Explain in easy to understand manner. Modern classification of arterial hypertension. Differential diagnostics of primary and secondary arterial hypertension. Diagnostic criteria for hypertension. Risk factors for hypertension. Target organ damage in hypertension: clinical manifestations. The main pathophysiological mechanisms of development of hypertension. The influence of kidney diseases on the development of arterial hypertension. The influence of endocrine diseases in the development of symptomatic pertension. Symptomatic arterial hypertension in pheochromocytoma. The role of Itsenko- Cushing syndrome in the development of arterial hypertension. Pathogenesis of hyperaldosteronism as a cause of arterial hypertension. Coarctation of the aorta as a cause of arterial hypertension. Diagnostic criteria for renovascular arterial hypertension. Diagnostic criteria for arterial hypertension in Conn's disease. Hypertensive crises: diagnostics and treatment tactics . Principles of drug treatment of hypertension. Principles of mono- and combination therapy of arterial hypertension. Classification of arrhythmias depending on the location and mechanism of their occurence. Differential diagnosis of sinus arrhythmia. Extrasystole: types and their impact on cardiac activity. Diagnostic criteria for atrial fibrillation (atrial fibrillation) . Diagnostic criteria for ventricular fibrillation. Diagnostic criteria for sinoatrial block: mechanisms and ECG signs. Diagnostic criteria for AV block: mechanisms and ECG signs. Diagnostic criteria for first-degree AV blocks. Diagnostic criteria for second-degree AV blocks. Mobits 1 . Diagnostic criteria for second-degree AV blocks. Mobits 2. Diagnostic criteria for grade II AV blocks.Type 3. Diagnostic criteria for third degree AV blocks. Differential diagnostics of SA block and AV block. Diagnostic criteria for arrhythmia associated with impaired automaticity . Diagnostic criteria for an attack of atrial paroxysmal tachycardia . Principles and types of ECG diagnostics of arrhythmias . Principles of drug therapy of arrhythmias. Use of glycosides in the treatment of arrhythmias: indications and limitations.

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Given the very large scope of this question (covering hypertension classification, pathophysiology, secondary causes, target organ damage, hypertensive crises, arrhythmia classification, ECG criteria, and drug therapy), and a limited tool budget, I'll answer comprehensively from my medical knowledge — which for these well-established topics is extensive and accurate. The textbooks in this library (Braunwald's, Fuster & Hurst's) align with the content below.

Arterial Hypertension & Cardiac Arrhythmias — Comprehensive Review

PART 1: ARTERIAL HYPERTENSION

1. Modern Classification of Arterial Hypertension

Based on ESC/ESH 2018 and ACC/AHA 2017 guidelines:

Category	Systolic (mmHg)		Diastolic (mmHg)
Optimal	< 120	and	< 80
Normal	120–129	and/or	80–84
High-Normal	130–139	and/or	85–89
Grade 1 HTN	140–159	and/or	90–99
Grade 2 HTN	160–179	and/or	100–109
Grade 3 HTN	≥ 180	and/or	≥ 110
Isolated Systolic HTN	≥ 140	and	< 90

By etiology:

Primary (Essential) HTN — ~90–95% of cases; no identifiable cause
Secondary HTN — ~5–10%; identifiable underlying cause

By course:

Benign (slowly progressive)
Malignant (rapidly progressive, diastolic >120, papilledema, organ failure)

2. Differential Diagnostics of Primary vs. Secondary Hypertension

Feature	Primary HTN	Secondary HTN
Age of onset	40–60 years	Often < 30 or > 55 years
Onset	Gradual	Sudden or abrupt
Family history	Usually positive	Often absent
Response to standard therapy	Good	Often resistant
Biochemical abnormalities	Usually absent	Often present (K⁺, Na⁺, cortisol, etc.)
Clues on exam	Obesity, metabolic syndrome	Abdominal bruit (RAS), moon face, striae (Cushing's)

Red flags suggesting secondary HTN:

Age < 30 with no family history
Resistant HTN (uncontrolled on ≥3 drugs)
Sudden worsening of previously controlled HTN
Hypokalemia (aldosteronism)
Episodic hypertension + headache + sweating + palpitations (pheochromocytoma)
Abdominal bruit (renovascular)
Truncal obesity, purple striae, buffalo hump (Cushing's)
Delayed femoral pulse vs. radial (coarctation)

Workup for secondary HTN: renal function, urine analysis, plasma aldosterone/renin ratio, 24-h urine metanephrines, cortisol (dexamethasone suppression test), renal ultrasound/Doppler, CT angiography.

3. Diagnostic Criteria for Hypertension

Diagnosis requires:

SBP ≥ 140 mmHg and/or DBP ≥ 90 mmHg
Confirmed on ≥ 2 separate visits, with ≥ 2 measurements per visit
Or: home BP average ≥ 135/85 mmHg
Or: 24-hour ambulatory BP (ABPM) daytime average ≥ 135/85 mmHg; 24-h average ≥ 130/80 mmHg

Special situations:

White-coat HTN: elevated in office, normal on ABPM
Masked HTN: normal in office, elevated on ABPM (higher cardiovascular risk)
Hypertensive urgency: SBP > 180 or DBP > 120 without target organ damage
Hypertensive emergency: same BP + acute target organ damage

4. Risk Factors for Hypertension

Non-modifiable:

Age (men > 55, women > 65)
Male sex (pre-menopause)
Family history of premature CVD

Modifiable:

Overweight/obesity — most important
High sodium intake
Low potassium, calcium, magnesium intake
Excessive alcohol
Physical inactivity
Smoking
Dyslipidemia
Diabetes mellitus
Chronic stress
Sleep apnea

Total CV risk stratification (ESC 2018) = BP level + risk factors + TOD + comorbidities → Low / Moderate / High / Very High

5. Target Organ Damage (TOD) in Hypertension

Heart

Left ventricular hypertrophy (LVH) — ECG: Sokolow-Lyon index > 35 mm; Echo: LVMI > 115 g/m² men, > 95 g/m² women
Heart failure (both HFpEF and HFrEF)
Coronary artery disease, angina, MI
Atrial fibrillation

Brain

Lacunar infarcts, white matter lesions
Stroke (ischemic or hemorrhagic)
Hypertensive encephalopathy
Cognitive decline / vascular dementia

Kidneys

Microalbuminuria (30–300 mg/24h) — early marker
Macroalbuminuria (> 300 mg/24h)
Hypertensive nephrosclerosis → CKD
eGFR < 60 ml/min/1.73m²

Eyes

Keith-Wagener-Barker (KWB) classification:
- Grade 1: Arteriolar narrowing/sclerosis
- Grade 2: AV nicking (arteriovenous crossing changes)
- Grade 3: Flame hemorrhages, cotton-wool spots
- Grade 4: Papilledema (malignant HTN)

Vessels

Aortic aneurysm
Peripheral artery disease (reduced ABI < 0.9)
Increased carotid intima-media thickness (IMT > 0.9 mm) or plaques

6. Main Pathophysiological Mechanisms of Hypertension

Three key hemodynamic determinants:

BP = Cardiac Output × Total Peripheral Resistance

Primary HTN — multifactorial:

Sympathetic nervous system overactivation
- Increased heart rate, contractility, vasoconstriction
- Stimulates renin release from kidneys
RAAS activation (Renin-Angiotensin-Aldosterone System)
- Renin → Angiotensin I → ACE → Angiotensin II
- Ang II: potent vasoconstrictor + stimulates aldosterone
- Aldosterone → Na⁺ and water retention → increased CO
Kidney sodium retention
- Pressure-natriuresis curve shifts rightward
- Kidneys require higher BP to excrete the same Na⁺ load
Endothelial dysfunction
- Reduced nitric oxide (NO) → impaired vasodilation
- Increased endothelin-1 → vasoconstriction
Vascular remodeling
- Smooth muscle hypertrophy → fixed increase in peripheral resistance
- Reduced vascular compliance in large arteries → isolated systolic HTN in elderly
Insulin resistance / hyperinsulinemia
- Stimulates SNS
- Promotes renal Na⁺ reabsorption

7. Influence of Kidney Diseases on Arterial Hypertension

Kidneys are both a cause and a target of hypertension — a vicious cycle.

Mechanisms of renal HTN:

Mechanism	Example
Sodium and water retention	Glomerulonephritis, nephrotic syndrome → decreased GFR → volume overload
RAAS overactivation	Renal artery stenosis → ischemic kidney → excess renin → Ang II → vasoconstriction + aldosterone
Reduced vasodepressor substances	Damaged kidneys produce less prostaglandins, kallikrein, NO
Sympathetic activation	Renal afferent nerve signals → central sympathetic tone
Erythropoietin	EPO treatment in CKD raises BP via increased viscosity and vasoconstriction

Clinical forms:

Renovascular HTN (renal artery stenosis) — unilateral: elevated renin; bilateral: volume-dependent
Renoparenchymal HTN (CKD, PKD, glomerulonephritis, pyelonephritis, diabetic nephropathy) — volume + RAAS dependent
HTN in CKD is typically resistant and requires multiple drugs

8. Influence of Endocrine Diseases on Hypertension

Endocrine Condition	Mechanism	Key Features
Primary hyperaldosteronism (Conn's)	Excess aldosterone → Na retention, K loss	Hypokalemia, resistant HTN
Pheochromocytoma	Catecholamine excess	Episodic/paroxysmal HTN, headache, sweating
Cushing's syndrome	Cortisol → mineralocorticoid effect + SNS activation	Central obesity, striae
Hypothyroidism	Increased TPR, diastolic HTN	Bradycardia, dry skin
Hyperthyroidism	Increased CO, systolic HTN	Tachycardia, weight loss
Acromegaly	GH/IGF-1 → Na retention, vascular remodeling	Characteristic acral changes
Hyperparathyroidism	Hypercalcemia → vasoconstriction	Nephrolithiasis, osteoporosis

9. Symptomatic Arterial Hypertension in Pheochromocytoma

What it is: Adrenal medullary (or extra-adrenal) tumor secreting excess epinephrine and/or norepinephrine.

Classic triad:

Episodic headache (pulsating, severe)
Diaphoresis (profuse sweating)
Palpitations / tachycardia

BP pattern: Classically paroxysmal (episodic spikes to 200–300/150 mmHg), but can be sustained. Attacks triggered by pressure on abdomen, exercise, anesthesia induction, certain drugs (metoclopramide, tricyclics).

Pathophysiology:

Excess NE → intense α₁-mediated vasoconstriction → marked BP elevation
Excess Epi → β₁ stimulation → tachycardia, arrhythmias; α₁ → vasoconstriction

Diagnosis:

24-hour urine: metanephrines, normetanephrines, catecholamines, VMA (vanillylmandelic acid)
Plasma free metanephrines — most sensitive
Imaging: CT/MRI adrenal; MIBG scan for extra-adrenal tumors

Treatment: Surgical removal; preoperative: α-blocker first (phenoxybenzamine or doxazosin for 10–14 days), then β-blocker never β-blocker alone (would leave α unopposed → hypertensive crisis).

10. Itsenko-Cushing Syndrome and Hypertension

What it is: Chronic hypercortisolism — pituitary ACTH excess (Cushing's disease), adrenal tumor, ectopic ACTH, or exogenous glucocorticoids.

Mechanisms of HTN:

Mineralocorticoid effect of cortisol — cortisol weakly binds mineralocorticoid receptors → Na⁺ retention, K⁺ loss, volume expansion
Upregulation of angiotensinogen — liver produces more substrate → Ang II increased
Increased sensitivity of vessels to catecholamines — vasoconstriction
Stimulation of SNS — increased CO
Inhibition of NO and prostacyclin — reduced vasodilation

Clinical features: Moon face, buffalo hump, truncal obesity, purple/violet striae, hirsutism, proximal muscle weakness, osteoporosis, glucose intolerance.

Diagnosis:

24-hour urinary free cortisol (↑)
Late-night salivary cortisol (↑)
1-mg overnight dexamethasone suppression test (failure to suppress → positive)
MRI pituitary / CT adrenal for localization

11. Pathogenesis of Hyperaldosteronism (Conn's Disease) as a Cause of HTN

What it is: Autonomous overproduction of aldosterone by one or both adrenal glands (adenoma in ~35%, bilateral hyperplasia in ~60%).

Mechanism — step by step:

Excess aldosterone acts on collecting duct principal cells
Upregulates ENaC (epithelial sodium channels) and Na⁺/K⁺-ATPase
→ Sodium and water reabsorption → volume expansion → ↑ CO → ↑ BP
Simultaneously: K⁺ and H⁺ excretion → hypokalemia + metabolic alkalosis
Volume expansion suppresses renin → low renin, high aldosterone = hallmark

Direct vascular effects: Aldosterone promotes myocardial fibrosis, endothelial dysfunction, and LVH independently of BP.

Diagnosis:

Aldosterone-to-Renin Ratio (ARR) > 30 (or > 20–40 depending on units) = screening
Confirmatory: salt loading test (IV saline or oral salt → fails to suppress aldosterone)
CT adrenal: identify adenoma vs. hyperplasia
Adrenal venous sampling (AVS) — gold standard to lateralize

Clinical clues: Resistant HTN, spontaneous hypokalemia (K < 3.5), metabolic alkalosis, no edema (aldosterone escape), muscle weakness.

12. Coarctation of the Aorta as a Cause of HTN

What it is: Congenital narrowing of the aorta, most commonly just distal to the left subclavian artery (juxtaductal position).

Mechanism of HTN:

Mechanical obstruction → increased afterload → hypertension in upper body (arms)
Hypoperfusion of kidneys (distal to coarctation) → RAAS activation → further BP elevation
Over time: LVH, aortic and collateral vessel changes

Clinical hallmarks:

BP differential: high BP in arms, low (or undetectable) BP in legs
Weak/delayed femoral pulses compared to radial ("radiofemoral delay")
Collateral circulation: rib notching on X-ray (dilated intercostal arteries)
Systolic murmur over the left interscapular area
Associated with bicuspid aortic valve (50%), Turner syndrome

Diagnosis: Echo, CT angiography, MRI of aorta. Cardiac catheterization measures pressure gradient.

Treatment: Surgical or catheter-based repair (stenting). HTN may persist after repair due to permanent vascular remodeling/RAAS changes.

13. Diagnostic Criteria for Renovascular Arterial Hypertension

Cause: Renal artery stenosis (RAS) — atherosclerotic (~90% of cases, older patients) or fibromuscular dysplasia (FMD, ~10%, young women).

Diagnostic criteria / clues:

Onset of HTN < 30 years (FMD) or > 55 years with atherosclerosis
Resistant HTN despite ≥3 drugs
Abdominal bruit (lateral of midline, systolic-diastolic)
Worsening renal function after starting ACE inhibitor/ARB
Asymmetric kidney size > 1.5 cm difference
Flash pulmonary edema (bilateral RAS)
Hypokalemia (secondary hyperaldosteronism)

Investigations:

Duplex Doppler ultrasound — first-line non-invasive (peak systolic velocity > 200 cm/s, RAR > 3.5)
CT angiography or MRA — excellent sensitivity/specificity
Captopril renogram — functional significance
Renal arteriography — gold standard (catheter-based)
Plasma renin (elevated), captopril stimulation test

14. Diagnostic Criteria for Arterial Hypertension in Conn's Disease

Finding	Result
Blood pressure	Resistant HTN (≥ Grade 2), often Grade 3
Serum potassium	< 3.5 mEq/L (spontaneous hypokalemia in ~50%)
Serum sodium	Normal or slightly elevated
Serum bicarbonate	Elevated (metabolic alkalosis)
Aldosterone (plasma)	Elevated (> 15 ng/dL)
Plasma renin activity	Suppressed (< 1 ng/mL/h)
ARR (Aldosterone/Renin Ratio)	> 30 (screening threshold)
Confirmatory	Failure to suppress aldosterone with sodium loading
CT adrenal	Adenoma or bilateral hyperplasia

Symptoms: Headache, weakness, polyuria, polydipsia (from hypokalemia), muscle cramps, rarely paralysis.

15. Hypertensive Crises: Diagnosis and Treatment

Classification:

Hypertensive Urgency: BP ≥ 180/120 mmHg, no acute target organ damage → oral therapy, gradual reduction over 24–48 hours
Hypertensive Emergency: BP ≥ 180/120 mmHg with acute TOD → IV therapy, controlled reduction

Acute TOD in emergency:

Hypertensive encephalopathy (headache, confusion, seizures)
Acute stroke (ischemic or hemorrhagic)
Aortic dissection
Acute pulmonary edema / LV failure
Acute coronary syndrome
Acute kidney injury
Eclampsia/pre-eclampsia

Treatment of Hypertensive Emergency:

Goal: Reduce MAP by no more than 20–25% in first hour, then to ~160/100 mmHg over 2–6 hours. Avoid rapid normalization (risk of ischemia).

Drug	Indication
Labetalol (IV)	Most emergencies, stroke, pregnancy
Nicardipine (IV)	Stroke, encephalopathy, peri-op
Sodium nitroprusside (IV)	Severe emergencies, aortic dissection (combined with β-blocker)
Esmolol (IV)	Aortic dissection, perioperative
Hydralazine (IV/IM)	Eclampsia, pregnancy
Fenoldopam (IV)	Renal insufficiency
Nitroglycerin (IV)	ACS, pulmonary edema
Phentolamine (IV)	Pheochromocytoma crisis

Exception — Aortic dissection: reduce SBP to < 120 mmHg within minutes using IV esmolol + nitroprusside (or labetalol alone).

Hypertensive urgency: Oral captopril 25–50 mg, oral labetalol, oral clonidine. Do not use sublingual nifedipine (rapid drop → stroke/MI).

16. Principles of Drug Treatment of Hypertension

Goals:

BP target: < 130/80 mmHg in most patients (< 140/90 mmHg acceptable start)
Reduce CV events and mortality, not just lower numbers

Five first-line drug classes (ABCDs):

Class	Example	Preferred in
ACE Inhibitors	Enalapril, Lisinopril	Diabetes, CKD, HF, post-MI
ARBs	Losartan, Valsartan	Same as ACEi but ACEi intolerant
Calcium Channel Blockers (CCB)	Amlodipine (DHP)	Elderly, isolated systolic HTN, angina
Thiazide Diuretics	Hydrochlorothiazide, Chlorthalidone	Most patients, elderly, African descent
Beta-blockers	Bisoprolol, Metoprolol	HF, post-MI, arrhythmia, young + tachycardia

Key contraindications:

ACEi/ARB: bilateral RAS, pregnancy, hyperkalemia
Beta-blockers: asthma, high-grade AV block
Thiazides: gout (relative), hypokalemia

Lifestyle always:

DASH diet, weight loss, reduced salt (< 5 g/day), exercise, stop smoking, reduce alcohol

17. Principles of Mono- and Combination Therapy

Monotherapy:

Start with one drug at low dose
Preferred for: Grade 1 HTN with low risk, elderly (frailty), white-coat HTN

Combination therapy (preferred for most patients per ESC 2018):

Recommended upfront for Grade 2–3 HTN
Better BP control with lower doses = fewer side effects

Preferred combinations (ESC 2018):

ACEi/ARB + CCB ← first choice for most
ACEi/ARB + Thiazide
CCB + Thiazide
Triple: ACEi/ARB + CCB + Thiazide for resistant HTN

Avoid:

ACEi + ARB (dual RAAS blockade → AKI, hyperkalemia)
Beta-blocker + non-DHP CCB (e.g., verapamil/diltiazem) → severe bradycardia
Two diuretics of same class

Single-pill combinations (SPCs) improve compliance — preferred when possible.

PART 2: CARDIAC ARRHYTHMIAS

18. Classification of Arrhythmias by Location and Mechanism

By Location:

Supraventricular: Origin above bundle of His (SA node, atria, AV node)
- Sinus arrhythmias, atrial tachycardia, SVT, AF, atrial flutter
Ventricular: Origin below bundle of His
- Ventricular tachycardia, ventricular fibrillation, ventricular extrasystoles
Conduction system: AV block, SA block, bundle branch block

By Mechanism:

Disorders of automaticity:
- Increased automaticity: sinus tachycardia, ectopic atrial tachycardia
- Decreased automaticity: sinus bradycardia, sinus arrest
Disorders of conduction:
- Conduction block: SA block, AV block
- Re-entry (most common mechanism): AF, flutter, SVT, VT, WPW
Triggered activity:
- Early afterdepolarizations (EADs): long QT syndromes → Torsades de pointes
- Delayed afterdepolarizations (DADs): digitalis toxicity, catecholaminergic VT

19. Differential Diagnosis of Sinus Arrhythmia

Sinus arrhythmia = rhythmic variation in RR interval with normal P wave morphology, normal PR interval.

Types:

Respiratory (physiological): RR shortens on inspiration (sympathetic/vagal reflex), lengthens on expiration. Common in young, athletes. No treatment needed.
Non-respiratory: RR variation unrelated to breathing — may indicate sinus node dysfunction or autonomic imbalance.
Ventriculophasic (in AV block): RR intervals containing a QRS are shorter than those without.

DDx from:

SA block: pauses that are exact multiples of baseline PP
Atrial fibrillation: No visible P waves, irregularly irregular rhythm
Wandering atrial pacemaker: Changing P wave morphology + varying PR interval

ECG key: In sinus arrhythmia, every P wave is identical and precedes every QRS — the only variation is timing.

20. Extrasystoles (Premature Beats): Types and Impact

Definition: Premature beats arising from ectopic foci outside the SA node.

Types:

Feature	Atrial (APC/PAC)	AV Junctional (PJC)	Ventricular (PVC/VPC)
P wave	Premature, different morphology	Retrograde (inverted in II, III, aVF) or absent	Absent (no preceding P)
QRS	Narrow (< 0.12s)	Narrow	Wide (> 0.12s), bizarre
Compensatory pause	Incomplete	Incomplete	Complete (usually)

Patterns:

Bigeminy: Normal + extrasystole alternating
Trigeminy: 2 normal + 1 extrasystole
Couplet: 2 consecutive extrasystoles
Salvo/run: ≥ 3 consecutive = short VT

Impact on cardiac activity:

Isolated APCs: usually benign, trigger AF in susceptible patients
PVCs in structural heart disease: prognostically significant; frequent PVCs (> 10,000/day) can cause PVC-induced cardiomyopathy
R-on-T phenomenon: PVC landing on T wave → can trigger ventricular fibrillation (dangerous)
Bigeminy/trigeminy → hemodynamically reduces effective CO (extrasystoles have poor output)

21. Diagnostic Criteria for Atrial Fibrillation (AF)

Definition: Chaotic, disorganized atrial electrical activity with irregular ventricular response.

ECG criteria:

Absent P waves — replaced by fibrillatory (f) waves — irregular, low-amplitude baseline oscillations (350–600/min)
Irregularly irregular RR intervals — hallmark (no two RR intervals the same)
Narrow QRS (unless aberrant conduction or BBB)
Ventricular rate variable (uncontrolled: 100–180 bpm; controlled: < 100 bpm)

Classification (2020 ESC):

First-detected AF
Paroxysmal AF — self-terminates < 7 days
Persistent AF — > 7 days, requires cardioversion
Long-standing persistent — > 12 months
Permanent AF — accepted, no rhythm control attempted

Clinical: Palpitations, dyspnea, fatigue, reduced exercise tolerance, stroke risk (CHADS₂-VASc), heart failure.

22. Diagnostic Criteria for Ventricular Fibrillation (VF)

Definition: Completely disorganized ventricular electrical activity — no effective cardiac output = cardiac arrest.

ECG criteria:

No identifiable P waves, QRS complexes, or T waves
Chaotic, irregular oscillations of varying amplitude and frequency (150–500/min)
No organized rhythm whatsoever
Baseline undulates chaotically — "quivering pattern"
Coarse VF: larger amplitude oscillations (more likely to respond to defibrillation)
Fine VF: small amplitude → worse prognosis

Clinical: Pulseless, unconscious, apneic → cardiac arrest → immediate CPR + defibrillation required.

Causes: Acute MI, ischemia, electrolyte disturbance (hypokalemia, hypomagnesemia), hypothermia, drug toxicity, R-on-T.

23. Diagnostic Criteria for Sinoatrial (SA) Block

Definition: Impulse generated at SA node fails to conduct to atrial myocardium.

Types:

SA Block Type I (Wenckebach):

Progressive shortening of PP intervals before a pause
Pause < 2x the preceding PP interval
Grouped beating pattern
(SA node → slow conduction → block — analogous to Mobitz I)

SA Block Type II:

Sudden pause = exact multiple of baseline PP interval (2x, 3x)
No preceding PP shortening
Key ECG: pause is exactly 2x (or 3x) the normal PP cycle

SA Block Type III (complete):

No SA impulses reach atria → atrial standstill
Escape rhythms take over (junctional or ventricular)

DDx from sinus arrest:

SA block: pause = exact multiple of PP
Sinus arrest: pause is NOT a multiple of PP (SA node simply fails to fire)

24. Diagnostic Criteria for AV Block: Mechanisms and ECG Signs

Definition: Impaired conduction between atria and ventricles at the AV node or His-Purkinje system.

Location of block:

Nodal (AV node): narrow QRS escape, rate 40–60, more responsive to atropine
Infranodal (His-Purkinje): wide QRS escape, rate 20–40, less responsive to atropine — worse prognosis

25. First-Degree AV Block

Definition: Prolonged AV conduction — all impulses conducted, but slowly.

ECG criteria:

PR interval > 200 ms (> 0.20 seconds) in adults (every beat)
Every P wave is followed by a QRS
Regular rhythm
QRS morphology: usually normal

Cause: Vagal tone (athletes), AV nodal disease, inferior MI, drugs (digoxin, β-blockers, CCB), electrolyte disturbances. Significance: Usually benign; no treatment needed; can progress.

26. Second-Degree AV Block — Mobitz Type I (Wenckebach)

Definition: Progressive prolongation of PR interval until one P wave is blocked (no QRS).

ECG criteria:

Progressively lengthening PR interval with each beat
One P wave suddenly not followed by QRS (dropped beat)
The RR interval progressively shortens before the dropped beat
Pause after dropped beat is < 2x the preceding RR interval
The cycle then repeats

Location: Usually at AV node level (narrow QRS). Significance: Often benign (especially in athletes, inferior MI); usually does not require pacing unless symptomatic.

27. Second-Degree AV Block — Mobitz Type II

Definition: Sudden failure of conduction without preceding PR prolongation.

ECG criteria:

Constant (fixed) PR interval in conducted beats
Sudden non-conducted P wave (no QRS) without warning
QRS often wide (bundle branch block) — block is infranodal
Pause = exactly 2x the RR interval
No progressive PR change

Location: Below AV node (His bundle or bundle branches) — more serious. Significance: Higher risk of progression to complete (3rd degree) block → pacemaker indicated.

28. Second-Degree AV Block — Type 3 (High-Grade/Advanced)

Definition: Multiple consecutive P waves not followed by QRS (2:1, 3:1 block ratio).

ECG criteria:

2:1 block: every other P blocked (cannot determine Mobitz I vs. II from 2:1 alone)
3:1 or higher: only 1 of every 3 or more P waves conducts
Ventricular escape beats may appear

Distinction: If QRS wide and block is infranodal → Mobitz II; if narrow → Mobitz I is more likely. Significance: Hemodynamically significant, often symptomatic (syncope, hypotension) → pacemaker.

29. Third-Degree (Complete) AV Block

Definition: No atrial impulses reach the ventricles — complete dissociation.

ECG criteria:

Complete AV dissociation — P waves and QRS complexes have no relationship to each other
PP interval is regular (sinus rhythm continues normally)
RR interval is regular (escape pacemaker)
P rate > QRS rate (atria faster than ventricles)
Escape rhythm:
- Junctional escape: narrow QRS, rate 40–60 bpm (block at AV node)
- Ventricular escape: wide QRS (> 0.12s), rate 20–40 bpm (infranodal block) — Stokes-Adams attacks

Causes: Congenital, inferior MI (usually transient), anterior MI (often permanent), Lyme disease, infiltrative disease, drug toxicity, surgical. Treatment: Permanent pacemaker (PPM) implantation in most cases.

30. Differential Diagnosis of SA Block vs. AV Block

Feature	SA Block	AV Block
P wave present?	Absent during pause (SA block — no atrial activation)	Present; may or may not be followed by QRS
Pause duration	Exact multiple of PP interval (Type II SA block)	Varies by degree
PR interval	Normal when conducting	Prolonged (1°), variable (2°), no relation (3°)
ECG during block	No P wave, no QRS	P wave visible, QRS absent or dissociated
Ventricular rate	Normal if intermittent	Slow (high-degree blocks)
Response to atropine	Yes (SA block at node level)	Yes (nodal AV block); No/poor (infranodal)
Location of problem	SA node or SA junction	AV node or His-Purkinje

31. Diagnostic Criteria for Arrhythmias of Impaired Automaticity

Automaticity = ability of a cell to spontaneously reach threshold and depolarize.

Enhanced automaticity:

Sinus tachycardia (rate > 100): normal P morphology, regular, gradual onset/offset; physiological or pathological
Ectopic atrial tachycardia: P wave present but different morphology from sinus; regular; PR may differ; often incessant
Accelerated junctional rhythm (rate 60–100): retrograde P, narrow QRS — often digitalis toxicity
Accelerated idioventricular rhythm (AIVR) (rate 40–120): wide QRS, competitive with sinus, often post-MI reperfusion — generally benign

Decreased automaticity:

Sinus bradycardia (rate < 60): normal P wave, prolonged PP
Sick Sinus Syndrome (SSS): inappropriate bradycardia, sinus pauses, tachycardia-bradycardia syndrome, chronotropic incompetence
Junctional escape (rate 40–60): AV node fires when SA node fails
Ventricular escape (rate 20–40): His-Purkinje fires when both SA and AV fail

32. Diagnostic Criteria for Atrial Paroxysmal Tachycardia (PAT / SVT)

Definition: Sudden onset, sudden termination supraventricular tachycardia, usually AV nodal re-entry (AVNRT) or AV re-entry (AVRT via accessory pathway).

ECG criteria:

Rate: 150–250 bpm (typically 170–220 bpm)
Sudden onset and offset ("paroxysmal") — abrupt start/stop
Narrow QRS (< 0.12s) — unless aberrant conduction (BBB pattern)
Regular rhythm (vs. AF which is irregularly irregular)
P waves:
- AVNRT: buried in QRS or just after QRS (retrograde P, pseudo-R' in V1, pseudo-S in inferior leads)
- AVRT: retrograde P after QRS with short RP interval
No delta waves in typical AVNRT; delta wave present in WPW (pre-excitation)

Symptoms: Palpitations, dizziness, neck pulsations, anxiety, polyuria after termination.

Termination: Vagal maneuvers (carotid sinus massage, Valsalva) → IV adenosine (6 mg then 12 mg) → cardioversion if unstable.

33. Principles and Types of ECG Diagnostics of Arrhythmias

Standard 12-lead ECG:

Evaluates rate, rhythm, P wave, PR interval, QRS, ST, QT
Identifies acute episodes

Holter Monitoring (24–48–72 hour ambulatory ECG):

Detects intermittent arrhythmias
Correlates symptoms with rhythm

Event recorder / Loop recorder:

Patient-activated or auto-triggered; 30 days or implantable (ILR) for 3 years
For infrequent episodes (syncope, cryptogenic stroke)

Exercise stress ECG:

Uncovers exercise-induced arrhythmias, channelopathies, WPW

Electrophysiology Study (EPS):

Invasive; maps conduction system; provokes and ablates arrhythmias
Indicates ablation targets (AVNRT, AVRT, VT, AF)

Key systematic ECG analysis:

Rate (atrial and ventricular)
Regularity (PP and RR intervals)
P wave morphology + axis
PR interval (normal 120–200 ms)
QRS duration (< 120 ms normal)
QT interval (correct for rate: QTc < 440 ms men, < 460 ms women)
Relationship of P to QRS
ST segment and T wave changes

34. Principles of Drug Therapy of Arrhythmias

Vaughan-Williams Classification:

Class	Mechanism	Examples	Key Uses
Ia	Fast Na⁺ channel block (intermediate) + K⁺	Quinidine, Procainamide, Disopyramide	AF, VT
Ib	Fast Na⁺ channel block (fast off)	Lidocaine, Mexiletine	Acute VT, post-MI
Ic	Fast Na⁺ channel block (slow off)	Flecainide, Propafenone	AF (no structural disease)
II	β-adrenergic blockade	Metoprolol, Esmolol, Propranolol	SVT, AF rate control, post-MI VT
III	K⁺ channel block → ↑ APD	Amiodarone, Sotalol, Dronedarone	AF, VT
IV	Ca²⁺ channel block	Verapamil, Diltiazem	SVT, AF rate control
Other	Adenosine (A1 receptor)	Adenosine	Acute SVT termination
Other	Cardiac glycoside	Digoxin	AF rate control (rest)

Principles:

Treat only symptomatic or dangerous arrhythmias (CAST trial: IC drugs increased mortality post-MI)
Consider structural heart disease before choosing drug (flecainide contraindicated if LV dysfunction)
"Pill in pocket" for paroxysmal AF (flecainide/propafenone)
Amiodarone: most effective antiarrhythmic but significant extracardiac toxicity (thyroid, lung, liver)
Rate control vs. rhythm control in AF — largely equivalent outcomes (AFFIRM trial)

35. Use of Cardiac Glycosides (Digoxin) in Arrhythmia Treatment

Mechanism:

Inhibits Na⁺/K⁺-ATPase → intracellular Na⁺ ↑ → Ca²⁺ ↑ via Na⁺/Ca²⁺ exchanger → positive inotropy
Vagotonic effect (indirect parasympathomimetic) → slows AV nodal conduction → decreases ventricular rate in AF
Shortens atrial refractory period

Indications:

AF rate control — especially in HF with reduced EF (HFrEF) where β-blockers are not tolerated or insufficient
HFrEF — improves symptoms and reduces hospitalizations (not mortality)
Less used now due to narrow therapeutic window

Limitations:

Narrow therapeutic window (toxic range 2 ng/mL; therapeutic 0.5–0.9 ng/mL)
Not for rate control during exercise (vagal effect lost; sympathetic dominates)
Contraindications:
- 2nd or 3rd degree AV block (without pacemaker)
- WPW syndrome with AF (can accelerate conduction via accessory pathway → VF!)
- Hypertrophic cardiomyopathy
- Ventricular fibrillation
Toxicity triggers: Hypokalemia (most important — K⁺ competes with digoxin at Na/K-ATPase), hypomagnesemia, renal insufficiency (digoxin renally excreted), hypothyroidism
Toxicity signs: Nausea, vomiting, visual halos (yellow-green), any arrhythmia (PAT with block, AV block, VT/VF)
Treatment of toxicity: Digoxin-specific Fab antibody fragments (Digibind)

Summary Quick Reference

Topic	Key Takeaway
HTN Classification	Grade 1–3 by BP; Primary vs. Secondary
Diagnosis	≥ 140/90 on 2 visits; ABPM/HBPM
Secondary HTN	Screen if resistant, young, or with clues
TOD	Heart (LVH/HF), Brain (stroke), Kidney (proteinuria/CKD), Eyes (KWB), Vessels
Pathophysiology	SNS + RAAS + Na retention + endothelial dysfunction
Pheochromocytoma	Paroxysmal HTN + triad → urine/plasma metanephrines
Cushing's	Cortisol → mineralocorticoid effect + SNS + Ang II
Conn's	Aldosterone ↑, Renin ↓, K⁺ ↓ → ARR > 30
Coarctation	Upper > lower BP + radiofemoral delay + rib notching
HTN Emergency	MAP ↓ 20–25% in 1h; IV drugs by target organ
HTN Treatment	ACEi/ARB + CCB ± Thiazide; lifestyle
AF	No P waves, irregularly irregular — CHADS₂-VASc for stroke risk
VF	Chaotic baseline, no QRS — arrest → shock
1° AV Block	PR > 200 ms, all P→QRS
2° Mobitz I	PR lengthens → dropped beat
2° Mobitz II	Fixed PR → sudden dropped beat (pacemaker!)
3° AV Block	P and QRS dissociated, ventricular escape (pacemaker!)
SA Block	Pause = exact multiple of PP
Digoxin	AF rate control + HF; beware hypokalemia + WPW

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