein B (apoB)
Protein that carries LDL
Helps LDL bind to cell wall.
Contributes to atherogenesis, MI, ASCVD risk
Screen if TH>200
High risk if level >130
Lipoprotein (a)
Genetically determined more potent subfraction of LDL.
Can cause atherosclerosis
How is VLDL calculated
Triglycerides/5
How is LDL calculated
TC-HDL-(TG/5)
What lipids are directly measured in lipid panel (not calculated)
Total cholesterol (HDL+LDL+VLDL)
HDL
Triglycerides
What lipids are calculated in lipid panel (not directly measured)
LDL
VLDL
Non-HDL cholesterol
Surrogate marker for apolupoprotein B containing particles
Measured directly and less sensitive to fasting status
Better predictor of CV risk than LDL
Goal is 30 points higher than LDL goals
Men cholesterol goal
TC: <200
Non-HDL: <130
LDL: <100
HDL: >60 is best. <40 is too low
Women cholesterol goal
TC: <200
Non-HDL: <130
LDL: <100
HDL: >60 is best. <50 is too low
Normal triglyceride level
<150
Borderline high triglycerides
150-199
High triglycerides
200-499
Very high triglycerides
> 500
Cardiac calcium score
Non-contrast cardiac gated CT.
Repeat every 3-7 years
Most useful in people with inttermediate risk of ASCVD
Levels of calcium score
0: no evidence of CAD
1-10: minimal evidence of CAD
11-100: Mild evidence of CAD
101-400: moderate evidence of CAD
>400: Extensive evidence of CAD
Levels of 10-year ASCVD
<5%: Low risk
5-7.4%: borderline risk
7.5-19.9%: Intermediate risk
>20%: high risk
Atherosclerosis
Plaque with large amounts of cholesterol build up in arterial walls
Associated with high LDL low HDL
Smaller LDLs are more dangerous bc can squeeze into spots
Antibodies to oxidized LDL play role in plaque growth and destabliztion
Familial hyper-cholesterolemia
Defective or absent LDL receptors
Homozygotes have LDL levels 8x normal
Heterozygotes have LDL levels 2-3x normal
Familial hypertriglyceridemia other names
AKA lipoprotein lipase deficiency, Fredrickson type 1, familial chylomicromnemia
Familial hypertrigyveridemia causes
Abnormality of lipoprotein lipase that is responsible for the ability of tissues to take up triglycerides from chylomicrons
Famililial hyperglyceridemia complicatoins
Recurrent pancreatitis
Hepatosplenomegaly
Dysbetalipoproteinemiia
Elevated levels of remnant lipoproteins
Rare familial disease
Associated with premature ASCVD
Familial combined hyperlipidemia
Polygenic combo of lipid abnormalities
Usually on genes LDLR, APOB, or PCSK9
Clinical presentation of dyslipidemia
Asymptomatic usually
Found in labs
Screening and fam history
Can have eruptive xanthomas or tedinous xanthomas, or retinalis
Non-pharmalogic treatment for dyslipidemia
Better diet
Exercise
Quit tobacco
Eat soluble fiber
Mediterranian diet (fish and plants)
Replace saturated fat with monounsaturated fat
Number one way to raise HDL
Stop smokingv
Diet guide to help with dyslipidemia
Total fat 27-30%
Sat fats <7%
20-30 grams of soluble fiber
Plant stanols and sterols
What does weight loss do for dyslipidemia
Lower LDL
Raise HDL
What does modest alcohol use do for dyslipidemia
Raise HDL
Contraindicated in those with high triglycerides
Statins
-statins
First line med against dyslipidemia
Lowers LDL
Raises HDL
Lowers Triglycerides
Decreases hsCRP
Statin side effects
Myalgia
Rhabdomyolysis
CK elevations
Myositis
Elevated transaminases
Diabetes development
When is a statin contraindicated
Liver failure
Low intensity statin
<30% LDL lowering
Pravastatin 10-20mg
Lovastatin 20mg
Moderate intensity statin
30-50% LDL lowering
Pitavastatin 2-4mg
Simvastatin 20-40mg
Pravastatin 40-80mg
Atorvastatin 10-20mg
Rosuvastatin 5-10mg
High intensity statin
50% LDL lowering
Atorvastatin 40-80mg
Rosuvastatin 20-40mg
What happens when you double the dose of statin med
LDL reduced by 7%
When to give moderate intensity statin
Presence of ASCVD and age >75
Age 40-75, diabetes, and LDL>70
Age 40-75, LDL 70-189, CVD risk >7.5%
When to give high intensity statin
Presence of ASCVD adn age 40-75
Primary LDL elevation >190
CVD risk >7.5% or other risk enhancing criteria
Cholesterol absorption inhibitors
Ezetemibe
Inhibits cholesterol transporter.
Monotherapy or added to statin
Reduces LDL 15-20%.
NOT for liver failure
PCSK 9 inhibitors
-ocumab
Inhibits LDL receptor degradation.
Monotherapy or added to statin
Decreases LDL and Lipoprotein (a)
Reduces CV events and deat
SC injection every two week
Adenoside triphosphate citrate lyase inhibitor
Bempedoic acid
Decreases LDL by about 18%
Upregulates LDL receptors in the liver
Caution in tendon rupture and hyperuricemia
Cholestyramine, colesevelam, colestipol
Bile acid sequestriants
Binds bile acids in the intestine
Good. option for pregnancy or liver disease
Can cause Triglyceride increase
Apheresis
Used in treatment of people with homozygous familial hypercholesterolemia.
Removes LDL directly from blood with machine.
Pts need AV fistulas
LDL lowered by 65-70% per treatment
Niacin
Good for raising HDL
Take with ASA or NSAID one hour before dose.
Need nicotinic acid for benefit
When to treat triglycerides
> 500 or 150-499 with CVD and well controlled LDL on maximally tolerated statin or other LDL lowering agent
How to treat triglycerides through diet
Avoid alcohol and simple sugars
Limit refined starches and sat and trans fats
Restrict overall calories
Secondary causes of high triglycerides
Obesity
Hyperglycemia
Alcohol abuse
CKD
Oral contraceptive/estrogen
Thiazide diuretics
Meds for high triglycerides
Statins
Omega-3 preparations/fish oils
Fibric acid derivatives
Omega-3 peparations/fish oil
Med for high triglycerides
Icosapent ethyl, omega-3-acid-ethyl
Antiplatelet, anti-inflammatory, anti-arrhythmia
Don’t give if have fish allergy or bleeding risk
Fibric acid derivatives
High triglycerides
Gemfibrozil, fenofibrate
Peroxisome proliferative-activated receptor-alpha (PPAR-alpha) agonist
Reduces TG and raises HDL
Side effects of hepatitis, choleithiasis, and myositis
When to check Lp(a)
Once in every adult’s life
Those with premature CVD
High risk ASCVD
Familial hypercholesterolemia
Recurrent pregnancy loss
High Lp(a) treatment
-PCSK 9 inhibitors (-ocumab)
Muvalaplin
Angina
Chest pain
Coronary vasospasm symptoms
Acute onset chest pain
Angina pain at rest
More common in women
Causes of coronary vasospasm
Cold, emotional stress, vasoconstricting medications.
Usually involves right coronary artery
History of vasospastic disorder
Coronary vasospasm diagnostics
Troponin levels (takes a while to be positive)
ECG - ST elevation
Coronary vasospasm treatment
CALCIUM CHANNEL BLOCKERS
Nitrates
AVOID beta blockers
Cocaine induced MI treatment
Calcium channel blockers and nitrates
Aspirin, heparin until CAD ruled out
NO beta blockers
Primary prevention of Coronary artery disease
BP<130/80
LDL<100
A1C<7
No smoking
Exercise
Target BMI
Secondary prevention of coronary artery disease
Diagnosis of DM, PAD,CVA/TIA,CKD
BP<130/80
LDL<55
A1C<7
Antiplatelet (aspirin)
Statin (moderate or high)
GLP-1 for diabetes
ACE/ARB or SGLT2 for CKD
NSTEMI ECG
Possibly ST depression
Troponin elevation
STEMI diagnostics
Active angina
Troponin elevation
ST elevation
Q wave development old aor infarct
New left bundle branch block (LBBB) looks same
NSTEMI treatment
Beta blockers
Aspirin
Statin
STEMI treatment
Heart Cath (ALWAYS)/reperfusion
Beta blocker
Aspirn
Statin
What causes ST elevation
Muscle dying
Stable angina
Chest pain
No symptoms while at rest
No ECG changes
No troponin elevation
Lasts less than 20 minutes
Stable angina treatment
Beta blocker, aspirin, high intensity statin treat disease
Nitrates, ronolazine, CCB treat symptoms
Unstable angina symptoms
Chest pain at rest
Last >30 mins
Unstable angina treatment
Heart cath
What conditions provoke or exacerbate ischemia in stable angina pectoris
Hyperthermia
Hyperthyroidism
Cocaine
HTN
Anxiety
Hypertrophic cardiomyopathy
Aortic stenosis
Stable angina diagnostics
Negative troponin
EKG usually normal
Stress test or stress echo to check for blockage
Cardiac CTA
Unstable angina diagnostics
Negative troponin
Elevated cardiac enzymes
Usually ST depression
NSTEMI diagnostics
Troponin positive
No ST elevation
Unstable angina and NSTEMI treatment
Morphine
Oxygen
Nitroglycerine
Aspirin
Beta blockers
Antiplatelet
Statin
NOT fibrolytics
How blocked does an artery have to be before stent is put in
70%
If it hasn’t reached that much, give statin
Normal ejection fraction
> 55%
Ideally >65%
ST elevation of V2-V4
Anterior wall
LAD
Prone to ventricular arrhythmias and shock
Widow maker
ST elevatoin of I, avL, V5, V6
Lateral wall
Circumflex artery
Not as bad
ST elevation of II, III, aVF
Right coronary artery
GIVE IV FLUIDS
Transient AV blocks
Stemi treatment
MONA-BAS
Aspirin
P2Y12 inhibitor
Anticoagulation
Reperfusion within 12 hours of onset stmptoms
Fibrinolytic therapy
Reperfusion therapy
Primary percutaneous coronary intervention.
Better than thrombolysis
Give fibrinolytics within 30 mins if stent can’t be put in within 90 mins.
Stent is standard for pts with acute MI
Who would you use a bare metal stent in
Someone with bleeding issues and can’t be on DAP (dual anti-platelet)
Fibrinolytic agents
-plase
Given for STEMI
Fibrinolytic absolute contraindications
Previous hemorrhagic stroke within a year
Intracranial neoplasm
Head trauma
Active internal bleeding
Suspected aortic dissection
Fibrinolytic relative contraindiations
BP>180/110
CVA>3 months ago
Bleeding/surgery within 4 weeks
Intracranial tumor
Pregnancy
Traumatic prolonged CPR
Dementia
Post fibrinolytic management
Conitinue with aspirin and anticoagulatoin until revascularization or for duration of hospital stay.
PPI for GI bleed prophylaxis
What NOT to do after reperfusion therapy
CCB
Nonsteroidal antiinflammatories
Post reperfusion therapy management
Statins
Beta blockers
ACEi if EF<40%
Aldosterone antagonist if EF<45%
What not to give after reperfusion therapy
CCB
NSAIDs
Acute coronary syndrome treatment
DAP for one year
Elective or stable PCI
Primary percutaneous coronary intervention
Needs to be done within 90 mins of noticed STEMI
Bare metal stent or drug eluding stent
What to do if post MI pt is in shock and you hear a murmur
Get an echocardiogram
Acute LV failure presentation
Dyspnea
Diffuse rales
Arterial hypoxemia
Diuresis
What to give if pt in post MI shock
Fluids (not if rhalles in lungs)
Ionotropic agents
Mechanical support
In that order
Acute LV failure treatment
Morphine sulfate in acure pulmonary edema
IV nitroglycerine
IV inotropic agents avoided if possible
RV infarction
Consider with inferior infarctions with low BP, raised venous pressure, clear lungs.
Hypotention made WORSE with diuretics, nitrates, and opiods
RV infarction treatment
FLUIDS FLUIDS FLUIDS
500mL of 0.9% saline
LV aneurysm
Post MI
Delineated area of scar bulges paradoxically during systole causing ST elevation.
May require surgical repair
Myocardial rupture
Usually 2-7 days post infarction and involves anterior wall.
No saving them
Pericarditis post MI complication
Audible friction rub with chest discomfort.
High dose aspirine and colchicine
Dressler syndrome (post MI syndrome)
1-12 weeks post MI
Autoimmune with pericarditis, fever, leukocytosis, pericardial leural effusions.
Treat with high dose aspirin and colchicine
Mural Thrombus
Common in large anterior infarcctions 6 weeks post MI
Give anticoagulants (start with heparin then warfarin)
How long does it take tropoonin to show up positive
4-8 hours after symptoms
Tunica intima
Innermost layer of artery.
Endothelial cells
Most responsive
Tunica media
Thick middle layer of artery
Tunica advenita
Thin outermost layer of artery
Thinnest layer
Aneurysm
Dialation of aorta>3cm
Involves all three layers of vessel wall
Weakness in the wall
Dissection
Tear of tunica intima creates false lumen
Rupture
Full-thickness tear of aorta
Thoracic aortic aneurysm
Involves aortic root, ascedning aorta, arch, and descending aorta above diaphragm
Thoracoabdominal aortic aneyrism
involves descending thoracic aorta and abdominal aorta
Abdominal aortic aneurysm
Involves descending aorta below diaphragm
Where do most aneurysms occur
Below level of renal arteries
Causes of aortic aneurisms
Primary connective tissue disorders
Turner syndrome
Menke’s syndrome
Focal medial agenesis
Tuberious scierosis
Poststenotic and arteriovenous fistula and amputation related
Injury
INflammatory stuff
Infection
Graft failure
Abdominal aortic aneurysm risk factors
Age
Male
Tobacco
Alcohol
White
Fam history
HTN
Hyperlipidemia
Abdominal aortic aneurysm clinical findings
Can be asymptomatic and found on accident in CT
Probably ruptured if symptomatic
Mild to severe deep abdominal or flank pain that is exacerbated by palpation
Pain radiates to back
Poor prognosis for ruptured
Abd aortic aneurysm imaging
ABD ULTRASOUND
Abd CT
Abd aortic aneurysm surgical repair indications
> 5.5 cm
Rapid expansion in diameter (>0.5cm in 6 months)
Symptomatic
Giant cell arteritis/Temporal arteritis
Vasculitis that affects medium and larger arteries of head and neck
Giant cell arteritis/Temporal arteritis symptoms
Fever
Fatigue
Weight loss
Malaise
Temporal headache
Jaw claudation
Unilateral vision loss
Giant cell arteritis/Temporal arteritis work up
Temporal artery biopsy
Giant cell arteritis/Temporal arteritis treatment
High dose of steroids
Give even before biopsy comes back to be safe
Marfan syndrome clinical presetation
Connective tissue disorder
Tall with long extremities
Pectus excavatum or carinatum
Increased risk for aortic root aneurisms
Marfan syndrome treatment
Screening, monitoring with echocardiogram annually
Beta blockers
Ehlers-Danlos syndrome
Increased risk for aortic root aneurisms
13 genetic disorders affecting connective tisue.
Causes joint hypermobility tissue fragility, skin hyperextensibilty
Easy bruising
Joint dislocation
Chronic pain
Ehlers-Danlos syndrome treatment
Dcreening, monitoring, fertility counseling
Thoracic aortic aneurysm clinical findings
Can be symptomatic.
Symptoms dependent on where it is
Dysphagia, stridor, dyspnea
Uper extremity edema
Cehat pain
Thoracic aortic aneurysm imaging
CT ANGIOGRAPHY
Chest radiograph
Echo if probably a rupture
Thoracic aortic aneurysm surgical repair indications
Diameter >5.5cm
Symptoms
Pt with special genetic conditions lower threshold for surgery bc of risk of rupture
Aortic rupture cause
Blunt force trauma
High speed car accident
Aortic rupture clinical findings
Severe pain
Hypotention
Pulsatile abdominal mass
Aortic rupture imaging
Thoracic: chest CT or transesophageal echocardiogram
Abd: Abd CT scan
If hemodynamically unstable get to the OR STAT
Aortic rupture management
Surgery
50% survive
Aortic dissection
Spontaneous tear of tunica intima.
Blood dissects into tunica media
Repetitive torque during cardiac cycle
HTN
Aortic dissection risk factors
HTN
Abnormalities of smooth muscle, elastic tissue or collagen from Marfan or Ehlers-Danlos syndrome
Pregnancy
Bicuspid aortic calce
Aortic dissection clinical findings
Sudden onset severe persistent chest pain described as ripping, sharp, tearing.
Pain radiates down back, anterior chest, neck
HTN
Syncopy
Aortic dissection imaging
ECG
CT of chest and abdomen
CXR
MRI
Transesophageal echocardiogram
Aortic dissection surgical repair type A
Urgent intervention
Grafting and replacing arch and branches
Aortic dissection surgical repair type B
Malperfusion urgent pintervention.
Bypass surgery to restore flow to rest of tissue
Endovascular stenting
BP control
Thoracic stent graft repair
Aortic dissection management
Agressive BP cotntrol
Beta blockers
Nitroprusside
Peripheral artery disease risk factors
Coronary artery disease
DM
Metabolic syndrome
HTN
Tobacco
Dyslipidemia
Peripheral artery disease clinical findings
Intermittent claudication
Cramping of lower extremities
Cold, pale, shiny, hairless skin
Peripheral artery disease diagnosis
Ankle brachial index (ABI)
Ultrasound assessment
CT angiogram or MR angiogram
Peripheral artery disease management
Antiplatelet therapy (clopidogrel, aspirin)
High intensity statin
Glucose and BP control
Peripheral artery disease surgical intervention
Endovascular revascularization
Balloon angioplasty without stent replacement
Arthrectomy
Bypass
When to do surgery for peripheral artery disease
Significant pain
Disability
Inadequate response to treatmetn
Chronic limb threatening ischemia
Foot ischemic wounds
Ulceration and gangrene
Severe vascular insufficiency
Ischemic rest pain
Chronic limb threatening ischemia management
Refer for vascular evaluation if diabetic
Surgical repair (bypass)
Amputation
Thrombus
Blood clot from atherosclerotic plaque or stagnant blood flow from cardiac.
Occlusion of small distal arteries
History of peripheral artery disease
Embolus
Blood clot from vascular system that TRAVELS to distal area.
Occlusion of larger arteries
History of cardiac event
Acute limb ischemia clinical findings
Abrupt onset pain and extremity.
Pain
Pulselessness
Pallor
Paralysis
Paresthesia
Cold limbs
Acute limb ischemia diagnosis
Arterial doppler ultrasound
CT angiography
Acute limb ischemia clinical intervention
Anticoagulation
Endovascular revascularization
Phlebitis
Inflammation with superficial vein
Usually due to infection or trauma from needles and catheters
Phlebitis clinical presentation
Localized pain and burning along length of vein
Tenderness
Erythema
Edema or bulging of vein
Phlebitis treatment
Warm compress
NSAIDs
Thrombophlebitis
Inflammatory reaction leads to formation of thrombus of superficial vein
Two types: superficial and septic
Superficial venous thromboflebitis
USUALLY AT SITE OF RECENT IV/PICC LINE
Can occur spontaneously in pregnant or postpartum.
Can be associated with trauma
Superficial venous thrombophlebitis clinical presentation
Dull pain in region
Tenderness along vein
Firm palpable cord
Superficial venous thrombophlebitis diagnostic imaging
Venous duplex ultrasound
Vein wall thickening (won’t compress)
Look for Virchow’s thriad
What is in Virchow’s triad
Caused by pulmonary embolism
Hypercoagulability
Vascular damage
Circulatory stasis
Superficial venous thrombophlebitis treatment
Supportive
NSAIDs
Compression socks
Extremity elevation
Septic thrombophlebitis
Usually involves inflammatino and suppuration within wall of vein
Septic thrombophlebitis risk factor
Burns
Glucocorticoid use
Injection drug use
Septic thrombophlebitis clinical presentation
Proximal estension of induration
Pain
Fever
Chills
Fluctuance or prurulent drainage
Septic thrombophlebitis labs
Blood culture
Usually caused by staph
Septic thrombophlebitis treatment
Remove catheter
Antibiotics (penicillin or aminoglycoside)
Thrombophlebitis surgery
Rarely needed.
Ligation and devision of vein at junction of deep and superficial veins.
Surgical excision of vein
Varicose veins
Dilated tortuous superficial veins secondary to defective venous valves.
Weakness of vein wall and increased intraluminal pressure leads to REVERSE VENOUS FLOW.
Phlebitis and thromobosis of lower extremity most likely to occur in varicose veins
Varicose veins risk factor
Pregnancy
Oral contraceptives
Prolonged heavy lifting
Prolonged standing
Varicose veins clinical presentatino
Dull ache with pressure sensation worsened with prolonged standing
Releived with elevation
Spider veins
Telangiectasias
Most common vein to become varicose veins
Greater saphenous
Varicose vein treatment
Compression sovks
Leg elevation
Exercise
Could use surgery but not usually (sclerotherapy, endovenous ablation (only for superficial), vein stripping (not good))
Absolute contraindicatoins of varicose vein treatment
Acute SVT, DVT, hypercoagulability
Advanced PAD
Pregnancy
Concurrent general anesthesia
Immobilized state
Prior anaphylaxis to proposed slcerosing agent
Infectoin
Venous insufficiency
Vascular incompetency of either the deep or superficial veins
Results from centripetal return of venous blood and increased capillary pressure.
Valves get thickened or scared
Most commmonly associate with varicose veins, superficial thrombophlebitis, DVT, or trauma to leg
Venous insufficiency risk factors
History of DVT
Varicose veins
Venous insufficiency clinical presentation
Erythema
Leg pain
Hyperpigmentation
Edema
Pulse and temp are normal
Ulcers at MEDIAL malleolus
Stasis dermatitis
Atrophie blanche (atrophic hyperpigmented areas)
Venous insufficiency diagnostic studies
DUPLEX ULTRASOUND
Trendelenburg test
Venous insufficiency treatment
Elastic compression stockings
Leg elevatoin
Avoid long term sitting or standing
Wound care
Deep venous thrombosis
Presence of clot in deep vein
Mostly originate in the calf
Deep venous thrombosis risk factors
Intrinsic coagulopathy
Impaire fibrinolysis
Recent surgery
Trauma
Immobilization
Increased estrogen
Smoking
Malignancy
Prior DVT
Inflammation
Coronary arter disease
IV catheters
Deep venous thrombosis clinical presentation
Unilateral swelling/edema of lower extremity >3cm
Calf pain/tenderness
Warmth
Erythema
Homan’s sign
Lower extremety deep venous thrombosis
Most commonly begin in calf and propgate to popliteal , femoral, and iliac veins
Much more common than upper extremity
Upper extremity deep venous thrombosis
Usually caused by placement of pacemaker, internal cardiac defibrillators or indwelling central venous catheters.
Likelihood increases as catheter diameter and number of lumens increases
Homan’s sign
Sign of DVT
Pt supine
Calf pain when examiner dorsiflex foot
DVT diagnostics
Venous doppler ultrasound.
Venography
DVT management
Direct oral anticoagulants (DOAC)
DVT magement for first event
DOAC for 3-6 months
Unprovoked DVT treatment
Long term anticoagulation
Pregnancy DVT treatment
Low molecular weight heparin
Direct oral anticoagulants (DOAC)
DVT treatment
Apixaban
Rivaroxaban
Dabigatran
Prior t stopping you must know if there is any clot left with venous duplex ultrasound
What to give for warfarin toxicity
Vitamin K
Warfarin
Should be overlapped with heparin for five days and until INR>2 for 24 hours.
Avoid eating vegetables with increased vitamin K
DVT prevention
Considered on all hospital pts
Compression boots.
Bed exercise
Ambulation
PT consult
Types of cardiomyopathy
Hypertrophic
Restrictive
Dilated
Dilated cardioomyopathy cause
Ischemic
Idiopathic (viral)
DM, thyroid disease
Familial
Tacy mediated
Alcohol abuse
Meds
Restrictive cardiomyopathy causes
Amyloid
Infultrative disorders
Familial
Hypertrophic cardiomyopathy cause
Thickening of muscles impairs LV filling and movement.
LV wall >1.5 cm
Dilated cardiomyopathy
Left ventricle space enlarged
Left ventricle muscle thinned out
Dilated cardiomyopathy treatment
Beta blocker (carvedilol or metoprolol)
RAAS (ace/arb/arni)
MRA (spironolactone)
SGLT-2 (flozin)
Avoid nondihydropyridine CCB
What symptoms does left heart failure have
Pulmonary symptoms
Dilated cardiomyopathy symptoms
Dyspnea with exertion
Impaired exercise capacity
Dilated cardiomyopathy physical exam findings
Rales
Cardiomegaly
S3
Peripheral edema
Elevated JVP
Dilated cardiomyopathy diagnostics
BNP, CMP, CBC, TSH
ECHOCARDIOGRAM with dilated LV, decreased EF, and ventricular hypokenesis
Possibly heart cath and CXR
Tako-tsubo
Stress cardiomyopathy
Broken heart syndrome
Present with acute anterior MI wit apical left ventricular ballooning
Tako-tsubo treatment
Beta blocker
Ace/arb/arni
Spironolactone
Hypertrophic cardiomyopathy causes
Genetic most common
Hypertrophic cardiomyopathy symptoms
Dyspnea
Chest pain
Post exertional syncope
Sudden cardiac death
Hypertrophic cardiomyopathy clinical exam findings
harsh systolic murmur, S4
Bisferiens carotid pulse
Enlarged PMI
Murmur worsened with valsalva or standing (decreased venous return)
Murmur decreased with squating, supine, leg raise, hand grip (increased venous return)
Hypertrophic cardiomyopathy diagnostic tests
EKG with LVH, axis deviation
Asymmetric septal wall thickiening (>1.5cm)
Hypertrophic myopathy treatment
Beta blockers to decrease HR, as much as possible
non-dihydropyridine CCB
Avoid dehydration
Maintain normal sinus rhythm
Surgical myectomy
Alcohol septal ablation
Restrictive cardiomyopathy cause
AMYLOIDOSIS most common
Sarcoidosis
Carcinoid
Hemocromatosis
Fibrosis
Restrictive cardiomyopathy symptoms
Pulmonary and systemic congestion
Dyspnea
Peripheral edema
Palpitatoins
Fatigue
Weakness
Exercise intolerance
Amyloidosis symptoms
Common cause of restrictive cardiomyopathy
Periorbital purpura
Thickened tongue
Hepatomegaly
Diarrhea
Weight loss
Kidney and heart usually involved
Resitrictive cardiomyopathy physical exam findings
Right sided failure
Elevated JVP
Kussmaul’s sign (increased jugular venous pressure with inspiration)
S3
Ascites
Edema
Restrictive cardiomyopathy diagnostics
EKG with low voltage, LA enlargement, deep Q waves
Echocardiogram with thickened LV and RV walls and bilateral enlargement
BIOPSY
MRI
Pulm HTN
Restrictive cardiomyopathy treatment
Treat underlying disorder
Hemochromatosis (chelation)
Sarcoidosis
BB, Diuretics
Congestive heart failure
Hypervolemia due to impaired cardiac function
Congestive heart failure symptoms
Dyspnea on exertion
SOB
Orthopnea
Edema
Abd bloating/distention
Cough
Decreased apetite
“Normal” EF (55-65%)
Heart failure causes
Myocardial eschemia
Arrhythmia
Uncontrolled HTN causes hypertrophy
Diet/med noncompliance
Substance abuse
Anemia
Hyperthyroidism
Sepsis
Pulm emboli
Acute kidney injury
NYHA classes heart failure symptoms
Class I: no limitation
Class II: symptoms at normal activity (grocery shopping)
Class III: Symptoms at minimal activity (brushing teeth)
Class IV: symptoms at rest
Right sided heart failure symptoms
Pedal edema
Abd bloating
Nausea/ decrease apetite
Left sided heart failure symptoms
DOE/SOB
Orthopnea
Cough
Activity intolerance
Left sided heart failure physical exam findings
Rales/crackles/wheezes
Dullness to percussion
S3 or S4 gallop
Right sided heart failure physical exam findings
Distended neck veins
Elevated JVP
Abd distension
Pedal edema
Hepatojugular reflx
Ascites
Liver enlargement/tenderness
CMP of heart failure
Hyponatremic
Renal function
LFTs
Low albumin can cause edema
Heart failure ECG findings
LVH (uncontrolled HTN)
Afib/Aflutter
LBBB
Q waves
Heart failure CXR findings
Alveolar edema (bat wing opacities
Blunt margins
Kerley B lines
Dilated upper lobe vessels
Pleural effusion
Pulm edema
Heart failure diagnosis
Echo
BNP
Congestive heart failure treatment
Treat symptoms (loop for wet)
Treat underlying cause (HTN, Weight, OSA, etc)
Education (low Na diet, fluid restriction, exercise)
SGLT-2. BB, RAAS, Spironolactone (MRA)
What does a wide (0.15) QRS tell you about the vetricles
Ventricle contraction not synchronized.
Entresto
Sacubitril + valsartan
(arb + neprilysin inhibitor)
36 hour washout from ACEi
Watch BP
Watch GFR
Used in CHF
Drugs to avoid in heart failure when EF<40
NSAIDs/COX2 inhibitors
CCBs
Thiazolidinediones
Sulfonylureas
Preferred RAS agent in heart failure
ARNI unless too expensive or can’t handle side effects
Pericarditis
Acute inflammation of pericardium
Pericarditis causes
Mostly viral
Trauma, tumor
Uremia
MI, Medications
Other infectious
Rheumatoid, autoimmune, radiation
Periarditis symptoms
Pain on deep breath or cough
Leaning forward (tripod)
Pericarditis ECG
ST elevation in most leads (diffuse)
Pericarditis physical exam findings
Pericardial friction rub
Pericarditis diagnostics
CXR normal unless effusion
Echocardiogram
CBC, ESR, CRP (maybe troponin) elevated
Acute pericarditis treatment
Aspirin or NSAID + colchicine + exercise restriction
Keep seeing them once per week until symptoms better
NSAIDs stop 1-2 weeks after symptoms stop
Colchicine stays on for 3-6 months after symptoms stop
Who is at high risk of recurrent pericarditis
Autoimmune disease
Not treated with colchicine the first time
Most common side effect of cholchicine
GI upset
Constrictive pericarditis treatment
Shell around heart
Treated by diuretics, pericardietomy
Restrictive pericarditis treatment
Treat underlying disorder or transplant
Pericardial effusion
Extra fluid in pericardial space
Cardiac tamponade look on echocardiogram
Right ventricular collapse during diastole
Pericardial effusion physical exam findings
Muffled heart sounds
Dullness to percussion left lung over angle of scapula
Hypotension
Elevated JVP
Pericardial effusion diagnositics
Low QRS voltage with sinus tachycardia.
Varrying QRS voltages from being bounced around (electrical alternans)
CXR water bottle sign
Echocardiogram assesses hemodynamic impact
Pericardial effusion treatment
Monitor if stable
NSAIDs, corticosteroids, colchicine
Cardiac tamponade
Medical emergency
Pressure from pericardial effusion impairs cardiac output
Cardiiac tamponade presentation
Tachycardia
Tachypnea
Hypotension
Cardiac tamponade treatment
Pericardiocentesis (can be done at bedside)
Pericardial window for tamponade
Pericardiectomy for recurrent
NO vasodilators or diuretics
Pericardial tamponade diagnosics
EKG: low voltage, sinus tach
Echocardiogram: RV colapse during diastole
CXR: Enlarged cardiac silhoette
Right heart cath: equalization of pressures in diastole
Pericardial tamponade treatment
Urgent pericardiocentesis
Infective endocarditis most common cause
Streptococcus viridians
Staphlococcus arureus (IV drug use at tricuspid)
Enterococci (men with GI or GU procedure)
Mitral valve most commonly effected
Infective endocarditis physical exam
Fever
Murmur
Splinter hemorrhages
Janewayy lesions
Osler nodes
Janeway lesions
Infective endocarditis symptom
Painless on palm of hands
Osler nodes
Infective endocarditis symptom
Painful spots on pads of fingers
Roth spots
Infective endocarditis symptom
Red spots on retina
Major infectious endocarditis diagnosis
Blood culure positive for IE
TEE positive for vegetation
Minor infectious endocarditis symptoms
Fever
Roth spots
Osler nodes
Murmur
Janeway lesions
Anemia
Nail-bed hemorrhages
Emboli
Infective endocarditis treatment
3 Blood cultures
TEE if TTE not confirmed
Monitor
Valve replacement if fever after 7 days antibiotic therapy
How to prevent reccurent infective endocarditis
Antibiotic prophylaxis before dental, respiiratory, procedure involving skin/msk tissue
Dental hygiene
Rheumatic fever
Systemic immune response 2-3 weeks after strep pharyngitis
Affects heart, joint, skin, CNS
Mitral valve usually involved
Rheumatic fever presentation
Funny looking rash
Joint invilvement
Subcutaneous nodules
Erythema marginatum
Myocarditis
Rheumatic fever diagnosis
Positive throat culture
risng ASO titer
Rheumatic fever treatment
Bed rest
Fluids
Pinicillin (erythromycin if allergic)
Salicylates PRN for fever and joint pain
Myocarditis presentation
Inflammation of myocardium (acute or chronic)
Unexplained heart failure
Chest pain
Arrhythmia
Raised troponin
Fever
Malaise
Myocarditis ECG
Sinus tachycardia with nonsecific ST/T wave changes
Prolonged QRS
Myocarditis imaging
Echo to rule out effusion
Cath to rule out ischemia
Cardiac MRI
Myocarditis treatment
Manage HF and arrhythmia
ACE/ARB/ARNI, BB, SGLT2, MRA
S1
Closing of AV valves
S2
Closing of aortic and pulmonic valves
S3
Usually heard in CHF
Volume overload
Ken-TUUUUUU-cky
S4
Usually precedes S1
LVH/RVH, AS, PS
Te-nness-eee
Tricuspid endocarditis
Usually Staph aureus
Usually related to IV drug abuse
Tricuspid endocarditis diagnostics
EKG (heart block or conduction delay)
ECHOCARDIOGRAM to see enlargemenet of tricuspid valve
CXR (infiltrates, emboli, pulm vascular congestion, abcess)
Tricuspid endocarditis treatment
Abx for 6 weeks
Maybe surgery after infection cleared
Tricuspid regurgitation
Blood flows backwards through floppy valve
Tricuspid regurgitation causes
Primary: PM/ICD leads, chest trauma, ischemic heart disease effecting RV
Secondary: RA or RV dilation, most have pulm HTN
Tricuspid regurgitation clinical manifestations
JVD
RV heave
Edema
Murmur
Maybe S3
EKG can show RV hypertrophy
CXR can show RV enlargement
Tricuspid regurgitation diagnostics
ECHOCARDIOGRAM
Cardiac MRI
Right/left cardiac catheterization
Tricuspid regurgitation management
Surgical repair or replacement
Tricuspid stenosis
Rare
Present with fatigue, venous HTN
Rarely just tricuspid valve
Pulmonic insufficiency
Leads to RV enlargement and dysfunction. tricuspid dysfunction.
Usually asymptomatic for years
Related to CHF
Pulmonic insufficiency diagnostics
ECHOCARDIOGRAM
CMRI for quantification of RV health
Pulmonic insufficiency treatment
Surgical in extreme
Bioprostetchic
Transcatheter
Five major parts of Mitral valve
Annulus
Leaflets
Commissures
CHordae tendinae
Papillary muscles
Mitral valve prolapse clinical manifestations
Rare
Mild
Murmur
Non-ejection click early iin ccardiac cycle while sitting/standing or later in cycle with squating
LA dialation
Arryhythmias
CHF
Mitral valve prolapse diagnostics
Physical exam
ECHOCARDIOGRAM
Cardiac MRI quantification
Primary Mitral valve regurgitation causes
Rheumatic heart disease
IE
Trauma
Congenital malformations
Mitral annular calcification
Cardiac amyloidosis
Secondary Mitral valve regurgitation causes
Coronary disease
Dilated cardiomyopathy
HOCM
RC pacing
Afib
Mitral valve regurgitation clinical manifestation
CHF symptoms
LA and LV enlargement
Mitral valve regurgitation physical exam findings
LV enlargement
Murmur
S1 diminished
S2 split
S3 gallop
Murmur radiates to maxilla
Mitral valve regurgitation diagnostics
ECHOCARDIOGRAM showing regurgitant volume >60mL, regurgitant fraction >50%
EKG - LAE, broad P waves notched with increased amplitude
Mitral valve regurgitation treatment
Mitral ring
Resection
Alfieri stitch
Replacement
Mitral clip
Mitral stenosis
90% of cases are rheumatic fever
Mitral stenosis diagnositcs
Doming on Echocardiogram
Annular or single leaflet calcification
Mitral stenosis comorbitity
HF
Afib
Death usually caused by CHF
Can cause LA dilation
Mitral stenosis diagnostics
ECHO, TEE for 3d view to see if annular calcification
Mitral stenosis treatment
Slow the HR
Mitral valve replacement
Balloon for rheumatic disease NOT for annular
What separates the heart from everything else
Aortic valve
Aortic insufficiency
Blood sucked back into ventricle during diastole through non-compliant valve
CHF symptoms
Aortic insufficiency diagnostics
Echocardiogram (usually TTE but TEE can be used to see exact mechanism)
Diastolic murumur
Aortic insufficiency treatmetn
Usually volume management
Sometimes surgery if severe
Caths not good
Aortic stenosis cause
Calcium buildup
Can be born with native bicuspid valves
Aortic stenosis symptoms
DOE
Chest pain
Syncope
Activity intolerance first symptom
Aortic stenosis diagnostics
Echocardiogram
Murmur
S4
Aortic stenosis treatmen
TAVR
TAVR
minimally invasive treatment for aortic stenosis
Put metal thing on balloon and put it in Aortic valve.
Works really good
TAVR risk
Stroke
Might need pacemaker
Acyanotic Congenital heart disease
Left to right shunt
Oxygenated blood mixes with venous return
Cyanotic congenital heart disease
More dangerous
Right to left shung
Venous blood mixes with systemic flow
Common things that come with acyanotic congenital heart disease
Patent foramen ovale
Atrial septal defect
Ventricular septal defect
Patent ductus arteriosus
Coarctation of aorta
Patent foramen ovale
Cardiac lesion that persists into adulthood
Patent foramen ovale symptoms
Most asymptomatic
Stroke at young age
Patent foramen ovale diagnosis
Echocardiogram after stroke
Patent foramen ovale treatment
Could do surgical closure but not recommended
What happens during atrial septal defect
Blood moves from LA to RA bc high pressure in LA
RA becomes enlarge
Overtime blood will get shunted from RA to LA bc of change in pressure (Eisenmenger syndrome)
Eisenmenger syndrome
Atrial septal defect where blood is shunted from RA to LA so deoxygenated blood is getting pumped into circulation
Atrial septal defect symptoms
SOB
Tired
Poor weight gain
Cyanosis
Arrhythmias
HF symptoms
Murmur of atrial septal defect
Wide split S2
RV heave
Atrial septal defect diagnosis
Echocardiogram (bubble study)
ECG
CXR
Atrial septal defect treat
Usually closes itself by 2-3 y/o if <5mm`
Surgical closure
Long term consquences of atrial septal defect
Blood clots–>stroke
Arrhythmias
Recurrent infections
What happens in ventricular septal defect
Blood from LV flows into RV bc high pressure in LV causing RV hypertrophy
Eventually blood will go from RV to LV
Most common type of congenital heart disease
Ventricular septal defect
What is a preventable cause of ventricular septal defect
Fetal alcohol syndrome
Ventricular septal defect symptoms
Asymptomatic
Weakness
Poor feeding
CHF like symptoms
Murmur of ventricular septal defect
HOLOSYSTOLIC high pitched
Ventricular septal defect diagnosis
EKG
CXR
Echocardiogram (bubble study)
Ventricular septal defect treatment
Most close themselves by 2 y/o
Surgery closure if necessary
Flurosemide (loop diuretic)
Ductus arteriosus
Attaches pulmonary artery to aortic arch
Patent ductus arteriosus
Ductus arteriosus doesn’t close after birth causing connection between aorta and pulmonary artery.
Seen in premature babies
Associated with rubella
Patent ductus arteriosus pathophys
Fetal ductus anteriosus is kept open by low arterial oxygen and circulating prostaglandin.
Causes oxygenated blood from aorta and left heart to flow back into lungs.
Can develop into eisenmenger’s syndrome
Patent ductus arteriosus symptoms
Small can be asymptomatic
Continuous “washing machine” murmur
Wide pulse pressure
Hyperdynamic apical pulse
Poor feeding
Weight loss
Freq respiratory infections
Patent ductus arteriosus diagnosis
Echocardiogram
CTA/MRA
EKG
CXR
Ductus arteriosus treatment in newborns
Prostaglandin synthesis inhibitors (NSAIDs: ibuprofen, indomethacin)
Ductus arteriosus treatment in slightly older babies
Surgery
Symptomatic treatment with digoxin and flurosemide
Follow up after ductus arteriosus surgery
Prophylactic Abx for six months
Coarctation of aorta
Kinked aorta
Associated with bicuspid aortic valve
Associate with Turner syndrome
How long does it take ductus arteriosus to close
About 15 hours after birth
When do coarctation of aorta symptoms start
When ductus arteriosus closes.
So baby could seem normal for first few hours
Coarctation of aorta in neonate symptoms
HF
Shock
Pale
Irritable
DIaphoretic
O2 sat higher in arms than legs
Coarctation of aorta in older infants symptoms
Chest pain
Cold extremities
Claudication
Lower BP in lower extremities than in upper extremities
Coarctation of aorta in adults symptoms
Must be very small to go unnoticed this long.
HTN
Underdeveloped lower extremeties
Cold and painful feet/legs with edema
Coarctation of aorta murmur
Harsh systolic murmur at left sternal border
Coarctation of aorta diagnosis
Echocardiogram
CXR rib notching and 3 sign
Neonate treatment of coarctation of aorta
Give prostaglandins (-prost-) to keep the ductus arterosus open until angioplasty/stent
Coarctation of aorta follow-up
life long with cardiology.
Ned cardiology clearance for participation in sports.
Hypoplastic left heart syndrome
Left side of heart fails to develop so RV is bigger than LV
Hypoplastic left heart syndrome symptoms
May not appear until ductus arterious closes
Usually no murmur
Shock
Cyanosis
Respiratory distress
Cool extremities
Decreased peripheral pulses
Very sick
Hypoplastic left heart syndrome diagnosis
Echocardiogram
Hypoplastic left heart syndrome treatmen
Norwood in first two weeks
Bidirectional glenn shunt 4-6 months
Fontan 18 months-3yrs
Heart transplant
Hypoplastic left heart syndrome post-op
Chronic anticoagulation
Screen develoomental delay
Transposition of great vessels
Occurs when aorta and pulmonary artery are switched
Associated with maternal diabetes
Die within a year if not treated
Transposition of great vessels symptoms
Severe cyanosis (blue skin)
Tachypnea
Resp distress
Poor feeding
Absent lower pulses
Systolic murmur
Transposition of great vessels diagnosis
Echocardiogram.
Can be found in-utero on ultrasound
CXR heart has egg/potato appearance
Transposition of great vessels treatment
Prostaglandins to keep DA open
Surgical correction
Pulmonary atresia
occur when the pulmonary valve did not form
Complete obstruction of right ventricular flow into pulmonary trunk
Body might make abnormal connection between RV and coronary arteries and a VSD
Pulmonary atresia symptoms
Murmur if VSD
Crtical condition
Hyperdynamic apical impuls
Pulmonary atresia diagnosis
Echocardiogram
Possibly caught on prenatal ultrasound
Pulmonary atresia treatment
Prostaglandins to keep ductus arteriosus open
Surgical repair
Tetralogy of fallot
Pulmonary stenosis
Right ventricular hypertrophy
Ventricular septal defect
Overriding aorta
Tetralogy of falot symptoms
systolic crescendo-decrescendo ejection murmur
INcreased RV outflow tract obstruction
INcreased RV impuls4e at left lower sternal border
Baby might be asymptomatic until changes in heart structure causes right to left shunting
Tet spell
Tet spell
Transient occlusion of right ventricular outflow from tetralogy of falot leading to severe cyanosis spell.
Improves when having kid squat or pull legs up to chest
Clubbing
Tetralogy of falot diagnosis
Echocardiogram
CXR boot shaped heart
Tetralogy of falot treatmetn
Prostaglandin to keep ductus arteriosus open till surgery
Surgery in first year of life.
Treatment of tet spell
Knee-to-chest positioning
Supplemental oxygen
IV morphine
IV fluid bolus
Amiodarone
Class III antiarrhythmic med that fixes VT, SVT and prevents VT, Afib, VF
Amiodarone side effects
Corneal microdeposits
Thyrod dysfunction
Pulmonary fibrosis
Blue-gray skin
What to do when you put someone on amiodarone
Yearly eye exam, PFTs, TSH, CXR
Causes of sinus tachycardia
Exercse
Anemia
Dehydration
Shock
Hypoxia
Sepsis
Pulmonary disease
Hyperthyroidism
Pheochromocytoma
HF
Sinus tachycardia treatment
Identify underlying cayse
Beta blockers
Sinus bradycardia causes
AV blocking meds
Heightened vagal tone
Hypothyroidism
Hypothermia
Obstructive sleep apnea
Hypoglycemia
Sinus bradycardia workup
TSH
Holter
Echo
Treadmill
Sinus bradycardia treatment
Discharge av nodal slowing agents r/o underlying diseases
Atropine
Pacemaker
Dopamine
What are the qualifications for pacemaker
<30bpm
<35bpm with symptoms
>3 second pauses
3rd degree AV block
Sinus arrhythmia
Heart rate increases with inspiration and decreases with expiration
Multifocal atrial tacycardia
3 or more distinct P wave morphologies on EKG
Seen in severe COPD
No treatment, just happens
Premature atrial contraction
Abnormal P wave follwed by normal QRS
Focus in the atrium (not SA node) generates action potential before next scheduled SA node action potential.
Premature atrial contraction presentation
Asymptomatic to palpitations
Premature atrial contractions workup
CBC, TSH, Mg, BMP, ECG, holter
Premature atrial contractions treatment
Monitor
Avoid triggers
Beta blocker
CCB
First degree AV block
Fixed prolonged PR interval (>.20)
First degree AV block treatment
Monitor
Second degree AV block - Wenckebach
Progressive PR interal prelongation with each beat until P wave is not conducted
Second degree AV block - Wenckebach cause
Inferior MI
Second degree AV block - Wenckebach treatment
Monitor.
If symptomatic, give atropine, epinephrine, pacemaker
Second degree AV block - Mobitz II
Extra P waves with dropped QRS
Second degree AV block - Mobitz II treatment
Atropine
Transcutaneous pacing or pacemaker
Usually turns into 3rd degree block
3rd degree AV block
Complete block
No association between atrial and ventricular impulses
3rd degree AV block treatment
Trascutaneous pacing followed by pacemaker
Afib
No P waves
Varying R-R intervals
High risk of coagulation
What does Afib usually cause
Enlargement of left atria
Causing mitral widening and regurgitation.
Causing left atria to widen more and worsens Afib
Afib treatment
Anticoagulants
Cardioversion (shock them to reset heart, not permanent fix)
Antiarrhythmic medicine to make cardioversion last longer
Ablation works for longer until it heals (burning tissue in heart causing the bad electricity)
Lone Afib
Isolated occurrence
Cocaine
Reversible
Paroxysmal afib
Recurrent episodes <7 days
Persistent Afib
Recurrent episodes >7 days
Longstanding, persistent Afib
Had it for >12 months
Most common chronic arrhythmia
Afib
Afib risk factors
HTN
Valvular heart disease
CAD
Cardiomyopathy
COPD
Obesity
Sleep apnea
Excessive ETOH
Thyrotoxicosis
Afib symptoms
Asymptomatic
Palpitations
Fainting
SOB
Chest pain
Stroke
Afib work up
CBC
CMP
TSH
Holter
Echocardiogram
Sleep study (sleep apnea common in Afib)
What Afib patients to put on rate control
Old, asymptomatic, presered EF
Give beta blockers or CCB
What Afib patients to give rhythm control
Young, symptomatic, EF<45%, new onset, HCOM
Give flecainide, propafenone, sotalol, dofetilide, amiodarone, dronedarone
Cardioversion
Ablation
Cardioversion
Requires sedation
Shock the heart back into good rhythm
Pt must be on anticoagualnts
Aflutter
Sawtooth
Lack of P waves
Aflutter presentation
Asymptomatic
Palpitations
DOE
SOB
Aflutter workup
CBC
CMP
TSH
Holter
ECG
Echo
Treatment for stable aflutter
OACtx
Unstable Afluter treatment
Cardioversion
Ablation
Supraventricular tachycardia EKG
Narrow QRS tachycardia (160-200)
Supraventricular tachycardia presentation
Palpitations
SOB
DIaphroesis
Chest pain
Rapid breathing
Dizziness
Loss of conscousness
Supraventricular tachycardia workup
CBC
CMP
TSH
Supraventricular tachycardia treatment
Valsalva
IV adenosine
IV Calcium channel blockers
IV Beta blockers
Cardioversion if unstable
Ablation is cure
Premature ventricular contraction EKG
premature, wide QRS
Compensatory pause
Premature ventricular contractions presentation
Asymptomatic
Palpations
Premature ventricular contractions treatment
Beta-blockers
non-dihyrdopyridine CCB
Ventricular tachycardia
Wide QRS (>0.12)
>100bpm
Ventricular tachycardia treatment
Iniitial: urgent cardioversion, IV amiodarone, epinephrine, short acting beta blocker
Long term: Beta blockers/amiodarone, catheter ablation, implatable cardioverter defibrilator
Polymorphic ventricular tachycardia treatmetn
Torsades de pointes
IV magnesium after cardioversion
Ventricular fibrilation
Quivering ventricles with no cardiac output.
Looks like scribbles
Vfib treatment
SHOCK
Asystole
No electrical activity of heart
Asystole treatmetn
CPR
Epinephrine
Hyperkalemia look on EKG
Tall peaked T waves
Wide QRS
Increase of PR interval
Bradycardia
Hypocalcemia look on EKG
Prolonged QT interval
Hyper calcemia look on EKG
Shortened QT interval
Brugada sndrome
RBBB
Genetic disorder causing sudden cardiac death from polymorphic VTach or VFib .
Long QRS that looks like M in V1 an V2
Treatment is ICD
Wolff-Parkinson-White
Accessory patthway that connects electrical system of atria directly to ventricals allowing conduction to avoid AV node
Wolff-parkinson-White EKG
Delta wave
Shortened PR interval
Wolff-Parkinson-White treatment
Ablation
Main unique symptom of distributive shock
Warm extremeties
Distributive shock presentation
Low SVR
Normal/high CO
Low BP
High lactate
Warm extremeties
Tachypnea
Tachycardia
Bradycardia
Hypotension
AMS
Fever
Cough
SOB
Distributive shock cause
Anaphylaxis
Sepsis
Neurogenic
Adrenal insufficiency
Distributive shock treatment
IV antibiotics or fluid for sepsis
Epinephrine, corticosteroids, bronchodilators for anaphylactic
Cooling and supportive care for neurogenic
Hypovolemic shock presentation
High SVR
Low CO
Low PAP
Low CVP
Cold extremities
Massive bleeding
SOB
Hypovolemic shock treatment
IV fluids
Blood transfusion
Control hemorrhage and pressure
Check for hypercoagulability
Tourniquet
Cardiogenic shock
Cool extremities
LV or RV failure
Decreased cardiac output
Increased systemic vascular resistance
Cardiogenic shock presentation
Low CO
High SVR
Cardiogenic shock LV failure cause
Acute MI most common
Hypertrophic obstructive cardiomyopath
Myocarditis
Myocardial contusion
STEMI, BBB, abnormal axis
Cardiogenic shock right ventricular failure cause
Acute MI
Myocarditis
Post-cardiotomy
Cardiomyopathy
Pulmonary embolsim
Worsening pulmonary HTN
Cardiogenic shock mechanical dysfunction
Aortic regurgitation
Acute bacterial endocarditis
Mechanical valve dysfunction/thrombosis
Mitral regurgitation
Mitral and atrial stenosis
Ventricular septal defect or free wall rupture
Cardiogenic shock arrhythmia
Afib
Aflutter
VTach
Vfib
Bradycardia
Heart block
Metabolic cardiogenic shock
Calcium channel antagonist
Adrenergic receptor agonist
Thyroid disorders
Cardiogenic shock treatment
ICU, tele, pulm artery catheter, foley catheter to measure urine
Maintain O2
INtravenous inotropes and vasopreessors
Intraortic balloon pump tandem heart, left ventricular assist device
Obstructive shock
Blood obstructed from right to left heart.
Acute MI
Obstructive shock presentation
Low SVR
Low CO
High PAP
High CVP
Obstructive shock causes
Pulmonary embolism
Pericardial tamponade
Tension pneumothorax
Aortic stenosis
Arterial line
Put into artery to continuously monitor systemic blood pressure.
Used during hemodynamic instability, vasopressor requirement, Frequent arterial blood gases.
In radial, femoral, axillary, or dorsal pedis arteries
Central venous pressure monitoring
Measure pressure in right atrium an dvena cava
Needed to assess right ventricular function, systemic fluid status, rapid infusions.
In jugular, subclavian, or femoral veins
What does high central venous pressure mean
Overhydration
Heart failure
Pulmonary artery stenosis
What does low central venous pressure mean
Hypovolemic shock
Swan-Ganz catheter/Pilmonary artery catheter
Measures Central venous pressure and pulmonary artery pressure.
Shock definition
Inadequate O2 delivery, increased consumption, or decreased utilization to meet metabolic demands.
Can occur with normal or hypotensive BP.
Release of catecholamines triggered to try to raise BP
Pre-shock
Compensated
No end organ damage
Nonhemorrhagic hypovolemic shock cause
Vomiting
Diarrhea
Bowl obstruction
Pancreatitis
Burns
Neglect, environmental (dehydration)
Hemorrhagic hypovolemic shock cause
GI bleed
Trauma
Massive hemoptysis
AAA rupture
Ectopic pregnancy post partum bleeding
Cardiogenic shock pathophys
MI causes loss of 40% of LV
CO reduction causing lactic acidosis and hypoxia
Stroke volume reduced so tachycardia happens to compensate but makes ischemia worse
Beck’s triad
Pericardial tamponade (can cause onbstructive andcardiogenic shock)
Hypotension
Muffled heart sounds
JVD
Neurogenic (type of distributive) shock symptoms
After spinal injury
Sympathetic outflow is disruptie
Hypotension
Bradycardia
Usually only lasts a couple weeks.
Neurogenic shock treatment
Cooling
What to give if pt in shock and glucose is low
1 ampule of 50% dextrose IV
Hemorrhagic shock treatment
Blood
How much fluid to give to hypovolemic shock patient
1 liter
If that doesn’t fix BP give vasopressors
How much fluid to give pt in septic shock
30mL/kg of crysalloid solution (normal saline or LR)
If that doesn’t fix BP give vasopressors
How much fluid to give when pt in cardiogenic shock
250
If that doesn’t fix BP give vasopressors
DIstributive shock meds for vacoconstriction
Norepinephrine
Epinephrine
Dopamine
Vasopressin
Septic shock meds for vasoconstriction
Norepinephrine
First choice vasopressor in shock
Norepinephrine
Cardiogenic shock meds
Dobutamine
Amrinone
Milrinone
When to start antibiotics in septic shock
ASAP (within hour of recognition)
Treatment for shock caused by adrenal insufficiency
Corticosteroids (cortisol)
Sepsis definition
Organ dysfunction caused by dysregulated response to infection
What labs to order for septic pts
Blood culture
Lactic acid/lactate
CBC
UA
CXR
Head CT if AMS
What values show pt will have long ICU stay or die in hospital
RR>22
Systolic BP<100
Most common source of sepsis
Pneumonia
Then intraabdominal
ten GU sources
Sepsis risk factor
Immunosuppression
Pneumonia
Previous hospitalization
Predisposition to organ dysfunction
How to tell if there is kidney damage from sepsis
Decreased urine output
Pulmonary effects of sepsis
Inflammatory response happens causing interstitial edema causing pulmonary shunting and refractory hypoxemia
GI effects of sepsis
Hypomotility causing translocation of gut bacteria into circulation
Neurological effects of sepsis
Encephalopathy from ongoing inflammatory response disrupting BBB
Endocrine effects of sepsis
Decreased CRH
Diminished sensitivity to glucocorticoids
Decreased vascuar tone
Insuline resistance causing hyperglycemia
Procalcitonin
Elevated with bacterial infections
NOT viral
Lactic acid in septic patient
2-4 maybe something
>4 is bad
Hypotension symptoms
Dizziness with position changes
Nausea
Headache
AMS
Symptomatic and stable hypotension treatment
Fluids
Compression socks
Increase salt intake
Midodrine
Fludrocortisone
Symptomatic and unstable hypotension treatment
Fluids
Vasopressors IV (dopa, epi, norepi, neosynephrine)
Syncope
Abrupt, transient loss of consciousness due to decreased cerebral perfusion
Cardiac syncope
Structural heart disease (valvular, congenital, HCOM)
Arrhythmia
Symptoms usually only on exertion
Neurological syncope
Carotid sinus syndrome (hypersensitivity)
Vasovagal
Seizure
Orthostatic syncope
CNS disease (Parkinson’s, MS)
hypovolemia
Orthostatic hypotension
20mmHg systolic or 10mmHg diastolic pressure drop
Orthostatic hypotension cause
Meds
Adrenal insufficiency
Prolonged bedrest
Parkinson’s
Hypovolemia
Orthostatic hypotension treatment
Fluids
Remove vasodilators
Increase salt intake
Midodrine
Fludrocortisone
Syncope workup
Orthostatic BP
EKG
Echo to see if structural
Vasovagal syncope
Can be caused by stress
Sitting in hot tub too long and suddenly feel like need to throwup and shit at same time
Carotid sinus syncope
Pressure on carotid causes them to pass out
Need hydration and avoid neck pressure.
Possibly need pacemaker
Causes of hypotension
Meds
Adrenal insufficiency
Prolonged bed rest
Spanal cord transection
Parkinson’s
Hypovolemia
POTS
Orthostatic BP with associated inappropriate tachycardia in young women
POTS treatment
Difficult
Fluids and sometimes meds
Might need beta blocker to fix tachy but it messes with hypotension too
Labs of malnutrition before surgery
Hypoalbuminemia (<2.5)
Prealbumin (<10)
Transferrin (<100)
NPO pre-op status
Usually okay to have lear liquids up to two hours before surgery.
Light meal up to six hours before surgery
What to do with aspirin preop cardiac
Aspirin continues unless increased risk of bleeding
Stop 5 days prior if bleeding risk
Restrt as soon as no risk of bleeding 325mg/day
Other meds to consider before cardiac surgery
Give beta blockers atleast 24 hours before surgery
Amiodarone reduces postop arrhythmias
Statins good to give preop, continue if already on it
Prophylactic antibiotics in cardiac surgery
Mupirocin in nares pre-op
IV cephalosporin an hour preinsision.
Do not continue prophylactic antibiotics beyond 48 hours after surgery
Adenosine diphosphate inhibitors /P2Y12 inhibitors
Clopidogrel
Prasugrel
Ticagrelor
Cangrelor
Inhibit platelet aggregation
Get pt off of them before surgery if possible
IIb/IIIa inhibitors
Prevent platelet aggregation and fibrinogen binding
Stop 4-6 hours before incision
Enoxaparin (Lovenox) SQ
Postpone surgery 48 hours post last doase
Irreversibly inactivates factor Xa
Post op meds for radial artery conduit
Ca channel blockers to prevent spasms bc very muscular artery
Hemoglobin level wanted after cardiac surgery
> 7.5
What levels of drainage from chest tube tell you you need to reexplore pt after cardiac surgery
> 500mL during first hour
400 mL in each of first 2 hours
300mL in each of first 3 hours
1000mL total in first 4 hours
1200mL total in first 5 hours
Holosystolic murmur maybe S3
Tricuspid endocarditis
Late systolic murmur at apex no ejection click
Mitral prolapse
Holosystolic murmur at apex, blowing radiates to axilla
Mitral valve regurgitation
Diastolic murmur at apex with opening snap
Mitral stenosis
Diastolic murmur at RUSB
Aortic insufficiency
Holosystolic murmur at RUSB, crescendo decrescendo, radiates to carotids
aortic stenosis
What two murmurs are made worse while standing (decreased venous return)
Mitral valve prolapse and hypertrophic cardiomyopathy