Cardiology Flashcards
Autoregulation pathway of BP re: increased CO?
increased CO -> increased MAP - detected by aortic and carotid baroreceptors ->vasodilation -> reduced TPR = reduced CO
Pathway of pressure natriuresis (increased MAP)?
increased MAP -> increased renal perfusion = increased GFR = reduced aldosterone -> increase Na and H2O excretion (natriuresis)
Equation for BP
BP = CO x SVR
CO = HR X SV MAP = dBP + 1/3 pulse pressure
RAAS pathway
JG cells produce renin renin = angiotensinogen -> angiotensin I ACE = angiotensin I -> angiotensin II ang II = aldosterone production, systemic vasoconstriction, vasoconstriction of afferent and efferent arterioles aldosterone = Na reabsorption
Causes of primary HTN?
- lifestyle
- medication
- family history/ genetics
Causes of secondary HTN?
- endocrine (aldosterone, glucocorticoid, hyperthyroid, hyperparathyroid, chatecholamines)
- CKD (including PCKD)
- vascular (coarctation of aorta, renal artery stenosis)
- OSA
Rx than can induce HTN?
- NSAIDs
- corticosteroids
- exogenous androgens/ estrogens
- liquorice root (aldosterone-like), antidepressants
Will BP cuff that is too small over or under estimate BP?
- small = overestimate BP
Exam for end organ damage?
- fundoscopy (copper wiring, cotton wool spots, AV nicking, papilledema)
- signs LVH (loud S2, S4, sustained apex beat)
- signs CHF (elevated JVP, S3, lung crackles, ascites, leg edema)
- peripheral vascular exam (pulsatile abdo mass, no peripheral pulses)
Lab investigations with HTN?
- UA and Cr (CKD)
- electrolytes (hypoK with hyperaldosteronism)
- fasting glucose and lipid profile (CV risk)
- 12-lead ECG (LVH, prior MI)
Workup secondary causes HTN?
endocrine
- TSH, PTH, 24h urine metanephrines, aldosterone, renin, aldosterone/renin ratio, 24h urine free cortisol, dexamethasone suppression test
ckd
- serum Cr and estimated GFR
vascular
- trans thoracic echo, CT or MR angiography (coarctation)
- captopril renal scan, abdo US with doppler, MRI (renal artery stenosis)
osa
- sleep study
Dx HTN
- BP >140/90 on 3 occasions (or if end organ damage, kidney disease, DM)
- at least 1 home, ambulatory or 24h BP monitoring recommended
OR single measurement >180/90
office >140/90
ambulatory/home >135/85
24h average >130/80
Classify HTN
normal <120/80
preHTN 120-139/ 80-89
stage 1 HTN 140-159/ 90-99
stage 2 HTN >160//>100
Target organ damage from HTN
- cerebrovascular disease
- hypertensive retinopathy
- HF
- CAD
- CKD
- peripheral arterial disease
Tx HTN
Lifestyle
- Na <1.8g/d
- weight loss
- EtOH reduction
- exercise
- diet
target <140/90
DM target <130/80
first line rx
- thiazide diuretics
- ACEi/ARBs (non-black pt)
- long acting CCB
- b-blocker (<60yr)
AntiHTN for DM?
ACEI or ARB
AntiHTN for asthma?
CCB (nondihydropyridine)
AntiHTN for prior MI?
ACEI, b-blocker
AntiHTN for angina?
b-blocker, long acting CCB
AntiHTN for CKD?
ACEI, ARB (caution)
AntiHTN for CHF?
ACEI, b-blocker, aldosterone antagonist
AntiHTN for migraines?
b-blocker, long acting CCB
AntiHTN for raynaud, coronary spasm?
long acting CCB
Which anti-HTN causes dry cough? Why?
- ACEI -> bradykinin related
Define hypertensive urgency
- severely elevated BP (>180/120) without progressive target organ dysfunction
Define hypertensive emergency
- severely elevated BP PLUS evidence of impending or progressive target organ dysfunction
How to tissues maintain perfusion relatively constant with increased BP?
- arterial and arteriolar vasoconstriction -> prevents pressure being transferred to smaller, more distal vessels
How do arteries and capillaries becomes damaged with severe HTN?
- autoregulation fails = increased arteriole and capillary pressure = damage vascular wall, disruption of endothelium (breakthrough vasodilation)
How does RAS exacerbate HTN?
- renin-angiotensin increases BP -> natriuresis and renal vascular injury -> increased renin which increases angiotensin II = HTN exacerbated
Mechanism HTN medication causes ischemic damage?
- rx can cause BP autoregulation curve to shift and respond at lower BP = ischemic damage
Q = P/R
- if reduce P with rx but R same = reduce flow = ischemia
autoregulaiton -> artery and arteriole vasodilation -> tissue perfusion maintained during rx HTN
Cause of severe essential HTN?
- often medication noncomplicance or acute drug withdrawal
Case of secondary HTN emergency/urgency?
- acute renal failure
- renovascular HTN (CHF + HTN)
- thyrotoxicosis
- medication-related (cocaine, MAOI + tyramine food)
- advanced CKD with volume overload
- pheochromocytoma
- pregnancy
What is likely dx with arm-arm different >20/10?
- aortic dissection
Investigations with HTN emergency/ urgency?
- CBC, lytes, urea, Cr, UA, troponin, LFTs
- CXR, ECG
- CT head if six HTN encephalopathy, stroke
- CT angio or TEE if sx aortic dissection
secondary causes
- toxicology, TSH, urine for metanephrines, b-hCG
Urgently drop BP in hypertensive urgency and emergency?
No - no evidence for aggressive drop with urgency
Drop aggressively and admit to ICU if emergency
How much do you want to reduce BP in HTN emergency?
- 25% in first hour
- gradually after first hour
risk organ hypoperfusino with sudden fall in BP
target 160/100 in initial 6-24h then add PO
Rx HTN emergency?
- labetalol first line (except CHF)
- nitroprusside (caution CKD and increased ICP)
- nitroglycerine (use in coronary schema and HF)
- hydralazine (use for eclampsia)
Define chronic HTN in pregnancy
- HTN prior to pregnancy
- before 20wk GA
- persists >12 wk postpartum
Define gestational HTN
- new onset HTN after 20wk GA
- without proteinuria
Define preeclampsia
- new HTN
- proteinuria (>300mg/24h) after 20wk GA
Define chronic HTN with superimposed preeclampsia
- new (or 2-3x increased) proteinuria, thrombocytopenia, elevated AST/ALT after 20wk GA
- in women with preexisting HTN before 20wk GA
Define transient HTN in pregnancy
- postpartum return to normal BP by 12wk postpartum
- increased risk of HTN in future pregnancies
What fails to invade the myometrial portion of the uterus in preeclampsia?
- cytotrophoblast
Where is earliest pathological change with preeclampsia?
uteroplacental circuation
What happens to vessels in placenta with preeclampsia?
- vessels narrow (tortuous vascular channels don’t develop) causing placental hypo perfusion
What happens in ischemic placenta?
- release of pro inflammatory cytokines and mediators of oxidative stress -> increase capillary permeability and activate endothelial cells and coagulation system
- > preeclampsia
Sx preeclampsia?
- visual change
- new headache
- epigastric or RUQ pain
- rapidly progressive peripheral edema
- rapid weight gain
What is indicated by rollover test (>15mmHg rise in dBP from left lateral decubitus to supine)?
Preeclampsia
Lab testing with pregnancy HTN?
- urinalysis: 24h urine protein, urine dip (>300 = preeclampsia)
- CBC + peripheral blood smear, Hgb, LDH, hepatoglobin (anemia, with schistocytes, increased LDH and low hepatoglobin = hemolysis from severe preeclampsia)
- platelet (low = severe preeclampsia)
- Cr, uric acid (elevated = severe preeclampsia)
- AST, ALT (elevated = severe preeclampsia)
- PT, PTT, fibrinogen (elevated PT, PTT, and low fibrinogen = severe preeclampsia resulting in DIC)
How do you assess fetus with maternal HTN?
- NST or BPP
Management HTN pregnancy?
chronic - anti-HTN
gestational - antiHTN (BP >160/110); fetal well being assessed; deliver if term
preeclampsia- delivery (definitive tx)
- fetal well-being and lung maturity: betamethasone 12mg IM x2 q12h if <34wk GA
- anticonvulsant - during labor, planned delivery or corticosteroid administration -> Magnesium sulphate 4-6g IV over 20min then 2g/h infusion
- antiHTN - often avoided, may alter uteroplacental blood flow
Safe anti-HTN in pregnancy
- labetalol (or other beta-blocker except atenolol)
- methyldopa (mild, s/e common)
CI
- ACEI/ ARBS
- aldosterone antagonist
- > fetal renal abnormalities and death
What is the inability of the heart to supply the circulatory needs of the body or the ability to do so only at higher than normal filing pressures?
heart failure
Systolic vs. diastolic HF?
- low LV ejection fraction in systolic HF
Low output vs. high output HF?
- low BP, organ hypo perfusion in low output
Congestive vs. dry HF?
- pulmonary edema, orthopnea, ascites, leg deem in congestive
Left vs. right sided HF
- pulmonary edema in left sided
- ascites, leg edema in right sided
Acute decompensated vs. chronic HF
- rapid (<2wk) sx progression in acute
Causes of mortality with HF?
- arrhythmia 40%
- worsening HF 40%
- other 20%
Is ischemic or HTN most common cause of HF?
- ischemic (prior MI or severe CAD) is most common cause
- HTN is second most common cause
Sx HF
- SOB
- fatigue
- orthopnea
- PND
- peripheral edema (leg edema, ascites)
Investigation HF
- CBC, lytes, Cr, transferrin saturation (serum iron/ TIBC), ferritin, TSH
- ECG
- CXR
- transthroacic echocardiogram
- B-type natriuretic peptide (BNP) or NT-proBNP
Tx wet and warm HF
- diurectics
- vasodilators (IV nitroglycerine or nitropatch)
Tx dry and warm HF (well compensated)
- optimize chronic HF therapies (incl BB)
Tx dry and cold HF (over diuresis)
- reduce/hold diuretic
- carful volume replacement
Tx wet and cold HF (advanced)
- inotropes
+/- invasive hemodynamic monitoring (PA catheter) - philosophy of care of transplant assessment
Do increased perfusion and increased congestion result in wet and warm HF or wet and cold HF?
wet and warm
Increased perfusion and reduced congestion = _ HF?
dry and warm
Increased congestion and reduced perfusion = _ HF?
wet and cold
Tx chronic HF?
- ACEI if LVEF <40% (ARB if ACEI intolerant or hydralazine/ isosorbide denitrate)
- beta blocker if LVEF <40%
- aldosterone antagonist (spironolactone) if NYHA II-IV symptoms, LVEF <35%
life-prolonging devices (LVEF <35% with medical rx)?
- cardiac resynchronization therapy (prolonged QRS)
- implantable cardioverter defibrillator
+/- digoxin
treat comorbidities (HTN, lipids, DM, etc)
vaccinate - yearly influenza, q5yr S. pneumonia
Classification of:
- enalapril
- lisinopril
- perindopril
- ramipril
ACEI
Classification of:
- bisoprolol
- carvedilol
- metoprolol
B-blocker
Classification of:
- spironolactone
- eplerenone
Aldosterone antagonist
Classification of:
- candesartan
- valsartan
ARB
Classification of:
- hydralazine
Vasodilator
Classification of:
- verapamil
- diltiazam
Non-DHP CCB
cardiac effect
Classification of:
- nifedipine
- amlodipine
DHP CCB
vascular > cardiac effect
NYHA functional classification of HF
- limitation of physical activity
- degree of comfort at rest
- sx with ordinary physical activity
Class I-IV
What is a physiologic state of overwhelming reduction in systemic tissue perfusion leading to a change in tissue O2? What can result?
Hypotension
- reversible at early stage
Cellular O2 deprivation -> cellular hypoxia
- ion pump dysfunction across cell membrane
- intracellular edema
- intracellular contents leak into extracellular space
- intracellular pH derangement
Causal conditions of hypotension?
Distributive (reduced SVR)
- sepsis, anaphylaxis, other
Reduced CO (increased SVR)
- hypovolemia
- cardiac dysfunction -> intrinsic vs. extrinsic (obstructive)
What is Beck’s triad?
- muffled heart sounds
- jugular venous distention
- hypotension
- > cardiac tamponade (+ pulses paradoxus)
5 common features of shock?
- hypotension (sBP <90 or drop >40 in sBP)
- cool, clammy skin (except distributive shock)
- oliguria (<0.5mL/kg/h)
- change in mental status (agitation -> confusion -> obtundation)
- metabolic acidosis
other: tachycardia, orthostatic hypotension, poor skin turgor, reduced sweat, dry mucous membranes
Hypotension workup
- CBC, lytes, LFT, Cr clearance, amylase/lipase, fibrinogen degradation product, lactate, cardiac enzymes, ABG, toxicology, CXR, ECHO, EKG, troponin, pro-BNP, UA
Acute tx hypotension/shock
ABCs, airway, 100% O2, two large bore IVs
- Trandeleberg position to increase venous return, cerebral profusion
- automatic BP monitor, pulse O2, cardiac monitoring
- dx cause of shock
- ICU admission if IV vasopressors needed or refractory hypoTN
Dx
- dry conjunctiva and mucous membrane
- reduced JVP
- tachycardia
- tachypnea, Kussmaul breathing
- abdo tender, distended, no bowel sounds, pulsatile masses
- cold clammy skin
- agitation, confusion, delirium, obtunded, coma
- bright red blood per rectum, melena, occult blood in stool
Workup? Causes?
Hypovolemic shock
CBC, lytes, BUN, Cr, amylase, lipase, lactate
AXR, UA
Hemorrhage, third space loss, GI fluid loss
Dx
- scleral icterus
- increased JVP, pulsus parvus et tardus (AS)
- arrhythmia, tachy/bradycardia, S3 gallop, ventricular heave, murmur, rub, distant heart sounds, pulsus paradoxus
- crackles (CHF), no breath sounds, rub
- distended abdomen (hepatic congestion)
- agitation, confusion, delirium, obtundation, coma
- hemorrhoids
Workup? Causes?
Cardiogenic shock
CBC, lytes, BUN, Cr, D-dimer, cardiac enzymes, ABG, toxicology screen
CXR, EKG, PCWP in ICU
Ischemic/dilated cardiomyopathy, arrhythmia, mechanical (valvular - AS), PE, TP, tamponade
Dx
- flushy/ swollen face, angioedema
- reduced JVP, delayed carotid, meningeal sign
- tachycardia
- shallow breaths
- abdo tenderness, distension, rebound tenderness, absent bowel sounds, pulsatile masses
- skin warm, hyperaemic, rashes, petechia, urticarial, cellulitis
- agitation, confusion, delirium, obtundation, coma, spinal cord injury
- reduced anal tone
Workup? Causes?
Distributive shock
CBC with differential, lytes, lactate, toxicology screen, amylase, lipase, blood culture
spinal X-ray, EKG, ECHO
cardiac enzymes, TSH, procalcitonin
Sepsis, anaphylaxis, neurogenic, spinal shock
Variable to assess preload?
PCWP
Variable to assess pump function?
CO
Variable to assess after load?
SVR
Variable to assess tissue perfusion?
mixed venous O2 saturation
Targets for tx hypovolemic shock (non-hemorrhagic and hemorrhagic)?
nonhemorrhagic - bolus 1-2L crystalloid (NS, RL) sBP >90 MAP >60 urine output >0.5mL/kg/h
hemorrhagic
- transfuse + crystalloid
- hemoglobin >80-90 (Hat 30-35%)
Acidosis, hypothermia and hypocalcemia can happen with what treatment?
- massive transfusion
Septic shock management
- bolus 2-6L crystalloid/colloid to target CVP 8-12mmHg
- vasoactive agents for sBP>90 and MAP >65
- organ perfusion: RBC transfusion and inotropes pro
- empiric broad spectrum abx ASAP (pip-taco, imipenem)
Management neurogenic shock?
- methylprednisolone 30mg/kg over 15min then infusion 5.4 mg/kg/h x24h
Management carcinogenic shock?
- underlying cause
- optimize volume status
- add/substitute inotropes for hypo perfusion
- treat arrhythmias
Vasopressor or inotrope? Act on CO/ SVR/ HR?
NE
vasopressor
CO +
SVR +++
HR +
alpha adrenergic agonist, mild B1 adrenergic agonist
Vasopressor or inotrope? Act on CO/ SVR/ HR?
Dopamine
vasopressor
CO ++
SVR +++ (low dose can decrease)
HR +++
dopamine agonist and B1 agonist at intermediate-high doses
Vasopressor or inotrope? Act on CO/ SVR/ HR?
Phenylephrine
vasopressor
CO -
SVR +++
HR -
pure alpha adrenergic agonist
Vasopressor or inotrope? Act on CO/ SVR/ HR?
Vasopressin
vasopressor
CO -
SVR ++
HR -
ADH analog - vasoconstriction
Vasopressor or inotrope? Act on CO/ SVR/ HR?
Epinephrine
vasopressor
CO +++
SVR +++
HR +++
alpha and beta adrenergic agonist
Vasopressor or inotrope? Act on CO/ SVR/ HR?
dobutamine
inotrope
CO +++
SVR -
HR ++
strong beta1 adrenergic agonist
Vasopressor or inotrope? Act on CO/ SVR/ HR?
milrinone
inotrope
CO +++
SVR decreased
HR +
phosphodiesterase (PD3) inhibitor with positive inotropic and vasodilatory action
Define anaphylaxis
IgE mediated, immediate hypersensitive allergic reaction to protein substances
Ag exposure cascade
- mast cell -> stimulation by cell-bound IgE cross linking with Ag -> degranulation
- complement proteins -> anaphylatoxins C3a, C4a, C5a -> degranulation
- arachidonic acid -> precursor to PGs, prostacyclin, thromboxjnes and LTs -> degranulation
degranulation = released mediators from mast cells and basophils promote synthesis of other active substances
Are these mediators initial or late?
- histamine, tryplase, PGs, LTs, platelet activating factor
initial minutes
Are these mediators initial or late?
- cytokines (IL4, IL13, TNF)
hours later - released by same cells as early mediators
What is an anaphylactoid reaction?
- non IgE mediated
- direct release of mediators from mast cells
- immune complex/complement mediated
- arachidonic acid metabolism modulator
- multiple/ unknown mechanisms
Management anaphylactic reaction?
- ABCs
- IV access, O2, cardiac monitoring, pulse O2
- intubate if stridor, altered mental status, resp arrest
- hypotension - 1-2L bolus +/- vasopressors
- epinephrine 0.3-0.5mg IM 5min
- antihistamine (diphenhydramine) and IV corticosteroid (methylprednisolone)
+/- H2 receptor blocker (ranitidine) - mild bronchospasm = nebulizer salbutamol (2.5-5mg)
observe 8hr -> biphasic reaction
What is test to sx anaphylaxis?
Clinical diagnosis! Based on 1/3 criteria - acute onset - 2+ sx after exposure to Ag - reduced BP
Pathophys of angina?
MOD exceeds myocardial O2 supply -> stimulation of chemosensitive and mechanoreceptive receptors of unmyelinated cardiac nerve cells -> angina
WHO MI criteria?
2 out of 3:
- chest pain
- ECG-ST changes, T wave inversions
- increased cardiac enzymes
What causes downsloping or horizontal ST depression?
ischemia
What causes ST elevation or T wave inversion?
infarction
Likely dx?
- substernal pressure (+/- radiation to neck/ jaw/ shoulders/ L arm)
- with exertion/ stress
- relieved with rest (5-10min) or nitroglycerin (immediate)
typical angina
2 out of 3 sx = atypical angina
0 or 1 out of 3 = non cardiac pain
What can you hear on cardiac exam with angina?
S4 with chest pain due to impaired myocardial relaxation from schema
Angina workup
- resting ECG (may see ST)
- depression (ischemia) or Q waves
- cardiac enzymes - negative
- exercise stress test
Positive exercise stress test?
> 1mm ST depression with exercise (85% age-predicted maximal [220-age]HR) = +
What are causes of increased MOD (e.g. causing chest pain)?
- increased HR
- increased myocardial contractility
- increased myocardial work -> increased MOD
- increased after load + increased preload -> increased wall tension
Dx?
- new or rapidly worsening pattern of typical angina that severely limits usual activities or occurs at rest
unstable angina
Dx?
- sudden, severe chest pain pressure lasting >30min and associated with diaphoresis, nausea, malaise, sense of impending doom
NSTEMI/STEMI
Why can you hear new systolic murmur with ACS?
- in MI = mitral regurgitation due to papillary muscle dysfunction
ACS workup
- ECG
- cardiac enzymes
Dx?
- very severe, sudden onset sharp/tearing pain in chest and/ or back (mid scapular)
- HTN or hypotension
- asymmetric BP/ pulses in upper extremities (>20 mmHg difference)
aortic dissection
hypotension from tamponade or AI in ascending aortic dissection
Workup aortic dissection
CXR - widened mediastinum, pleural effusion
Contrast CT - identifies true lumen from false lumen (no contrast in false lumen)
TEE - assess pericardium, AI and safe in renal failure (no contrast)
MRI - gold standard, time consuming
Dx
- sudden, pleuritic pain and shortness of breath
- often unilateral
- unilateral reduced breath sounds on exam with hyper-resonance on percussion
Imaging?
tension pneumothorax
CXR - mediastinal shift, distinct pleural lining -> confirm with expiratory views
Dx - sudden, pleuritic pain with severe SOB \+/- syncope - tachypnea, tachycardia - may hear loud S2, feel parasternal heave or new RUSB systolic murmur
PE
- S2= pulmonic component
- parasternal heave = RV pressure overload
- RUSB systolic murmur = pulmonary insufficiency from pulmonary HTN = Graham Steel murmur
PE workup?
- d-dimer: high false positive rate
- ECG: sinus tachycardia +/- t wave inversion in V1-V3 from RV strain (S1, Q3, T3) pattern
- ABG: hypoxemia with A-a gradient
- Imaging: V/Q scan, contact CT chest, angiogram is confirmatory
Define aortic dissection
tear in aortic intima = blood accumulation in false lumen
Causes of pericarditis
- infectious
- post-MI (acute vs. subacute -> subacute is autoimmune aka Dressler syndrome)
- uremic
- CT disease
Life threatening causes of chest pain?
- angina
- ACS
- aortic dissection
- tension pneumo
- PE
Management stable angina?
- Nitroglycerine 0.4mg SL q5min x3
- ASA 81mg
- high dose statin (Lipitor, Crestor)
- antianginal medications: b-blocker (1st line), CCBs, long acting nitrates
- lifestyle
- stress test
- high risk = coronary angiography
Does PCI improve MI occurrence or death or help with symptom relief of stable angina?
- symptom relief
- does not prevent MI or death in stable angina
Treatment offered to pt with prognosis-altering CAD, pt refractory to medication?
CABG
What is similar in all cases of ACS re: pathophys?
- intra-coronary thrombosis
UA vs. NSTEMI vs. STEMI
UA
- sub-total occlusion by intra-coronary thrombus
- myocardial ischemia but no infarction
NSTEMI
- subtotal occlusion by intra-coronary thrombus
- myocardial infarction (non-transmural)
STEMI
- total occlusion by intra-coronary thrombus
- large, transmural infarction (if flow not immediately restored)
Management ACS
- stabilize and monitor: O2, IV access, cardiac monitoring, ASA 160mg PO, 12lead EKG
- SL nitroglycerine or IV; morphine for pain
- serial cardiac enzymes (repeat 6h)
Management UA/NSTEMI
medical + RF tx
- ASA 160mg load then 81mg daily
- anti platelet (clopidogrel) x1yr
- anticoagulant (LMWH unless GFR <30) x48-72h
- high dose statin (crestor, lipitor) x life
- b-blocker (metoprolol, bisoprolol) x1yr or longer
- ACEI (ramipril, lisinopril, coversly) x1yr or longer
- revascularize with PCI or CABG
- invasive - coronary angiography/ echo
- conservative - stress test/ echo, with coronary angiography if high risk stress test or EF <40%
TIMI risk score for UA/NSTEMI
age >65 = 1 >CAD RF = 1 Known CAD = 1 ASA in past 7d = 1 Recent severe angina = 1 troponin + = 1 ST deviation >0.5mm = 1
risk score /7
STEMI management
- urgent repercussion with primary PCI or thrombolysis (high risk from MI = PCI; high risk bleeding = PCI; time delay >60-90min to cath lab favours thrombolysis)
- dual anti platelet (ASA + clopidogrel) and anticoagulant (LMWH, heparin)
- ongoing cardiac monitoring in CCU for arrhythmia, recurrent CP
- coronary angiography in next 6-24h if thrombolysis; if unsuccessful then emergency rescue PCI
- optimize medical therapy and RFs
Aortic dissection types
De Bakey
- type I - proximal dissection
- type II - proximal dissection (isolated)
- type III - distal dissection
Stanford
- type A = proximal dissection
- type B = distal dissection
proximal dissection - surgical root repalcement
distal dissection = medical management
Management aortic dissection
- medical therapy, continuous BP monitoring in ICU
- IV anti-HTN
- HR aggressively controlled with b-blockers to reduce shear stress on tidal tear
- pain control with morphine
Dx
- pulses paradoxus
- tachycardia
- hypotension
- muffled heart sounds
- bottle shaped heart on CXR
pericardial tamponade
Management Pericarditis
r/o pericardial tamponade and secondary causes
- echocardiogram to assess size of effusion
- viral/idiopathic: NSAIDs, colchicine, corticosteroids (if refractory)
- large effusion/tamponade: pericardiocentesis
- recurrent large effusion/ tamponade: pericardial window
What is most common rhythm in sudden cardiac death?
VF
Management of cardiac arrest (in hospital)
- responsiveness/ confirm lack of pulse
- call for help
- BLS
- check heart rhythm, ensure IV access
- ACLS guidelines
Management asystole/PEA
- CPR
- epinephrine 1mg IV q3-5min
5Hs + Ts (reversible causes)
- hypoxia
- hypo/hyperK
- hypo/hyperglycemia
- hypovolemia
- hypothermia
- H+ (acidosis)
- tension pneumo
- tamponade
- toxins
- thromboembolism (PE)
- thrombosis (MI)
Management VF/ pulseless VT
- defibrillate 200J (biphasic) WITH CPR
- epinephrine 1mg IV q3-5min
- amiodarone 300mg IV if VF/ pulseless VT persists/ returns after 3 shocks
consider hypoMg and hypoK
Management stable severe tachycardia (VT or SVT)
- sx hypoperfusion -> present = cardioversion
- 12lead ECG if stable
- adenosine if regular HR
- irregular HR and a fib likely then give b-blocker, CCB or digoxin
Management severe bradycardia
- sx hypo perfusion -> atropine 1mg if present
- transcutaneous pa king or IV dopamine/ epinephrine (stimulate escape rhythm)
consider hyperK
Is mild therapeutic hypothermia a treatment option post-arrest?
Yes
- if GCS <14 and not rapidly improving, downtime 10min -1h, VT or VF initial rhythm or no CI to cooling
- > improves long term neurologic outcomes
Define syncope
- transient loss of consciousness due to global cerebral hypoperfusion
Equation for CO
CO = HR x SV
What 3 main factors determines SV?
- proload
- afterload
- contractility
What is ventricular volume at end of diastole?
Preload
- increased preload = increased SV
What is Starling law of heart?
- energy of contraction of muscle is proportional to initial length of muscle fiber
What is resistance to vernacular ejection?
Afterload
- caused by resistance to flow in systemic circulation
= SVR
What refers to degree of active constriction of vessels (mainly veins) which affects return of blood to the heart?
vascular capacitance
Increacred intravascular volume increases what?
increases vascular capacitance which increases preload
Ddx syncope
neurocardiogenic (most common, often benign)
- vasovagal
- situational
- carotid sinus hypersensitivity
- orthostatic
cardiac
- bradyarrhythmia
- tachyarrhythmia
- obstructive
psychogenic
- hyperventilation, panic disorder, malingering
cerebrovascular
- vertebrobasilar insufficiency, subclavian steal syndrome, carotid artery disease, bilateral TIA
pseudosyncope (no cerebral hypo perfusion)
- seizure
- hypoglycaemia
- hypoxia
- drug intoxication
Describe auto regulation of cerebral blood flow
increased vasodilators -> reduced cerebral arteriolar resistance -> reestablish cerebral blood flow
constriction of systemic vasculature of skin, splanchnic bed, muscles -> diverts blood to brain
increased sympathetic output -> increased contractility and peripheral resistance -> increased arterial pressure
Workup neuro causes syncope?
- heat CT
- EEG
- cerebral flow studies (Doppler)
Workup sudden dyspnea, risk PE with syncope?
V/Q scan
spiral CT
-> anticoagulate
Workup cardiac cause of syncope?
- CXR
- CCU admission
- echocardiogram
- cardiac enzymes (r/o MI)
- perfusion test
- functional assessment
+/- CTA
tx re: etiology
Workup unexplained syncope with abnormal EKG, hx of CAD?
- holter monitor
- loop monitor
- electrophysiology study
- tilt table test
- ECHO
- consider cardiology consult/EP, psychiatry
Standard investigation syncope?
ECG
CBC, lytes, urea, glucose/ chemstrip, Cr
- postural BP
Where are central pulses assessed? What are they assessed for?
- carotid and/or femoral arteries
- palpated for amplitude, contour, upstroke
Where are peripheral pulses assessed?
- radial, brachial, popliteal, posterior tibialis, dorsalis pedis
Ddx peripheral pulse deficit?
- dissection
- aortic coarctation
- peripheral vascular disease
What is laminar flow re: pulses?
- laminar flow aka streamline flow occurs when a fluid flows in parallel layers, with no disruption between the layers
- no current perpendicular to the direction of flow
Is laminar flow high or low momentum of diffusion? Convection? Pressure and velocity?
High momentum of diffusion
Low momentum of convection
Constant pressure and velocity
What is flow regime characterized by chaotic, stochastic property changes?
Turbulent flow
- includes low momentum diffusion, high momentum convection, and rapid variation of pressure and velocity
Types of abnormal pulses?
- small and weak
- large and bounding
- Bisferiens pulses
- pulses alternans
Does increase velocity cause laminar or turbulent flow?
- turbulent flow
- very low speed = blood flow laminar
- increase in velocity (narrowing blood vessels or increase flow rate) = turbulent flow
Ddx unequal or delayed pulses
- obstructive arterial disease (atherosclerosis)
- aortic disease
- Takayasu arteritis
Ddx rhythm irregular/ too fast/ too slow
- tachycardia
- bradycardia
- arrhythmia
Dx
- alternating weak and strong pulses with fixed cycle length
- present in systolic dysfunction/low EF
Pulses alternans
Dx
- biphasic pulse
- present in: AS plus AI, severe AI, HOCM
pulses bisferiens
Dx
- double peak, with weaker second beat
- present in: low arterial pressure/ PVR, very low EF, post AVR
dicrotic pulse
Dx
- slow rising, typically with an ascending notch
- present in aortic stenosis
Anacrotic pulse/ pulsus parvus et tardus
Dx
- rapid pulse then sudden collapse
- present in aortic insufficiency
Corrigan pulse (water hammer/ collapsing)
Dx
- exaggerated inspiratory decrease in arterial pulse amplitude
- present in cardiac tamponade, asthma, hypovolemic shock
Pulsus paradoxus
What is ankle-brachial index?
- grading of peripheral vascular disease
++ calcified vessels
1-1.3 normal ABI
low = peripheral vascular disease
What does brachio-femoral delay indicate?
coarctation of aorta
Define dyslipidemia
- one of more alterations in serum lipids (elevated fasting TC, LDL, TG, apoB, low HDL)
- increase risk of CVD -> atherosclerosis
What elevates LDL levels?
increased VLDL or reduced LDL catabolism
What does reverse cholesterol transport?
HDL
What changes occur in atherosclerosis?
- changes in blood vessel wall -> lipid deposition and cell proliferation
= narrow lumen and thrombus formation
High risk (FRS >20%) management and target?
Treatment
LDL <2mmol/L or >50% reduction win LDL-C
apoB <0.8g/L
Moderate risk (FRS 10-19%) management and target?
Treatment if LDL-C <3.5 mmol/L, TC/HDL-C ratio >5, hs-CRP >2mg/L (men >50, women >60)
Target <2mmol/L LDL or >50% reduction LDL-C
apo-B <0.8g/L
Low risk (FRS <10%) management and target?
Treatment if LDL-C <5mmol/L
Target >50% reduction in LDL-C
Who gets a screening fasting lipid profile?
- men >40yr and postmenopausal women (or >50yr)
- kids with fam hx hypercholesterolemia or chylomicronemia
- adults with RF: DM, smoker, HTN. BMI >27, family history of premature CAD, signs of hyperlipidemia, evidence of atherosclerosis, CT disease (RA, SLE, psoriasis), HIV on HAART, GFR <60, erectile dysfunction
What provides 10yr risk of CAD events based on RF (age, gender, TC, HDL-C, sBP, smoker, DM)?
Framingham risk score
What is similar to FRS but includes high-sensitivity CRP and family history of parent having MI <60yr?
Reynold’s risk score
Key points on physical exam for pt with hyperlipidemia?
- tendon xanthomas (high LDL-C)
- eruptive xanthomas (high TG-C)
- xanthelasma
- corneal arcus (ring-like appearance on cornea)
Drugs to treat lipid abnormalities?
HMG-CoA (simvastatin)
- reduces LDL
- inhibits cholesterol synthesis, up regulates LDL receptors
- s/e myopathy and hepatic dysfunction
Fibrates (gemfibrozil)
- reduce Tg through VLDL
- inhibits VLDL production
- s/e nausea, abdo discomfort, gallstone, myopathy
Niacin
- reduce LDL through VLDL
- inhibits VLDL production
- s/e flushing, hyperglycaemia, pruritus, gout, elevated liver function enzymes
Bile-acid binding resins (cholestyramine)
- depletes bile acids, up regulates LDL receptors
- s/e constipation, abdo discomfort, may bind other rx
Inhibitors of intestinal sterol absorption (ezetimibe)
- reduced LDL by preventing dietary cholesterol absorption
- s/e reversible impairment in hepatic function
Mitral stenosis, prosthetic mitral valve, short PR interval -> causes loud or soft S1 or S2?
Loud S1
Mitral regurgitation, COPD, long PR interval -> causes loud or soft S1 or S2?
Soft S1
HTN, aortic sclerosis, prosthetic aortic valve -> causes loud or soft S1 or S2?
Loud S2
Hypotension, severe aortic stenosis, HF/ low cardiac output -> causes loud or soft S1 or S2?
Soft S2
What causes split S2 (often heard LUSB)?
- normal (physiologic) due to pulmonary valve closure (p2) being slightly delayed after aortic closure (a2) during inspiration
- exaggerated:
delayed P2 with RBBB, PE;
early A2 with VSD, mitral regurgitation - fixed, split S2 with ASD
- paradoxical split (P2 before A2): LBBB, RV pacemaker
Etiologies S3?
low pitched sound just after S2 caused by large volume of blood entering ventricle in early diastole
- dilated cardiomyopathy with volume overload
- mitral/tricuspid regurgitation
- occasionally young athlete (hyper dynamic hearts)
Etiologies S4?
low pitched sound just before S1, caused by late filling into a stuff ventricle
- left ventricular hypertrophy (from HTN or hypertrophic cardiomyopathy)
- ischemia
- aortic stenosis
What is a high pitched sound in early systole (after S1) heard in pt with bicuspid aortic (or pulmonic) valve?
ejection sound
What is high pitched should in early diastole (after S1) heard in pt with rheumatic mitral (or tricuspid) disease?
opening sound
What is high pitched sound in mid-systole, caused by bowing of a myxomatous mitral valve, heard in pt with mitral valve prolapse?
mid-systolic click
What is classically a biphasic or triphasic scratching sound with systolic and diastolic components, caused by pericardial inflammation and rubbing between the visceral and parietal pericardium (best heard when pt leaning forward)?
Pericardial friction rub
What is a sound caused by turbulent blood flow, which could be occurring between chambers of the heart or across narrowed arterial vessels?
Murmur
Grade a murmur
Graded according to intensity (loudness)
Grade I - very faint, heard only when tuned in
Grade II - faint but can be identified after placing stethoscope on chest
Grade III - moderately loud
Grave IV - loud with palpable thrill
Grade V - very loud, with thrill, may be heard with stethoscope partly off chest
Grade VI - very loud, with thrill, heard without stethoscope
Are diastolic murmurs often innocent or pathologic?
Pathologic
What cardiac issues is Marfan associated with?
MVP
aortic regurgitation
What cardiac issue is Down syndrome associated with?
AVSD
Where is it best to palpate for systolic heave?
Left parasternal area - typically in right ventricular enlargement or pulmonary HTN
What and where is the apex beat?
- most inferolateral cardiac impulse palpated on chest
- should be in 4th intercostal space, in left midclavicular line
displaced if inferior or lateral to this = left ventricular enlargement (LVH also noted by sustained impulse)
What produces S1?
mitral valve closes (and tricuspid valve)
What produces S2?
AV valve closure
How do you describe a murmur?
- intensity (loudness /6)
- timing (re: systolic/diastolic)
- shape (crescendo, decrescendo, holosystolic, etc)
- location (aortic, pulmonic, tricuspid, mitral area)
- radiation (carotids, apex, back)
- pitch (low = bell, high = diaphragm)
- quality (harsh, blowing, musical)
- dynamic maneuver (handgrip, valsalva)
Ddx mid systolic murmur
- AS
- Ao valve sclerosis
- PS
- increased semilunar blood flow
- innocent mid systolic murmur
Ddx later systolic murmur
- mitral valve prolapse
- tricuspid valve prolapse
- papillary muscle dysfunction
Ddx holosystolic murmur
- MR
- TR
- VSD
Ddx continuous murmur
PDA
Ddx early diastolic murmur
- AR
- PR
Ddx mid diastolic murmur
- MS
- TS
- atrial myxoma
Ddx late diastolic murmur?
- complete heart block
Workup murmur?
ECHO (for all new systolic murmurs >=3/6; all diastolic murmurs; all murmurs with other sx cardiac disease)
CXR
ECG
cardiac catheterization
cardiology consult for pathologic murmurs
Mitral stenosis
- etiology
- sx and physical exam
- investigations
- management
Rheumatic heart disease, claficiation of leaflets
Sx - malar flush, AF, CHF
- mid-diastolic rumbling after OS at apex
- loud P2
- OS after S2
- low pitch tapping apex beat, thrill
- LLD position = increased murmur
Inv
- ECHO
- R heart cath - measure pulmonary pressures, PCWP
- CXR - LA, LV enlargement
- ECG - P mitral +/- AF
Tx
- medical - b-blocker and diuretics
- anticoagulate pt in AF
- surgical - balloon valvoplasty
Mitral regurgitation
- etiology
- sx and physical exam
- investigations
- management
- myxomatous degeneration
- ischemic heart disease, infective endocarditis, rheumatic heart disease, dilatation of LV
Sx - CHF (SOB, fatigue, leg deem, pulmonary deem, orthopnea, PND)
- high pitch holosystolic murmur at apex, radiates to axilla
- laterally displaced apex beat, parasternal heave
- handgrip = increases
Inv
- ECHO - color doppler = back flow from LV to LA
- ECG - P mitral, LVH +/- AF
- CXR - LA, LV nelargement
- Cath - can quantify regurgitation with LV contrast
Tx
- acute/hypotensive: IABP and surgery
- normotensive: nitroprusside, ACEI, hyralazine
- anticoagulation if AF
- surgery - repair vs. replacement
Mitral valve prolapse
- etiology
- sx and physical exam
- investigations
- management
- myxomatous degeneration (genetic variants of fibrillar, elastin, collagen I and II)
f: m = 3:1
Sx - usually asx, may lead to MR
- mid-systolic click
- late systolic murmur
Inv
- ECHO - thickened prolapsing valve +/- mitral regurgitation anatomy, regurgitant flow
- ECG - PACs, PVCs
Tx
- no tx unless mitral regurgitation
Aortic stenosis
- etiology
- sx and physical exam
- investigations
- management
- calcification of aortic valve
- bicuspid aortic valve, rheumatic heart disease
Sx - angina, CHF, syncope/ SCD
- mid-systolic, crescendo-decrescendo murmur at LUSB, radiating to carotids
- weak pulse with slow upstroke (pulsus parvus and tardus)
- soft S2
- sustained apical beat
Inv
- ECHO - measure transoartic gradient
- Cath - measure pullback gradient across aortic valve
- ECG: LVH
- CXR - cardiomegaly
Tx
- avoid after load reducers (fixed after load from AS) and b-blockers (fixed stroke volume, may depend on HR for CO)
- surgery - valve replacement (transcatheter valve if poor surgical candidate)
Hypertrophic cardiomyopathy
- etiology
- sx and physical exam
- investigations
- management
- mutation in genes that code for characteristics of heart muscle
sx- angina, CHF, syncope/SCD
- mid-systolic crescendo-decrescendo murmur at LUSB
- biphasic pulse
- increases with standing (from squat)
Inv
- ECHO - severe global or regional hypertrophy
- ECG - LVH, Q waves, T wave abnormalities
- Holter, exercise stress test - risk stratify
Tx
- medical - b-blocker, no competitive sports
- anticoagulant - if AF
- ICD if high risk SCD
- surgery - septal ablation (EtOH) or myomectomy if refractory sx
Aortic insufficiency
- etiology
- sx and physical exam
- investigations
- management
- aortic root dilatation (Marfan, HTN, idiopathic)
- bicuspid aortic valve, aortic dissection, syphilis
sx- angina, CHF
- 3 murmurs: high-pitched, blowing decrescendo diastolic murmur at LLSB; mid-systolic murmur at base; Austin Flint - low pitched
Inv
- ECHO - regurgitant flow from aorta to LV, LV dilated
- ECG - LAD, LVH
- Cath - quantity regurgitation with aortic root contrast injection
Tx
- acute/ hypotensive: inotropes (dobutamine) +/- vasodilators (nitroprusside)
- chronic: b-blockers (Marfan), vasodilators (hydralazine, nifedipine, ACEI), diuretics +/- digoxin
- surgery - valve and/or root replacement
Define palpitations
unpleasant awareness of the heartbeat; rapid, forceful or irregular
What is normal SA pacemaker function and impulse propagation?
- spontaneous depol of SA node -> atrial depol (P wave) -> impulse propagates slowing through AV node with normal delay in reaching His bundle (PR segment) -> impulse travels rapidly vis Purkinje fibres of bundle branches, reaching ventricular myocardium
Mechanism of arrhythmia?
- reentry (perpetual loop/ short circuit is formed, often due to additional conduction pathway)
- automaticity (focus other than SA node)
- triggered activity/ after depolarizations (oscillations in membrane voltage after preceding impulse, which can trigger depol)
Ddx palpitations
Cardiac
- arrhythmia - SVT, PACs, PVCs
- structural heart disease
Psych
- anxiety, panic, stress
Endocrine
- hyperthyroidism, hypoglycaemia, pheochromocytoma
Medications
- caffeine, nicotine, sympathomimetics
High output state
- anemia, pregnancy, fever, exercise, Paget disease
How does parasympathetic stimulation reduce pacemaker current to reduce HR?
via vagus nerve
How does sympathetic stimulation increase SA node automaticity and increase rate of pacemaker depol to increase HR?
b1 adrenergic receptor stimulation
Investigations for palpitations?
Vitals
Cardiac exam
ECG - rhythm strips and 12 lead
Labs - CBC, lytes, TSH (r/o anemia, hypo/hyperK, hyperthyroidism)
+/- trans thoracic echo to r/o structural heart disease
- ambulatory monitoring if dx unclear to capture event
Dx, acute/long-term rx?
Unstable arrhythmia
VT, VF, rarely AF/SVT
acute
- defibrillation or cardioversion
long-term
- AICD for unstable VT or VF
Acute/long-term rx?
VT (stable), SVT
12-lead ECG then cardioversion
long-term
- cardiologist tx - meds, RF ablation, ICD
Acute/long-term rx?
- sinus tachycardia
treat underlying cause
long-term
- n/a
Acute/long-term rx?
ectopic atrial tachycardia
b-blocker or CCB
long-term
- b-blocker or CCB
- RF ablation if meds fail
Acute/long-term rx?
PSVT (AVNRT or AVRT)
- vagal maneuvers, adenosine
long-term
- b-blocker, CCB if no accessory pathway (delta wave)
- RF ablation
Acute/long-term rx?
atrial fibrillation
b-blocker, CCB, digoxin
- rarely cardio version if unstable
long-term
- anticoagulation for most
- rate control: b-blockers, CCB, digoxin
- rhythm control: antiarrhythmics +/- RF ablation
Acute/long-term rx?
atrial flutter
- b-blocker, CCB, digoxin
long-term
- b-blocker, CCB, +/- digoxin
- RF ablation often needed as HR control can be difficult
Acute/long-term rx?
- multifocal atrial tachycardia
- b-blocker or CCB
long-term
- b-blocker or CCB
- RF ablation of AV node + pacemaker if meds fail
Is ventricular tachyarrhytmia narrow or wide QRS complex?
Wide
- narrow = SVT
Ddx SVT with regular P wave morphology
- sinus tach, sinoatrial node reentrant tacky if upright P before QRS
- AT if no sinus before QRS
- AVNRT if no P
- AVNRT, AVRT, non paroxysmal junctional tachycardia if retrograde P waves
- AFL if F waves at 300 bpm
Ddx SVT with irregular P wave morphology
- AFL if F waves at 300 bpm
- no P or fibrillation = AF
- multifocal atrial tachycardia if >3 morphology
Ddx ventricular tachyarrhytmia
- PVC if QRS >12s, bizarre QRS morphology or LBBB/ RBBB pattern
- VT if 3+ consecutive ventricular rate >100/min; rate 120-300 bpm; AV dissociation, capture beats, fusion beats, L axis deviation, mono/biphasic QRS in V1 with RBBB; concordance V1-V6
- VF if no true QRS complex
What can cause fatigue/palpitations, HF (HR >110 persistently), stroke?
A fib
When acute cardioversion be done for AF?
Yes, if <48hr
- when >48h or uncertain onset then anticoagulant x3-4wk or transesophageal echo (visualize LAA) to prevent CVA
- unless urgently required, i.e. patient unstable
Is rate or rhythm control better for long-term AF management?
Both equal for risk of death or stroke
When do you anticoagulant pt with A fib?
CHADS2-Vasc score >=2 (men with scores >=1)
- daily ASA if pt not receiving chronic anticoagulant
What is CHADS2 score? What does it estimate?
Estimate yearly CVA risk in AF
CHF = 1 HTN = 1 Age >75yr = 1 DM = 1 Hx stroke = 2
What is CHADS2-Vasc score? What does it estimate?
Estimates yearly CVA risk in AF
CHF = 1 HTN = 1 Age 65-75 = 1 Age >75 = 2 DM = 1 Stroke (or TIA) = 2 Vascular disease (MI, PAD, aortic plaque) = 1 Sex (female) = 1
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