Cardiology, Mhu, Mbbs Iv

Front 1

AF causes; structurally normal

Back 1

- Thyroid

- Alcohol binge (Associated with cytochrome P450 and free radical production) - If <48 hours duration, cardiovert

- Familial

- Lone AF

Front 2

AF causes; structurally abnormal

Back 2

Incidence increases with age

1. Atrial distension (most common):

a. IHD b. Valvular heart disease c. OSA

?secondary to an inflammatory condition involving myeloperoxidase

Front 3

AF hx

Back 3

- More SOB and lethargic than previously

- If very rapid AF, more CHF symptoms

- Lifetime risk over the age of 40 years is ~25%.

Front 4

AF PE

Back 4

- Irregular pulse

- Hyperthyroid s/s

- Mitral valve stenosis

 Classic cause of AF - due to atrial stretch; often secondary to RHF

 Loud S1 heard with the bell at the mitral area

 Malar flush/mitral facies

Front 5

Af complications

Back 5

Haemodynamic - AF affects ventricular filling and contraction rate

Thromboembolic - atrial clot formation

Front 6

AF haemodynamic changes

Back 6

3 main changes:

Pulse deficit

 Short diastolic filling time means some ventricular contractions are too weak to be perceived at the wrist=>Disparity of the heart rate at the apex by auscultation and to the wrist. Difference of <15bpm is reasonable.

Reduced stroke volume (fibrilliation=> dec atrial contribution to V filling)

Treppe phenomena HF, inc HR past a certain point is assoc. w decrease in contractility d/t saturation of the Na+Ca++ Exchange therefore rapid AF with concurrent systolic dysfunction → cause tachyarrhymia-induced cardiomyopathy

Front 7

AF tx

Back 7

- Rate control

- Cardioversion (for new AF): amioderone (SE: pulm fibrosis)

- Anticoag

- Ablation (75% effective)

- Treat aetiology

- AV blockers: (Some block potassium channels)

- Na channel block - B blockers - K chan block - CCB

Front 8

AF causes; Pirates

Back 8

P - Pulmonary embolism, pulmonary disease, post-operative Ischemic heart disease,

I - idiopathic (“lone atrial fibrillation”)

R - Rheumatic valvular disease (mitral stenosis or regurgitation)

A - Anaemia, alcohol (“holiday heart”), age, autonomic tone (vagal atrial fibrillation)

T - Thyroid disease (hyperthyroidism)

E - Elevated blood pressure (hypertension), electrocution

S - Sleep apnea, sepsis, surgery

Front 9

APO

Back 9

cardiac dysfunction=>elevated pulmonary venous pressure=>Inc capillary hydrostatic press =>accumulation of fluid with a low-protein content in the lung interstitium and alveoli

Front 10

APO causes

Back 10

- Imbalance of Starling forces

- Damage to the alveolar-capillary barrier

- Lymphatic obstruction

- Idiopathic mechanism

Front 11

APO complications

Back 11

- Respiratory failure

- Respiratory fatigue (lethargy, fatigue, diaphoresis, worsening anxiety)

- Cardiac arrythmia=>sudden cardiac death

Front 12

APO s/s

Back 12

Severe dyspnoea, distress, pallor, sweating, tachycardia and poorperipheral perfusion.

Delirium and falls in the elderly

Front 13

Diastolic heart failure

Back 13

Defined as an LVEF >40%.

Diastolic - LV filling abnormal.

- Ventricles can’t relax therefore fillinadequately and Hypertrophy (concentric).

- LVEF maintained. Diastolic dysfunction is characteristic of both Hypertrophic CM and restrictive cardiomyopathy (RCM)

Front 14

Systolic Heart Failure

Back 14

Defined as an LVEF <40%

Dec. in myocardial contractility => dec. LV EF.

CO maintained by:

- LV enlargement=>inc. Stroke Vol

- Frank-Starling =>inc SV

Eventually above fails=>dec CO => Dilated cardiomyopathy

Front 15

Praecordial lead summary

Back 15

Front 16

Lead summary

Back 16

Front 17

Septal leads

Back 17

V1, V2

Front 18

Anterior leads

Back 18

V3, V4

Front 19

Inferior leads

Back 19

II, III, Avf

Front 20

Lateral leads

Back 20

I, AvL, V5, V6

Front 21

Pericarditis s/s

Back 21

Chest pain (praecordial or retrosternal, referral to the trapezius ridge, neck, left shoulder, arm.)

- low-grade intermittent

- fever,dyspnea/tachypnea, cough, dysphagia

Front 22

Causes pericarditis

Back 22

- Idiopathic

- Viral, bacterial, and tuberculous infections

- Inflamm disorders, eg. RA, SLE, scleroderma, rheumatic fever (most common= sterile inflamm)

- Metabolic eg. renal failure, hypothyroidism, and hypercholest

- CVS disorders, eg. acute MI, Dressler syndrome, & aortic dissection

- Misc.causes, such as iatrogenic, neoplasms, drugs, irradiation, cardiovascular procedures, and trauma

Front 23

Pericarditis ix

Back 23

- ECG (Widespread concave ST elev+ PR depres, recip ST depression + PR elevation in lead aVR (± V1). Sinus tachy also common d/t pain/ pericardial effusion)

- Echocardiography

-CXR

- CBE; serum electrolyte, BUN & creatinine levels, ESR, CRP levels, LDH, and serum glutamic-oxaloacetic transaminase (SGOT; AST)

Front 24

Pericarditis tx

Back 24

- NSAIDsx14 days mainstay of pain relief, prednisalone to stop recurrence

- O2

- Pericardiocentesis, pericardial window or pericardectomy

- Treat cause

Front 25

Functions of the pericardium

Back 25

1. Mechanical - limits acute dilation=> maintains ventricular compliance + preserves Starling curve + distributes hydrostatic forces. + creates a closed chamber with subatmospheric pressure =>aids atrial filling +lowers transmural cardiac pressures

2. membranous function = shields to friction + infection/inflam extension

3. Anatomically fixes the heart.

Front 26

Uraemic pericarditis. Patho

Back 26

- kid failure=>metabolic toxins =>Inflamm visceral & parietal layers of peri. (multifactorial b/c occurs in dialysis px)

- Correlation b/w degree & duration azotemia exists

- BUN) usually >60

- Assoc. w hemorrhagic (more common d/t uraemia induced platelet dysfunct) or serous effusion

Front 27

Pericarditis patho

Back 27

Acute inflam + PMN infiltrate + pericardial vascularization => fibrinous rxn=> exudates+ adhesions=>serous or hemorrhagic effusion

Front 28

Causes of granulamatous pericarditis

Back 28

Tuberculosis, fungal infections, rheumatoid arthritis (RA), andsarcoidosis.

Caseation is TB until proven otherwise

Front 29

Chronic pericarditis

Back 29

Irrad, CVS surg, suppurative/caseous pericarditis, (sometimes simple fibrinous exudate)=>Adhesive mediastinopericarditis=>pericard potential space obliterated=>adhesion parietal layer to neighbour structs=>systolic contraction ribs +diaph&pulsus paradoxus.

inc. workload =>+++cardiac hypert &dilatation, (mimics cardiomyop).

Front 30

Constrictive pericarditis

Back 30

Causes: Suppurative, caseous, haemorrhagic pericarditis=> heart encased scar or calcification (concretio cordis)

- Heart can't hypertrophy or dilate d/t rigid box.

- More freq comp. of bact peritonitis

Front 31

Pericardial effusion hx

Back 31

Chest pain, pressure, discomfort, Light-headedness, syncope, Palpitations, Cough, Dyspnea, Hoarseness, Anxiety and confusion, Hiccoughs

tx same as pericarditis

Front 32

Cardiac Tamponade

Back 32

- Commonest in malignant pericarditis

- Blood more common fluid that trans/exudate as it accumulates faster

Front 33

Pericardial effusion PE

Back 33

Classic Beck triad of pericardial tamponade: Hypotension, muffled heart sounds, jugular venous distention

- Pulsus paradoxus, friction rub, Tachycardia, Tachypnea, Dec breath sounds, Ewart sign: (Dullness to percussion beneath the angle of left scapula), Hepatosplenomegaly, Weakened peripheral pulses, oedema, and cyanosis

Front 34

Pulsus Paradoxus

Back 34

Abnormally large decrease (>10 mm Hg) in systolic BP & pulse wave amplitude during insp.

Normally dec press in inhalation & inc during exhalation

Indicates: cardiac tamponade, pericarditis, COA, croup, & obstructive lung disease

Front 35

Broad complex tachycardia ddx

Back 35

VT, SVT with BBB or SVT with AV conduction over an accessory AV pathway, pacemaker rhythm

Front 36

Causes of SVT w BBB and SVT with AV conduction over an accessory AV pathway (causes are the same)

Back 36

Atrial tachy, atrial flutter, atrial fibrillation, AV nodal tachycardia, orthodromic circus movement tachycardia

Front 37

Hallmark of VT on ECG

Back 37

Dissociation b/w atrial and ventricular activity with tachycardia, broad QRS (some form of VA conduction can be present during VT, especially at slow VT rate)

Front 38

Capture beats in VT description

Back 38

Run of V tach and then a beat with normal AV conduction that has a normal sinus morphology

Front 39

Fusion beats VT description

Back 39

- Occurs when a supravent & vent impulse coincide to produce a hybrid complex

- Means there's two foci of pacemaker cells firing simultaneously: a supraventricular pacemaker (e.g. the sinus node) and a competing ventricular pacemaker (source of ventricular ectopics).

- Intermediate width and morphology to the SV & V complexes.

Front 40

Back 40

VT fusion beat (first narrow complex), followed by two capture beats

Front 41

Factors contributing to QRS width

Back 41

- Beats arising lat wall of vent makes wider QRS (takes longer to spread through both vents), closer to septum = narrower (more simultaneous conduct both vents)

- Scar tissue, vent hypertrophy also play a role

Front 42

Axis determination

Back 42

1. find isoelectric lead

2. go 90 away from it (because impulse must be running equally toward and away from isoelectric lead). This means axis could be either end of this lead.

3. Look at this new lead, if it is mostly positive, impulse travelling towards lead, if mostly negative travelling away. This is accurate to 30 degrees

4. Looking at isoelectric lead, is it truly isoelectric or slightly more pos or neg? If pos, shift your found lead 15 degrees towards your isoelectric lead. If neg, shift 15 degrees away from isoelectric lead and you have your axis!

Front 43

Normal cardiac axis

Back 43

+90 to -30 degrees

Front 44

Left axis Deviation

Back 44

-30 to -90 degrees

Front 45

Right axis deviation

Back 45

+90 to +180 degrees

Front 46

Width of QRS to qualify as wide complex

Back 46

>120ms (or >3 small squares).

Front 47

SVT hallmarks

Back 47

Rate that is exactly 150/min and a narrower (than VT) QRS-complex width (120-140ms).

Front 48

Factors that make VT more likely in BCT

Back 48

More common generally (80%, but up to 95% in IHD). More likely with extreme right axis, minor rate variation and chest lead concordance.

Clinically: patient unstable, with cardiac failure, a midline sternotomy scar, a pacemaker or ICD, cannon a-waves or heart sound fluctuations (esp S1)

Front 49

Px to be considered for cardioversion

Back 49

- New-onset AF

- SymptomaticLV dysfunction secondary to AF

- Reversible cause of AF (e.g. post surgical / post infection)

- Reasonable chance of maintaining sinus rhythm: Previous successful cardioversion, Minimal dilatation of the left atrium, No significant mitral valve disease

Front 50

AVNRT tx

Back 50

- Induce AV node blockade and the tachycardia is terminated:

- Mechanical (vasovagal manoeuvres, carotid sinus massage)

- Chemical (adenosine, beta blockers, verapamil)

Front 51

AVRT tx

Back 51

- AVOID AV node blockade as this can promote conduction down the AP and AFib can transmit to VF.

- Electrical cardioversion is the best initial option although flecainide can be used to chemically cardiovert.

- Ablation of the pathway is a curative option.

Front 52

Indications for cardiac stress test

Back 52

- Px with intermediate risk ACS

- Perform within 72 hrs

- Need two neg troponins + pain free + ECG changes resolved or static

- If px can't exercise=>pharma stress test (eg. dobutamine stress echocardiogram, adenosine stress MRI or a myocardial perfusion scan)

Front 53

Cardiac tamponade s/s

Back 53

- SOB

- Tachycardia

- Poorly perfused peripheries

- Elevated JVP

- Pulsus paradoxus

- Musculoskeletal pain

- Fever

- Dysphoria

Front 54

Tamponade MGMT

Back 54

- Emergency!

- Emergency subxiphoid percutaneous drainage

- Echocardiographically guided pericardiocentesis

- Percutaneous balloon pericardiotomy

Front 55

Paroxysmal AF

Back 55

- Eps stop spontaneously

- Increasingly frequent eps

- Up to 90% of episodes of paroxysmal atrial fibrillation are asymptomatic

Front 56

Persistent AF

Back 56

Episodes of continuous AF that last more than 7 days and do not self-terminate

Front 57

Long-standing persistent AF

Back 57

Episodes of continuous AF that last more than 12 months

Front 58

Nonvalvular AF

Back 58

AF in the absence of rheumatic mitral valve disease, a prosthetic heart valve, or mitral valve repair

Front 59

AF treatment: rhythm

Back 59

- More hospital admissions and adverse cardiac events than rate control.

- Pharmacological or ablation by catheter or surg

- Pharm: amioderone, ibutilide, flecainide, sotalol

Front 60

Af treatment: rate

Back 60

Tx of choice

B-blocker first line (metoprolol, propranolol), then ca channel blockers (diltiazem, verapamil), maybe digoxin but it is not good in exercise so they pair it with one of the above

Front 61

Markers of disease in IHD

Back 61

-Elevated lipoprotein

-Hyperhomocysteinemia

-Elevated high-sensitivity C-reactive protein (hsCRP)

-Coronary artery calcification

-Carotid IMT/plaque

-Ankle-brachial index

Front 62

Atherosclerosis mech

Back 62

endothelial damage=>cytokines=>recruitment of monocytes=>MO+oxidation of LDLs=>engulf ox-LDLs=>become foam cells=>this is fatty streak/lipid core of plaque=>cytokines+GF=>smooth muscle recruitment into intima=>intimal hyperplasia=>releases matrixformation of fibrous cap=>protrudes into lumen=>grows, can occlude lumen or rupture=>embolus/thrombus

Front 63

Printzmetal's angina

Back 63

• myocardial ischemia secondary to coronary arteryvasospasm, with or without atherosclerosis

• rarely assoc w infarct or LV dysfunction


• typically occurs between midnight and 8 am,unrelated to exercise, relieved by nitrates


• typically ST elevation on ECG


•diagnosed by provocative testing with ergot vasoconstrictors (rarely done)

•treat with nitrates and Calc Channel Blockers

Front 64

Syndrome X

Back 64


• typical symptoms of angina but normal angiogram


•may show definite signs of ischemia with exercise testing


• thought to be dueto inadequate vasodilator reserve of coronary resistance vessels

• betterprognosis than overt epicardial atherosclerosis 


Front 65

ACS definition and NSTEMI/STEMI diff

Back 65

- Unstable angina, NSTEMI and STEMI

NSTEMI meets criteria for myocardial infarction without ST elevation or BBB

STEMI meets criteria for myocardial infarction characterized by ST elevation or new BBB

Front 66

Silent MI RFs

Back 66

>30% of MIs are unrecognized or “silent” due to atypical symptoms – more common in women, DM, elderly, post-heart transplant (because of denervation)

Front 67

Ix ACS

Back 67

• ECG

• CXR

• labs:

- Troponin I and T for myocardial damage immediately and 8hrs later

- CBE

- INR/PTT

- electrolytes + Mg, glucose

- Urea+creat

- serum lipids (draw w/i 24-48 h because values are unreliable from 2-48 d post-MI)

Front 68

Cardiac biomarkers for MI

Back 68

Troponin I and T: peak in 1-2hrs, stay elevated for up to 2 wks

CK-MB: peaks in 1 day, lasts 3 days

AST and LDH: also increased in MI (low specificity)

Front 69

DDx Trop I or T elevation

Back 69

Absolutely indicative of cardiac damage

MI, CHF, AFib, acute PE, myocarditis, chronic renal insufficiency (this will be constantly raised, but in cardiac damage will rise&fall),sepsis, hypovolemia

Front 70

DDx CK-MB elevation

Back 70

Rises in all muscle damage (trops specific to cardiac)

MI, myocarditis, pericarditis, muscular dystrophy, cardiacdefibrillation, chronic renal insufficiency, etc.

Front 71

Tx: chronic stable angina, principles

Back 71

- Reduce myocardial oxygen demand and/or increase oxygen supply

- Lifestyle modification (diet, exercise)

- tx of RFs: statins, antihypertensives,

- Pharmacological therapy to stabilize the coronary plaque to prevent rupture and thrombosis

Front 72

tx Chronic stable angina

Back 72

1. lifestyle

2. antiplatelet: Acetylsalicylic acid (ASA) or clopidogrel

3.B-blocker (metoprolol/atenolol:cardioselective)

4. GTN for sx relief (dec preload (veno dilatat) + afterload (art dilatat), + increase coronary perfusion.

5. CCB: 2nd line or in combo (amlodapine)

6. ACEI or ARB (ramipril): to decrease RFs (HTN, renal fcn, DM)

7. revascularisation

Front 73

ACS MGMT

Back 73

- Assess: ECG, bloods (trops, lipids)

- Immediate: cannula, pain relief, aspirin 150-300mg

- Ticagrelor/Clopidogrel

- Enoxaparin (LMWH)

- Reperfuse if: new BBB, >1mm ST elevation in 2 contig limb leads or >2mm in 2 contig chest leads. w/i 90 mins of pres

- If not PCI=>fibrinolysis w tPA

- B blockers: unless low BP/cardiogenic shock, 2/3rd degree heart block, PVD

Front 74

Contraindications to thrombolysis in STEMI

Back 74

- Prior intracranial hemorrhag

- Known structural cerebral vascular lesion

- Known malignant intracranial neoplasm

- Significant closed-head or facial trauma (≤3 mo) - Ischemic stroke (≤3 mo)

- Active bleeding

- Suspected aortic dissection

Front 75

Cardiomyopathy HARD mneumonic

Back 75

Hypertrophic: genetic, affects sarcomeres, most common cause sudden cardiac death in young athletes

Aryythmogenic RV

Restricted

top three: HF and preserved EF

Dilated: HF and dec EjectFrac

Front 76

Causes of dilated cardiomyopathy

Back 76

Idiopathic, infectious (myositis), alcohol, familial, collagen vasc. disease

Front 77

Restrictive cardiomyop

Back 77

- Connective tissue diseases

- Haemochromotosis

Front 78

Secondary causes of cardiomyop

Back 78

- HTN

- DM

- Valvular path

- Post MI

Front 79

Myocarditis

Back 79

- Cause of dilated cardiomyop

- Can be acute or chronic

- Can be: idiopathic, infectious (viral most comm), toxic (catecholamines, chemo, cocaine), eosinophilic (antibiotics, diuretics, lithium, clozapine), connective tissue disease (SLE, RA, sarcoid), autoimmune

Front 80

Infectious causes myocarditis

Back 80

Viral: (most common) parvovirus, flu, coxsackie B, polio, HIV, mumps

Bact: S.aureus, c.perfringens. diphtheriae, mycoplasma, rickettsia

Fungi

Spirochetes (lyme disease)

Chagas disease, toxoplasmosis

Front 81

Presentation cardiomyopathies

Back 81

All present like CHF, arrythmias plus other heart sounds signs and palpation bull

Front 82

Heart failure pressure overload causes and result

Back 82

- Causes: AS, coarctation aorta or HTN

=>compensatory hypertrophic (concentric)=> interstitial fibrosis

Front 83

HF vol overload causes and results

Back 83

- Aortic or mitral regurg, patent ductus arteriosus, ventricular septal defect, previous MI, dilated cardiomyopathy (alcohol, familial, myositis, CT disease)

=>LV dilation (eccentric)

findings:

- apex beat displaces, S3, cardiothoracic ratio>0.5, dec LVEF

Front 84

Mitral stenosis remodelling

Back 84

- LVhypertrophy (concentric, pressure overload), LA hypertrophy (both)

- Causes pulm HTN=>RV dilation=>tricuspid regurg=>inc. JVP, peripheral oedema, liver congestion,ascites

- Commonly causes by rheumatic fever

Front 85

Mitralregurg remodelling

Back 85

LV and LA dilation (vol overload)

Front 86

Aortic stenosis remodelling

Back 86

- Pressure overload=>LV Concentric hypertrophy=>diastolic failure.

- In severe AS, atrial contraction v v important for diastolic filling of LV. Thus, development ofAF in AS often leads to HF d/t aninability to maintain CO.

Front 87

AorticRegurg

Back 87

volume overload=>eccentric hypertrophy=> Systolic dysfunction

Front 88

Bradyarrythmias causes

Back 88

- Sinus bradycardia

- Sinoatrial block

- Sinus arrest

- AV block (2/3rd degree)

- Junctional rhythm

- idioventricular rhythm

Front 89

Regular tachyarrythmias, Narrow QRS

Back 89

SVTs

- Sinus tachycardia

- Atrial tachy

- Junctional tachy

- AVNRT

- AVNRT (orthodromic)

- Atrial flutter

Front 90

Regular tachyarrythmias, Wide QRS

Back 90

- SVT with BBB

- Ventricular tachy

- AVRT (antidromic)

Front 91

Irregular tachyarrythmias Narrow QRS

Back 91

- AF

- A flutter with variable block

- multifocal atrial tachy

- premature atrial contraction

Front 92

Irregular tachyarrythmias wide QRS

Back 92

- AF with BBB

- A flutter w BBB and variable block

- Polymorphic VT (torsades)

- Premature vent contraction

Front 93

JONEs criteria

Back 93

- Major criteria:

- Sydnham's chorea

-

Front 94

IE mneumonic

Back 94

B - 2x positive blood cultures (step viridans)

E - echo evidence of IE (vegetations >2mm)

Is - immune complex deposition (osler's nodes, glomerular nephritis)

Very - vascular phenomenon

Painful - 1 positive blood culture

Every - echocardial evidence but not enough to fulfil major criteria

Fricken - fever

Morning - drug use/prosthetic valve, predisposing heart cond

Front 95

3 patterns of AF

Back 95

Paroxysmal

persistent

permanent

Front 96

HAS BLED score

Back 96

- For people anticoagulated w AF

HTN (>160, uncontrolled)

Abnormal kidney or liver fcn

Stroke hx

Bleeding

Labile INR

Elderly >65

Drugs or alcohol

1 pt each, score ≥3= high risk

Front 97

Eisenmenger syndrome

Back 97

- Any untreated congenital cardiac defect (commonly PDA) w intracardiac communication=>pulm HTN=>reversal of flow=>cyanosis

- Previous L=>R shunt is converted to R=>L shunt b/c of elevated pulmonary artery pressure + assoc pulm vascular disease

- Represents irreversible pulm HTN and inoperable heart defect

Front 98

Coarctation aorta

Back 98

- Common defect (5-8% congenital heart defects)

- Constricted aortic segment comprised of local medial thickening w infolding of medial and neointimal tissue.

- Usually just distal to lef subclavian artery

- Usually dilation of descending aorta

- Often assoc w bicuspid aortic valve and VSD

- Sometimes missed until px gets CHF (common in infancy) or hypertension (common in older kids)

- Increased and ventricular hypertrophy

Front 99

Ventricular septal defect

Back 99

- Accounts for >20% congenital heart disease

- Left=>Right shunt:

*Inc LV volume

*XS pulmonary blood flow

*reduced systemic CO

*inc pulm artery pressure

=>inc venous return to LA=>LV=>LV dilation + hypertrophy

s/s:

- lack of adequate growth

- Inc sweating/fatigue w feeding d/t inc sympathetic output

- exertional dyspnea, cyanosis, chest pain, syncope, and hemoptysis in eisenmenger

ix:

- Echo

- CXR

- ECG

tx:

- Good prognosis in children, small defects need no tx, medium defects tx for CHF

- Most spontaneously close by age 2

Front 100

Patent ductus arteriosus

Back 100

- Persistent communication b/w descending aorta and pulmonary artery

- L=>R shunt=>pulmonary htn=>dec pulm compliance

- Can present at any age

*new murmur well after adolscence in adult+pulm congestion + dec exercise tolerance

*hoarse, dry cough, lower resp tract infections, atelectasis, pneumonia

*lifet-hreatening pulm overcirculation straight after birth in newborn, failure to thrive, feeding trouble

*mostly asymptomatic

*frank CHF rare in infancy

*adults can present w s/s heart failure, atrial arrhythmia, differential cyanosis

Front 101

Coarctation aorta presentation

Back 101

- BP discrepancies b/w the upper + lower limb

- Reduced or absent lower extremity pulses

- Differential cyanosis (pink upper extremity, blue lower)

- Strong pulse upper limb, weak lower limb

- Murmur: non specific but usually systolic in left infraclav area + under L scapula, ejection click maybe (bicuspid aortic valve)

Front 102

S3

Back 102

- low-pitched, early diastolic sound audible during the rapid entry of blood from the atrium to the ventricle.

- if coming from LV, listen at apex w patient in left lateral decubitus position with breath held at end expiration

- When it is of RV origin, S3 listen L lower sternal border or the xiphoid with the patient in supine position.

- Best heard with the bell of the stethoscope.

Front 103

Conditions assoc with patho S3

Back 103

- Systolic and/or diastolic ventricular dysfunction

- Ischemic heart disease

- Hyperkinetic states:

*Anaemia

*fever

*pregnancy

*thyrotoxicosis

*AV fistula

- MR or TR

- Chronic AR with systolic dysfunction

- Systemic and pulmonary hypertension

- Acute aortic regurgitation

- Volume overload

- Renal failure

Front 104

Mitral stenosis description

Back 104

- Holodiastolic with pre-systolic accentuation due to the atrial kick

- Tapping heart beat

- Usually described as low-pitched, decrescendo, and rumbling

- Patient in the left lateral decubitus position

- “opening snap” (stenotic valve suddenly halts its normal opening at the start of diastole)

Front 105

S4

Back 105

- Late diastolic sound that corresponds to late ventricular filling through active atrial contraction.

- Low-intensity sound heard best with the bell

- Listen in the same spots as for S3

Front 106

Conditions assoc w S4

Back 106

Ventricular hypertrophy

- LV hypertrophy (systemic hypertension, hypertrophic cardiomyopathy, AS)

- RV hypertrophy (pulmonary hypertension, pulmonary stenosis [PS])

- Ischemic heart disease - Acute MI, angina

Ventricular aneurysm

- Hyperkinetic states that cause forceful atrial contraction

Front 107

Austin flint murmur

Back 107

- Mid-diastolic, low-pitched rumbling heard at the apex

- Occur in aortic regurgitation due to the vibration of the anterior leaflet of the mitral valve as it is buffetted simultaneously by the blood jets from the left atrium and the aorta

Front 108

Pulmonary regurg

Back 108

- Early diastolic

Causes:

*postvalvulotomy

*endocarditis

*marfan synd

*congenital (tetralogy of fallot, VSD, pulm stenosis

Front 109

Tricupsid prolapse

Back 109

Late systolic murmur

Front 110

Malignant hypertension complications

Back 110

End organ damage:

- Acute pulmonary oedema

- Aortic dissection

- Pre-eclampsia

- Subarachnoid haemorrhage

- Hypertensive encephalopathy

- Acute kidney injury

- Vascular damage to eyes as seen on fundoscopy

- Fibrinoid necrosis of arterioles and small arteries

- Red blood cells are damaged as they flow through vessels obstructed by fibrin deposition, resulting in microangiopathic hemolytic anemia

Front 111

ddx Malignant htn

Back 111

- Complications of pregnancy

- Cocaine

- Monoamine oxidase inhibitors (MAOIs), or oral contraceptives

- Withdrawal of alcohol, beta blockers, or alpha stimulants

- Renal artery stenosis

- Pheochromocytoma

- Aortic coarctation

- Hyperaldosteronism

- Hyperthyroidism/hypothyroidism can cause hypertension.The following conditions should also be considered when making the diagnosis: stroke, intracranial mass, head injury, epilepsy or postictal state, connective-tissue disease (especially lupus with cerebral vasculitis), drug overdose or withdrawal, cocaine or amphetamine ingestion, acute anxiety, and thrombotic thrombocytopenic purpura.